Examination Notes in Psychiatry

Examination Notes in
Psychiatry
This page intentionally left blank
Examination Notes in
Psychiatry
4th edition
PETER BUCKLEY MD MRCPsych

Professor and Chairman, Department of Psychiatry,
Medical College of Georgia, Augusta, Georgia, USA
DEL PREWETTE MD
Child and Adolescent Psychiatry Fellow, Palmetto
Health/University of South Carolina School of
Medicine, Columbia, South Carolina, USA
JONATHAN BIRD BSc MB ChB FRCPsych

Consultant Neuropsychiatrist, The Burden Centre
for Neuropsychiatry, Bristol, and Honorary Senior
Lecturer, Division of Psychiatry, University of Bristol,
Bristol, UK
GLYNN HARRISON MD FRCPsych

Norah Cooke Hurle Professor of Mental Health,
University of Bristol, Bristol, UK
Hodder Arnold
A MEMBER OF THE HODDER HEADLINE GROUP
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Contents
Preface vii
1 Research methodology and statistics 1
2 Descriptive psychopathology 13
3 Schizophrenia 24
4 Affective disorders 43
5 Neurotic disorders 60
6 Personality: development and disorders 77
7 Eating disorders 86
8 Human sexuality 96
9 Alcohol dependence 109
10 Drug dependence and gambling 123
11 Suicide and non-fatal deliberate self-harm 134
12 Uncommon psychiatric syndromes 144
13 Organic psychiatry 150
14 Psychiatric aspects of epilepsy and sleep disorders 175
15 EEG and brain imaging in psychiatry 185
16 Psychophysiological, somatoform, dissociative and related disorders 195
17 Psychogeriatrics 205
18 Forensic psychiatry 215
19 Child psychiatry 233
20 Mental retardation 253
21 Drug therapy 266
22 Physical treatments 289
23 Psychotherapy 297
24 Community-orientated psychiatry 312
25 Specific psychiatric problems of women 318
26 Transcultural psychiatry 328
27 Psychiatry and the Internet 333
Index 337
Preface
As with any subject worthy of human study and endeavour, pshychiatry develops,
understandings change, new facts emerge or old ones are seen in a new light. Since the
first edition of this book some 20 years ago there have been tremendous advances in
neuroscience and, as a result, major new insights into the functioning of the brain
have emerged. Yet, at the same time, major changes are also taking place in the organ-
ization and delivery of mental health services throughout the world.
We hope that the fourth edition of this widely read text will prove even more useful
to mental health trainees of various disciplines (psychiatrists, psychologists, nurses and
other professionals), to interested medical students, and to mental health clinicians
wishing to prepare lectures or brush up on the main essentials of psychiatry. This edi-
tion has been almost totally revised and, inevitably, expanded. Almost every subject
has been revisited in the light of the most current knowledge and theories. ‘New’
conditions (e.g. Internet addiction) and new investigations (e.g. functional MRI) sit
beside all the old favourites.
References are included where these are considered to be ‘key’ papers or reviews
which could be quoted and which readers should look up for themselves. There are
also suggestions for further reading.
Finally, we would reiterate what we have written in previous prefaces, that this book
is not intended as a substitute for wider reading or experience, but as a detailed and
comprehensive aide-mémoire. In order to gain fluency in the subject, readers might
carry it with them, rehearse its content, follow up its references, debate its currently
received wisdom and enjoy the fruits of their labours by achieving the success that
their endeavours deserve.
Peter Buckley
Del Prewette
Jonathan Bird
Glynn Harrison
Acknowledgements
Material in Tables 3.1, 3.3, 4.1, 5.1, 6.1, 7.3, 7.4, 8.1, 16.1, 18.1 and 19.1 is reproduced,
with permission from: The ICD-10 classification of Mental and Behavioural Disorders:
Diagnostic Criteria for Research. Geneva, World Health Organization, 1993.
Material in Tables 3.2, 3.8, 7.3, 7.4 and 18.1 is reproduced, with permission from:
The Diagnostic and Statistical Manual of Mental Disorders, Copyright 2000. American
Psychiatric Association.
Research methodology and 1
statistics
PHILOSOPHY OF SCIENCE
Science is only one approach to understanding the world. According to Popper, it involves:
• Hypothesis formulation.
• Observation based on the hypothesis.
• Attempts to falsify the hypothesis.
• Control of variables.
• Predictions based on the hypothesis.
• Replication of results.
HOW TO DO RESEARCH
1 Find a problem – from everyday practice, past research or theory.

2 Formulate a testable hypothesis on the basis of observation and a literature search.
3 Define the variables to be studied.
4 Design an experiment to measure the variables and thus to test the hypothesis.
5 Run a pilot experiment to explore difficulties.
6 Seek funding.
7 Redesign the experiment as necessary.
8 Run the main experiment.
9 Collect and analyse the data.
10 Publish so as to allow for replication.
PLANNING RESEARCH
Write a protocol:
• Title
• Introduction – survey of background information and reasons for doing the research
2 RESEARCH METHODOLOGY AND STATISTICS
• Statement of hypotheses to be tested

• Description of method:
– Sample and target populations
– Method of sample selection
– Information to be gathered
– Methods of gathering information
– Design of study
– Discussion of reliability and validity
– Statistical methods to be used and power calculation
• Facilities and resources required:
– Personnel
– Equipment
– Space
– Time
– Costs
• Ethical aspects and responsibility for the experiment
• Anticipated problems.
BASIC DEFINITIONS
VARIABLES
Variables are any constructs or events which research studies.
• Independent variable – the antecedent condition manipulated by the experimenter
(e.g. drug levels).
• Dependent variable – the variable used to measure the effect of the independent
variable (e.g. recovery rates).
• Confounding variable – any extraneous variable whose potential influence on the
dependent variable has not been controlled for; a source of error (e.g. age or sex
imbalances).
• Controlled variable – a variable whose influence is kept constant by the experi-
menter (e.g. other medications).
• Uncontrolled variable – a variable which is not manipulated or held constant,
though it may be measured (e.g. life events).
RESEARCH DESIGN
Simple designs may be:
• Cross-sectional in time
• Longitudinal in time.
They may also be:
• Between-group
• Within-group
• Within-individual.
BASIC DEFINITIONS 3
Designs may also be:

• Cross-over – patients used as their own controls.
• Longitudinal – in time.
• Double-blind – observer and patient are unaware of independent variables when
assessing dependent variables.
• Latin square – variables are allocated randomly to subjects and longitudinally
in time.
Longitudinal designs may be:
• Retrospective – observations in the present to elicit information about past events;
may be methodologically unsatisfactory owing to information bias.
• Prospective (cohort study) – ongoing gathering of information after the event stud-
ied; may be difficult and expensive but methodologically sounder.
• Mixed – retrospective study to elicit desired group of subjects, then prospective
follow-up.
Research may be:
• Normothetic – information derived from classifying a number of events and
experiences.
• Ideographic – information derived from a single event or individual.
• Operationally defined – precise definition of terms used, in measurable quantities
or attributes; these are essential for effective research and communication.
RELIABILITY
Reliability is the extent to which there is repeatability of an individual’s score or other
test result.
• Test–retest reliability – high correlation between scores on the same test given on
two occasions.
• Alternate-form reliability – high correlation between two forms of the same test.
• Split-half reliability – high correlation between two halves of the same test.
• Inter-rater reliability – high correlation between results of two or more raters of the
same test.
Inter- or intra-reliability is measured using intraclass correlation coefficient (ICC – range
0–1; ICC of ⭓0.7 is acceptable).
VALIDITY
Validity is the extent to which a test measures what it is designed to measure.
• Predictive validity – ability of the test to predict outcome.
• Content validity – whether the test selects a representative sample of the total tests
for that variable.
• Construct validity – how well the experiment tests the hypothesis underlying it.
The ‘reliability paradox’ is that a very reliable test may have low validity precisely
because its results do not change; i.e. it does not measure true changes.
SAMPLE SELECTION (see also Chapter 21)

• Target population – the whole population from whom information could be
gathered (e.g. all chronic schizophrenics). This is studied in a census.
• Sample population – the subsection of a target population which is actually under
study (e.g. the chronic schizophrenics in one area). This is studied in a survey. A
sample population should be selected in such a way that generalized inferences
may be made. Such inferences are always statements of probability.
• Bias – the difference between the sample population result and the true target
population result. Bias is caused by inaccurate sampling.
• Random sampling – selection of a sample population such that each member of the
target population has a calculable, non-zero and usually equal probability of being
selected.
• Stratified sampling – the target population is divided into a number of strata (e.g.
age groups) and sampling occurs within each stratum.
• Multiphase sampling – some information is gathered from the whole sample popu-
lation, but additional information is gathered from subsamples.
• Multistage sampling – further information is gathered at a later date from the ori-
ginal sample population.
A control group is used to hold constant or eliminate any possible confounding vari-
ables. It is a sample population which receives no treatment or some standard treat-
ment, as a comparison with the population which does receive the experimental
treatment or manipulation.
MEASUREMENT IN PSYCHIATRIC RESEARCH
QUESTIONNAIRES, INTERVIEWS AND CASE-NOTE STUDIES
Aims may be:

• To identify psychiatric cases
• To diagnose psychiatric disorder accurately
• To assess severity and change in severity.
Collect information by:
• Document studies – case notes, which are retrospective, not written with research in
mind; journal articles; official studies, e.g. census.
• Mail questionnaires – cheap and easy but low response rate, hence sampling bias.
• Self-rating questionnaires – cheap, easy, sensitive to changes, but may be answered
inaccurately due to misunderstanding; cannot be complex.
• Observer-rater interview – may be structured, semi-structured or informal; allow
great flexibility and accuracy but are expensive and require training. See Table 1.1.
SOURCES OF ERROR
• Response set – subject always tends either to agree or to disagree with questions.
• Bias towards centre – subject tends to choose the middle response and shun extremes.
MEASUREMENT IN PSYCHIATRIC RESEARCH 5
Table 1.1 Commonly used psychiatric instruments

Evaluation Scale Comments
General health General Health Questionnaire Commonly used screening, used in primary care
(GHQ) and general population studies.
Global Clinical Global Impressions (CGI) Global observation of severity of psychiatric
assessment/screening illness, 7-point scale.
Nurses Observation Scale for Very commonly used observational scale, mostly
Inpatient Evaluation (NOSIE) used for inpatients with psychosis.
Global Assessment Scale (GAS) Evaluates social functioning and severity of
symptoms.
Hopkins Symptom Checklist 90-item checklist of 9 symptom dimensions,
(SCL-90) with 3 global indices of distress.
Structured interview NIMH Diagnostic Interview (DIS) Generates Research Diagnostic Criteria
schedules diagnosis.
Schedule for Affective Disorders Generates RDC or DSM-III-R diagnosis of
and Schizophrenia (SADS) psychotic disorders.
Schedule for Clinical Assessment Incorporates Present Status Examination 10
in Neuropsychiatry (SCAN) with an updated CATEGO program.
Evaluates different time periods – primary and
secondary and lifetime.
Generates both ICD-10 and DSM – IV diagnoses.
Structured Clinical Interview for Generates DSM-III-R diagnosis.
DSM-III-R (SCID)
Schizophrenia Brief Psychiatric Rating Scale Widely used measure of psychotic symptoms
(BPRS) (not just schizophrenia) and psychopathology,
18 items.
Comprehensive Assessment of Evaluates major psychoses re: symptoms, past
Symptoms and History (CASH) history, premorbid function and cognitive status.
Schedule for the Assessment of Details hallucinations, delusions, bizarre
Positive Symptoms (SAPS) behaviour, formal thought disorder.
Schedule for the Assessment of Details alogia, affective blunting, avolition,
Negative Symptoms (SANS) asociality, attentional impairment.
Positive and Negative Symptoms Developed from BPRS, more detailed, more
Scale (PANSS) structured, includes general psychopathology
section.
Depression Beck Depression Inventory (BDI) Self-rating, 21 items.
Hamilton Depression Scale (HamD) Observer rating, 17 items and severity
dimension, widely used in depression research.
Zung Depression Scale Self-rating, 20 items.
Mania Young Mania Scale 11-item observer scale.
Anxiety Hamilton Anxiety Rating Scale 14-item observer scale covering psychic and
(HARS) somatic dimensions.
Zung Anxiety Scale Combined observer and brief report formats,
20 items.
Obsessive–compulsive Maudsley Obsessional– Self-report, 30 items.
disorder Compulsive Inventory (MOCI)
Yale-Brown Obsessive– Observer scale, 19 items.
Compulsive Scale (YBOCS)
Psychosomatic/eating Eating Attitudes Test (EAT) Self-report on eating behaviour.
disorders McGill Pain Questionnaire Detailed self-report.
Psychosocial Adjustment to Self-report and interview – based on adjustment
Illness Scale (PAIS) to (chronic) illness.
Personality Eysenck Personality 90-item questionnaire yielding sub-scales of
Questionnaire (EPQ) neuroticism, extroversion, psychoticism, lie
score.
(Continued)
Table 1.1 Continued

Evaluation Scale Comments
Minnesota Multiphasic Personality Self-rating questionnaire, validated on

Inventory (MMPI) psychiatric patients not normally given
‘personality profile’.
Personality Assessment Scale Produces 5 diagnostic categories plus
(PAS) dimensional trait scores.
Substance abuse CAGE Cut down on drinking; annoyed by others
criticizing; guilty over drinking; eye-opener.
Michigan Alcoholism Screening 25-item interview or 10-item self-report formats.
Test (MAST)
Severity of Alcohol Dependency Measures impact of alcoholism.
Questionnaire (Stockwell
Questionnaire)
Child disorders Child Behaviour Checklist (CBCL) Many versions according to child’s age,
self-report/parent/teacher informant.
Child Assessment Schedule Semistructured interview schedule.
Geriatric disorders Mini Mental Status Examination Very widely used 19-item test.
(MMSE)
Katz Activity of Daily Living Index 6-item observer scale for staff and/or family
members.
Mental retardation Adaptive Behaviour Scales (ABS) 110-item observer scale of social life,
symptoms and behaviour.
• Social acceptability – subject chooses the acceptable answer rather than the
true one.
• Halo effect – answers are chosen to ‘fit’ with previously chosen answers; responses
become what is expected by the observer.
• Hawthorne effect – researchers alter the situation by their presence.
PSYCHOMETRIC TESTING
Psychological tests must be:

• Standardized – as regards both the procedure (i.e. it is repeatable) and the scores
produced (i.e. it is related to normative data).
• Reliable.
• Valid.
Psychological tests may assess general intelligence, personality or neuropsychological
status:
• General intelligence, e.g.:
– Stanford–Binet – in which mental age is assessed as a ratio of chronological age,
giving a mean IQ of 100.
– Wechsler Adult Intelligence Scale – a series of subtests of verbal and performance
aspects of intelligence allows more detailed breakdown of scores and assessment
of discrepancies.
STATISTICS 7
• Personality, e.g.:
– Minnesota Multiphasic Personality Inventory
– Eysenck Personality Inventory
– Projective tests – which analyse fantasy material (e.g. Rorschach Ink Blot Test,
Thematic Apperception Test).
• Neuropsychological status:
– Usually aimed at assessing whether diffuse or focal brain change is present,
whether localization of pathology is possible, and what rehabilitation measures
might help.
– Screening tests used include Bender Gestalt, Benton Visual Retention Test, Trail
Making Task, Memory for Designs, WAIS, Wechsler Memory Scale.
– Batteries of tests are often used – e.g. the Halstead–Reitan and Luria–Nebraska
batteries.
Also assess interests, aptitudes and attitudes.
PSYCHOPHYSIOLOGICAL TECHNIQUES
These are the quantification of biological events as they relate to psychological

variables.
• Tend to measure non-specific arousal.
• Measure base levels, degree of response and habituation (the reduction of response
with repeated stimuli).
• Measures taken include:
– Sweat gland activity – galvanic skin response (GSR)
– Forearm blood flow
– Electromyography
– Electroencephalography
– Pulse
– Blood pressure
– Salivation
– Pupil size.
STATISTICS
DESCRIPTIVE STATISTICS
These simply summarize the data.
MEASURES OF CENTRAL TENDENCY

• Mode – the most commonly occurring score.
• Mean – sum of scores divided by number of scores.
• Median – the middle score, i.e. the score below which 50% of scores fall.
MEASURES OF DISPERSION
• Range – from largest to smallest score.
• Variance – a measure of the dispersion of data about the mean; the average squared
deviation from mean.
• Standard deviation – 64% of scores in a normal distribution fall within one stand-
ard deviation either side of the mean; square-root of the variance.
• Standard error – an estimate of the discrepancy between sample mean and
true population mean; standard deviation divided by square-root of number of
cases.
• Z score – number of standard deviations on each side of the mean.
• Skewness – measures deviation from the normal distribution curve.
• Kurtosis – measures peakedness or flatness of curve.
INFERENTIAL STATISTICS
These assess the meaning of the data.

• Null hypothesis – The first step in the decision-involving process. The hypothesis
that there is no significant difference between comparison groups or any difference
is only due to chance. P (probability) value ⫽ 0.01 says there is a one-in-a-hundred
chance of finding any given difference.
• Type I error – null hypothesis is erroneously rejected (i.e. there is no difference but
an apparent one is shown). Multiple comparisons (‘throwing the dice’) increase
the risk of type I error; this may be taken into account by resetting the probability
level using a Bonferroni correction test.
• Type II error – null hypothesis is erroneously accepted (i.e. a true difference is not
shown). Small sample sizes predispose to type II errors. The power of a study to
detect differences (␣ value) is related to sample size.
• Correlation coefficient (CC) – measures the statistical relationship between two
variables, without assuming that either is dependent or independent; i.e. no
causality is assumed (CC ⫽ 1.0 implies exact similarity; CC ⫽ 0.0 implies no
relationship).
• Pearson’s product moment correlation – the most widely used parametric test of cor-
relation (r ⫽ ⫺1 implies inverse relationship; r ⫽ ⫹1 implies positive relationship;
r ⫽ 0 implies no relationship).
• Spearman’s rank correlation (rs) – non-parametric equivalent test to Pearson’s,
for ordinal data.
• Regression coefficient (R) – measures strength of dependency of one variable on the
independent variable; R2 describes the amount of shared variance between these
variables.
• Regression analysis – determines the predictive power of each successive variable
upon the outcome variable; uses multivariate statistical tests (e.g. MANOVA), with
each variable independently entered into a regression equation or model.
• Parametric statistics – assume a normal distribution (see Table 1.2).
• Non-parametric statistics – do not assume a normal distribution; less powerful, less
dependent upon sample size (see Table 1.2).
STATISTICS 9
Table 1.2 Parametric and non-parametric tests

Parametric tests Non-parametric tests
(Student’s) t-test Chi-squared (␹2)

Analysis of variance (F test/ANOVA) Analysis of variance
Analysis of covariance (ANCOVA) Mann–Whitney U test
Kruskal–Wallis analysis of covariance (ANCOVA)
Student’s t-test can use paired or non-paired relationships between variables, so that either within-subject or between-subject
comparisons can be studied.
ANOVA may be one- or two-way ANOVA (takes multiple relationships into account).
ANCOVA ‘partials out’ an observed effect that may contribute to group difference (e.g. gender, educational status).
• Factor analysis – segregates data into the minimum number of dimensions that
define a group (e.g. principal component analysis, principal factor analysis,
eigenvalue determination, verimax factor rotation). It is used, e.g., to generate posi-
tive, negative and disorganization syndromes in schizophrenia (see Liddle, 1987).
• Cluster analysis – segregates data into groups, but with some overlap; e.g. Pakel’s
classification of depression (see Chapter 4).
• Meta-analysis – statistical technique in which related data from numerous studies
on a topic are pooled to determine the size and strength of a proposed association;
e.g. treatment response in schizophrenia and dose of atypical antipsychotics (see
Leucht et al., 2003).
THE PLACEBO EFFECT
A placebo is any therapeutic procedure (or that component of a therapeutic proced-

ure) which is given deliberately to have an effect, or which unknowingly has an effect
on the patient’s symptom, disease or syndrome, but which is objectively without spe-
cific activity for the condition treated. The placebo is also used to describe an adequate
control in experimental studies. A placebo effect is defined as the changes produced by
placebo.
The placebo effect is influenced by:
• Expectations of the patient – general characteristics of placebo responders are:
younger patients of lower intelligence, higher levels of anxiety, extraversion, and
possibly more females than male.
• Status and attitude of the person prescribing.
• Nature of the placebo – tablet size, shape, colour, etc. (e.g. smaller tablets viewed as
more potent).
• Condition being treated – possibly more effective in acute complaints, including
headache, sickness, postoperative pain.
Modes of action are not understood. It is unlikely that it works purely by suggestion, as
patients with hysterical conversion symptoms respond poorly.
Side-effects are often reported: frequently dry mouth, headache, nausea and drowsi-
ness. More severe reactions have been reported, including hypersensitivity reactions
and withdrawal phenomena.
DESIGNING A TRIAL
See Freeman and Tyrer (1992).
Patient selection
Specify inclusion and exclusion criteria, source of recruitment, diagnostic criteria
(operationally defined).
Treatment
Prepare active drug in a form identical to the placebo or to a comparison drug. Ensure
that new drug and standard drug have similar bio-availability. Compliance should be
assessed in outpatients at least by a tablet count. Plasma drug level may also be monitored.
Control group
Important variables influencing response must be spread across the treatment and
control groups (i.e. age, sex, duration of symptoms). Randomization must be ensured.
Crossover designs, where patients receive two or more treatments one after the other,
should ensure ‘order effect’. Ensure adequate ‘washout’ to avoid overlapping of patients,
and exclude rapid placebo responders.
Evaluation
Each outcome variable should be precisely defined, objective and reliably detected.
Use standardized rating scales with training of observers for inter-rater reliability.
Ensure ‘blindness’ as far as possible.
Trial size
The number of subjects needed should be calculated from the proportion of patients
expected to respond, and the smallest difference between treatments considered worth
measuring. Power analysis should be part of the initial protocol.
Analysis and presenting results

Explain all patient withdrawals. Present each patient’s responses, where possible, to
demonstrate variations. For treatment studies with missing data points, survival
analysis or ‘intent-to-treat’ statistical approaches as appropriate.
Subject data to statistical analysis ensuring correct methods are used in view of
numbers of patients, spread of data, etc. Remember that the more significance tests
used, the more likely are some false positives to appear by chance (type 1 error) unless
a ‘multiple contrast’ adjustment is used. Consult a statistician at time of trial design,
not after conclusion.
Conclusions should present a balanced appraisal of evidence. Avoid illustrations
and diagrams which exaggerate treatment differences.
REVIEWING A RESEARCH PUBLICATION
• Title and abstract – should be interesting, informative.

• Introduction – should provide review of topic, contain key references and provide a
clear rationale as to why study was performed.
REFERENCES AND FURTHER READING 11
• Methods – ideally, readers should be able to perform study on the basis of the depth
of description. Sample should be appropriate in selection and size; also, well-
matched with controls.
• Results – clearly stated, no excess of analyses (Bonferroni correction, if needed).
Tables and figures enhance clarity and interpretation of results.
• Discussion – major findings should be explicitly stated; should not be overinter-
preted. Methodological constraints should be acknowledged.
• References – should be scholarly. Other relevant work of the authors cited; not
under/over-referenced. Readers need to know some background of topic to judge
merit of the study, its importance – breaking new ground or replication?
EVIDENCE-BASED MEDICINE (EBM) AND PSYCHIATRY
• EBM is the integration of the best research evidence with the expertise of the clin-
ician in delivering care to individual patients (Sacket et al., 2000).
• Swift access to the latest published scientific data is available from numerous com-
mercial, as well as free, Internet sites (see Chapter 26).
• EBM allows guidelines to be formulated that aid the clinician in making an accur-
ate diagnosis and prescribing the most effective treatment.
• The central limitation of EBM involves the reliability of the scientific evidence.
In psychiatry, EBM is further encumbered by the relative lack of neuropathology
with many psychiatric illnesses and the complexity of psychosocial aspects of
individuals.
REFERENCES AND FURTHER READING
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Cooper B (2003) Evidence-based mental health policy: a critical appraisal. Br. J. Psychiatry 183, 10.
Croudace T, Evans J, Harrison G et al. (2003) Impact of the ICD-10 Primary Health Care (PHC)
diagnostic and management guidelines for mental disorders on detection and outcome in
primary care: cluster randomized controlled trial. Br. J. Psychiatry 182, 20.
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Scientific, Oxford.
Edwards E, Kornacki MJ, Silversin J (2002) Unhappy doctors: what are the causes and what can
be done? BMJ 324, 83.
Everitt BS, Dunn G (1992) Applied Multivariate Data Analysis. Edward Arnold, Oxford.
Freeman C, Tyrer P (1992) Research Methods in Psychiatry: a Beginner’s Guide, 2nd edn. Gaskell,
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beyond the conventional randomized controlled trial. Br. J. Psychiatry 180, 1.
Gilbody SM, House AO, Sheldon TA (2002) Outcomes research in mental health: a systematic
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Descriptive psychopathology 2
Descriptive psychopathology attempts to portray in words, as subtly and accurately as

possible, the nature of experiences, perceptions and behaviour. It defines, differentiates
and inter-relates such experiences.
It owes a great deal to the philosophical discipline called ‘phenomenology’ – a
method (developed by Husserl) of scrupulously inspecting one’s own conscious
processes, without assuming anything about external causes or consequences of those
‘phenomena’ and without altering the phenomena by observational methods.
This school of thought has influenced psychiatry through the philosopher/
psychiatrist Karl Jaspers. The development of sympathy and intuitive understanding
allows for the objective observation of phenomena in others, by relating them to
phenomena in ourselves.
Descriptive psychopathology may be seen, with epidemiology, as a scientific basis for
the practice of psychiatry. It should not be confused with ‘dynamic psychopathology’ – the
attempt to explain the phenomena of mental disorder in terms of psychodynamic
theories of aetiology.
DISORDERS OF APPEARANCE AND BEHAVIOUR
Appearance (state of health, posture, cleanliness, clothing, self-care) is an important

indication of other mental functions. Mood may be expressed in the form of:
• Appearance (facial expression, posture)
• Manner (response to others)
• Motility (degree and form of movements).
MOTOR DISORDERS (OF GENERAL BEHAVIOUR)
The degree and quality of activity are important. There may be increased restless
motor activity in agitation or in hypomania, but the quality will differ.
14 DESCRIPTIVE PSYCHOPATHOLOGY
The form of abnormal movements may be classified (after Hamilton, 1974) as

follows.
DISORDERS OF ADAPTIVE MOVEMENTS

• Expressive behaviour – e.g. tearfulness, unhappy facial expression, paucity of move-
ments or downcast appearance in depression; laughing, expansive gesturing and
overactivity in hypomania.
• Obstruction – seen in catatonia and consisting of irregular hindrance and blocking
of movements.
• Mannerisms – abnormal, repetitive goal-directed movements (e.g. bizarre methods
of walking or eating) commonly seen in chronic schizophrenia.
NON-ADAPTIVE MOVEMENTS
Spontaneous movements – habitual, not goal-directed
• Tics are sudden involuntary twitchings of groups of muscles, particularly facial
(seen in extreme form in Gilles de la Tourette syndrome).
• Static tremor of hands, head or upper trunk indicates anxiety, hyperthyroidism,
hysteria or ‘essential’ tremor, lithium toxicity, parkinsonism.
• Spasmodic torticollis involves spasm of neck muscles with twisting of head, which
may become permanent.
• Chorea is abrupt, random jerky movements resembling fragments of goal-directed
behaviour.
• Athetosis is slow, semi-rotary writhing movements.
• Orofacial dyskinesia is restless movements of tongue, mouth and facial muscles
(seen in the elderly and following chronic neuroleptic ingestion).
• Stereotypies are regular, repetitive non-goal-directed movements; e.g. repetitive
foot tapping, body rocking. Stereotyped utterances can occur. Stereotypies are seen
in chronic schizophrenia, mental handicap and infantile autism.
Induced movements
• Automatic obedience – the subject does whatever is asked of him or her.
• Echopraxia – the subject imitates the movements of the interviewer.
• Echolalia – words or phrases are imitated.
• Perseveration – the senseless repetition of a previously requested movement; i.e.
the repetition of a response after withdrawal of the stimulus. Special variants of
this are palilalia (the perseverated word is repeated with increasing frequency) and
logoclonia (perseveration of the last syllable of the last word). These are seen in
organic disorders and occasionally in catatonia.
• Forced grasping – the offered hand is repeatedly grasped and shaken, despite
requests not to do so. Seen in frontal lobe lesions.
• Mitmachen – the body can be put into any posture, despite instructions to resist.
• Mitgehen – an extreme form of mitmachen in which very slight pressure leads to
movement in any direction.
• Negativism – apparently motiveless resistance to suggestion or attempts at
movement.
DISORDERS OF PERCEPTION 15
Disorders of posture
• Postural mannerisms – strange and abnormal postures adopted habitually.
• Perseveration of posture – may be seen in schizophrenia and lesions of the mid-
brain. If the subject’s body is placed in an awkward posture and left, the posture is
held for a period before slowly relaxing, despite asking the patient to relax. If a
plastic resistance is felt to initial movement, this is termed ‘waxy flexibility’ (or
flexibilitas cerea).
DISORDERS OF PERCEPTION
SENSORY DISTORTIONS
Sensory distortions are changes in the quality, intensity or spatial form of a percep-
tion. Examples are:
• Hyperacusis – in mania, hyperthyroidism.
• Hypoacusis – in some acute organic states.
• Xanthopsia, micropsia – produced by psychedelics and temporal lobe lesions.
SENSORY DECEPTIONS
Hallucinations
Hallucinations are perceptions which arise in the absence of any external stimulus
(Esquirol, 1833). They are actual sense deceptions, not distortions of real perceptions.
Hallucinations are perceived as being located in the external world. They are per-
ceived as having the same qualities as normal perceptions – i.e. vivid, solid.
Hallucinations are not subject to conscious manipulation, in the same sense that
normal perceptions cannot be produced or dismissed at will.
Illusions
Illusions are distortions of perceptions of real objects; e.g. flowery wallpaper is per-
ceived as swarming snakes. Illusions are perceived as having the same qualities as
normal perceptions, but often are more fleeting than hallucinations.
Pseudohallucinations
Pseudohallucinations are not perceived by the actual sense organs, but experienced as
emanating from within the mind. They are a form of imagery. Although vivid they
lack the substantiality of normal perceptions.
Pseudohallucinations are located in subjective rather than objective space. They are
not subject to conscious control or manipulations.
Other mental images

• Eidetic images – previous perceptions are reproduced as a mental image of vivid
intensity and uncanny detail. May be regarded as a form of pseudohallucination.
• Pareidolia – vivid mental images occurring without conscious effort when perceiv-
ing an ill-defined stimulus; e.g. glowing fire.
DISORDERS OF THOUGHT
DISORDERED CONTENT
DELUSIONS
A delusion is a fixed false idea held in the face of evidence to the contrary, and out of
keeping with the patient’s social milieu.
• Held unshakeably.
• Not modified by experience or reason.
• Content often bizarre.
• Not dependent on disintegration of general intellectual functioning or reasoning
abilities.
• Often infused with a sense of great personal significance.
Types
• Autochthonous or primary delusions have no discernible connection with any pre-
vious interactions or experiences. They arise fully formed as sudden intuitions, like
sudden ‘brainwaves’. They are often preceded by a period of ‘delusional mood’ (or
‘delusional atmosphere’) in which the subject is aware of something strange hap-
pening; he/she then suddenly realizes the personal significance of this feeling with
a complete delusional understanding. This period of delusional perception is seen
as having two stages: first, the real perception of some object or event and, second,
the delusional misinterpretation of that event.
• Secondary delusions emerge understandably from other psychic experiences or current
preoccupations; e.g. prevailing affect, fears, personal stress, habitual attitudes of mind.
• Overvalued ideas are intense preoccupations with marked associated emotional
investment. The patient holds tenaciously to the idea, demonstrably false, with vir-
tual certainty but not unshakeable conviction.
OBSESSIONS AND COMPULSIVE PHENOMENA

• ‘Obsession’ refers to impulses and thoughts.
• ‘Compulsion’ is confined to motor acts.
Obsessional phenomena describes persistent intrusion into consciousness of unwanted
thoughts, feelings or impulses, despite the individual’s recognition of their senseless
nature and resistance to them.
Although rejected by the individual, phenomena are owned as being ‘his’ or ‘hers’ (cf.
passivity phenomena experienced as being something imposed from outside). Thoughts
are often of a repugnant or bizarre nature, e.g. violent, sexual and blasphemous themes.
These thoughts are resisted initially, at the cost of mounting anxiety. Resistance may
lessen after time.
PASSIVITY PHENOMENA
Passivity phenomena are a variety of phenomena which have in common the apparent
disintegration of boundaries between the self and the surrounding world. The individual
DISORDERS OF THOUGHT 17
experiences outside control of, or interference with, his/her thinking, feeling, perception
or behaviour.
• Thought insertion and withdrawal – the experience of thoughts being put into or
taken out of the mind by some external agency or force.
• Thought broadcast – the experience that others can read or hear the individual’s
thoughts as they are ‘broadcast’ from him or her.
• ‘Made actions’ – either simple motor actions or more complex patterns of behav-
iour are experienced as being caused by an outside agency.
DISORDERED FORM OF THINKING
ACCELERATED TEMPO
This produces increased rate of delivery of speech (‘pressure of speech’) and ‘flight of
ideas’. There is loss of coherent goal-directed thinking with increasingly obscure asso-
ciations between ideas. Vague connections may be prompted by rhyme, sounds of words
(‘clang associations’) and associations only acceptable in other contexts. Punning is
a common feature.
It is characteristic of hypomania, mania and may occur in delirium, and in rare
organic states, e.g. hypothalamic lesions.
DECREASED TEMPO – PSYCHIC RETARDATION

Subjectively experienced as ‘muzziness in thinking’ or difficulty in concentration,
leading to difficulty in decision-making and pseudo-dementia. It is characteristic of
retarded depressive states; said to occur rarely in manic stupor.
SCHIZOPHRENIC THOUGHT DISORDER

Bleuler considered disturbance of association of ideas to be a fundamental feature of
schizophrenia. In contrast to the thought disorder of hypomania, the logical associ-
ations between ideas are not only loosened, but often incomprehensible to the listener.
See also Table 2.1.
• Omission – a sudden discontinuation of a chain of thought.
• Derailment – a disruption of the continuity of speech by the insertion of novel and
inappropriate material to the chain of thought.
• Fusion – a merging and ‘interweaving’ of separate ideas.
• Drivelling – refers to the muddling of elements within an idea to the extent that
the meaning is totally obscured to a listener.
Table 2.1 Some descriptive terms

Clinician Descriptive terms
Bleuler (1951) Loosening of associations, condensation

Cameron (1944) Overinclusive thinking
Goldstein (1944) Concrete thinking
Schneider (1959) Derailment, drivelling, desultory thinking, fusion, omission, substitutions
• Desultory thinking – ideas are expressed correctly in terms of syntax and grammatical
construction, but juxtaposed inappropriately. The ideas would be comprehensible if
expressed in another context or in isolation.
Other features of schizophrenic thought disorder

• Thought blocking – a sudden cessation of speech mid-sentence with an accompany-
ing sense of subjective distress. A patients may complain that his/her mind has
‘gone blank’ or that his/her thoughts have been interfered with.
• Clang associations
– Verbal stereotypy – repetition of a word or phrase which has no immediate rele-
vance to the context.
– Condensations – common themes from two or more separate ideas are combined
to form an incomprehensible concept.
DISORDERS OF EMOTION
• Mood – the emotional ‘tone’ prevailing at any given time. A ‘mood state’ will last
over a longer period.
• Affect – synonymous with ‘emotion’ and also meaning a short-lived feeling state.
Related to cognitive attitudes and understandings, and to physiological sensations.
When examining for disorders of emotion, look for:
1 The quality of the emotion: anxiety, sadness, cheerfulness, suspiciousness, irritabil-
ity, apathy
2 The appropriateness of the emotion to what is being said and to behaviour
3 The constancy of the emotion at interview and what factors appear to influence it.
ABNORMAL EMOTIONAL PREDISPOSITION

Abnormal emotional predisposition is found in disorders of personality and signifies
a consistent tendency to particular stereotyped emotional expressions. Thus a person
may be:
• Dysthymic – always tending to be sad and miserable.
• Hyperthymic – always tending to be overcheerful, unrealistically optimistic.
• Cyclothymic – tending to marked swings of mood from cheerful to unhappy.
• Affectless – emotionally cold and indifferent.
ABNORMAL EMOTIONAL REACTIONS

• Anxiety is a fear with no adequate cause. Fear and anxiety may be normal experi-
ences, but are regarded as pathological if they are excessive or prolonged, or inter-
fere markedly with normal life. Anxiety is usually accompanied by somatic and
autonomic changes.
• Depression is a feeling of misery, inner emptiness, hopelessness and helplessness,
accompanied by morbid preoccupations. Such emotions may be normal in the
bereaved, but are regarded as pathological if excessive, prolonged, and accompanied
DISORDERS OF SELF-AWARENESS 19
by disturbance of appetite, sleep, concentration, etc., or by depressive delusions.

Depression is often associated with (or may present as) somatic complaints,
hypochondriasis or a feeling of bodily insecurity.
• Euphoria and ecstasy are excessive and unrealistic cheerfulness and a feeling of
extreme well-being.
• Apathy is the loss of all feeling. No emotional response can be elicited.
ABNORMAL EXPRESSION OF EMOTION

• Denial or dissociation of affect – as seen in hysteria (la belle indifférence) or occa-
sionally in situations of extreme danger.
• Emotional indifference – as may be seen in ‘psychopathic’ disorder. Expected emo-
tional response is not shown to others, or to his/her own antisocial behaviour.
• Perplexity – anxious and puzzled bewilderment. Seen in early schizophrenia and
confusional states.
• Emotional incongruity – the abnormal presence or absence of emotions; e.g. fatu-
ous euphoria in a situation which would normally evoke a depressed mood. The
criterion of ‘understandability’ is therefore employed; i.e. the mood is not under-
standable to the ‘normal’ person. Emotional incongruity is characteristic of acute
schizophrenic disorder.
• Emotional blunting – insensitivity to the emotions of others and a dulling of the
normal emotional responses. It is characteristic of chronic schizophrenia.
• Emotional lability – rapid fluctuations of emotion. The emotions may be appropri-
ate in a less intense form, but the rapid change is not. Emotional lability is seen in
organic disorders, brain stem lesions, mania, and some personality disorders.
• Emotional incontinence – an extreme form of emotional lability, with complete
loss of control over the emotions. It is seen in organic disorders, especially
pseudobulbar palsy.
DISORDERS OF SELF-AWARENESS
Self-experience has four aspects, according to Jaspers (1959):

• Awareness of the existence of activity of the self
• Awareness of the unity of the self at any one time
• Awareness of the continuity of self-identity through time
• Awareness of the self as distinct from the outside world.
The final three aspects may be abnormal in schizophrenia.
AWARENESS OF THE EXISTENCE OF ACTIVITY OF THE SELF

All psychic life involves the experience of a unique and fundamental activity of the
self. All emotions, behaviour, ideas, etc., are experienced as ‘being mine’. This experi-
ence is absent in depersonalization, in which the sense of awareness of existence as a
person is altered or lost. This is often accompanied by derealization, the loss of the
sense of reality of surroundings. These experiences may be seen in dissociative hysteria,
temporal lobe epilepsy, extreme fatigue or anxiety and psychotic illness of all sorts.
The alteration of awareness of one’s activities (moods, thoughts, acts) as belonging

to the self is seen in passivity experiences. In these the mental phenomena are often
seen as being under the passive influence of some outside force or person. This is the
elementary, primary experience of being actually and directly influenced. This is char-
acteristic of schizophrenia.
DISORDERS OF INTELLECTUAL FUNCTIONS
CONSCIOUSNESS
Consciousness is the state of awareness of the self and its environment. Reduced levels
of consciousness are seen in:
• Clouding of consciousness – disorientation in time, place, person, disturbances of
perception and attention and subsequent amnesia.
• Drowsiness – further reduction in level of consciousness, with unconsciousness if
unstimulated, but can be stimulated to a wakeful state.
• Stupor – further loss of responsiveness, which can be only aroused by considerable
stimulation. Awareness of environment is often maintained in depressive or catatonic
stupor, but not in organic stupor (cf. neurological and psychiatric definitions).
• Coma – profound reduction of conscious level with very little or no response to
stimulation.
ATTENTION AND CONCENTRATION
The intensity and extent of attention may be abnormal, as may the ability to sustain
attention (i.e. to concentrate). Attention may be intensified in a restricted area in those
with preoccupations (depressive, hypochondriacal, etc.). Attention may be reduced or
absent in certain restricted areas in those with hysterical denial.
Attention may be easily distracted in hypomania or organic psychoses. In the latter,
the ability to concentrate may be very variable.
Tests of attention
1 Reverse order of months of year.
2 Subtraction of serial 7s from 100.
3 A series of digits repeated forwards and backwards.
Record time and accuracy for these tests.
MEMORY
Memory involves the registration of data, the retention in the mind and recall at will –
both immediately and at a later time. Thus anything interfering with registration (e.g.
alcohol, organic psychosis, head injury), retention (e.g. Korsakoff ’s psychosis) or
recall (organic or hysterical amnesia) will lead to defect of memory.
INSIGHT 21
Tests of memory
1 Recall of past personal life events which can be corroborated.
2 Recall of recent personal life events. Note any specific periods of amnesia (e.g. retro-
grade or anterograde amnesia) or any particular topics which are forgotten (e.g.
hysterical amnesia).
3 Short-term memory can be tested using recall of a simple name and address after
5 minutes, repeating a sentence (e.g. Babcock sentence) and digit span.
4 General knowledge tests (e.g. names of royal family, prime minister, recent events
in the newspapers, dates of first and second world wars).
Note any confabulation to fill in the memory gaps with false information.
LANGUAGE FUNCTIONS (PARTICULARLY CENTERED IN THE TEMPORAL LOBE)
Language functioning is tested both by listening to spontaneous conversation and by

direct testing. Observe any errors in the form of:
• Dysarthria – disorder of articulation of speech.
• Neologizing – new words which do not exist.
• Paraphasia – words which are slightly incorrect.
• Dysphasias:
– Receptive – disorder of the comprehension of words due to dysfunction of
Wernicke’s area in the temporal lobe.
– Expressive – disorder of expressing thoughts in the correct form of words, due to
dysfunction of Broca’s area in the posterior frontal lobe.
– Intermediate, particularly nominal dysphasia – inability to name objects cor-
rectly. This should always be tested for in assessment of intellectual function.
Test by using a series of objects.
• Perseveration – inappropriate repetition of a previous name, word, theme or act.
VISUOSPATIAL FUNCTIONS (PARTICULARLY CENTRED IN THE PARIETAL LOBE)
Visuospatial functioning is tested by observation and by direct testing. Test the ability
to copy an asymmetrical object, to draw a clock face, to construct a star from match-
sticks (constructional dyspraxia). Test right–left orientation and ability to name fin-
gers (finger agnosia). Observe any difficulty in dressing and in finding his/her way
about (dressing apraxia, topographical disorientation).
INSIGHT
Insight according to Lewis (1934) is a ‘correct attitude to morbid change in oneself ’.

The concept is multidimensional, incorporates both current and retrospective
components, and is usually not an ‘all-or-none’ phenomenon (Amador and David,
2004).
According to Amador et al. (1993), insight includes:

• Recognition of illness (signs, symptoms, etc.)
• Attribution of illness (attributes of illness phenomena to a mental disorder)
• Awareness of treatment – benefit–compliance
• Awareness of social consequences of illness – e.g. disability, involuntary commital to
hospital, response/concern of relatives.
Partial insight (i.e. retrospective insight) may not be the same as pseudo-insight.
Medication compliance and awareness of illness are separate but overlapping con-
structs which contribute to insight (Amador and David, 2004).
Issues: Is loss of insight consequent upon cognitive deficit, perhaps with a specific
pattern of localization (e.g. parietal), or is persistent symptomatology only partially
related to these factors?
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Amador XF, Strauss DH, Yale SA, Flaum MM et al. (1993) Assessment of insight in psychosis.
Am. J. Psychiatry 150, 873.
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4th edn: DSM-IV-TR. American Psychiatric Association, Washington, DC.
Boyce WT, Essex MJ, Woodward HR et al. (2002) The confluence of mental, physical, social, and
academic difficulties in middle childhood. I: Exploring the ‘head waters’ of early life mor-
bidities. J. Am. Acad. Child Adolesc. Psychiatry 41, 580.
Chessick RD (2002) Psychoanalytic peregrinations. IV: What is phenomenology? J. Am. Acad.
Psychoanal. 30, 673.
Fabrega H (2001) Culture and history in psychiatric diagnosis and practice. Psychiatr. Clin. North
Am. 24, 391.
Flashman LA (2002) Disorder of awareness in neuropsychiatric syndromes: an update. Curr.
Psychiatry Rep. 4, 246.
Flashman LA, McAllister TW (2002) Lack of awareness and its impact in traumatic brain injury.
NeuroRehabilitation 17, 285.
Hamilton M (ed.) (1974) Fish’s Clinical Psychopathology. Wright, Bristol.
Harrison PJ (1991) Are mental states a useful concept? Neurophilosophical influences on phe-
nomenology and psychopathology. J. Nerv. Ment. Dis. 179, 309.
Jaspers K (1959) General Psychopathology, 7th edn, trans. Hoenig J and Hamilton M. Manchester
University Press, Manchester.
Leff JP, Isaacs AD (eds) (1981) Psychiatric Examination in Clinical Practice, 2nd edn. Blackwell
Scientific, Oxford.
Lewis A (1934) The psychopathology of insight. Br. J. Med. Psychol. 14, 332.
Manschreck TC (1992) Delusional disorders. Psych. Ann. 22(5).
Markova IS, Berios GE (1992) The meaning of insight in clinical psychiatry. Br. J. Psychiatry
160, 850.
Maser JD, Patterson T (2002) Spectrum and nosology: implications for DSM-V. Psychiatr. Clin.
North Am. 25, 855.
McDougall GM, Reade B (1993) Teaching biopsychosocial integration and formulation. Can.
J. Psychiatry 38(5), 359.
McGuire MD, Marks I, Neese RM et al. (1992) Evolutionary biology: a basic science for psychi-
atry? Acta Psychiatr. Scand. 86, 89.
Miller LJ, O’Connor E, DiPasquale T (1993) Patients’ attitudes toward hallucinations. Am. J.
Psychiatry 150(4), 584.
Mortimer AM (1992) Phenomenology: its place in schizophrenia research. Br. J. Psychiatry
161, 293.
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Sims A (ed.) (1988) Symptoms of the Mind: an Introduction to Descriptive Psychopathology.
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Disorders: Clinical Descriptions and Diagnostic Guidelines. WHO, Geneva.
Schizophrenia 3
CONCEPTS
Modern concepts of schizophrenia are in part a distillation of historical concepts. No

distinct aetiology or pathophysiology is presumed.
There have been several early clinical descriptions: demence précoce (Morel, 1856);
dementia paranoides (Kahlbaum, 1860); katatonia (Kahlbaum, 1868); hebephrenia
(Hecker, 1870).
EARLY CLINICAL CONCEPTS

• Greisinger (1870): ‘unitary psychosis’ – schizophrenia as part of a single psychotic
disorder.
• Kraepelin (1893): dementia praecox – chronic disorder distinct from ‘manic depres-
sive insanity’; onset in adolescence; progressive deterioration in mental function
(84% of his patients); four subtypes (hebephrenic, catatonic, paranoid, simplex);
‘single morbid process’, presumed organic.
• Bleuler (1911): the schizophrenias – collection of psychoses with fundamental
symptoms (‘four As’) representing the splitting (‘schizo’) of psychic functions.
(Hallucinations, etc., are secondary phenomena of lesser importance.)
– Ambivalence (coexisting conflicting ideas)
– Loosening of associations
– Affective incongruity and blunting
– Autism (withdrawal).
• Jaspers (1913): schizophrenia characterized by non-understandability of mental
functions (‘praecox feeling’).
EARLY SOCIOLOGICAL CONCEPTS

Schizophrenia is: not an illness but a myth; a role forced upon the individual; a product
of society; a sane reaction to an insane world.
DEVELOPMENT OF OPERATIONAL CRITERIA 25
OTHER CONCEPTS/CLASSIFICATIONS
• Langfeldt (1939): process schizophrenia (insidious onset, chronic course) versus
schizophreniform (acute onset, affective symptoms, good outcome).
• Leonhard (1957): systemic schizophrenia (catatonia, hebephrenia, paraphrenia)
versus non-systemic (affect-laden paraphrenia, schizophasia and periodic
catatonia).
• Strömgen (1968): brief reactive psychosis (‘psychogenic psychosis’).
• Schneider (1959): strict phenomenological approach, devoid of aetioloical theory.
SYMPTOM RANKING
First-rank symptoms (FRS), in the absence of organic illness, signify schizophrenia:

• Hearing thoughts spoken aloud.
• ‘Third person’ hallucinations.
• Hallucinations in the form of a commentary.
• Somatic passivity.
• Thought withdrawal or insertion.
• Thought broadcasting.
• Feelings or actions experienced as under the control of an external force.
• Delusional perception (see Chapter 2).
Second-rank symptoms (other hallucinations, etc.) have less diagnostic significance.
Schneider’s FRS have been very influential, but have limitations:
1 Specificity – occur in other ‘functional psychoses’ – about 20 per cent in psychotic
depression and 40 per cent in acute mania.
2 Sensitivity – about 20 per cent of chronic schizophrenics never showed FRS.
3 Prognosis – FRS have no predictive/prognostic value.
DEVELOPMENT OF OPERATIONAL CRITERIA
Influential Bleulerian and sociological views led to a diffuse (over-diagnosable) and

unreliable concept of schizophrenia (especially in the USA) compared with phenom-
enological (Kraepelinian, Schneiderian) concepts in Europe. Regional differences were
exposed in a USA/UK project (1972) and International Plot Study of Schizophrenia
(IPSS).
Pressure to standardize the diagnosis led to development of operational, atheoreti-
cal, diagnostic criteria:
• Research diagnostic criteria (RDC) – illness duration of at least 2 weeks,
Schneiderian plus other criteria emphasized.
• Feighner’s criteria – 6 months’ duration, more restrictive, favour poor prognosis.
• Catego – computerized diagnostic algorithms generated from Present State
Examination. Updated now to Catego 5 generated from SCAN-PSE-10.
26 SCHIZOPHRENIA
• DSM criteria (Diagnostic and Statistical Manual of Mental Disorders, American

Psychiatric Association) – successive sets of diagnostic criteria (DSM-III, 1980;
DSM-III-Revised, 1987; DSM-IV, 1994; DSM-IV-TR, 2000) essentially favouring
a more ‘Kraepelinian’ concept of schizophrenia. DSM-V is under development
and is likely to reflect more trait/dimensional approaches as well as neurobiologi-
cal distinctions.
• Multiaxial system:
– Axis I – major clinical syndrome.
– Axis II – developmental or personality disorder.
– Axis III – psychosocial stressors (1–7 scale).
– Axis IV – highest level of functioning in past year (GAF: 10–100 scale).
CURRENT DIAGNOSTIC CRITERIA
• ICD-10 (International Classification of Diseases, 10th edn; WHO, 1992; see Table 3.1).
This groups together schizophrenia, schizotypal states and delusional disorder. It has
greater congruence with the DSM system (see below), but differs because there is
more reliance on FRS. Only one month’s illness duration is necessary. The category of
post-schizophrenic depression is included.
• DSM-IV (APA, 1994; see Table 3.2). This was developed from DSM-III-Revised.
There is greater emphasis on negative symptoms. Delusional disorder is not classi-
fied separately. There is no mention of prodromal symptoms. Schizoaffective dis-
order is not classified under Mood.
Table 3.3 compares ICD-10 and DSM-IV.
Table 3.1 ICD-10 criteria for schizophrenia
A minimum of 1 very clear symptom (and usually ⭓2 if less clear-cut) from groups (a)–(d) below, or symptoms
from ⭓2 of the groups (e)–(h), which have been present for most of the time during a period of 1 month
or more:
(a) thought echo, insertion, withdrawal, broadcasting

(b) delusions of control, influence, passivity; delusional perception
(c) hallucinatory voices of running commentary, third-person discussion, or other types of voices coming from
some part of the body
(d) persistent delusions of other kinds that are culturally inappropriate and completely impossible
(e) persistent hallucinations in any modality: daily for weeks/months, or accompanied by half-formed non-
affective delusions, or with persistent overvalued ideas
(f) breaks in thought fluency, i.e. incoherence, irrelevant speech, neologisms
(g) catatonic behaviour: excitement, stupor, mutism, posturing, waxy flexibility, negativism
(h) negative symptoms: apathy, paucity of speech, blunted emotions, social withdrawal; not due to depression or
neuroleptic medication
(i) a significant and consistent change in the overall quality of some aspects of personal behaviour (loss of interest,
social withdrawal, aimlessness)
Subtypes: paranoid, hebephrenic, catatonic, undifferentiated, post-schizophrenic depression, residual, simple

schizophrenia.
DEVELOPMENT OF OPERATIONAL CRITERIA 27
CURRENT CONTROVERSIES ON THE NATURE OF SCHIZOPHRENIA
Clinical heterogeneity is not disputed, but underlying aetiological mechanism(s) are

still unclear (Hirsch and Weinberger, 2003).
VIEW 1
Schizophrenia is a single aetiopathological process leading to diverse manifestations
(e.g. neurosyphilis).
VIEW 2
There are multiple disease entities of different aetiopathological processes leading to
schizophrenia (e.g. mental retardation, epilepsy).
Table 3.2 DSM-IV criteria for schizophrenia
A. Characteristic symptoms: ⭓2 of the following, present for a significant time period during 1 month (or less if
successfully treated):
(1) delusions
(2) hallucinations
(3) disorganized speech (e.g. frequent derailment or incoherence)
(4) grossly disorganized or catatonic behaviour
(5) negative symptoms (e.g. affective flattening, alogia, avolition)
[NB: Only one ‘A’ symptom is required if delusions are bizarre or hallucinations consist of a voice keeping up a
running commentary on the person’s behaviour or thoughts, or two or more voices conversing.]
B. Social/occupational dysfunction: For a significant time-period since the illness onset, ⭓1 major area of
functioning such as work, interpersonal relations or self-care is markedly below the level achieved prior to the
onset (or of onset in childhood/adolescence – failure to achieve expected level of interpersonal, academic, or
occupational achievement).
C. Duration: Continuous signs of illness for ⭓6 months; period must include at least one month of symptoms
that meet criterion ‘A; (i.e. active-phase symptoms), and may include periods of prodromal or residual
symptoms. During prodromal or residual periods, illness may manifest by only negative symptoms or
⭓2 symptoms listed in criterion ‘A’ present in attenuated form (e.g. odd beliefs, unusual perceptual
experiences).
D. Schizoaffective and mood disorder exclusion: Schizoaffective disorder and mood disorder with psychotic
features have been ruled out since: (1) no major depressive or manic episodes occurred concurrently with
active-phase symptoms; or (2) if mood episodes occurred during active-phase symptoms, their total duration
was brief relative to the duration of active and residual periods.
E. Substance/general medical condition exclusion: Not due to the direct effects of a substance (e.g. drugs of
abuse, medication) or a general medical condition.
Subtypes:
• Paranoid – prominent delusions and/or auditory hallucinations.
• Catatonic – dominated by stupor, negativism, posturing.
• Disorganized – prominent disorganization of speech and behaviour, inappropriate/flat affect.
• Undifferentiated – prominent delusions, hallucinations, disorganization; but not meeting criteria of other
types.
• Residual – meets ‘A’ criteria but criteria for other subtypes no longer met; yet some continuing disturbance
(i.e. negative symptoms).
Schizophreniform disorder: Meets ‘A’, ‘D’ and ‘E’ criteria but episode greater than 1 month, less than 6 months.
28 SCHIZOPHRENIA
Table 3.3 ICD-10 and DSM-IV classifications of schizophrenia and schizophrenia-like disorders
ICD-10 DSM-IV
Schizophrenia Schizophrenia
– paranoid – paranoid
– hebephrenia – disorganized
– catatonic – catatonic
– undifferentiated – undifferentiated
– residual – residual
Post-schizophrenic depression
Simple schizophrenia
Other schizophrenia
Unspecified schizophrenia
Schizoaffective disorder Schizoaffective disorder
Schizotypal disorder
Persistent delusional disorder Delusional disorder
Acute and transient psychotic disorder Brief psychotic disorder
Induced psychotic disorder Schizophreniform disorder
Shared psychotic disorder
Psychotic disorder
Other non-organic psychotic disorder caused by Psychotic disorder
a medical condition
Unspecified non-organic psychosis Substance-induced psychosis
Psychotic disorder not otherwise specified
VIEW 3
There are specific symptom clusters within schizophrenia reflecting different disease
processes that combine differently in patients.
Type I/type II syndromes (Crow, 1980)

• Type I – acute, positive symptoms, good response to neuroleptics, good prognosis,
brain structurally normal, presumed dysfunction in dopamine system.
• Type II – chronic, negative symptoms, poor treatment response and prognosis,
abnormal cerebral structures (ventriculomegaly, cortical atrophy).
Positive and negative symptoms (Andreasen et al., 1990)

• Positive symptoms – hallucinations, delusions, formal thought disorder, bizarre
behaviour.
• Negative symptoms – affective blunting, alogia (impoverished thinking and speech),
avolition/apathy, anhedonia/asociality, disturbance of attention.
The positive/negative dichotomy is less influential now. There is large symptom
overlap in patients, and inconsistency of neuroimaging and biochemical research.
Three patterns of symptoms are now advocated.
Positive, negative, disorganization syndromes

• Positive syndrome – reality distortion syndrome: delusions, hallucinations.
• Negative syndrome – psychomotor poverty syndrome: negative symptoms.
• Disorganization syndrome – disorganization: positive formal thought disorder,
inappropriate affect, poverty of content of speech.
EPIDEMIOLOGY 29
Cognitive impairment (Sharma and Antonova, 2003)

Kraepelin originally considered cognitive deficits as a major aspect of schizophrenia.
This is again considered a core facet, especially since subtle deficits (e.g. poor scholas-
tic performance, memory loss) may antedate psychotic symptoms. Cognitive impair-
ment is also a stronger predictor (than other symptoms) of poor function and
vocational performance.
Deficit syndrome (Carpenter et al., 1988)

Primary, enduring negative symptoms (restricted affect; diminished emotional range;
poverty of speech; diminished sense of purpose and social drive) reflect a distinct
neural substrate. There is emphasis on distinguishing primary from secondary negative
symptoms (secondary to positive symptoms, depressed mood, parkinsonism).
NEURODEVELOPMENTAL VERSUS NEURODEGENERATIVE HYPOTHESES
• Neurodevelopment (Lewis and Levitt, 2002; Keshavan and Murray, 2004) – static
lesion from CNS disruption in utero; typical symptoms emerge later. Evidence
includes:
– Post-mortem and neuroimaging findings.
– Excess of obstetric complications, minor physical anomalies, abnormal
dermatoglyphics.
– Season of birth phenomenon.
– Epidemiological association with prenatal exposure to influenza infection.
• Neurodegenerative – progressive degeneration (Kraepelin). Evidence includes:
– Deteriorative course of illness.
– Gliosis seen in earlier post-mortem (PM) studies, but not found in recent PM
studies.
CONTINUUM OF PSYCHOSIS (GREISINGER, 1870; CROW, 1990)
This view holds that there is a single psychosis, with schizophrenia most severe, affective
disorders least severe, schizoaffective disorders occupying an intermediate position.
EPIDEMIOLOGY
See Jones and Buckley (2003).
INCIDENCE
• 15–20 per 100 000 per year.
• 6–8 fold increased incidence among Britains of Afro-Caribbean family descent
(Harrison et al., 1988).
• Lifetime risk: 0.9 per cent.
• Median age at onset: males ⫽ 28 years, females ⫽ 32 years.
30 SCHIZOPHRENIA
• Other gender differences: males – more obstetric complications, poorer premorbid

adjustment, poorer prognosis, less genetic predisposition(?), more structural brain
abnormalities.
• Increased incidence of winter births (esp. if low genetic risk).
• Increased obstetric complications, left-handedness, abnormal determatoglyphics.
• There is much interest in a reported association of possible exposure during 2nd
trimester to 1957 A2 influenza.
• Substance abuse co-morbidity is now a significant problem (see Chapter 10).
PREVALENCE
• 0.5–1 per cent; higher in Sweden, Croatia, Southern India; lower among US
Hutterites.
• Increased prevalence among lower social classes – the breeder hypothesis (poor social
conditions inducing schizophrenia) versus the social drift hypothesis (patients drift
down the social scale while paternal occupations show normal class distribution).
• Increased prevalence in urban versus rural settings, especially for males.
MORTALITY
Between 4 and 10 per cent die by suicide (see Chapter 11). There are also increased
cardiovascular and respiratory deaths, and deaths by homicide.
AETIOLOGICAL FACTORS
GENETICS
Family studies
See Table 3.4. There is a 0.5 per cent morbid risk in relatives of normal subjects.
Twin studies
Twin studies address the nature/nurture issue. Monozygotic:dizygotic (MZ:DZ)
rate ⫽ 48%:4%, suggesting a strong genetic component (especially for paranoid sub-
type). However, MZ twins discordant for schizophrenia show more brain abnormali-
ties than the normal co-twin (Suddath et al., 1990).
Table 3.4 Family studies

Relationship to schizophrenic Morbid risk (%)
Parent 5
Sibling 10
Child of schizophrenic 14
Child of two schizophrenics 46
AETIOLOGICAL FACTORS 31
Adoptive studies
Adoptive studies test for genetic versus environmental influences by examining rates
of schizophrenia in adopted-away offspring of schizophrenic and of normal parents.
Results: 10 per cent and 13 per cent, versus 0 per cent from normal parents.
Schizophrenia spectrum
‘Good genetics requires good phenotypes’ (Kendler and Diehl, 1993) – unclear whether
genetic liability is restricted (to schizophrenia only) or broad (many disorders)? Studies
(Kendler and Diehl, 1993) suggest a moderate inheritance risk which includes
schizophrenia-like personality disorders and schizophrenia-like non-affective psychoses.
See Table 3.5.
Molecular genetics
This is a major focus of research (Waterwort et al., 2002). How many genes are
involved? Where are they? How common are they? What is their functional impact:
• Effect on cellular processes (functional genomics)?
• Effect on protein development and expression (proteomics)?
Genome-wide scans provide evidence (but confusing and inconsistent) of suscepti-
bility genes on chromosome 5, 6, 8, 10, 13, 15, 22; research is complicated by differing
thresholds Lod score values for linkage analysis, diagnostic variability, phenocopy
selection.
Recent focus has been on candidate genes; e.g. chromosome 15 abnormal alleles at
the locus of the alpha-7 nicotinic acetylcholine receptor subunit gene, and abnormal
alleles on chromosome 6 region related to dysbindin (a developmental protein) gene.
Polymorphisms of COMT (catechol O-methyltransferase) gene are associated with
poorer prefrontal cortex functioning in schizophrenia (Weinberger et al., 2001).
There is intense interest in examining genes regulating neurodevelopment (e.g. SNAP
23 – synaptosomal-associated protein 23, neuroregulin) to determine whether these are
differentially expressed (under/over-expressed, different alleles) in schizophrenia.
The genetics of treatment response (pharmacogenetics) is now also a major focus
(Malhotra, 2001).
Vulnerability markers
• Evoked potential (P 300) abnormalities in ‘unaffected’ first-degree relatives.
• Smooth-pursuit eyetracking abnormalities in 34 per cent of parents of schizo-
phrenics (Holzman et al., 1974) and in schizotypal patients (Siever et al., 1993).
Table 3.5 Schizophrenia spectrum

Prevalence rate Morbid risk (%)
Schizotypal/paranoid Schizophreniform Affective disorder
personality disorder schizophrenia-like
psychoses
1st-degree relative of schizophrenics 8 3.7 25

1st-degree relatives of healthy controls 2 1.5 23
32 SCHIZOPHRENIA
High-risk studies
Repeated, longitudinal evaluations (cognitive, neurological, psychiatric) of children of
schizophrenic parents suggest early, subtle manifestations of schizophrenic genotype
(CNS soft signs, attentional deficits, social deficits – ‘pandysmaturation’; Fish et al.,
1992). The general pattern of CNS maldevelopment permits evaluation of relative
genetic and environmental contributions to illness (Cannon et al., 1993).
Prodromal studies
There is intense interest in early detection of psychosis in the prodrome stage
(McGorry et al. 2003; McGlashan, 2003). Educational programmes may help bring
patients into treatment earlier – shorten the duration of untreated psychosis (DUP)
which may be ‘biologically toxic’. Early use of antipsychotics may delay onset of
psychosis (McGorry et al., 2002). These approaches are contentious and of ethical
concern (McGlashan, 2001).
NEUROCHEMISTRY
Dopamine hypothesis
This view postulates dopamine (DA) overactivity in mesolimbic pathways. It is a very
influential theory, largely based on:
• Amphetamine-induced schizophrenia-like psychosis – amphetamine increases DA

release.
• Antipsychotics block DA (especially D2) receptors to an extent which correlates with
clinical potency.
• Cis-fluphenthixol (DA blocker) is clinically effective but transfluphenthixol (no DA
blockade) ineffective.
• Post-mortem studies (although contaminated by neuroleptic treatment) show
increased DA and DA receptors in caudate and nucleus accumbens.
• Direct evidence (PET studies of neuroleptic-native patients) is conflicting and con-
troversial: increased DA receptors (Johns Hopkins group – Wong et al., 1986) ver-
sus no increase (Karolinska Institute group – Farde et al., 1987).
• Relationship between plasma homovanillic acid, psychopathology and response to
neuroleptics (Kahn and Davidson, 1993).
Recent theories include: deficit in corticofugal/corticothalamic DA inhibitory out-

put (Carlsson, 1995); DA receptor supersensitivity occurs with neuroleptic treatment
(Grace, 1992); interaction of DA with other neurotransmitters.
Serotonin (5-HT)
• LSD (5-HT agonist) induces psychosis; m-chlorophenyl-piperazine (MCPP; a
5-HT agonist) worsens psychosis.
• Ritanserin (5-HT2/5-HT1c antagonist) improves psychosis; clozapine (5-HT2
antagonist) is an effective treatment for psychosis.
There is a suggested mechanism of 5-HT modulatory effect on DA system.

Noradrenaline
• There is evidence for over- and underactivity; clozapine induces potent noradren-
ergic blockage.
Other neurotransmitters, neuropeptides/phospholipids

• GABA – reduced GABA receptors in hippocampus on PM studies.
• Glutamate – excess glutamate receptors in frontal cortex in PM studies; hypothesis
of decreased glutamatergic inhibition of subcortical and mesiotemporal DA
neurones.
• Possible abnormalities of cholecystokinin (CCK), neurotensin.
• Abnormalities of essential fatty acid metabolism (brain membrane components).
• Application of molecular genetics and proteonomic techniques likely to yield more
complex changes at subcellular level.
NEUROPATHOLOGY
Schizophrenia is not ‘the graveyard of neuropathologists’.

• There is a 6 per cent decrease in brain weight and 4 per cent reduction in anterior–
posterior length.
• There are inconsistent findings in cortex, corpus callosum, basal ganglia, thalamus.
• Temporal lobe(s) are implicated (left ⬎ right) – reversed planum temporale asym-
metry; decreased area of hippocampus, amygdala, parahippocampal gyrus;
reduced cell number and abnormal cellular arrangement (pre-alpha cell migratory
failure during 2nd trimester) in hippocampus and entorhinal cortex.
NEUROIMAGING
• Early CT studies showed non-specific ventricular enlargement, cortical sulcal

prominence.
• PET and MRI studies show that frontal and temporal lobes are major sites for
abnormalities (see Chapter 15).
• Current evidence favors generalized cortical tissue loss and functional disconnec-
tivity in schizophrenia. There may be progressive tissue loss in patients with more
active illness (Mathalon et al., 2001) which may represent complex disease–host
interaction (Weinberger and McClure, 2002).
• Structural brain abnormalities are subtle but reproducible (Shenton et al., 2001).
Family members ‘at risk’ also show similar but more subtle brain changes (Lawrie
et al., 2002; Seidman et al., 2002).
PSYCHOPHYSIOLOGY AND IMMUNOLOGY
• Evoked potential (P 300) – failure of sensorimotor gating (impaired prepulse inhib-

ition; Braff, 1993); related to earlier theories of defective filter (Broadbent) and
overarousal (Venables).
34 SCHIZOPHRENIA
• Abnormal smooth-pursuit eye movements – may infer dysfunction in frontal eye

fields region (Leve et al., 1993).
• Immunological interest stems partly from epidemiology: geographical variations
in prevalence, increased urban prevalence, season of birth phenomenon, associ-
ation with prenatal exposure to influenza – direct viral CNS toxicity? immuno-
logical response? epiphenomenon (e.g. temperature)?
• Inconclusive immunological findings – increased B lymphocytes, decreased T lym-
phocytes, increased CSF antibodies to some viruses.
• There is a negative association with rheumatoid arthritis.
LIFE EVENTS
Vulnerability–stress models of schizophrenia propose a strong relationship between

inherent vulnerability and life stressors to induce/exacerbate symptoms of schizo-
phrenia. This is a heuristic model, yet there is only moderate support for the influence
of stress/life events (LEs) (more evident in other disorders, especially depression) and
many methodological difficulties, including retrospective falsification, defining
period of observation for LEs, measurement of LEs.
FAMILY DYNAMICS
Early theories included a schizophrenogenic mother, double-blind communication, skew

and schism of marital roles, abnormal family communication. All are disregarded now.
Recent emphasis has been on relatives’‘expressed emotion’ and relapse, but a meta-analy-
sis of twin studies confirmed a small but significant effect of shared environment over
and above that of the genetic contribution. Also, there is evidence from high-risk studies
(Tienari et al., 2004) for a possible aetiological role of family relational style (‘con-
stricted’/lacking boundaries/critical) via gene–environment interactions.
MANAGEMENT
NEUROLEPTICS/ANTIPSYCHOTIC MEDICATIONS (see Chapter 21)

There has been a gradual shift from older (conventional, ‘typical’) antipsychotics to
newer (atypical, second-generation) antipsychotics: clozapine, risperidone, olanzap-
ine, quetiapine, ziprasidone, aripiprazole, sertindole, zotepine. In a US multicentre
trial of treatment-refractory patients (Kane et al., 1988), 30 per cent were treated
with clozapine, compared with 4 per cent with chlorpromazine. By 12 months,
60–70 per cent showed improvement.
Other atypical antipsychotics are first-line and maintenance treatment choices.
Evidence for the superiority of atypicals (over conventionals) is under debate for
positive symptoms, but is stronger for negative symptoms.
Cognitive benefits are subtle but major (Sharma and Antonova, 2003). There are
possibly broader effects beyond psychosis, including a possible antisuicidal effect of
MANAGEMENT 35
clozapine (Meltzer et al., 2003) and a possible antiaggressive effect (Buckley et al.,
2003).
However, medication and treatment compliance is a major challenge (Lacro et al., 2002).
ELECTROCONVULSIVE THERAPY (ECT) (see Chapter 22)

Electroconvulsive therapy may be helpful in catatonic states, occasionally in secondary
depression.
PSYCHOSOCIAL TREATMENTS (see Chapter 24)

Psychosocial treatments aim to maximize abilities and minimize disabilities.
Components include:
• Cognitive retraining
• Crisis management
• Education
• Vocational rehabilitation
• Family therapy
• Group therapy
• Social skills training.
Psychoeducational and family intervention strategies are used. High expressed
emotion of relatives (HEE: critical comments, hostility, emotional over-involvement;
rated from Camberwell family interview) is predictive of relapse (Vaughn and
Leff, 1976; see Table 3.6). Intervention strategies aim to reduce HEE and relapses
(see Table 3.7).
Consumer movement now encourages ‘recovery’ approaches involving consumer
support groups, and peer-support treatment programmes (Thompson et al., 2001).
PSYCHOTHERAPY
Psychotherapy is supportive, practical problem-oriented, and encourages compliance.
Cognitive–behavioral therapy (CBT) is now advocated for persistent delusions
Table 3.6 Relapse rates in 9 months after discharge

Relapse rate
(%)
Patient on neuroleptics, low expressed emotion (EE) family 12

Patient on neuroleptics, high EE family, less than 35 hours’ 42
contact weekly
No neuroleptics, high EE family, more than 35 hours’ 92
contact
Table 3.7 Intervention strategies

Relapse 0–9 months Relapse 0–24 months
(%) (%)
Family intervention 10 33
Routine treatment 48 71
36 SCHIZOPHRENIA
and hallucination. CBT can be adapted to address compliance issues – ‘compliance

therapy’.
PROGNOSIS
• Good prognosis – 1/3.

• Intermediate prognosis – 1/3.
• Poor prognosis – 1/3.
The illness course may plateau after the first 5 years (Carpenter and Strauss, 1991).
WHO-coordinated IPSS, DOSMeD and ISoS studies (initial report, 1973; Jablensky
et al., 1992; Harrison et al., 2001) indicate a more benign course in developing
countries.
PREDICTORS OF POOR OUTCOME

• Male gender.
• History of obstetric complications.
• Abnormal premorbid personality.
• Low IQ.
• Single status.
• Early age at onset.
• Insidious onset.
• Substance abuse.
• Family history of schizophrenia.
Enduring negative symptoms early in the course predict a poor outcome. The dura-
tion of active psychosis without/prior to neuroleptic treatment predicts a poor
response to neuroleptics and poor outcome.
SCHIZOAFFECTIVE DISORDER
Kasanin (1933) described patients with illness of both affective and schizophrenic
symptoms, with sudden onset after a stressor, and good premorbid adjustment.
Subsequent definitions and application of different diagnostic criteria led to confusion
and poor reliability of schizoaffective (SA) disorder – ␬ ⫽ 0.19 for concordance among
seven diagnostic criteria (Brockington and Leff, 1979). See Table 3.8.
Table 3.8 DSM-IV criteria for schizoaffective disorder
A. Uninterrupted period of illness during which, at some instances, either a major depressive or manic episode is
concurrent with symptoms satisfying criterion ‘A’ for schizophrenia.
B. Delusions or hallucinations present for 2 weeks during the same period of illness in the absence of
prominent mood symptoms.
C. Mood symptoms present for significant extent of total duration of active and residual phases of the illness.
D. Exclusion of substance/general medical condition.
Subtypes: bipolar, depressive.
DELUSIONAL DISORDER 37
SA is unlikely to be either:
• Co-occurrence of schizophrenia and affective disorder in a patient.
• A separate disease entity.
SA is more likely to be either:
• A subtype of schizophrenia.
• A subtype of affective disorder.
• A heterogeneous disorder, intermediate between schizophrenia and affective dis-
order (i.e. continuum model).
Available data from family and twin studies suggest a continuum.
A schizodepressive subtype is more related to schizophrenia; a schizomanic subtype is
more related to affective disorder.
MANAGEMENT OF SCHIZOAFFECTIVE DISORDER

Treatment is individualized according to the pre-eminence of either schizophrenic or
affective symptoms.
• Lithium or valproic acid – most beneficial for mainly affective SA patients; schizo-
phrenic symptoms, less response.
• Neuroleptics – used in combination with lithium or antidepressant; more effective
than neuroleptic monotherapy.
• ECT – useful in patients with mainly affective symptoms, perplexity, or a family
history of SA.
PROGNOSIS OF SCHIZOAFFECTIVE DISORDER

The prognosis is intermediate between schizophrenia and affective disorder.
Schizomanics have a more episodic course and better outcome; schizophrenic symptoms
are associated with poor outcome.
Early onset is associated with schizophrenic symptoms and poor outcome (see
Table 3.9).
DELUSIONAL DISORDER
Delusional disorder is a contentious nosological entity. Is it a distinct mental disorder

(‘paranoia’), or a milder form of schizophrenia (‘late paraphrenia’ ‘senile schizophre-
nia’), or part of a spectrum of disorders (‘paranoid spectrum’: Munro, 1992)?
Table 3.9 Schizoaffective disorder (SA) and schizophrenia

SA Schizophrenia
(%) (%)
Cologne follow-up study Very poor outcome 6 52

Marneros et al. (1989) Very good outcome 51 12
38 SCHIZOPHRENIA
Table 3.10 DSM-IV criteria for delusional disorder
A. ⭓1 month duration of non-bizarre delusions.

B. Never had any criteria ‘A’ for schizophrenia.
C. Functioning not markedly impaired and behaviour not obviously odd/bizarre (apart from impact of delusion).
D. Mood episodes, if ever present, brief in duration relative to total duration of illness.
E. Exclusion of substance/general medical condition.
Subtypes:
• Persecutory.
• Jealous (corresponds to description of ‘morbid jealously’ – Shepperd, 1961).
• Erotomanic (corresponds to description of ‘de Clerambaut’s Syndrome, see Chapter 15).
• Somatic (corresponds to description of ‘monosymptomatic hypochondrical psychosis – Munro, 1992).
• Grandiose.
• Mixed and unspecified.
Table 3.11 Clinical differential diagnosis of delusional disorders

Disorder Delusions Hallucinations Other clinical attributes
Paranoia Present, well Present but not Personality well preserved

encapsulated prominant
Paraphrenia Multiple Prominent Illness suggestive of paranoid
schizophrenia, but with
preservation of rapport and affect
Paranoid schizophrenia Multiple Prominent Thought-disorder, blunted affect,
suspiciousness; social isolation
Personality disorder Absent Absent Anger, suspiciousness, but no
psychotic features
Obsessive–compulsive disorder Absent Absent Obsessions may appear bizarre
(‘overvalued ideas’), not
delusional
Organic delusional syndrome Present, single Often present Other organic features usually
or multiple evident
Adapted from Munro (1992).
Genetic and outcome studies support the present classification under the rubric of
schizophrenia/related psychotic disorders. See Tables 3.10 and 3.11.
MANAGEMENT OF DELUSIONAL DISORDER

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Affective disorders 4
CLASSIFICATIONS
Classification is unsatisfactory and continues to be contentious. There is ongoing

debate as to whether the forms of affective disorder described below represent sep-
arate disorders or a continuum of severity. See Table 4.1.
Primary versus secondary

Is mood disturbance independent, or a manifestation of either another psychiatric
disorder or physical illness? There is little clinical difference, and neurobiological
parameters (e.g. dexamethasone suppression test) do not discriminate.
Unipolar versus bipolar (Leonard, 1962; Angst, 1966; Perris, 1966)

• Unipolar – ⭓3 complete episodes of depression, never manic.
• Bipolar – ⭓1 episode of depression and of mania, or multiple episodes of mania:
– I – major depressive and manic episodes, or manic episodes alone
– II – major depressive episodes, but manic or hypomanic episodes only attribut-
able to treatment (electroconvulsive therapy, antidepressants).
Bipolar patients are more likely to have earlier and more acute onset, and tend to
have a different pattern of familial inheritance.
ENDOGENOUS (‘MELANCHOLIA’)/PSYCHOTIC VERSUS NEUROTIC/REACTIVE DEPRESSION

It is contentious as to whether these terms specify distinct subgroups of aetiological
and clinical significance or whether they describe a continuum of severity.
Nomenclature is confusing: ‘psychotic’ is used by the British to describe major depres-
sion (‘endogenous’) with or without psychosis, while US authors refer to ‘psychotic’
solely in a phenomenological context.
Melancholia refers to severe depression with anhedonia, diurnal variation in mood,
lack of reactivity, psychomotor retardation or agitation, early morning wakening, and
anorexia/marked weight loss.
Neurotic and reactive depression were originally thought to be more clearly associ-
ated with precipitating ‘life events’, although this distinction is less clear now. Attempts
44 AFFECTIVE DISORDERS
Table 4.1 ICD-10 and DSM-IV classification of affective disorders

ICD-10 DSM-IV
Depressive episode Depressive disorders

Mild (without/with somatic symptoms) Major depressive episodes
Moderate Mild
Severe (without/with psychotic symptoms) Moderate
Severe
Recurrent depressive disorder – without psychotic features
Mild, moderate, severe – with psychotic features
In remission [Mood congruent or mood incongruent]
Other/unspecified In partial remission
In remission
In full remission
Single
Recurrent
Bipolar affective disorder Bipolar disorder
Current episode hypomania Hypomanic episode
Current episode manic (without/with psychotic symptoms) Manic episode
Other/unspecified episodes Mild
Moderate
Current episode depression Severe
– mild – without psychotic features
– moderate – with psychotic features
– severe (without/within psychotic symptoms) [Mood congruent or mood incongruent]
In partial remission
Current episode mixed In full remission
Currently in remission
Other/unspecified Bipolar I disorder
– single manic episode
– most recent episode
– hypomanic/mixed/depressed/unspecified
Bipolar II disorder
Manic episode
Hypomania
Mania (without/with psychotic features)
Other/unspecified episodes
Persistent mood disorders
Cyclothymic disorder Cyclothymic disorder
Dysthymia Dysthymic disorder
NOS Depressive disorder
Other/unspecified
Other/unspecified mood disorders Mood disorder due to medical condition or
substance abuse
to discriminate subgroups further have examined melancholic versus non-melancholic,

psychotic versus non-psychotic, or characteristics on the basis of cluster analysis of
symptoms. Overall, research supports the continuum viewpoint.
Cyclothymia There is recognition in ICD-10 and DSM IV of Kraepelin’s original con-
cept of patients with less severe mood disturbance and persistent instability of mood
with chronic course. It is common in relatives of patients with major affective disor-
der. Some patients in middle age eventually develop major affective disorder superim-
posed on cyclothymia.
CLINICAL FEATURES 45
Dysthymia This is equated in ICD-10 and DSM-IV to chronic, low-grade ‘neurotic’

depression which is rarely severe enough to fulfill the criteria for recurrent depressive
disorder (mild or moderate). It is frequently complicated by superimposed major
depressive episodes – ‘double depression’. Boundaries between dysthymia, chronic
unremitting major depression and depressive personality traits are controversial.
CLINICAL FEATURES
MAJOR DEPRESSIVE ILLNESS (‘PSYCHOTIC’/RETARDED/‘ENDOGENOUS’)
Mood
• Persistent depression of mood.
• Qualitatively different from normal unhappiness.
• Loss of reactivity to circumstances (‘autonomous’).
• Diurnal rhythm.
• Pervasive.
Speech and cognition
• Decreased tempo and reduction in quantity of speech.
• Guilt, self-blame, worthlessness and hypochondriasis.
• Impaired concentration or slowed thinking, indecisiveness, not associated with
incoherence or loosening of associations.
• Suicidal, morbid and paranoid ideation.
Somatic/biological/behavioural features
• Poor appetite, weight loss or, less commonly, increased appetite or significant
weight gain.
• Insomnia or hypersomnia – characteristic early morning wakening but also onset
of insomnia.
• Psychomotor retardation, agitation – loss of energy and fatigue, decreased libido
and loss of interest in pleasure and work activities.
‘HYPOMANIC’ AND ‘MANIC’ STATES
Mood
• Persistent elevation of mood.
• Irritability a common feature.
• May be intermingled with transient depression of mood (‘manic’/‘hypomanic’
may be used to indicate degree of severity, or presence or absence of delusions and
hallucinations).
Speech and cognition

• Pressure of speech, increased tempo of thinking, impaired concentration and
‘flight of ideas’.
• Distractibility, attention easily drawn to irrelevances.
• Inflated self-image (grandiose, expansive).
Somatic/biological/behavioural features
• Increased drive and activity: physical, social, work, libido.
• Excessive activity in risk-taking pursuits, indiscretion socially.
• Insomnia often earliest sign, but no fatigue (EEG shows reduction in delta sleep)
• Appetite good; weight loss is due to overactivity.
EPIDEMIOLOGY
Statistics vary widely, depending on diagnostic criteria and ‘caseness’ issues.

Depressive symptoms are very common (13–20 per cent point prevalence).
Results of an epidemiologic catchment area study were:
• 1 month prevalence of 2.2 per cent for major depression.
• Lifetime prevalence of 5.8 per cent for major depression.
• Lifetime prevalence of 0.012 per cent for bipolar disorder.
Females are more affected than males. Lifetime prevalence for males is 2.3–4.4
per cent and for females, 4.9–8.7 per cent. Lifetime incidence for males is 10 per cent
and for females, 20 per cent.
The lifetime prevalence for bipolar type I is 0.8 per cent. For type II it is 0.5 per cent.
There are no consistent gender differences in rates of bipolar disorder.
Other observations
• There is concern over increased depression and bipolar illness in young people.
• Onset:
– Bipolar disorder most often in mid-20s.
– Unipolar disorder in late 20s.
– Women have peak onset in 30s, males in 40s.
• There is a higher prevalence of depression in lower social group females (Brown
and Harris, 1978).
• Prevalence is higher in urban areas and among the divorced.
• Ethnic differences in the USA appear more related to social class differences.
Depression may be becoming more common. From 1910 to 1950 the risk of depres-
sion rose in each generation with associated earlier age at onset – the ‘birth cohort effect’.
Unipolar depression was the biggest cause of lifetime disability in the WHO Global
Burden of Disease study.
GENETICS
Family studies
High rates of mood disorders have been found in first-degree relatives of bipolar
patients – about 20 per cent. The rate of mood disorder in first-degree relatives of
unipolar patients is about 10 per cent.
Table 4.2 Percentages of parents affected

Biological Adoptive
Bipolar adoptees 28 12
Bipolar non-adoptees 26 –
Normal controls 5 9
Unipolar forms tend to ‘breed true’, but bipolar forms are associated with elevated
risk of both unipolar and bipolar disorder in relatives.
Twin studies
• Unipolar – MZ:DZ ⫽ 54%:24%.
• Bipolar – MZ:DZ ⫽ 79%:19%.
Adoptive studies
Mendlewicz and Rainer (1977) studied relatives of adult bipolar probands who
had been adopted early in life and compared them with those of normal adoptees,
biological parents of patients with poliomyelitis and bipolar non-adoptees (see
Table 4.2).
Molecular genetics
This is a major area of research. For bipolar disorder, genome-wide search reveals
evidence of susceptibility genes on chromosomes 4, 12, 13, 18, 21 and 22 (Berrettini,
2001; Liang et al., 2002; Sklar, 2002; Shaw et al., 2003). Chromosomes 13 and 22 are
also associated with schizophrenia (see Chapter 3).
For unipolar depression, studies suggest that genetic factors may account for 40–70
per cent of the risk. Genome-wide search reveals susceptibility genes on chromosomes
1, 2, 5, 8, 10, 11, 15, 18, 19 (Zubenko et al., 2003).
NEUROCHEMISTRY
NEUROTRANSMITTER ABNORMALITIES
Serotonin
Evidence includes:
• Decreased:
– Plasma tryptophan
– CSF 5-hydroxyindoleacetic acid (5-HIAA) (especially in suicides)
– Platelet 5-HT uptake
– 3H-imipramine binding in platelet, in frontal cortex, and in hippocampus
– Prolactin response to neuroendocrine challenge tests (intravenous tryptophan,
oral fenfluramine) – responses are then normalized with antidepressant therapy.
• Increased:
– 5-HT2 receptor binding in platelets, in cortex of suicides.
Noradrenaline
Evidence includes:
• Decreased:
– Growth hormone response to neuroendocrine challenge tests (amphetamine,
clonidine, desipramine)
– Platelet CAMP turnover with stimulation by clonidine.
• Increased:
– Platelet ␣2-adrenergic-receptor binding
– Beta-adrenergic receptors in suicides.
• Normal:
– CSF, plasma, urinary measures of noradrenaline and MHPG.
Acetylcholine
There is little evidence of abnormality, apart from the cholinergic basis for sleep dis-
turbances in affective disorder (see Chapter 14), findings which are consistent with
postsynaptic muscarinic supersensitivity.
Dopamine
There have been mixed results in studies of neuroendocrine responses to either apo-
morphine or amphetamine.
NEUROENDOCRINE ABNORMALITIES
• There is blunted growth hormone in response to insulin challenge, and blunted
thyroid-stimulating hormone in response to TRH.
• Hypercortisolaemia and loss of normal circadian rhythm of cortisol.
• Failure of cortisol suppression in a dexamethasone suppression test (DST) is seen
in 50–60 per cent of depressed patients. Initial optimism that this would be a ‘trait’
marker rather than a ‘state’ marker has not held up, and DST non-suppression is
seen also in alcoholism, anorexia nervosa, schizophrenia, etc.
Neurochemical and neuroendocrine studies are difficult to assimilate and to detect
a consistent pattern for various reasons:
• There is uncertainty about the origin of metabolites; i.e. does plasma MHPG
reflect central noradrenaline metabolism?
• Effects of diet and menstrual status need to be accounted for. Some of these
(e.g. appetite) are behavioural features of depression.
• There are varying methodologies, assay techniques, etc.
• There are variable criteria for affective illness and patient selection between studies
(e.g. unipolar vs. bipolar).
Collectively, the results suggest the overall possibility of:
• Subsensitivity of noradrenaline postsynaptic receptors
• Presynaptic 5-HT dysfunction.
It is most likely that there is an interaction between two or more neurotransmitter
systems, perhaps modulated by neuropeptides.
NEUROPEPTIDES
The exact role of neuropeptides on mood is unknown. Elevated corticotropin releas-
ing factor (CRF) is associated with depression, and CRF neural pathways interact
extensively with serotonergic and noradrenergic systems. Administration of CRF in
animal studies produces depressive behavior. Research into the effect of CRF receptor
antagonists on depression is ongoing.
Antagonists to human substance P (neurokinin 1) receptors were originally developed
as a treatment for pain but did not meet with success. However, their efficacy for
improving depressive symptoms has been demonstrated in a placebo-controlled trial
(Kramer et al., 1998) and further research is under way (Stout et al., 2001).
PSYCHOIMMUNOLOGY
• There are decreased numbers of natural killer cells, and T-cell replication.
• There is decreased interleukin-2.
• There is increased monocyte activity.
Immune deficits are thought to be related to the end-products of sympathetic ner-
vous system and hypothalamic–pituitary–adrenal axis activation (i.e. glucocorticoids
and catecholamines), which modulate the immune system.
Animal models support the involvement of catecholamine and glucocorticoid lympho-
cyte receptors in the immune alterations related to depression (Silberman et al., 2004).
NEUROIMAGING/NEUROPATHOLOGY (see Chapter 15)
MRI studies suggest a reduction of hippocampus and caudate nucleus size in depres-
sion. PET studies indicate reduced metabolic activity and perfusion in cingulate
gyrus, dorsolateral prefrontal cortex and left angular cortex (pronounced in depres-
sive ‘pseudodementia’ patients).
In stroke victims, dysphoria is associated with lesions in the anterior left hemi-
sphere, whereas euphoria is associated with right hemispheric strokes.
ORGANIC CAUSES
See Table 4.3.
Table 4.3 Examples of high prevalence of depression

in medical illness
Patient population Patients with depression
Cancer outpatients 33%

Cancer inpatients 42%
CVA 47%
MI 45%
Parkinson’s disease 39%
Endocrine disorders
• Hypothyroidism • Cushing’s syndrome
• Hyperparathyroidism • Addison’s disease
Infective causes
• Post-influenza • Infectious mononucleosis
• Brucellosis • Hepatitis
Metabolic causes
• Iron-deficient anaemia • Hypercalcaemia
• B12/folate-deficient anaemia • Hypomagnesia
Neurological causes
• Post CVA • Intracranial tumours
• Multiple sclerosis • Epilepsy
• Parkinson’s disease
Depression, particularly epilepsy – associated with non-dominant (right-sided)
temporal lesions, although later refuted in several studies.
Drugs
• Reserpine • Steroids
• Alpha-methyldopa • Barbiturates
• L-dopa • Prolonged use of amphetamines
The oral contraceptive pill is no longer considered to be ‘depressogenic’.
PSYCHOLOGICAL THEORIES
Psychodynamics
• Loss of love object.
• Regression to primitive emotional level where lost object is ‘incorporated into self ’
and bitterly attacked by superego.
• Depressive position characterized by guilt, helplessness, and fear of the loss
of love.
Early childhood experiences

Bowlby emphasized early maternal deprivation, but research has been complicated by
poor methodology.
The observed relationship between prolonged absence of a parent during early
life and subsequent depression (Brown et al., 1986) seems more related to the absence
of care rather than the specific figure (maternal vs. paternal) or type of separation
(death, divorce).
Cognitive/behavioural theories
• Wolpe – depression is conditioned by repeated losses in the past.
• Seligman – ‘learned helplessness’ is a consequence of repeated exposure to uncon-
trollable traumas.
• Beck – there is a ‘negative cognitive trait’ of self-defeating thoughts.
Premorbid personality
Early research suggested that depressed patients were premorbidly more introverted,
shy and obsessional, while manic patients had vivacious, cyclothymic personalities.
However, depression compounds ‘retrospective’ assessment, and in more recent research
premorbid characteristics show only a minor association.
SOCIOLOGICAL THEORIES
Brown and Harris (1978) described high rates of depression among inner-city
London lower social group females. This suggested vulnerability factors which predis-
pose to depression only in the presence of provoking agents.
Vulnerability factors
• Excess of threatening life events or major difficulties prior to onset of depression.
• Unemployed status.
• Unsupportive relationship with spouse or partner.
• Three or more children under age of 15 living at home.
• Loss of mother before age 11.
Subsequent studies (Brown et al., 1986) only partly replicated Brown and Harris’
hypothesis, and further suggest that low self-esteem is a major vulnerability factor.
LIFE EVENT STUDIES
Methodological problems include: colouring of retrospective information by depres-

sion (‘search for meaning’); inadequate controls; separating dependent life events
(may be secondary to depression, e.g. marriage break-up) from independent life
events (e.g. job loss due to business liquidation); difficulty in corroborating history.
Nevertheless, there seems to be an excess of life events preceding depression as well
as mania.
INTEGRATIVE MODELS OF DEPRESSION
A review of animal studies supports an integrative model of depression based on a

stress paradigm (Newport et al., 2002):
1 Disrupted parenting which produces stress.
2 Stress results in hypersecretion of CRH.
3 CRH elevation causes hyper-responsivity in the hypothalamic–pituitary–adrenal
axis.
COURSE AND PROGNOSIS
These are dependent on concepts and definitions of affective disorder used in studies and
clinical policies. The original Kraepelinian view of good outcome of ‘manic–depressive
insanity’ (relative to the chronicity of schizophrenia) is now questioned.
Short-term prognosis
Approximately 67 per cent of patients respond to treatment within 8 weeks. Even
when treated, the risk of recurrence of major depression is substantial:
• 50 per cent after one episode
• 70 per cent after two episodes
• 90 per cent after three episodes.
Thirty per cent of patients will become chronically depressed.
Long-term prognosis
Inter-episode intervals of depression and mania tend to lengthen over time, although
this pattern is reversed in elderly people, where affective episodes also last longer and
are more likely to leave residual symptoms.
In a 25-year follow-up (Angst and Preisig, 1995), 13 per cent of patients failed to
recover and had continued symptoms and disability, resembling dysthymia rather
than major depression; severity of initial psychopathology was predictive of outcome.
Thirteen per cent died of suicide.
In an 18-year follow-up (Lee and Murray, 1988), 25 per cent had poor outcome
(death, continued disability); only 11 per cent recovered and showed no further
psychiatric morbidity. Severity of the initial psychopathology was predictive.
Predictors of poor outcome

• Early onset.
• Severity of symptoms at index admission.
• Co-morbid personality disorder.
• Co-morbid dysthymia – ‘double depression’.
TREATMENT
PSYCHOTHERAPY (see Chapter 23)
COGNITIVE BEHAVIOURAL THERAPY (CBT)

This is systematic treatment aimed at challenging ‘logical errors’, ‘automatic thoughts’
and ‘generalizations’. Research supports its effectiveness in the treatment of depres-
sion. It needs to be of at least 16-weeks duration, and appears to be as effective as
pharmacotherapy in reducing later relapse.
The use of CBT as a maintenance treatment needs further research. There is no
consensus that combined CBT plus medication is better than either modality singly.
TREATMENT 53
INTERPERSONAL PSYCHOTHERAPY (IPT)

This is exploration of the origins of depression in terms of interpersonal losses, role
disputes and transitions, social isolation, and/or deficits in social skills. It is effective in
the acute treatment of depression, particularly for vocational and social sequelae of
illness. The efficacy as maintenance therapy is still under investigation.
PHYSICAL APPROACHES
PHARMACOLOGY (see Chapter 21)

Numerous antidepressant medications are available. Claims for the superiority of an
individual antidepressant are unsubstantiated, and this is also true overall, even for
comparison of newer antidepressants (SSRIs, etc.).
The newer antidepressants – SSRIs and SNRIs – are safer in overdose, and have more
tolerable side-effects than older antidepressants (TCAs and MAOIs). MAOIs are best
used for ‘atypical depression’ and are not generally used as a first-line drug in major
depression.
Recent research indicates that patients with recurrent depression should receive long-
term maintenance treatment at the dose that produced the initial response (Kupfer
et al., 1992).
COMBINATION THERAPIES
Combination therapies are reserved primarily for treatment-resistant depression (see
later). The addition of low-dose lithium to an antidepressant regimen may augment
the effect. Atypical antipsychotics given in combination with SSRIs have shown clinical
efficacy.
Lithium
• Treatment of mania (3–4 days for therapeutic effect) – 75 per cent response rate.
• Prophylaxis for bipolar disorder usually commenced when there are two or more
affective disturbances within 2 years.
• 50 per cent of patients relapse within 3 years, with poor compliance with medica-
tion being the key factor.
Valproate
Valproate is another first-line agent in mania. Patients with mixed affective disorder
may respond better than those with ‘pure’ mania (McElroy et al., 1992).
Carbamazepine
The overall response rate in mania is 65 per cent; i.e. less than with lithium. It is gen-
erally used as a second-line drug, for treatment resistance or lithium intolerance.
There is no evidence yet to support its use in unipolar disorder.
Atypical antipsychotics
Atypical antipsychotics are effective for the management of acute mania.
ELECTROCONVULSIVE THERAPY
See Chapter 22.
Sleep deprivation
Total sleep deprivation is reported to induce rapid clinical improvement in about
30 per cent of patients. REM deprivation (causing ‘REM pressure’) results in improve-
ment in 30–60 per cent. The mechanism is unclear – it may restore circadian rhythm
through an improved sensitivity of neurotransmitter/melatonin.
MANAGEMENT OF TREATMENT-RESISTANT DEPRESSION
1 Review the diagnosis, physical investigations and social/family factors. Pay particular
attention to interpersonal and family dynamics that may inhibit resolution of symp-
toms. Continue with periodic review/update of diagnosis, management, etc.
2 Enhance present physical treatments:
– Maximize dose of antidepressant.
– Switch to a different class of antidepressant if failure follows an adequate trial.
3 Add in:
– Atypical antipsychotic
– Lithium.
4 Physical treatment measures (see Chapter 22):
– Electroconvulsive therapy
– Vagal nerve stimulation (VNS)
– Transcutaneous magnetic stimulation (TMS).
OTHER SYNDROMES
MIXED AFFECTIVE STATES

During transition from mania to depression and vice versa, Kraepelin held that mood,
cognition and behaviour may vary independently, producing ‘mixed’ states. There are
six combinations:
1 Manic stupor (elation, increased thought tempo, motor retardation).

2 Excited (agitated) depression (decreased thought, depressed mood, overactivity).
3 Anxious mania (increased thought tempo, overactivity, anxious mood).
4 Unproductive mania (decreased thought tempo, overactivity, elation).
5 Depression with flight of ideas (depressed mood, motor retardation, increased
thought tempo).
6 Inhibited mania (decreased thought tempo, motor retardation, elation).
States were usually transitional, but sometimes persistent. Some studies suggest
up to 30 per cent of bipolar patients present with mixed symptoms in their first
episode.
OTHER SYNDROMES 55
BEREAVEMENT REACTIONS
Uncomplicated bereavement or typical grief
1 ‘Stunned’ phase – emotions blunted – lasts few hours to 2 weeks.
2 Mourning phase – intense yearning and distress – autonomic features – unhappi-
ness, futility, anorexia, restlessness, irritability, preoccupation with deceased –
transient hallucinatory episodes and guilt-denial.
3 Acceptance and readjustment – several weeks after onset of mourning.
The duration of typical grief varies with culture – on average 6–12 months.
Atypical grief
• Chronic grief – typical depressive illness may emerge with morbid preoccupation
with worthlessness, prolonged functional impairment, marked psychomotor
retardation. Other features include: excessive guilt, denial, identification, antisocial
behaviour.
• Inhibited grief or delayed grief.
• Non-specific and mixed reactions – psychosis, neurosis, etc.
ATYPICAL OR ‘MASKED’ DEPRESSION
This is illness presenting as either (1) physical conditions or (2) non-affective psychi-
atric disorders:
• Chronic pain, hypochondriasis, somatoform disorders, conversion disorders –
usually show absence of significant organic pathology, poor response to medical
treatment and some depressive features.
• Pseudodementia, anxiety states, behavioural change (e.g. shoplifting in middle-
aged women).
SEASONAL AFFECTIVE DISORDER (SAD)

There is a history of major affective disorder with at least three previous winter
depressive episodes. There is onset and remission of each depressive episode; these
occur within specific 60-day periods of each other.
Seasonal mood disturbances outweigh (by more than 3:1) any non-seasonal mood
disturbance (if present). There is an absence of a clear-cut seasonally changing psy-
chosocial variable.
‘Atypical’ depressive features can be anxiety, irritability, increased fatigue, increased
sleep, appetite, weight gain (‘carbohydrate craving’). Mild ‘hypomania’ is often experi-
enced in summer.
The true prevalence is unknown. Four per cent of a population in Washington (USA)
had winter SAD (Kasper et al., 1989). More females than males are affected, although
this may be a selection bias.
Pathophysiology
Pathophysiology is unknown. The dysregulation of melatonin postulate is:
• Melatonin deficit.
• ‘Phase shift’ in normal circadian output of melatonin.
• Dopamine-mediated abnormality in melatonin secretion.
Treatment
Ultraviolet light therapy (bright, but not dim) suppresses blood melatonin – unclear
whether morning therapy is best time of day.
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Neurotic disorders 5
ANXIETY DISORDERS
See Table 5.1.

Anxiety disorders include various combinations of mental and physical manifestations
of anxiety not attributed to real danger and occurring either in attacks (panic disorder) or
as a persisting state (generalized anxiety disorder). Other neurotic features may be pres-
ent (obsessional or hysterical symptoms) but do not dominate the clinical picture.
Table 5.1 ICD-10 and DSM-IV classifications of anxiety-related disorders

ICD-10 DSM-IV
Phobic anxiety disorders Phobic anxiety disorders

Agoraphobia Agoraphobia
– with panic disorder
– without panic disorder
Social phobias Social anxiety disorder
Specific (isolated) phobias Specific phobia
Other phobias
Other anxiety disorders

Panic disorder Panic disorder
– with agoraphobia
– without agoraphobia
Generalized anxiety disorder Generalized anxiety disorder
Mixed anxiety and depressive disorder
Other anxiety disorders Anxiety disorder due to physical illness or
substance abuse
Obsessive–compulsive disorder Obsessive–compulsive disorder
Reaction to severe stress and adjustment Reaction to severe stress and adjustment
Acute stress reaction Acute stress disorder
Post-traumatic stress disorder Post-traumatic stress disorder
Adjustment disorders
ANXIETY DISORDERS 61
‘Anxiety’ suggests (Lewis):

• An emotional state with the subjectively experienced quality of fear.
• An unpleasant emotion which may be accompanied by a feeling of impending
death.
• A feeling directed towards the future, perceiving a threat of some kind.
• A subjective bodily discomfort and manifest bodily disturbance.
There may be no recognizable threat – or one which, by reasonable standards, is out
of proportion to the emotion it seemingly provokes.
PANIC DISORDER
Recurrent attacks of panic (anxiety) occur unpredictably and unexpectedly, though

certain situations (e.g. being away from one’s secure surroundings – panic disorder
with agoraphobia) may become associated with them.
Clinical symptoms
• There is sudden onset of intense apprehension, anxiety, fear, often with feeling of
impending doom or even death. Feelings of unreality may occur.
• Somatic effects can include dyspnoea, palpitations, chest pain, choking or smother-
ing sensations, paraesthesias, flushes, sweating, faintness, etc.
• There may develop ‘anticipatory fear’ of loss of control, so the individual becomes
afraid of being left alone in public places. Anticipatory fear may itself precipitate
an attack.
GENERALIZED ANXIETY DISORDER
There is a generalized persistent anxiety without the specific symptoms that characterize
phobic anxiety disorder or panic disorder.
Clinical symptoms
• There is subjective apprehension, fear, worries (see above).
• Motor tension.
• Autonomic hyperactivity.
• Vigilance and scanning – the person complains of feeling ‘on edge’, has difficulty
sleeping, has interrupted sleep or fatigue on waking.
EPIDEMIOLOGY OF ANXIETY DISORDERS
An anxiety disorder often begins in early adult life, but may occur for the first time in
middle age. Women are more affected than men.
There is a 4–7 per cent prevalence in the normal population. It accounts for 27 per
cent of psychiatric consultations in general practice, and 8 per cent of psychiatric
outpatients.
62 NEUROTIC DISORDERS
PREDISPOSING FACTORS FOR ANXIETY DISORDERS
GENETICS
• There is a problem of small samples and diagnosis.
• MZ:DZ ⫽ 65%:13% (Slater and Shields).
• There is some evidence of genetic influence on neurotic ‘traits’ measured by per-
sonality tests and reflected in autonomic reactivity (e.g. GSR habituation).
EARLY CHILDHOOD
• Separation experiences.
• Childhood trauma.
• Undue emphasis on achievement.
• Demands for excessive conformity.
OTHER
• Current situational stress, uncertainty, conflict.
• Biological factors (see p. 66)
COURSE AND COMPLICATIONS OF ANXIETY DISORDERS
There is a variable course and prognosis – the more chronic and established the condi-
tion, the worse the prognosis.
Males are (?) more likely to improve than females. Premorbid stability has an
important influence. Agoraphobia may develop, or secondary depression.
Alcohol abuse and abuse of anxiolytics are not uncommon.
TREATMENT OF ANXIETY DISORDERS
Reassurance, counselling and social intervention should be aimed at current situational

stresses.
PSYCHOTHERAPY
• Cognitive–behavioural: more effective in panic disorder. Identify and ‘label’ mor-
bid anticipatory thoughts and replace with realistic cognitions.
• Insight-orientated: explore covert conflicts.
• ‘Anxiety management’ training:
– Distraction techniques.
– Cognitive control.
– Breathing/relaxation exercises – reduce chronic hyperventilation.
– Education – somatic effects of anxiety and overbreathing.
DRUG THERAPY
• Serotonin reuptake inhibitors are a first-line treatment. They are more effective
than benzodiazepines in reducing anxiety, anger, and hostility in the long term.
PHOBIC DISORDERS 63
• Benzodiazepines provide symptomatic relief in the short term.

• Azapirones are equal in efficacy to benzodiazepines in reducing anxiety, but are
more effective at reducing anger and hostility.
• Beta-blockers are not useful in panic disorder, otherwise they reduce anxiety-
related symptoms in adequate dosage.
• MAOIs have anxiolytic properties. There is some evidence for usefulness in panic
disorders.
• Novel antianxiety agents – Venlafaxine blocks the reuptake of serotonin as well as
noradrenaline (norepinephrine) and provides long-term relief from anxiety.
PSYCHOSURGERY
Surgery is reserved only for cases of chronic, intractable, incapacitating anxiety that is
unresponsive to other measures.
PHOBIC DISORDERS
In phobic disorders (Marks):

• Fear is out of proportion to the demands of the situation.
• It cannot be explained or reasoned away.
• It is beyond voluntary control.
• The fear leads to an avoidance of the feared situation.
CLINICAL SYNDROMES RELATED TO EXTERNAL STIMULI
AGORAPHOBIA
Agoraphobia is strictly a fear of open spaces, but the term is often used for fear of
shopping, crowds, etc.
Agoraphobia accounts for 60 per cent of phobic patients seen by psychiatrists;
66 per cent are female. Most develop symptoms between the ages 15 and 35.
Other non-phobic symptoms are common, including generalized anxiety, panic
attacks, depression and depersonalization.
Predisposing and associated factors

• Passive, anxious and dependent premorbid personality.
• Stable family.
• Similar to general population in terms of education, social class.
• Often precipitated by major life event.
• History of childhood fears and enuresis.
• Higher incidence of sexual problems in female group compared with control
population.
Course and prognosis

There is a fluctuating course, once established. It may persist for many years.
SOCIAL PHOBIA
Social phobia accounts for 8 per cent of phobic patients seen by psychiatrists; 60 per
cent are women. It usually develops after puberty and peaks in late years.
It is a persistent, irrational fear of, and compelling desire to avoid, situations in
which the individual may be exposed to the scrutiny of others. There is also fear that
the individual may behave in a manner (e.g. blushing, shaking, vomiting) that will be
humiliating or embarrassing.
Social phobia is probably not a homogeneous clinical entity but may represent
the prominent symptomatic manifestation of a wide variety of psychological
disorders.
ANIMAL PHOBIAS AND OTHER SPECIFIC PHOBIAS

These account for 17 per cent of phobic patients seen by psychiatrists. Women suffer
more than men from animal phobias, otherwise the sex incidence is equal. Onset is in
childhood for animal phobias.
There is a persistent, irrational fear of, and compelling desire to avoid, an object or
a situation – other than being alone in public places away from home (agoraphobia)
or embarrassment in certain social settings (social phobia). There is relative absence of
other psychiatric symptoms. It tends to pursue a continuous course.
ILLNESS PHOBIA
Illness phobia accounts for 15 per cent of phobic patients consulting psychiatrists. It
occurs equally in both sexes.
Illness phobia is a persistent, intense fear of illness, focused on specific disorders
such as cancer, heart disease or veneral illness, or an intense fear of death and dying.
There are chronic ruminations but no apparent attempts at resistance. A previous ill-
ness in a relative or individual may act as the precipitant.
The patient may have other mental illness (e.g. depression), and illness phobia fades
as this is treated.
TREATMENT OF PHOBIC DISORDERS
All treatment rests on careful assessment with respect to:

• The degree to which the manifest anxiety is a reflection of basic personality traits,
or may be considered to be a state arising in the setting of relatively normal per-
sonality structure.
• The presence or absence of stress supposed to be related to the course of the
condition.
• The presence of any dangerous coping strategies (e.g. alcohol abuse).
• The attitudes of others, especially family, towards the patient’s illness. Is the dis-
order being covertly encouraged?
• The presence or absence of secondary gain factors.
• The presence or absence of other clinical syndromes (e.g. depression).
PHOBIC DISORDERS 65
BEHAVIOUR THERAPY
Systematic desensitization
There is gradual exposure to the phobic stimulus with increasing intensity until the
patient habituates and the avoidance response is extinguished. This is combined with
relaxation training, then practice in fantasy before situational exposure.
Good response is associated with:
• Phobias that are specific.

• Good relaxation response.
• Patient motivation.
• Encouragement and support from the therapist.
• Positive involvement of relatives.
Poor response is associated with:
• The presence of free-floating anxiety.

• Poor motivation.
• The presence of secondary gain.
• Severe obsessions.
Flooding (implosion)
This can be in fantasy or in real life. There is supervised maximum exposure to the
feared stimulus until anxiety reduction/exhaustion. This is effective (especially expos-
ure in vivo) for phobias where free-floating anxiety is prominent.
Modelling
The patient observes the therapist (the model) engaging in non-avoidance behaviour
with the feared stimulus.
There is some evidence that a combination of flooding, associated modelling and
moderate doses of diazepam given 4 hours before sessions is particularly effective in
treating agoraphobia.
DRUG THERAPY
• SSRIs are the drug treatment of choice and are well tolerated with no abuse
potential.
• Benzodiazepines are effective but only for short-term management of fear-associated
anxiety until other measures are successful.
• Beta-blockers are effective for short-term management of performance fears.
• MAOIs and TCAs are less effective and have a greater side-effect burden.
PSYCHOTHERAPY
Behavior therapy is effective using either systematic desensitization or flooding.
Cognitive–behavioural therapy is effective at modifying dysfunctional thoughts
involving fear.
BIOLOGICAL ASPECTS OF ANXIETY
The following abnormal autonomic responses to stimuli in anxious patients may

indicate underlying dysfunction of the autonomic nervous system, reflecting increased
sympathetic tone or parasympathetic abnormalities.
Cardiac function
• Higher basal rate.
• Less deceleration after stress.
• More beat-to-beat fluctuation.
• Increased awareness of heart function.
Electrodermal response
• Increased skin conductance.
• Decreased habituation.
• More spontaneous fluctuation.
Peripheral blood flow

• More vasodilation.
• Decreased renal and splanchnic flow.
Neurotransmitter abnormalities
Findings conflict, probably owing to differences in diagnostic groups studied.
• Circulating adrenaline – increased.
• Circulating noradrenaline – ? increased.
• Platelet MAO – increased.
• Central noradrenaline and 5-HT – increased activity.
Responses to sodium lactate infusion

Sodium lactate provokes panic attacks in susceptible patients, compared with controls.
Imipramine is effective in blocking lactate-induced panic.
Panic is provoked because of:
• Abnormal metabolism.
• Production of alkalosis.
• Reduction of ionized calcium.
• Interaction with hyperactive ␤-adrenergic receptors.
Mitral valve prolapse (MVP)

Studies (see Pariser et al., 1979) have suggested a 40–50 per cent incidence of MVP
in patients with panic disorder or agoraphobia. Incidence in the general population
is 6–20 per cent.
Evidence does not suggest that MVP causes panic attacks (e.g. patients with panic
disorder and MVP respond to imipramine as patients solely with panic disorder, but
MVP persists).
POST-TRAUMATIC STRESS DISORDER 67
Both MVP and panic may form part of a general syndrome of primary autonomic
dysfunction.
or
MVP may act as an autonomic precipitant interacting with a predisposition (genetic)
to panic disorder.
Hyperventilation syndrome
Physiological effects of reduced PCO2:
• Vasoconstriction of cerebral arteries.
• Reduced availability of O2 in oxyhaemoglobin.
• Increased irritability of autonomic sensory and motor nervous system.
• Bronchoconstriction and tachycardia.
• Exaggerated sinus rhythm.
Symptoms produced:
• Light-headedness or faintness.
• Breathlessness and palpitations.
• Sweating, fatigue and stiffness.
• Dry mouth with aerophagy and globus.
• Chronic malaise.
Some researchers think that hyperventilation causes panic attacks, others that it is
merely a consequence (see diagram below).
Anticipatory
cognitions
Panic attacks Hyperventilation
Symptoms
POST-TRAUMATIC STRESS DISORDER (PTSD)
Familiar terms are ‘combat neurosis’, ‘shell-shock syndrome’ and ‘traumatic neurosis’ in
the UK – stemming from experiences in war, but PTSD is also now seen as a response
to natural disasters (e.g. Hillsborough deaths Pugh and Trimble, 1993; Australian bush
fire-fighters McFarlane et al., 1990; Coconut Grove fire), to rape, to traffic accidents, to
trauma, etc.
Rates of PTSD are related to specific types of traumatic events (Kessler et al., 1995):
• rape – 65 per cent
• combat – 38.8 per cent
• natural disaster – 3.7 per cent
• criminal assault – 1.8 per cent.
The lifetime prevalence in the community is 1–9 per cent. Chronic PTSD is seen in
1.3 per cent of males and in 4.7 per cent of females (Breslau et al., 1995).
There are high rates of co-morbidity (Kessler et al., 1995):
• alcohol abuse/dependency – 52 per cent
• depression – 48 per cent
• substance dependency – 34 per cent
• social phobia – 28 per cent
• generalized anxiety disorder – 17 per cent
• panic disorder – 7 per cent.
CLINICAL FEATURES OF PTSD
1 There has been exposure to a traumatic event, lying outside normal human experi-
ence and which would clearly cause suffering in almost everyone. The person’s
response involves intense fear, helplessness.
2 There is persistent re-experiencing – recurrent nightmares, flashbacks, reliving of
episode, psychological distress and/or physiological reactivity on exposure to cues
which resemble/symbolize the trauma.
3 There is persistent avoidance of stimuli related to the trauma.
4 Symptoms of hyperarousal are present – hypervigilance, startle reflexes, sleep dis-
turbance, decreased habituation to auditory stimuli.
5 There is psychosocial impairment: ICD-10 criteria emphasize onset within 6 months
of the traumatic event.
AETIOLOGY OF PTSD
There has been much debate about the extent of individual determinants of PTSD.
Not everyone experiencing major trauma develops PTSD, and the neurobiological
basis is not clear.
• PTSD may be due to a complex neurobiological response mechanism that engen-
ders maximal and sustained response to stress.
• There is evidence of increased hypothalamic–pituitary–adrenal axis reactivity.
• Lower basal cortisol levels and more glucocorticoid receptors are seen in individ-
uals with PTSD.
• Elevated catecholamine levels may account for some PTSD symptoms.
• Smaller hippocampal volumes are seen in those with PTSD.
• A previous traumatic event and/or prior history of psychiatric illness are predis-
posing factors for PTSD.
OBSESSIONAL/COMPULSIVE STATES 69
MANAGEMENT OF PTSD
• Rule out a physical illness or cause.

• Rule out alternative psychiatric illness and/or detect and treat secondary disorder –
depression, substance abuse, suicidal behaviour.
• Suicidal behaviour in Vietnam survivors related to ‘combat guilt’ (Hendin and
Haas, 1991).
• Consider cognitive–behavioural therapy, with graded exposure to imagery. Some
evidence points to the efficacy of therapy involving saccadic eye movements.
• Psychoeducation – explanation regarding stress.
• Interpersonal psychotherapy.
• Psychodynamic psychotherapy.
• Relaxation training.
• Group therapy.
• Drugs:
– SSRIs are a first-line treatment.
– Atypical antidepressants – nefazodone, venlafaxine.
– Mood stabilizers useful.
– Atypical antipsychotics.
– Antiadrenergics.
– Imipramine, amitryptiline shown to be effective.
– MAOIs sometimes used but side-effect tolerability poor.
– Benzodiazepines not generally recommended because of liability of abuse and
chronicity of PTSD.
PROGNOSIS FOR PTSD
Prognosis is good if:

• Healthy premorbid function.
• Brief trauma of lesser severity.
• No personal or family history of psychiatric illness.
• Good social support.
The condition becomes chronic in a minority, and the course is fluctuating.
Emphasis today is towards early intervention and prevention – ‘debriefing’ to avert the
development of chronic PTSD. In a preliminary trial, a ‘morning after pill’ of propranolol
immediately in the emergency department after a traumatic event was encouraging.
There is increasing PTSD research and research on ‘resilience’ (what characteristics
make people able to cope with adversity), particularly global terrorism.
OBSESSIONAL/COMPULSIVE STATES
Obsessions are recurrent, persistent ideas, thoughts, images or impulses that the patient
regards as alien and absurd, while recognizing them as products of his/her own mind.
Attempts are made to ignore and suppress them.
Table 5.2 Phenomenology of obsessional–compulsive states
Obsessional doubting – 42%. Aggressive thoughts – 28%.

Fears of contamination – 45%. Checking compulsions – 63%.
Bodily fears – 36%. Washing – 50%.
Insistence on symmetry – 31%. Counting – 36%.
From Rasmussen and Tsuang (1986).
Compulsions are voluntary motor actions which are reluctantly performed despite
being regarded as alien or absurd. The act is performed with a subjective sense of com-
pulsion coupled with a desire to resist it (at least initially). When the individual does
attempt to resist, there is a mounting sense of tension which can only be relieved by
yielding.
The phenomenology of obsessional–compulsive states is shown in Table 5.2.
Symptoms may complicate:
• Depressive illness (found in 30 per cent) – low rate of suicide in depressed patients
with obsessive–compulsive disorder (OCD).
• Schizophrenic disorder.
• Early dementia and other organic brain syndromes.
• Anorexia nervosa.
• Generalized anxiety state.
Fears of harming a baby may occur as part of puerperal illness.
EPIDEMIOLOGY OF OCD
The sex distribution is equal. The most common age at onset is early adulthood:
• 65 per cent of patients onset ⬍25 years.
• 15 per cent after age 35 years.
• Mean age at onset ⫽ 20 years.
• Mean age of presenting to psychiatric services ⫽ 27.5 years (Rasmussen and Tsuang,
1986).
Prevalence
• 0.5 per cent of general population, but recorded lifetime rates of 2–3 per cent in
ECA study (overestimated).
• 1 per cent of psychiatric outpatient and inpatient population.
• 4 per cent of the ‘neurotic’ group.
AETIOLOGY OF OCD
GENETICS
Up to 20 per cent of first-degree relatives have subclinical OCD symptoms. There have
been few twin studies: MZ ⫽ 50–80 per cent; DZ ⫽ 25 per cent. The condition is
strongly linked to Tourette’s disorder.
OBSESSIONAL/COMPULSIVE STATES 71
NON-GENETIC FACTORS
Neurochemistry and neuroanatomy
Glutamatergic-serotonin modulation in the caudate nucleus is thought to be involved.
The primary pathology may be in the caudate nucleus. The frontal lobe also is impli-
cated. PET studies show glucose hypermetabolism in fronto-orbital gyrus and caudate
nuclei (Baxter et al., 1992); these abnormalities are normalized with effective pharma-
cotherapy (Swedo et al., 1992, Rosenberg et al., 2000).
PANDAs
Paediatric autoimmune neuropsychiatric disorders are associated with streptococcal
infection. They are characterized by the abrupt onset of OCD or tics and are thought
to be the result of an autoimmune response to group A ␤-haemolytic streptococcal
infection.
Premorbid personality
The meticulous (‘anankastic’) type personality is associated in 15–35 per cent. Concern
is with orderliness, cleanliness, checking, rigidity.
Psychoanalytic theory
Freud’s views were expounded in his lecture ‘Notes upon a Case of Obsessional Neurosis’
(the Rat Man):
• Defensive regression to pregenital anal-erotic stage of development.
• Defensive mechanism against aggressive and cruel impulses.
• Key defences: reaction formation, undoing, isolation (see p. 298).
Psychological theory
One view is that OCD is a defect of the arousal system (Beech). Major defensive reac-
tions are precipitated by minor alterations to incoming stimuli, perceived as danger-
ous and threatening. The defensive response is thus seen as preventive or placatory
activity aimed at controlling unpleasant internal states.
Learning theory cannot account fully for obsessional phenomena, which are not a
motor response to an anxious thought, but simply the repetitive intrusion into con-
sciousness of an anxious thought or impulse alone.
TREATMENT OF OCD
Psychotherapy
Cognitive–behavioural therapy has been shown to decrease symptomology (Benazon
et al., 2002). Ruminations are more difficult to treat. ‘Thought stopping’ may be helpful.
Loop-type techniques also are helpful.
Drugs and surgery

SSRIs are effective in relieving symptoms and also cause normalizing changes in neu-
rochemistry in the caudate nucleus, as seen by proton magnetic resonance spectroscopy
(Rosenberg et al., 2000).
Fluoxetine, sertraline, citalopram, clomipramine, paroxetine and fluvoxamine have

all been used, but there is no clear superiority of any one agent. Combining serotoner-
gic drug treatment with CBT exposure and response prevention is the mainstay of
treatment.
Case reports of atypical antipsychotic utilization exist and further research is needed.
Psychosurgery (anterior cingulotomy, subcaudate tractotomy, limbic leucotomy,
capsulotomy) is indicated only in severe cases of chronic, incapacitating illness when
other methods have failed (Sachdev et al., 1992).
COURSE AND PROGNOSIS OF OCD
With treatment, the majority of individuals diagnosed with OCD experience a chronic,
fluctuating course. About half of those with OCD will experience partial remission;
and of those, half will experience relapse. Only 12 per cent achieve full remission.
Monitor treatment with Yale–Brown Obsessive Compulsive Scale (YBOCS).
Poor prognostic factors are:
• Co-morbid psychiatric disorder.
• Earlier onset, longer duration of illness.
• Poor insight into the illness.
• More severe, bizarre symptoms – symmetry, ordering, hoarding obsessions.
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Personality: development 6
and disorders
Personality can be defined as the distinctive, enduring patterns of behaviour (includ-

ing thought, perception and emotions) that characterize each individual’s interaction
with the social and personal situations of his or her life.
PERSONALITY DEVELOPMENT THEORIES
FREUD
• The oral stage relates to narcissism, dependence, envy, jealousy.
• The anal stage relates to obsessionality, orderliness, obstinacy, frugality; also rage
and sadomasochism.
• The phallic stage relates to competitiveness and ambition.
Character is that pattern of adaptation to instinctual and environmental forces
which is habitual for the individual. It results from a combination of: innate biological
predisposition, id forces, early ego defences, environmental influences and early iden-
tification and imitation. Character traits owe their existence to successful repression,
leading to persistence. Neurotic symptoms result from a failure of repression.
ADLER
Lifestyle is the individual’s active adaptation to the social milieu. The individual is motiv-
ated by a striving for superiority as a defence against the helplessness of inferiority.
HORNEY
Horney emphasizes the important effect of culture. There are three character types
depending on the predominant mode of relating to others: compliant/self-effacing,
aggressive/expansive, detached/resigned.
SULLIVAN
The individual has two major goals (and states): satisfactions (of biological needs) and
security (in relationships with others). Anxiety is the response to adult disapproval
and personality development is the process of learning to deal with this anxiety.
78 PERSONALITY: DEVELOPMENT AND DISORDERS
ERIKSON
Personality development takes place through (potentially) eight ‘stages’. These are a
series of alternative attitudes which develop into a ‘sense of the attribute’. ‘Epigenesis’
refers to the process of development of the ego through these stages.
1 Basic trust versus mistrust (oral/sensory) – awareness of consistency and continu-
ity, leading to ego identity.
2 Autonomy versus shame and doubt (muscular/anal) – self-control vs. loss of
self-esteem.
3 Initiative versus guilt (locomotor/genital) – planning tasks, but failure leads to guilt.
4 Industry versus inferiority (latency) – recognition is won by doing things, the dan-
ger is inferiority.
5 Identity versus role confusion (puberty) – may lead to the ‘identity crisis’, between
inner sense of continuity and outer vulnerability in one’s meaning for others.
6 Intimacy versus isolation (young adulthood) – the capacity to commit oneself to
others.
7 Generativity versus stagnation (adulthood) – productivity/creativity or self-absorption.
8 Integrity versus despair (maturity) – in the awareness of the closeness of death.
MEYER
Pathological personality reactions are regressions to former, previously protective phylo-
genetic reactions which are now maladaptive. Symptoms are the individual’s attempt to
cure himself or herself. Personality disorder results from disorganization of habits.
PIAGET
Piaget investigated the development of cognition in children. Human intelligence is
an extension of biological adaptation, has a logical substructure and develops in four
stages (another ‘epigenetic’ theory).
1 Sensorimotor (0–2 years) – learns object permanence, differentiates self from
objects, aware of effects of self on objects.
2 Preoperational (2–7 years) – uses symbols, language develops, egocentric.
3 Concrete operational (7–12 years) – capable of logical thought, develops concept of
conservation, classifies, relates.
4 Formal operational (12⫹) – capable of abstract thought, hypothesis, concerned
with ideologies.
PERSONALITY DISORDERS
DEFINITIONS
DSM-IV and ICD-10 presume a major category of personality disorders (PDs), with
features (see Table 6.1):
• Deeply ingrained, maladaptive patterns of behaviour.
• Recognizable in adolescence or earlier.
PERSONALITY DISORDERS 79
Table 6.1 ICD-10 and DSM-IV classification of personality disorders

ICD-10 DSM-IV
Cluster A
Paranoid Paranoid
Schizoid Schizoid
Schizotypal
Cluster B
Antisocial Dissocial
Emotionally unstable Borderline
Impulsive type Histrionic
Borderline type Narcissistic
histrionic
other specific (includes narcissistic)
Cluster C
Anxious (avoidant) Avoidant
Dependent Dependent
Anankastic Obsessive–compulsive
Pers. disorder unspecified Pers. disorder mixed
Pers. disorder NOS
Notes: Enduring change not attributable to gross brain damage or disease.

Affective (cyclothmic) pers. disorder, which was under this category in ICD-9, now categorized under Mood
Disorders.
Paranoid – pervasive mistrust, cold affect and hypersensitive.
Schizoid – social withdrawal, social discomfort, bland constricted affect, aloof and insensitive.
Schizotypal – eccentric, magical thinking, isolated, ideas of reference, illusions, tangential
communications. More common in relatives of patients with schizophrenia.
Dissocial – see Chapter 18.
Borderline – self detrimental impulsivity, unstable, intense relationships, intense affect, identity
confusion, shifts of mood, chronic anhedonia. Frequently co-morbid substance abuse, eating
disturbance, hypersexuality, self-mutilation. Prone to brief psychotic episodes (micropsychoses).
Histrionic – colourful, dramatic, superficial, unable to maintain deep relationships, self centred and dependent.
Narcissistic – self important, attention demanding, unable to empathize and exploitative.
Avoidant – shy, hypersensitive to rejection, socially withdrawn and low self-esteem.
Dependent – lacking in self confidence, requires others to assume responsibility and subordinates own needs to
those of others.
Obsessive–compulsive – perfectionistic, orderly, devoted to work and emotionally constricted.
• Continuing throughout most of adult life.

• The patient or others have to suffer.
• An adverse effect on the individual or society.
Particularly notable points are that great care must be taken in the diagnosis of per-
sonality disorder during an episode of another psychiatric disorder (e.g. affective dis-
order). Also, distinctions on the one hand from ‘normality’ and on the other from
chronic neurotic and psychotic disorders are not clear. Distinguish between behaviour
and personality.
Some regard ‘personality disorder’ as fundamentally a social diagnosis – the assign-
ment of a sick role to those whom society finds troublesome. This is a pejorative diag-
nosis, a diagnosis of despair (Lewis and Appleby, 1988).
There is a large overlap between PDs: 54 per cent of patients with DSM-III-PD met
criteria for another PD (Pfohl et al., 1986).
EPIDEMIOLOGY
PD rates are variable, and unreliable, being very dependent on sampling, assessment
and definition:
• General population – 10 per cent.
• Epidemiological Catchment Area (ECA) study – 6 per cent.
• A prison population – 20–80 per cent.
• Psychiatry outpatient attenders – 10–40 per cent.
• Primary care attenders – 7 per cent (one-third of those with ‘conspicuous’ psychi-
atric morbidity will have PD).
CLASSIFICATION AND MEASUREMENT
DIMENSIONAL APPROACHES
The trait approach (Cloninger, 1987) considers personality as a constellation of traits –
a set of dimensions along each of which any individual will vary. Differences between
normal and abnormal are viewed as quantitative.
The dimensional approach is also applied along psychiatric ‘continua’; e.g. schizo-
phrenic spectrum disorders, borderline spectrum.
Approaches may show overlap on psychobiological measures.
Typical assessments
These include (see Chapter 1):
• Catell Sixteen Personality Factor Test (16PF).
• Minnesota Multiphasic Personality Inventory (MMPI).
• Eysenck Personality Inventory (EPI).
CATEGORICAL (TYPOLOGICAL) APPROACH

Personality types are recognizable as consistent groupings of characteristics. This
approach is less theoretically sound, but intuitive, convenient, and widely used in clin-
ical practice. Early examples include:
• Hippocrates – choleric, phlegmatic, sanguine, melancholic.
• Kretschmer (1921) – endomorph (social, relaxed), ectomorph (restrained, aloof),
mesomorph (muscular, active).
• Schneider (1923) – 10 types of ‘psychopathic personality’.
• Henderson (1939) – ‘aggressive’, ‘creative’, ‘inadequate’ subtypes of psychopaths.
AETIOLOGICAL THEORIES
Theories are diverse. Many researchers tend to favour a specific theory, although the
biopsychosocial model may be a more appropriate and integrative approach.
PERSONALITY DISORDERS 81
PSYCHODYNAMIC THEORY
Defensive, non-adaptive personality patterns develop as a result of a disruptive early
environment. Under the personality dysfunctioning lies defective and infantile ego
functions (see Chapter 23); e.g. poor impulse control, defective object relations, intoler-
ance of affect, unstable identification and super-ego lacunae.
Borderline PD uses primitive defence mechanisms (splitting, projective identifica-
tion) which may result from pathological early object relations and difficulties at the
separation/individuation stage of development.
Reality testing is distorted by intense internal needs and conflicts, leading to habit-
ual distortion of thought, judgement and perception obvious to others but not the
individual.
Poor self-image is combined with infantile feelings of entitlement. Aggressive impulses
are poorly integrated, resulting in persistently disturbed relationships with others.
Such mechanisms develop as responses to early childhood relationships, and particu-
lar personality traits relate to particular disturbances of upbringing. Psychodynamic
development may be halted at a particular stage owing to environmental stress, or the
individual may regress to that stage under further stress later in life.
BEHAVIOURAL PSYCHOLOGY (SKINNER)

‘The self is a repertoire of behaviour appropriate to a given set of contingencies.’
Behaviour is shaped and maintained by its consequences. Personality is governed by
environmental forces.
GENETICS
Diagnostic imprecision causes difficulties. Central markers include serotonin dysreg-
ulation in sociopathy, borderline PD and impulse disorders, sleep and dysregulation
and eye-tracking abnormalities (see Chapter 3). Peripheral markers include platelet
MAO, DST suppression.
• Polymorphisms in the COMT gene are associated with anger-related traits
(Rujescu et al., 2003).
• An association has been shown between a functional promoter polymorphism in
the dopamine D2 receptor gene and detached personality trait, as seen in schizoid
or avoidant behavior (Jonsson et al., 2003).
• Criminality, social introversion, pattern of crime (sexual, violent criminal career)
have all been shown to have higher MZ concordance.
• Danish adoption studies:
– Biological father criminal – 21 per cent criminality in adoptees.
– Neither father criminal – 10 per cent criminality in adoptees.
– Both fathers criminal – 36 per cent criminality in adoptees.
• XYY individuals show evidence of increased criminality independent of low IQ
and socioeconomic status.
• XY individuals show greater aggression and greater reported/detected criminality
than XX.
• There is a prominent influence in schizotypal (see Chapter 3), antisocial PD (see
Chapter 18).
• Female criminals have higher genetic loading than males.

• Relatives of females with Briquet’s syndrome/somatization disorder have high
rates of antisocial PD.
SOCIOCULTURAL FACTORS
Social learning theory emphasizes personality traits of children derived from the
shaping influence of parents (direct reinforcement or modelling). Most likely this is a
complex interaction; e.g. match of temperament with parental expectations, subcul-
tural expectation.
TEMPERAMENT
The New York Longitudinal Study followed 133 subjects from infancy to adulthood.
Behaviour is said to consist of:
• Abilities (the ‘what’).
• Motivations (the ‘why’).
• Temperament (the ‘how’).
Nine categories of temperament are defined (e.g. biological rhythmicity, activity
level, mood, withdrawal, adaptability). Three temperamental constitutions are found:
• The easy child (40 per cent) – regular, positive, adaptable.
• The difficult child (10 per cent) – irregular, negative, not adaptable.
• The slow-to-warm-up child (15 per cent) – mildly negative, slow to adapt.
Temperament is partly governed by genetics, not by sex or parental attitudes
(except parental conflict, which related to early adult adjustment).
Continuity of temperament over time from infancy was very evident given stability
of the environment. The difficult child was most vulnerable to development of behav-
iour disorders. Optimal development depends on consonance between individual and
environment – ‘goodness of fit’.
DEVIANT CHILDREN GROWN UP

Children referred to a child guidance clinic were followed up at 30 years. Conduct-
disordered children were particularly likely to become sociopathic adults, with more
criminality, marital discord and occupational failure. Psychiatric disorders were also
more common. Severity and variety of conduct disorder were predictive.
NEGATIVE CHILDHOOD EXPERIENCES

Childhood sexual abuse (CSA), physical abuse and early separation or loss are associ-
ated with PD. However, these are non-specific risk factors; e.g. CSA is not a specific
risk factor for borderline PD.
Decreased ‘social integration’, by failing to provide containment for impulsivity,
may be related to PDs characterized by poor impulse control.
ASSESSMENT AND TREATMENT
Multidimensional
• Rule out any organic cause, such as focal or diffuse brain disorder, toxic or meta-
bolic disorder, seizure disorder.
• Rule out other or evaluate for co-morbid psychiatric disorder. Ensure that the
problem is persistent since adolescence, not episodic.
• Hospitalization is probably best avoided (brief if required for crisis such as
co-morbidity, suicidality/deliberate self-harm). The person may function better
in a partial hospitalization setting.
Pharmacotherapy
SSRI therapy decreases impulsivity in borderline personality and is useful for co-morbid
depression. Mood stabilizers are effective in managing mood lability, anger and aggres-
sion. Atypical antipsychotics are preferred for cognitive–perceptual disturbances.
Psychotherapy
There is some evidence for the role of dialectical behaviour therapy in deliberate
self-harm (DSH).
CAT therapy carries some weak evidence.
Group therapy may be more useful than individual for some PDs (not for paranoid
disorders).
PROGNOSIS
A 10- to 25-year follow-up of borderline PDs showed a range of outcomes:

• Suicide – 3–9 per cent (co-morbidity, depression)
• ‘Clinical recovery’/maturation out of behavioural difficulties – 50–60 per cent.
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Eating disorders 7
OBESITY
Obesity has been defined as a body mass index (BMI) above 30. In England, 17
per cent of males and 21 per cent of females are obese. It is the most common nutri-
tional disorder in the UK. There has been an alarming increase in the number of chil-
dren who are obese. Obesity is most common in lower social class, middle-aged
females.
Obesity is associated with an increased risk of cardiovascular disorders (MI, CVA,
hypertension), diabetes, cancer (breast, ovarian, colon), osteoarthritis, sleep apnoea
and accidents.
AETIOLOGY OF OBESITY
Basically, obesity results from food intake in excess of energy requirements.

• Emotional factors – Boredom, loneliness or stress may contribute to excessive food
intake.
• Environmental factors – There may be a more sedentary lifestyle due to techno-
logical advances. There is greater availability and consumption of energy-dense foods.
• Learned behaviour – Food is given by parents at times of stress, and guilt evinced if
the food is not taken.
• Organic – Organic causes are rare for extreme obesity: hypothyroidism,
hypopituitarism, hypoglycaemic attacks, hypothalamic damage (? ventromedial
nucleus).
• Molecular/genetic:
– Genetics are thought to account for 25–70 per cent of variations in bodyweight.
– Adoption studies support a genetic contribution to weight.
– Early-onset obesity is related to mutation in genes for leptin, leptin receptor,
prohormone convertase 1 and proopiomelanocortin (POMC).
– Abnormal hormonal regulation of neural circuits that control food intake and
energy expenditure appear to be involved in obesity.
ANOREXIA NERVOSA (AN) 87
MANAGEMENT OF OBESITY
Diet
A calorie-controlled diet to decrease energy balance by 500–600 kcal/day will result in
weight loss of about 0.5–1.0 kg/week. Numerous types of diets exist, but there is a high
relapse rate associated with dieting alone.
Psychotherapy
Group psychotherapy may be particularly helpful. Marital therapy may be necessary
to alter family patterns. Ultimately, management may require inpatient supervision in
a therapeutic milieu.
Behaviour therapy
Self-monitoring is the key to behaviour therapy. Regulation of environmental cues
for eating, alteration of eating behaviour and self-reinforcement in weight loss
(also group reinforcement, e.g. ‘Weight Watchers’) has proven effective. Cognitive fac-
tors are important: guilt and feelings of failure are common, so attempt to reduce
these.
Drug therapy
Orlistat (inhibits fat absorption by inhibiting lipase) and sibutramine (enhances sati-
ety via noradrenergic/serotonin reuptake inhibition) show effectiveness in promoting
weight loss.
Surgical therapy
Surgery is generally limited to those with morbid obesity (BMI ⬎ 40). Gastric bypass,
gastric banding, and vertical banded gastroplasty are effective in providing sustained
long-term weight loss.
ANOREXIA NERVOSA (AN)
EPIDEMIOLOGY OF AN
• Anorexia nervosa is the third most common chronic illness in teenage females
(Lucas et al., 1991).
• Annual incidence:
– 14.6/100 000 for females.
– 1.8/100 000 for males.
– Unclear whether incidence is increasing – some increase suggested for 15- to
24-year age-group.
• Prevalence – 0.5–3.7 per cent in adolescent/early adult females. There are higher
rates in certain groups; e.g. ballet dancers, gymnasts.
• AN is over-represented in higher social classes (I & II).
• 90 per cent of females have onset within 5 years of menarche.
• Seasonal pattern of onset (maximum May)?
88 EATING DISORDERS
Table 7.1 Predisposing factors for AN

Predisposing factors Precipitating factors Perpetuating factors
Individual Leads to dissatisfaction with Dieting to feelings of Starvation symptoms

Familial body weight and shape self-worth and control and reactions from others
Cultural
Adapted from Garner (1993).
Adverse life effects are more evident in ‘late onset’ (⬎25 years) AN. Eighty-four
per cent of AN patients have a lifetime diagnosis of another psychiatric disorder
(Halmi et al., 1991), with major depression in 68 per cent of patients.
AETIOLOGY OF AN
The aetiology is multifactorial (see Table 7.1).
Psychological factors
There are inconsistent data on personality disorder – high rates of avoidant personality
have been described. A specific association with childhood sexual abuse is overestimated.
• Body image disturbance is a core feature – body shape misperception or
disparagement.
• Morbid fear of fatness, pursuit of thinness, weight phobia – body thinness is viewed
as a cognitive construct equated with self-worth and control. Twenty-five per cent
of AN patients are overweight before onset.
• Psychodynamics – regression to the ‘prepubertal’ state; fear of becoming a sexual-
ized adult; fixation at the oral (pregenital) stage.
Familial factors
There are high rates of psychiatric illness – particularly depression, alcoholism,
psychosexual disturbances and obsessive–compulsive disorder (OCD) in mothers
(Halmi et al., 1991).
Earlier descriptions emphasize the family as the site of pathology: a dominant, intru-
sive mother; a passive, ineffectual father; an enmeshed, overprotective, rigid family struc-
ture with conflict avoidance. It is unclear whether these characteristics are cause or effect.
Twin studies affirm genetic and non-genetic environmental contributions.
Cultural factors
• The western ‘thinness-conscious’ culture.
• Role conflict – changing expectations for and by women.
• Food as a form of communication.
Biological factors
• Familial aggregation – association with (unipolar) depression may suggest genetic
predisposition.
ANOREXIA NERVOSA (AN) 89
Table 7.2 Medical complications and laboratory abnormalities in AN
Neurological ‘Pseudoatrophy’ on brain-imaging, EEG abnormalities and seizures; peripheral neuritis;

anatomic dysfunction
Cardiovascular Bradycardia; hypotension; decreased heart size; QT prolongation; arrhythmias; oedema
Metabolic Dehydration hypoglycaemia, hypercholesterolaemia; ↑ plasma amylase, ↑ liver function
tests; ↓ plasma proteins (oedema) ↓ K+, ↓ Mg2+, ↓ CA2+, ↓ phosphate
Endocrine ↑ GH, cortisol (positive dexamethasone suppression test) ↓ gonadotropin, oestrogens,
testosterone ↓ T3 (sick euthyroid syndrome)
Haematological Normochronic, monocytic or iron-deficient anaemia, leucopenia, relative lymphocytosis,
hypocellular marrow
Gastrointestinal Swollen salivary glands; dental caries, erosion of enamel (vomiting), delayed gastric
emptying; acute gastric dilations (bulimic episodes, vigorous refeeding, constipation;
acute pancreatitis
Renal Partial diabetes insipidus; pre/acute/chronic renal failure
Musculoskeletal Osteoporosis, stress fractures; stunted growth; muscle cramps
Other Hypothermia, bacterial infections (TB, staph), lanugo (hair on trunk); normal secondary
sexual hair pattern unaffected; low birthweight, ↑ miscarriage and congenital malforma-
tion, perinatal mortality if patients conceive before complete restoration of weight
• Twin studies – MZ:DZ ⫽ 54%:9%.

• Neurochemical abnormalities have been postulated:
– Deficiency in serotonin may contribute to blunted satiety responses.
– 5-HT abnormalities persist even after weight restoration (Kaye et al., 1991).
– Cholecystokinin (CCK) may also cause dysregulation of satiety.
– Abnormalities in hypothalamic–pituitary–gonadal axis (see Table 7.2) also are
implicated.
– Blunted prolactin (5-HT mediated).
– Response to D-fenfluramine challenge (Monteleone et al., 2000).
However, neurochemical hypotheses are difficult to establish, since many of the
abnormalities may reflect secondary effects of starvation.
CLINICAL FEATURES AND DIFFERENTIAL DIAGNOSIS OF AN
These are described in current diagnostic criteria (see Table 7.3).
Differential diagnosis
• Psychiatric – depression, schizophrenia, OCD, psychotic disorder.
• Medical – hypopituitarism, thyrotoxicosis, diabetes mellitus, neoplasia, reticulosis,
malabsorption.
MANAGEMENT OF AN
General principles
• Use a multifaceted approach (APA, 2000; Royal College of Psychiatrists, 2000):
– Detect and treat medical complications.
– Encourage a ‘normal’ balanced diet to regain ‘normal’ weight.
– Educate about diet and exercise.
90 EATING DISORDERS
Table 7.3 IDC-10 and DSM-IV diagnostic criteria for anorexia nervosa
ICD-10 DSM-IV
1. Bodyweight ⭐15% of expected Quetelet’s A. Refusal to maintain bodyweight ⭓ minimal normal

body-mass index ⭐17.5 (weight (kg)/[height (m)]2) weight for age and height
2. Self-induced weight loss B. Intense fear of fatness
Avoidance of ‘fattening foods’ ⭓1 of: C. Body-image disturbance
– self-induced vomiting D. Amenorrhoea in post-menarchal females
– self-induced purging Subtypes: restricting, binge eating/purging
– overexercising
– misuse of diuretics/stimulants
3. Body image distortion
Dread of fatness a persistent ‘overvalued’ idea
4. Abnormalities of hypothalamic–pituitary–gonadal axis
Amenorrhoea; ↓ libido, decreased potency in males
↑ GH, cortisol; ↓ T3
5. If onset is prepubertal, this sequence of pubertal
events is delayed
Behavioural approaches
• Encourage a regular diet (3000 kcal daily) to attain 1.5 kg weekly weight gain;
smaller intake if severe weight loss (tube or IV feeding rarely necessary); restora-
tion to at/near ideal bodyweight as target – i.e. body mass index of 20–25.
• Nurse supervision during and after meals helps to avoid surreptitious vomiting,
disposal of food and/or over-exercising.
Psychological approaches
Cognitive–behavioural therapy (CBT), psychoanalytic psychotherapy and family
therapy are effective in producing weight gain (Dare et al., 2001).
Education: dietary, exercise; body function/sexual and psychological maturation;
life skills support.
Pharmacological approaches
There is a limited role. Atypical antipsychotics have been shown to result in weight
gain. Antidepressants and anxiolytics can be given as clinically indicated. SSRIs may be
beneficial.
PROGNOSIS FOR AN
The prognosis is generally poor. There are high drop-out rates from treatment, and no
consistent evidence that treatment clearly alters outcome.
One 20-year follow-up (Zipfel et al., 2000) showed:
• 50.6 per cent recovered.
• 10.4 per cent still had DSM-IV criteria.
• 15.6 per cent died.
There is a high mortality from complications of AN, including suicide. Even ‘recov-
ered’ anoretics show psychopathology.
BULIMIA NERVOSA (BN) OR ‘DIETARY CHAOS SYNDROME’ 91
Factors indicating poor prognosis

• Older age at onset.
• Premorbid obesity.
• Illness duration ⬎6 years.
• Personality disturbance.
• Bulimic behaviour.
• Male gender.
BULIMIA NERVOSA (BN) OR ‘DIETARY CHAOS SYNDROME’
Note that a further category has been proposed in DSM-IV – ‘binge-eating disorder’:
• Recurrent distressing episodes of uncontrolled overeating.
• Not satisfying the diagnostic criteria for BN.
It is unclear whether this group differs in pathophysiology, treatment outcome, etc.
EPIDEMIOLOGY OF BN
• 80 per cent of US students have reported binge eating.

• Bulimia nervosa affects 4 per cent of female adolescents.
• Peak onset is later than for AN – late adolescence or early 20s.
• A history of longstanding dietary difficulties is common.
• BN is more common than AN. About 30 per cent of BN cases have a prior history
of AN.
AETIOLOGY OF BN
This is multifactorial; factors are similar to those in AN (see above).
Psychological factors
• There are high rates of depression/dysphoria, alcohol abuse, personality distur-
bance (borderline, labile).
• There is poor self-esteem and sense of personal control.
Familial factors
There are high rates of psychiatric disturbance, particularly depression.
Cultural factors
As for AN (see above).
Biological factors
• Twin studies – MZ:DZ ⫽ 22%:9%.
• Serotonin dysfunction is more extensively studied in BN:
– Deficits in CSF 5-HIAA persist after treatment.
– Blunted GH response to D-fenfluramine challenge.
92 EATING DISORDERS
Table 7.4 ICD-10 and DSM-IV criteria for bulimia nervosa

ICD-10 DSM-IV
1. Persistent preoccupation with eating; craving A. recurrent episodes of binge eating

for food; episodes of overeating
2. Attempts to counteract the ‘fattening’ B. recurrent inappropriate compensatory behaviour to
effect of food by ⭓1 of: prevent weight gain
– self-induced vomiting C. A and B occur for ⭓ twice weekly for 3 months
– alternate periods of starvation
– purgative abuse
– diuretic/stimulant misuse
3. ‘Morbid dread of fatness’
• Dopamine abnormalities also found – ↓ CSF HVA.

• CCK also is implicated in dysregulation of appetite in BN.
CLINICAL FEATURES OF BN
See Table 7.4.

• Patient has a defined weight threshold.
• In contrast to AN, weight may be normal (typical bulimia nervosa – F50.3, ICD-10).
• Body-shape disturbances are somewhat less prominent in BN.
• There are similar medical and psychiatric complications to AN. Medical complica-
tions are generally less frequent or severe.
MANAGEMENT OF BN
As with AN, the approach is multifaceted. Most are treated as outpatients. The criteria
for hospitalization are similar to AN (see above).
Psychological approaches
• Psychoeducation, nutritional counselling, relaxation training are all used.
• CBT:
– Intensive, weekly over 5 months.
– Many components include self-monitoring (diary-keeping).
• Self-reporting – establish cognitive and behavioural strategies to alter low frustra-
tion tolerance, poor impulse control, negative self-concept, poor recognition and
identifications of emotions.
• CBT is more effective than interpersonal therapy (Agras et al., 2000).
• CBT is most effective for attitudes to weight and shape.
• CBT is more effective in the short term than antidepressants. A combination of
CBT and antidepressants may be best.
• Group psychotherapy can be used. Family therapy also is helpful, where clinically
indicated. Self-help and support groups are beneficial.
Pharmacological approaches
SSRI antidepressants are effective independent of mood status, at dosages similar to
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PROGNOSIS FOR BN
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Human sexuality 8
NORMAL BEHAVIOUR
EPIDEMIOLOGY
Kinsey et al. (1948, 1953)

• 93 per cent of men and 28 per cent of women masturbated by age 20.
• Males show peak of sexual activity in late adolescence.
• Women show peak of sexual activity in their 30s.
• 75 per cent of males achieve orgasm within 2 minutes of penetration.
• Recent US studies show 45–90 per cent of adolescent males and 25–40 per cent of
adolescent females masturbate.
Johnson et al. (2001)

UK survey 1999–2001.
• 29.8 per cent of males, 21.1 per cent of females reported having two or more het-
erosexual partners within previous year of study (51.9 per cent of males, 38.7 per
cent females in 16–24 age-group).
• 5.4 per cent males had a history of having had a homosexual partner (10.5 per cent
males in London).
• 2.0 per cent males, 0.6 per cent females reported ever injecting illicit drugs.
Centers for Disease Control and Prevention (2002)

US high school survey 1991–2001.
• 42.9 per cent of females, 48.5 per cent of males had experience with sexual
intercourse.
• In general, teens are less sexually active and more likely to use condoms since 1991.
• A 16 per cent decrease in sexual experiences among high school students.
• A 24 per cent decrease in multiple sex partners.
SEXUAL DYSFUNCTIONS 97
PHYSIOLOGY
Masters and Johnson (1966) and Kaplan (1978)

Phases of response cycle:
• Desire – affected by personal, social, cultural, hypothalamic and hormonal factors.
• Arousal – excitement, mediated by parasympathetic nervous system. Genital vaso-
constriction leads to erection in male or swelling and lubrication in female.
• Plateau – maintenance of arousal state.
• Orgasm – emission, in male only. Ejaculation or, in female, ejaculatory equivalent.
Both mediated by sympathetic nervous system.
• Resolution – with a longer refractory period in the male (can be 24 hours if over 60
years) and very short refractory period in the female (allowing for multiple orgasms).
NEUROPHYSIOLOGY
• Exact mechanism of orgasm unknown.
• Dopaminergic effects result in increased sexual activity. Antidopaminergic drugs
cause decreased sexuality and impotence.
• Noradrenergic effects (␣2 receptors) reduce sexual activity.
RELATIONSHIP BEHAVIOUR
Consider:
• Communication – within the relationship.
• Commitment – to the relationship.
• Conflict – within the relationship.
• Context – of the sexual encounter (culture, personal, surroundings).
SEXUAL DYSFUNCTIONS
See Table 8.1.
DEFINITIONS
Male
• Erectiled dysfunction (‘impotence’) – inability to sustain an erection adequate for
penetration. Commonest disorder presenting in males at clinic.
• Ejaculatory impotence – inability to ejaculate despite adequate erection. Uncommon.
• Premature ejaculation – ejaculation before, during or immediately after penetration.
Usually in young men. Common.
Female
• Anorgasmia (‘frigidity’) – orgasm achieved rarely or never.
• Vaginismus – involuntary contraction of vaginal introitus in response to attempts
at penetration.
98 HUMAN SEXUALITY
Table 8.1 ICD-10 and DSM-IV classification of sexual disorders

ICD-10 DSM-IV
Sexual dysfunction Sexual desire disorders

Lack of sexual desire Hypoactive sexual desire
Sexual aversion/lack of enjoyment Sexual aversion
Sexual arousal disorders
Failure of genital response Female sexual arousal disorder
Male erectile disorder
Orgasm disorders
Orgasmic dysfunction Female orgasmic disorder
Male orgasmic disorder
Premature ejaculation Premature ejaculation
Sexual pain disorder
Non-organic vaginismus Vaginismus
Non-organic dyspareunia Dyspareunia
Excessive sexual desire
Sexual dysfunction due to general medical condition
Substance-induced sexual dysfunction
Disorders of sexual preference Paraphilias
Exhibitionism Exhibitionism
Fetishism Fetishism
Fetishistic transvestism Transvestic fetishism
Paedophilia Paedophilia
Sadomasochism Sexual sadism
Sexual masochism
Other disorders of sexual preference Voyeurism
Paraphilia NOS (necrophilia, zoophilia, etc.)
Sexual disorders NOS
Gender identity disorders Gender identity disorders
Transsexualism Gender identity disorder
Dual-role transvestism Gender identity disorder NOS
Gender identity disorder of childhood
Other gender identity disorders
Psychological and behavioural disorders associated
with sexual development and orientation
Either sex
• Low sex drive.
• Dyspareunia – pain on intercourse.
CLASSIFICATIONS
Can be classified as:
• Primary or secondary; i.e. no history of normal function or onset later in life after a
period of normal functioning.
• Symptomatic or functional; i.e. due to organic or psychological cause.
Can be further classified as:
• Acute or insidious onset.
• Total or partial.
• Global or situational.
– or according to stage affected (see Table 8.2).
Table 8.2 Classification of dysfunction according to stage affected

Stage Male Female
Initiation Avoidance, low drive

Arousal Premature ejaculation Lubricative failure
Erectile impotence
Penetration Lack of urge to penetrate Vaginismus
Orgasm Ejaculatory impotence Anorgasmia
ASSESSMENT
AIMS OF ASSESSMENT
1 To define the dysfunction.
2 To assess whether it is organic, functional or both. Often a mild dysfunction due to
organic causes (e.g. diabetes mellitus) can lead to ‘performance anxiety’, and thus to
a much worse ‘functional’ disorder.
3 To determine the immediate causes.
4 To assess the couple’s resources and motivation.
5 To decide on the correct management and likely prognosis.
Always see the sexual partner; see both partners together also if possible.
The problem
• Exact nature of problem, precise examples sought.
• Frequency and timing of dysfunction.
• Total or partial? If partial, seek situational circumstances.
• Any sign of normal function, e.g. morning erections in male.
• Mode of onset: acute or insidious, primary or secondary?
• Duration of problem.
• Course of problem: constant or fluctuating?
Current influences
• Environmental conditions: sexual stress, relationship with partner, other stresses,
timing and setting of sexual encounters.
• Personal variables: sexual knowledge and experience, emotional reaction (guilt,
anxiety), cognitive avoidance, contraceptive habits, fear of conception.
• Organic condition: important in only about 10 per cent presenting to a psych-
iatrist. Age is often an important factor.
• Consequences of problem: avoidance of intercourse, partner’s reaction.
Resources
• Personal resources: motivation, honesty, flexibility, ability to verbalize, history of
sex drive.
• Sexual relationship: commitment, willingness to be involved in treatment, conflict.
In 30 per cent, both partners have dysfunctions.
• Professional resources: time and personnel available to treat the disorder.
100 HUMAN SEXUALITY
PROGRAMME OF ASSESSMENT
History
• Take a full history of the complaint: look for precise diagnosis, indication of aetiology
and prognostic signs.
• Family background and personal history: parental relationships, attitude to sex.
• Sexual and marital history: degree of sexual knowledge, past sexual experiences,
relationship with sexual partner, contraceptive methods, children, attitudes to
pregnancy.
• Drug and alcohol abuse.
Examination
• Assess mental state: depression, anxiety.
• Physical examination, including genitalia.
Investigations
Physical investigations may be indicated, particularly with impotence and if there is
total absence of any sign of erection in a man with previously normal sexual history.
Include urinalysis for sugar, liver function tests, testosterone level. The nocturnal penile
tumescence strain gauge is a useful diagnostic tool.
Intersexual disorders:
• Virilizing adrenal hyperplexia (adrenogenital syndrome) – commonest female

intersex disorder, autosomal recessive, XX genotype, excess of androgens from in
utero.
• Turner’s syndrome (X genotype) – see Chapter 20. Usually assigned as females
because of female-looking genitalia.
• Klinefelter’s syndrome (XXY genotype) – males with low androgen production,
rudimentary sex organs.
• Testicular feminization syndrome (Y genotype) – X-linked recessive, end-
organ insensitivity to androgens; assigned as females because of female-looking
genitalia.
• Enzymatic disorders (5␣-reductase deficiency; 17 hydroxysteroid deficiency) – low
testosterone results in ambiguous genitalia and female habitus; assigned as
females.
• Hermaphroditism – true hermaphrodite (46XX or 46XY) is rare, possesses both
testes and ovaries; pseudohermaphroditism usually results from endocrine or
enzymatic defect in person with normal chromosomes; gender assignment accord-
ing to morphology or genitalia.
AETIOLOGY
Previous experiences
• Restrictive upbringing leading to intrapsychic conflict.
• Traumatic early sexual encounters.
• Abnormal family relationships.
Current circumstances
• Sexual stresses (e.g. concerning contraception or pregnancy).
• Non-sexual stresses (e.g. lack of privacy, recent childbirth).
• Relationship difficulties (e.g. partner rejection, sexual sabotage).
• Ignorance or guilt resulting in failure to engage in effective sexual behaviour.
• Psychiatric disorder (e.g. depression, schizophrenia with sexual delusions).
• ‘Performance anxiety’ – fear of failure arising from demand for performance by
partner or excessive need to please partner.
• ‘Spectatoring’ – observing own behaviour and not allowing automatic responses
or recognizing erotic sensations.
Organic factors
An organic cause of impotence is suggested by:
• Penis never fully turgid/generalized dysfunction (i.e. not situational).
• No associated significant life event.
• Previous uninterrupted period of normal sexual function.
• Sexual interest being maintained.
Age
Erectile dysfunction increases dramatically with age: 0.1 per cent under 20 years;
7 per cent 40–50 years; 75 per cent over 70 years.
General illness
• Endocrine – diabetes mellitus, thyroid disorder, HPA axis disorder.
• Cardiovascular – atheromatous, Leriche’s syndrome, heart failure.
• Hepatic – cirrhosis.
• Renal/urological – Peyronie’s disease, hydrocele, varicocele, renal failure.
• Others – respiratory failure, intersex disorders, congenital (severe) hypospadias.
Local disorders
Look for urethritis, balanitis, penile or vaginal trauma, chordee, castration, radical
surgery (prostatectomy, colostomy, etc.).
Drugs
• Decreased libido – antipsychotics, antiandrogens, antidepressants (most varieties
but SSRIs least likely); alcohol increases libido acutely but libido reduces with
chronic misuse.
• Impaired erection – antipsychotics, antidepressants, beta-blockers.
• Priapism – may occur with antipsychotics.
• Impaired ejaculation – antipsychotics, antidepressants.
• Hyperprolactinenia – secondary to antipsychotic therapy causes amenorrhoea in
females; sometimes also breast engorgement/galactorrhea.
TREATMENT OF SEXUAL DYSFUNCTION
Attend to any organic cause, if possible, but only 10 per cent of cases of impotence
presenting to psychiatrists (and a much lower proportion of other dysfunctions) have
102 HUMAN SEXUALITY
an organic cause, and this is often not reversible. Psychological factors almost always
play an important part, and these can be treated.
Behaviour therapy
This is the treatment of choice. ‘Masters and Johnson’ techniques are used. It is short-
duration, symptom-focused therapy, seeing the couple together after initial individual
interviews.
The aim is to reduce performance anxiety, reduce spectatoring and reduce the pressure
of sexual demands on the self and from the partner. Autonomic responses (erection,
orgasm, etc.) are not concentrated on. Instead, increased pleasure and confidence and
reduction of anxiety are aimed at, with the presumption that normal sexual activity
will follow.
Therapy may be performed intensely every day for 2 weeks, but under the NHS
weekly therapy sessions for 6–10 weeks are more common and almost as successful.
Sequence of therapy
1 Supply and discuss sexual information (anatomy, physiology, partner discord, erro-
neous beliefs).
2 Direct attempts to modify attitudes by explanation, by sanctioning behaviour, etc.
3 Establish effective communications, assumption of joint responsibility.
4 Explain ‘giving to get’ (i.e. mutual exchange of rewards).
5 Define and discuss precise goals of therapy.
6 Clear sexual assignments are given, explained and discussed (‘homework’). Couple
set aside a time each day for these and report back.
7 Homework starts with ‘non-demand pleasuring’ (or ‘sensate focus technique’).
Prohibit coition for the first week or more. Couple take turns in caressing each other,
avoiding genital areas initially. This is discovery of what is pleasurable, mutual
enhancement of non-orgasmic sexual pleasure, without being concerned about erec-
tions, orgasms or performance. This is therefore a form of desensitization.
8 Discuss resistances, guilt and anxieties when reporting back in therapy sessions.
Couple progress from caressing non-sexual areas (back, legs, etc.) to caressing sex-
ual areas (breasts, vulva, penis), but not aiming at orgasm or penetration.
9 Progress is made to specific techniques as appropriate:
– Erectile impotence – gradual introduction of penis with female superior or side
by side. Then male relaxes and enjoys it. Instruction given to focus on erotic sensa-
tions and stop rationalizing (‘get out of your head and into your body’). May
proceed to extravaginal orgasm before finally achieving intravaginal orgasm.
– Ejaculatory impotence – vigorous penile stimulation with lotion or cream, grad-
ually bringing penis nearer to vagina and continuing stimulation as inserted.
– Premature ejaculation – Seman’s technique. Female squeezes base of penis or
glans as orgasm approaches (initially extravaginally, then intravaginally), thus
preventing ejaculation, and then proceeds to arousal again. May be repeated
several times before ejaculation is allowed.
– Vaginismus – relaxation training, gradual approach to intercourse as for erectile
impotence. Vaginal dilators may be used initially.
– Anorgasmia– masturbation, use of vibrators, gradual progress to coitus with clit-
oral stimulation.
PARAPHILIAS 103
Drug and physical therapies

Modern treatments include:
• Oral phosphodiesterase type 5 inhibitors: sildenafil, vardenafil, tadalafil – caution
with heart disease.
• Intracavernosal penile injections (effect lasts 1–2 hours) of prostaglandin E1.
• Penile prosthetic implants.
• External vacuum devices.
• Penile surgery – microrevascularization, penile vein ligation.
• Hormone replacement – testosterone.
Psychotherapy
It is rarely useful to enter into prolonged analytic therapy unless sexual dysfunction is
part of an extensive neurotic or personality problem. Broader marital therapy sessions
may be indicated.
PROGNOSIS FOR SEXUAL DYSFUNCTION
Good prognosis is indicated by:

• Previously normal sexual function.
• Acute onset.
• Short duration of dysfunction.
• High motivation.
• Involved, motivated partner.
• Absence of other psychological problems.
• Marked improvement in first few therapy sessions.
Cure rates with behavioural therapy (Masters and Johnson):
• Primary impotence – 50 per cent.
• Secondary impotence – 70–80 per cent.
• Premature ejaculation – 100 per cent.
• Female dysfunction – 80 per cent.
These figures are from uncontrolled series and may be over-optimistic.
PARAPHILIAS
EXHIBITIONISM
Exhibitionism is deliberate exposure of genitalia by an adult male in the presence of

an unwilling female and not as a prelude to sexual intercourse. ‘Indecent exposure’ is
the criminal offence.
Victims are usually strangers, especially pubertal girls. Exposure is often regarded
by the victim as a nuisance rather than a danger. Reaction of the family is often worse
than the victim’s own reaction and may lead to greater disturbance in the victim.
No personality difference is found between those exposed to and those not.
104 HUMAN SEXUALITY
CLASSIFICATION (ROOTH, 1971)

• Type 1 – 80 per cent of cases. Inhibited young men, emotionally immature, strug-
gle against the impulse, usually expose flaccid penis, feel guilty afterwards. Good
prognosis.
• Type 2 – 20 per cent of cases. Sociopathic personality, expose erect penis, often
masturbate while exposing, little guilt, may take sadistic pleasure. Worse prognosis.
EPIDEMIOLOGY
• Commonest single sexual offence.
• 3000 convictions per year in England and Wales.
• Peak age of onset is 15–25 years.
• Incidence in persons under 25 years has doubled since 1945.
• 75 per cent are under 40 years.
• 5 per cent are subnormal or psychotic.
• Personality factors – immature, passive, obsessional if type 1.
• Enjoyment of risk taking.
• Dissociative behaviour in response to stress or depression.
• Witness response (fear or disgust) may reinforce behaviour.
• Often poor sexual performance – with impotence or premature ejaculation and
increased masturbation.
• Possibly close ambivalent relationships with mother and poor distant relationship
with father.
MANAGEMENT
The first court appearance is often sufficient deterrent. Psychiatric management is
suggested if there has been more than one offence:
• Aversive behavioural techniques (e.g. covert sensitization).
• Group therapy with other exhibitionists may be helpful.
• Injections with antiandrogen compounds – long-acting agonists of luteinizing
hormone-releasing hormone – may help control sexual impulses.
PROGNOSIS
Good: 80 per cent only offend once.
Poor prognostic indicators (type 2)

• Exposure to children aged under 10.
• Previous convictions for other offences.
• Attempt to contact victim physically.
• Late onset associated with psychosis or brain damage.
Good prognostic indicators (type 1)

• Stable personality.
• Regular work record.
PARAPHILIAS 105
• Heterosexual relationship.
• Sympathetic wife.
PAEDOPHILIA
Paedophilia is defined as erotic attraction to prepubescent children. There are no

accurate data available on prevalence. Fifty per cent are relatives or friends of the tar-
get child. Seventy per cent of children participate actively.
Characteristically there are three groups of offenders:
• Immature adolescents.
• Middle-aged men with marital difficulties.
• Elderly, socially isolated men.
INCEST
Characteristically there are three types of incestuous father:

• Endogamic – confining all his sexual and social activities to his family. Often yearn-
ing for a sexually inaccessible person.
• Paedophilic – and hence attracted to daughters.
• Promiscuous – ignores sexual taboos, part of general hedonism.
TRANSVESTISM
Transvestism is a disturbance of general role behaviour – i.e. cross-dressing. It is not a

disorder of core gender identity. Transvestism is not itself an offence, though the per-
son may be charged with ‘behaviour likely to cause a breach of the peace’ or with theft
of women’s underwear.
EPIDEMIOLOGY
There are possibly 30 000 transvestites in the UK. Fifty per cent are married. Thirty-
five per cent of men are homosexual (most of women are homosexual). Fifteen per
cent are permanent cross-dressers.
Transvestism is most common in social classes II and III.
CLINICAL FEATURES
• Usually evident before age 10.
• May develop increasingly prominent female interests.
• May use female clothing for fetishistic masturbation.
• Older transvestites often belong to clubs and act socially as females.
106 HUMAN SEXUALITY
TRANSSEXUALISM
Transsexualism is disturbance of the core gender identity, usually a biological male who
is convinced that he is female. It is not itself an offence, but the person may be charged
with ‘breach of the peace’.
CLINICAL FEATURES
• Many have been fetishistic transvestites before becoming fully transsexual and
homosexual in orientation.
• Usually convinced of ‘wrong sex’ before age 8.
• Often has poor work record, difficulty in forming relationships, low sex drive.
MANAGEMENT
Transsexualism tends to be intractable, but the person may fluctuate in the desire for
sex-change surgery. Surgery should be postponed until the person has lived as the
opposite-sex person for 2 years.
Pre- and post-surgical counselling is necessary. Success is related to premorbid per-
sonality, acceptance of surgical limitations, effectiveness and motivation to maintain
opposite-sex lifestyle.
Hormone therapy is mainly of cosmetic benefit.
HOMOSEXUALITY
Gender identity appears to be established by age 3 years, in most in response to social

factors – sex assignment and rearing. Gender constancy is acquired later and may also
reflect social factors.
Homosexuality is not regarded as a psychiatric disorder. However, conflict arising
from homosexuality may precipitate psychiatric ill-health:
• Interpersonal problems in relationship(s) – as with a heterosexual relationship.
• Sexual dysfunction – behavioural approaches as in heterosexual therapy may
be used.
• Psychiatric ill-health – depression, anxiety, etc. Counselling, psychotherapy and
pharmacotherapy may be used as appropriate.
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Alcohol dependence 9
ICD-10 AND DSM-IV
ICD-10 and DSM-IV emphasize a spectrum of psychological and physical effects:
• Alcohol abuse.
• Alcohol dependence (see Chapter 10 for definition).
• Alcohol intoxication.
• Alcohol withdrawal.
• Alcohol delirium.
• Alcohol persisting dementia.
• Alcohol persisting amnestic disorder.
• Alcohol psychotic disorder – with delusions or with hallucinations.
• Alcohol mood disorder.
• Alcohol anxiety disorder.
• Alcohol sexual dysfunction.
• Alcohol sleep disorder.
EPIDEMIOLOGY OF DEPENDENCE
National Institute on Alcohol Abuse and Alcoholism (NIAAA) (2000) guidelines for
safe use of alcohol:
• Men – two drinks per day.

• Women – one drink per day.
• Men and women older than 65 years – ⭐1 drink per day.
• Standard drink (USA) ⫽ 12 g of alcohol:
– one 12 oz bottle of beer (4.5 per cent strength);
– one 5 oz glass of wine (12.9 per cent);
– 1.5 oz of 80-proof distilled spirits.
110 ALCOHOL DEPENDENCE
Table 9.1 SAMHSA 2002 National Survey in USA

Use of alcohol in age groups Previous month (%) Previous year (%)
12–17 years 17.6 34.6

18–25 years 60.5 77.9
26–34 years 61.4 77.9
35 ⫹ years 52.1 66.1
Table 9.2 Per capita consumption of alcohol (litres of pure alcohol) by country
Country 1997 1998 1999 2000
Romania 11.4 13.3 12.2 12.3

Rep. Ireland 9.7 9.7 11.0 10.8
France 10.9 10.8 10.7 10.5
Germany 10.8 10.6 10.6 10.5
UK 8.2 8.0 8.4 8.4
Russia 7.5 8.1 8.7 8.1
USA 6.6 6.6 6.7 6.7
Japan 6.4 6.5 6.6 6.5
Adapted from NTC Publications (2002). World Drink Trends. NTC Publications Ltd,
Henley-on-Thames, UK.
General surveys
See Table 9.1 for results of a national survey in the USA, and Table 9.2 for per capita
consumption in various countries.
The National Center for Social Research (2002) survey among secondary school
pupils in England showed that 4 per cent of 11- to 15-year-olds used alcohol in the
previous week.
Hospital/practice surveys
Thirty per cent of patients in general health care have alcohol-related disabilities.
Hospital admission rates

• 25 per cent of emergency hospital admissions in England and Wales are attribut-
able to excessive alcohol consumption.
• Alcoholism accounts for 10 per cent of all psychiatric admissions in the UK.
• 7.9 per cent of the US population needed treatment for an alcohol problem
in 2002.
Prevalence among specific groups

• There has been a disproportionate rise in females – 6 per cent have alcohol-related
disabilities.
• There has been a rise in adolescent drinking – 4 per cent of US high school
students abuse alcohol daily.
• 35 per cent of homeless have alcohol disorders.
• In the elderly, alcohol abuse is surreptitious and effects more marked.
• 4–6 per cent of the medical profession abuse alcohol.
EPIDEMIOLOGY OF DEPENDENCE 111
Table 9.3 Odds ratios for co-morbid diagnoses

Co-morbid diagnosis Odds ratio
Antisocial personality 21.0

Drug dependence 11.2
Mania 6.2
Schizophrenia 4.0
Panic disorder 2.4
Major depression 1.7
Adapted from Helzer and Pryzbeck (1991).
Co-morbidity
Forty-seven per cent of alcoholics meet criteria for another psychiatric disorder (see
Table 9.3).
Curran et al. (2003) measured co-morbid substance use disorders in emergency
room patients who had a primary psychiatric diagnosis and found the following
rates:
• Schizophrenia – 16.1 per cent.

• Bipolar – 15.6 per cent.
• Depression – 17.3 per cent.
• Anxiety – 5.7 per cent.
Age and sex

The age of onset of alcoholism is in the late teens or 20s for males. The course is often
insidious. Recognition of alcohol dependence is often not until the 30s.
Onset is later in females. They are more likely to drink alone, delay seeking treat-
ment, have higher rates of co-morbid depression, stronger genetic predisposition to
alcoholism and more physical complications – especially cirrhosis.
• Overall sex ratio – male:female ⫽ 4:1.

• Higher rates are in urban areas.
• Marital status – often divorced or separated.
• Social class – lowest prevalence in ‘middle’ social groups.
High-risk occupational groups

• Those who manufacture or sell alcohol.
• Commercial travellers, frequent overseas travellers.
• Entertainers, doctors, journalists.
Permissive factors include job mobility, with absence of restraining structures of

home/regular workplace; absence of supervision at work; ready availability of alcohol.
Ethnic factors
Dependence is high in North American, Afro-Caribbean and Irish; low in Jewish and
in Chinese – may relate to different isoenzymes of acetaldehyde dehydrogenase.
AETIOLOGY OF DEPENDENCE
GENETICS
Family studies
• There is a sevenfold increase in risk of alcoholism among first-degree relatives of
alcoholics versus controls.
• Twin studies – MZ:DZ ⫽ 70%:43% for males (Pickens et al., 1991), 47%:32% for
females (Kendler et al., 1992).
Adoption studies
Danish, Swedish and US (Iowa) studies indicate:
• Sons of alcoholics are four times more likely to be alcoholic than sons of non-
alcoholic, whether raised by alcoholic biological parents or by non-alcoholic
adoptive parents.
• Sons of alcoholics raised by non-alcoholic adoptive parents are no more susceptible
to another non-alcoholic adult psychiatric disorder.
• There is a higher rate of childhood conduct disorder in male offspring of alcoholics.
• Alcoholism and antisocial personality are genetically independent disorders for
both males and females.
Cloninger (1987) proposed, on the basis of Swedish data, type I/II subgrouping of
alcoholism:
• Type I – predominantly female, later onset than type II, not associated with antisocial
behaviour, higher psychological dependency, more guilt, more related to environmen-
tal factors than genetic, abusers show high traits of dependency and harm avoidance.
• Type II – predominantly males, onset usually before 25 years, high genetic com-
ponent, parental alcoholism, parental antisocial behaviour, more alcohol-related
aggression, more legal problems, less likely to achieve abstinence, more impulsive/
antisocial personality traits.
Chromosomes
Variations in allele compositions for alcohol dehydrogenase and aldehyde dehydroge-
nase may contribute to risk patterns for alcoholism among oriental populations.
Vulnerability markers
Abnormalities in P3 event-related potential are associated with genetic risk for sub-
stance use disorders (Iacono et al., 2002).
MOLECULAR GENETICS
A number of alcohol-responsive genes have been found (Pandey et al., 2003).
Neuropeptide Y (NPY) is of particular interest; decreased expression of NPY has been
proposed as a substrate for the predisposition to alcohol-seeking behaviors and alco-
holism (Ilveskoski et al., 2001).
Mayfield et al. (2002) propose that alcohol alters genes expression involved in cAMP
signalling pathways that modulate alcohol sensitivity as well as withdrawal anxiety.
CLINICAL FEATURES 113
BIOCHEMICAL FACTORS
Alcohol has complex interactions with multiple systems (Ciraulo et al., 2003).
• Dopamine (DA) – Acute alcohol consumption stimulates DA release in nucleus
accumbens. Chronic alcohol use results in down-regulation of D2 receptors.
• Serotonin (5-HT) – Alcohol interferes with serotonin function. Greater reduction
of serotonin function is associated with impulsivity, aggression, suicidality and
psychiatric disorders.
• Growth homone (GH) – Chronic alcoholism is associated with reduced GH
response to stimulus challenge, and is reflective of severe dependence.
• Opioids – Endogenous opioid system mediates reinforcing effects of alcohol and
may be altered in those with high risk for alcoholism.
• Other receptor/neuropeptides.
PSYCHOLOGICAL FACTORS
Meszaros et al. (1999) used a ‘tridimensional personality questionnaire’ to measure
the three personality dimensions: novelty seeking (NS), harm avoidance (HA) and
reward dependence (Cloninger et al., 1987) in detoxified alcoholics and found that
NS is a strong predictor for relapse in detoxified males, and that HA predicts ‘early’
relapse (4 weeks) in females.
Operant conditioning: relief of withdrawal symptoms promotes further abuse.
SOCIOCULTURAL FACTORS
• Cultural values, role of alcohol in social activities.
• Per capita consumption and cultural patterns of alcohol usage correlate with
prevalence of alcohol-related disabilities.
• Peer-group pressures.
• Occupation-related factors.
CLINICAL FEATURES
The alcohol dependency syndrome (Edwards and Gross, 1976):

1 Stereotyped pattern of drinking – The ordinary drinker drinks in accordance with
variety of cues. The dependent drinker drinks to avoid symptoms of withdrawal;
‘personal drinking repertoire’ is increasingly narrowed.
2 Prominence of drink-seeking behaviour – The dependent drinker gives priority
to maintaining alcohol intake. Unpleasant consequences (social, financial, physical)
fail to deter.
3 Increased tolerance to alcohol – There is metabolic tolerance (increased liver clearance
makes relatively trivial contribution). Presumably, changes occur at synaptic junc-
tions. In later stages of dependence, tolerance may be suddenly lost (not known why).
4 Repeated withdrawal symptoms – Initially there are mild symptoms at any time of
day as alcohol levels fall. To incur symptoms, the individual generally has to con-
sume 200–300 g of alcohol a day for several years.
5 Relief or avoidance of withdrawal symptoms by further drinking.
6 Subjective awareness of compulsion to drink – The desire for a further drink is seen
as irrational, resisted, but the further drink is taken (analogous to classic descrip-
tion of compulsive disorder).
7 Reinstatement after abstinence – Many patients find abstinence surprisingly easy to
maintain in, say, a ward setting where drinking cues are removed. Relapse into the
earlier stage of dependence (reinstatement) is rapid (within 72 hours of drinking)
for those severely dependent and varies (weeks, months) for lesser degrees.
COMPLICATIONS OF ALCOHOL DEPENDENCE: ‘ALCOHOL-RELATED

DISABILITIES’
CNS EFFECTS
WITHDRAWAL SYMPTOMS
The spectrum of symptoms is wide: tremor, nausea (or retching), sweating (drenching
in early morning), mood disturbance (fearful, depressive), hyperacusis, tinnitus, itch-
ing, muscle cramps, sleep disturbance, perceptual distortions and hallucinations,
convulsions and fully developed syndrome of delirium tremens.
• Acute tremulousness – 34 per cent.
• Transient hallucinosis – 11 per cent.
• Auditory hallucinosis – 2 per cent.
• Convulsions – ⬍12 per cent.
• Wernicke–Korsakoff syndrome – ⬍3 per cent.
• Full-blown delirium tremens – 5 per cent.
Delirium tremens is typically seen 3–5 days after selective or absolute withdrawal,
although prodromal features occur earlier. Trauma or infection present from outset in
up to 50 per cent of cases and biochemical evidence of liver damage in up to 90 per cent.
There may be vivid hallucinations, delusions, profound confusion and inattention,
with agitation and restlessness, sleeplessness, autonomic overactivity and fearful affect.
Primary disorder of the reticular activating system is suggested by inattention, over-
arousal, insomnia and overactivity. There is a 10–20 per cent mortality rate related to
autonomic instability.
Alcoholic hallucinosis, in a restricted sense, applies to rare conditions in which audi-
tory hallucination occurs alone in clear consciousness. Voices are frequently offensive
and critical. This may be followed by secondary delusional interpretation. It usually
clears in a few days, where there is no evidence for association with schizophrenia.
WERNICKE–KORSAKOFF SYNDROME
Wernicke’s encephalopathy (also see Chapter 13)
This is caused by thiamine deficiency. There are acute degenerative changes in thalamus,
hypothalamus, mamillary bodies. Signs are:
• Confusion/clouding of consciousness.
• Ocular palsies and nystagmus.
COMPLICATIONS OF ALCOHOL DEPENDENCE 115
• Staggering gait.
• Peripheral neuropathy.
Treatment with thiamine is usually effective in promptly resolving ataxia and ocular
symptoms, but cognitive symptoms are slower to resolve.
Korsakoff syndrome
There are degenerative changes in upper brain stem, thalamus, hypothalamus and
mamillary bodies. Signs are:
• Inability to form new memories and retrograde amnesia extending to days/years.

• Confabulation – apparent recollection of imaginary events and experiences.
• Relative preservation of other intellectual functions and clear consciousness.
Wernicke’s encephalopathy and Korsakoff ’s psychosis may be viewed as successive

stages of the same disease process; i.e. Korsakoff ’s psychosis is the residual state of
which Wernicke’s encephalopathy is the acute organic reaction (see diagram below).
Wernicke syndrome Response to treatment

(thiamine)
84% cases
Resolution of symptoms
6%
20%
Thiamine treatment
Korsakoff’s syndrome
80%
Established Korsakoff’s
⫾ alcohol dementia
Prevention/treatment of Wernicke’s encephalopathy with thiamine may prevent

Korsakoff ’s psychosis. Only 20 per cent of patients with Korsakoff ’s psychosis show
any improvement when treated with thiamine.
ALCOHOLIC DEMENTIA
There is debate as to whether this is actually a manifestation of evolving Korsakoff ’s.
There are mild to moderate cognitive deficits, including impaired memory and judge-
ment, social and personal neglect, and paranoia.
Dementia rarely occurs before age 40 years. Females may be more at risk. It is usu-
ally accompanied by other CNS and liver evidence of alcohol damage. It is associated
with CT/MRI evidence of ‘atrophy’, especially in the frontal lobes.
In a small number of patients without full dementia who maintain abstinence, radio-
logical ‘atrophy’ reverses with time (see Chapter 15).
OTHER CNS EFFECTS

• Seizures.
• Myopathy – acute or subacute with more proximal muscle weakness. Women are
more susceptible than men.
• Optic atrophy – loss of visual acuity, central ⫹ colour vision, leading to blindness
associated with methanol poisoning, thiamine and B12 deficiency.
• Cerebellar degeneration.
• Marchiafava–Bignami disease – primary degeneration of the middle lamina of the
corpus callosum; cognitive and behavioural changes manifest by dementia, disinhibi-
tion and aggressiveness. Recurrent seizures and altered consciousness are late events.
• Central pontine myelinolysis – sudden-onset pseudobular palsy; quadriplegia, fatal
condition.
PSYCHIATRIC EFFECTS
• Co-morbidity (see above).

• Suicide and deliberate self-harm (see Chapter 11).
• Homicide.
• Other forensic disorders.
OTHER PHYSICAL EFFECTS
Respiratory
• Orofacial/laryngeal carcinoma.
• COPD/lung cancer related to 80 per cent smoking rate in alcoholics.
• Klebsiella pneumonia in alcoholics.
• Reactivation of primary TB focus in alcoholics.
Cardiovascular
• Cardiomyopathy.
• Hypertension – alcohol-associated may not respond well to antihypertensives.
• Sinus tachycardia with intoxication and withdrawal.
Gastrointestinal
• Gastritis.
• Barrett’s oesophagitis.
• Oesophageal varices.
• Mallory–Weiss oesophageal rupture.
• Peptic/gastric ulceration – in 20 per cent of alcoholics. Bleeding may be exacerbated
by vitamin K deficiency secondary to cirrhosis.
• Carcinoma of stomach.
• Possible association with large bowel/rectal carcinoma.
• Pancreatitis.
• Diabetes mellitus.
COMPLICATIONS OF ALCOHOL DEPENDENCE 117
Liver damage
Liver damage is related to lifetime intake, enhanced by nutritional deficiences. Fatty
infiltration is the earliest feature – decreased fatty acid oxidation.
• Alcoholic hepatitis – Acute episode resembles viral hepatitis: 10–30 per cent die, a
proportion go on to cirrhosis. Occurs usually after 10 years’ abuse.
• Cirrhosis – Up to20 per cent of chronic alcoholics suffer. Eighty per cent of all cases
of cirrhosis are related to alcohol abuse. Women are more susceptible. Vulnerability
may be due in part to histocompatibility antigen HLA-B8, found in approximately
25 per cent of the population. Alternatively, HLA-A28 may have a protective effect.
Note that hepatotoxicity may occur at ‘therapeutic’ doses of acetaminophen.
Haematological
• Macrocytosis – folate deficiency and direct toxic effect of alcohol.
• Anaemia:
– Iron deficiency – absorption, blood loss.
– B12 – nutritional deficiency.
– Malabsorption.
– Liver stores.
• Thrombocytopenia – splenic sequestration due to enlarged spleen secondary to
liver disease; suppression of platelet formation due to toxic effect of alcohol.
Neoplasm
May be orofacial, GI, respiratory, liver.
Fetal alcohol syndrome (FAS), or fetal alcohol spectrum disorder (FASD)

In FAS there are facial anomalies: microcephaly, short palpebral fissures, flat philtrum,
thin upper lip, small mid-face, low-set ears; mental retardation/low IQ, neurobehav-
ioral problems (ADHD in up to 50 per cent), low birthweight, skeletal defects, con-
genital heart disease, congenital renal disease.
• Incidence of 1.9 per 1000 live births in the USA.
• Alcohol in pregnancy is associated with increased stillbirth, increased neonatal
mortality.
• Effects of alcohol are thought to be dose-related.
Endocrine
There may be sexual problems and feminization in males – erectile impotence due to
impaired metabolism of estrogen by liver and suppression of testosterone production.
Menstrual irregularities occur in females.
SOCIAL EFFECTS OF ALCOHOL DEPENDENCE
Disabilities may precede the psychological and physical by several years. Family/mari-
tal difficulties include:
• Physical/sexual abuse of partner, ‘reactive’ psychiatric disorder (usually depres-
sion) in partner.
Table 9.4 Useful laboratory tests

Test Sensitivity Specificity
GGT 80⫹ 80⫹

MC V50⫹ 90⫹
AST 40⫹ 80
Alkaline phosphatase 60 50
AST/ALT ⬎ 2 is often seen in alcoholism.
• Increased divorce.
• Increased abuse of children.
• Increased risk of later alcoholism in children, developing other psychiatric disorders,
later marrying an alcoholic.
EFFECTS IN SOCIETY
The cost of alcohol-related disabilities is estimated to be between 2 and 6 per cent of

gross domestic product, with almost two-thirds accounted for by morbidity/prema-
ture mortality, and the remainder being for medical care, alcohol-related violent
crime and car accidents, and fetal alcohol syndrome.
• Employment – 21⁄2 times as many days off work, decreased productivity, more acci-
dents at work.
• Accidents – 80 per cent of fatal car accidents involve alcohol; 40 per cent of casu-
alty trauma involves alcohol.
• Crime – In the USA, 40 per cent of prison inmates are under the influence of alcohol
when crime committed; alcohol is consumed prior to almost half of all murders.
RECOGNITION AND DETECTION OF ALCOHOL DEPENDENCE
• A high index of suspicion is warranted.

• There is a 75 per cent chance if the patient smells of drink during consultation.
• There is a 20–30 per cent rate of alcohol abuse/misuse in general hospital patients,
and a high rate in casualty/emergency service users, vagrants. CAGE and MAST
questionnaires will improve detection in outpatient clinics and in primary care.
• Laboratory tests are helpful (see Table 9.4).
MANAGEMENT OF ALCOHOL DEPENDENCE
GENERAL GUIDELINES
Make an initial comprehensive, multidimensional assessment of alcohol-related dis-
abilities. Involve the spouse/significant relationship.
MANAGEMENT OF ALCOHOL DEPENDENCE 119
A goal-orientated treatment plan is required. Recent research suggests a better out-

come is achieved if treatment is tailored or ‘matched’ to patients’ attributes rather than
standardized.
There is some evidence that earlier-onset alcoholics with a family history of alco-
holism respond better to pharmacotherapy, specifically naltrexone (Monterosso et al.,
2001), while the less severely affected respond better to a cognitive–behavioural
approach (Litt et al., 1992).
Alcoholism with co-morbidity

• Patients need careful evaluation with collateral history.
• Relationship of co-morbidity (primary, secondary, co-related) needs to be
determined.
• Where the mechanism of depression is unclear, antidepressant medication should
be delayed until 2 weeks of abstinence.
• Inpatient treatment advocated for:
– Significant current or past psychiatric co-morbidity.
– Significant physical co-morbidity/complications of alcoholism.
– History of seizures, prominent DTs.
– Risk of suicide, homicide.
Characteristics of the patient are more predictive of response and outcome than
either setting or programme characteristics.
DETOXIFICATION
• Give attention to hydration and electrolyte balance; multivitamin, folic acid, and
thiamine given. Intramuscular/vascular thiamine should be given prior to any
glucose load to avoid depletion of thiamine stores and subsequent precipitation/
exacerbation of Wernicke–Korsakoff syndrome.
• Give attention to general medical conditions and the risk of respiratory depression/
infection. Co-morbid physical illness/sepsis are associated with high mortality in
acute Wernicke–Korsakoff syndrome.
• Benzodiazepines are the mainstay of withdrawal treatment, in tapering dose or
as-needed dose per CIWA scale (Sullivan et al., 1989); they are the treatment of choice
for withdrawal seizures/DT. Lorazepam or oxazepam (no metabolites/renal clear-
ance) are favoured in patients with liver dysfunction or the elderly.
• Give antipsychotics as needed for alcoholic hallucinosis.
• An ␣2-adrenergic blocker (clonidine) is useful to lessen noradrengergic symptoms.
• Anticonvulsants carbamazepine and divalproex have shown efficacy for detoxifica-
tion but are not in widespread use.
PHARMACOLOGICAL MAINTENANCE TREATMENTS

• Disulfiram – an aversive agent, inhibits aldehyde dehydrogenase. Problems with
compliance limits its efficacy.
• Naltrexone – an opioid blocker, reduces relapse rates (Pettinati et al., 2000).
• Acamprosate – restores NMDA receptor tone in the glutamate system and is shown
to increase abstinence rates. In combination with naltrexone it further enhances
relapse prevention (Kiefer et al., 2003).
• Serotonergic drugs – no consistency in studies as to relapse prevention. They are

used to treat co-morbid depression.
PSYCHOSOCIAL REHABILITATION
Principles of treatment
• ‘No cure’ – achieving abstinence ⫽ remission.
• All efforts are aimed at motivating the patient towards abstinence.
• Education is essential about addiction, compulsive behaviours, medical complications.
• Emotional insight is stressed.
• Involvement of family/significant relationships is critical to treatment.
• Induction into AA’s Twelve-Step Facilitation (TSF) Therapy is especially helpful
for alcoholics who drink heavily in social situations.
• Group/individual therapy aims at self-understanding and realization of the effect
of addiction on the patients’ life.
• Continued participation in support/follow-up programme, AA, etc., should be
encouraged.
Modalities
• Individual therapy:
– Cognitive–behavioral therapy (CBT) (see Chapter 23) is shown to have durable
effects.
– Motivational enhancement therapy (MET) motivates individuals to utilize their
own resources to effect change in their behaviour. It is most effective in alco-
holics with high levels of anger.
– Coping skills training.
• Group therapy.
• Couples therapy.
• Family therapy.
PROGNOSIS FOR ALCOHOL DEPENDENCE
Patient attributes rather than treatment factors are a better predictor of outcome.
There is a poor prognosis with:
• Established brain damage.
• Co-morbid psychiatric illness, especially antisocial personality disorder.
• Criminal history.
• Low IQ.
• Poor support.
• Low motivation.
Follow-up
• Sixty per cent with ‘good’ outcome at 20.8 months; 40 per cent in remission and
19 per cent with no more than three relapses and continuous sobriety 6 months
prior to survey (Castle Craig Hospital Extended Care Unit Follow-up Study, 1999).
• Self-reports for follow-up study are about 90 per cent reliable (Secades-Villa and
Fernandez-Hermida, 2003).
Anderson P, Cremona A, Paton A et al. (1993) The risk of alcohol. Addiction 8, 1493.
Babor TF, Hofmann M, DelBoca JK et al. (1992) Types of alcoholics. I: Evidence for an empiric-
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Drug dependence and 10
gambling
ICD-10 AND DSM-IV
SUBSTANCE DEPENDENCE
Substance misuse which results in clinically significant impairment or stress, as evi-
dent by ⭓3 of the following during a 12-month period:
1 Tolerance – markedly increased amounts of substance required to achieve intox-

ication or desired effect, or markedly diminished effect with continued use of the
same amount of the substance.
2 Withdrawal – Characteristic. Withdrawal syndrome for the substance, or the same
(or similar) substance is used to relieve or avoid withdrawal.
3 Substance is often taken in larger amounts or over a longer period than was
intended.
4 Persistent desire or unsuccessful efforts to reduce or control substance use.
5 Excessive time in activities necessary to obtain the substance, use the substance, or
recover from effects.
6 Loss or reduction in important social, occupational, or recreational activities.
7 Continued substance use despite knowledge of a persistent or recurrent physical/
psychological problem which is caused/exacerbated by the substance.
• With physiological dependence – evidence of tolerance or withdrawal.

• Without physiological dependence – no evidence of tolerance or withdrawal.
SUBSTANCE ABUSE (SA)

A. Pattern of substance misuse leading to clinically significant impairment or distress,
as manifested by ⭓1 of the following occurring during a 12-month period:
1 Recurrent substance use resulting in a failure to fulfill major role obligations at

work, school or home.
2 Recurrent substance use in situations in which it is physically hazardous.
3 Recurrent substance-related legal problems.
124 DRUG DEPENDENCE AND GAMBLING
4 Persistent substance use despite recurrent social or interpersonal problems having

origin in or caused or exacerbated by the effects of the substance.
B. Never met criteria for dependence for this class of substance.
EPIDEMIOLOGY OF SUBSTANCE ABUSE
Lifetime illicit drug use in the USA (SAMHSA Household Survey on Drug Abuse,
2002):
• Marijuana/hashish – 40.4 per cent.

• Cocaine – 14.4 per cent.
• Crack – 3.6 per cent.
• LSD – 10.4 per cent.
• Inhalants – 9.7 per cent.
• Methamphetamine – 5.3 per cent.
• Ecstasy – 4.3 per cent.
• Non-medical use of prescribed medications – 19.8 per cent.
Of the US population 8.3 per cent actively used illicit drugs in 2002; 3.3 per
cent needed treatment in 2002 for a drug problem, of which 0.6 per cent actually
received help.
Co-morbidity
• 45 per cent of patients with alcohol abuse/dependence have at least one other psy-
chiatric disorder.
• 72 per cent of patients with drug abuse/dependence have at least one other psychi-
atric disorder.
• Co-occurrence of substance and psychiatric disorders portends negatively for suc-
cessful treatment of either.
• Over half of schizophrenic patients in the USA have substance use disorder.
Possible associations:
1 Vulnerability hypothesis – SA may precipitate schizophrenia in predisposed indi-
viduals. It is unlikely as a primary cause.
2 Self-medication hypothesis:
– SA counteracts negative symptoms, depressed mood.
– SA counteracts side-effects of treatment.
Age, sex and class

• Eighty per cent begin SA before age 18, with peak abuse period in 20s–30s (20–24
for females, 20–30 for males). Risk lessens after age 40. Volatile SA (inhalants, etc.)
are mostly used by young adolescents.
• Overall – male:female ratio ⫽ 4:1.
• All classes are affected, but lower groups are over-represented, especially in the USA.
AETIOLOGICAL THEORIES OF SUBSTANCE ABUSE 125
Pattern of abuse
• Episodic abuse generally seen with less addictive drugs, continuous course with
highly addictive drugs.
• Cannabis is the first drug of abuse in 70 per cent of opiate addicts.
• Polysubstance abuse is common: 90 per cent of opiate abusers also abuse benzodi-
azepines (especially diazepam or temazepam, oral and IV).
• Other drug use is more ‘contained’:
– Volatile SA is often experimental; only 20 per cent become chronic abusers and
polysubstance abusers.
– Ecstasy (NMDA) is used mainly for recreational purposes – dance parties or
‘raves’.
• Only one-third of opiate users are in contact with treatment agencies at any time.
• Average duration of use before seeking treatment is 9 years.
• Average duration of intravenous use before seeking treatment is 4 years.
AETIOLOGICAL THEORIES OF SUBSTANCE ABUSE
Theories are diverse and conjectural. A multifactorial perspective is required.
GENETICS
Twin studies in adolescents suggest a modest influence of genetics in conveying liabil-
ity for non-alcohol substance use disorders (Hopfer et al., 2003).
PHARMACOLOGICAL AND PHYSIOLOGICAL THEORIES (also see Chapter 9)

Abnormalities are observed in many neurotransmitter systems:
• Opiate receptor.
• Dopamine.
• Serotonin.
There is intensive research on the neuropharmacology of craving:
• May relate to the ability to increase dopamine (DA) activity in nucleus accumbens.
• Reinforcing effects may occur from stimulation of corticofugal DA pathways.
PSYCHOLOGICAL THEORIES (see Table 10.1)

• Behavioural:
– Modelling.
– Primary direct reinforcement (psychic effect of SA promotes continued abuse).
– Secondary reinforcement (interaction of environmental cues and pharmaco-
logic effects of drug).
• Analytic – regression/fixation at oral stage of development (see Chapter 23).
• Sociocultural:
– 50 per cent of heroin addicts are from single parent/divorced families.
– There are high rates of parental alcoholism.
– Peer group activation (e.g. ecstasy abuse).
Table 10.1 Psychopharmacology and clinical characteristics of commonly abused drugs
Drugs Pharmacology Route of administration Psychic effects Physical effects Withdrawal effects Dependence Treatment
Opioids: Bind to opioid receptors; Oral, IV, IM, Euphoria, relaxation, Miosis, bradycardia, Craving, agitation, Yes Overdose:
heroin naltrexone, naloxone – subcutaneously drowsiness, personality itching, nausea, restlessness, cardiorespiratory
morphine competitive antagonists change, hypoactivity, constipation tachycardia, dilated support, naloxone
meperidine Tolerance develops with ↓ appetite, ↓ libido pupils, perspiration, Detoxification:
methadone usage; also cross-tolerance yawning, diarrhoea, methadone
pentazocine within opioid group abdominal cramps, buprenorphine,
Withdrawal commences ‘goose flesh’ clonidine
4–6 hours after last dose,
peaks 28–48 hours, lasts
7–10 days
Cocaine Blocks re-uptake of Chewing, sniffing, Euphoria, excitement, Mydriasis, tremor, ‘Crash’: craving, Yes ↓ Craving:
serotonin and smoking, IV confusion, paranoid tachycardia, depression, amantadine,
catecholamines, especially psychosis, formication perforated insomnia, propranolol for
dopamine – inhibits (‘cocaine bugs’) nasal septum, psychomotor severe craving
transporter uptake site; fever, seizures, agitation
various dopamine agonists/ cardiorespiratory
autoreceptors studied for arrest, CVA
↓ craving
Crack-cocaine – Smoking Extreme agitation, – – Yes –
psychosis
Amphetamines Sympathomimetics, Oral, IV Euphoria, excitement, Mydriasis, tachycardia, Dysphoria, anergia Yes Overdose:
detected by urinalysis hyperalertness, hyperreflexia sedation,
toxicology if ⭐48 hours irritability/aggression, Overdose: cardiac antiarrhythmic,
after last dose paranoia, psychosis, arrhythmia, acidify urine
hallucinosis hyperpyrexia Detoxification:
self-resolution;
neuroleptic only
if psychosis
prolonged
Hallucinogens Sympathomimetic; 5-HT Oral Depersonalization, Red eyes, mydriasis, None No Abstinence,
lysergic acid agonist; onset of effects in derealization, ataxia, tachycardia rehabilitation
diethylamide 1 hour, last 8–12 hours; hyperperceptualization,
(LSD) flashback may occur false sense of ability,
mescaline spontaneously even 1 year anxiety, ideas of
psilocybin after stopping LSD reference, impaired
(‘magic judgement, flashbacks,
mushrooms’) psychotic or
mood disturbance
Phenylcyclidine Receptor sites located Oral, IV, sniffing, smoking Hallucinations, paranoid Nystagmus, ↑ blood Craving, depression, Yes Desipramine for
(PCP) in calcium ion schizophreniform pressure anergia craving; haloperidol
channel of NMDA psychosis, depressed for agitation/
subtype of glutamate consciousness psychosis, avoid
aggression chlorpromazine
Overdose: with
hypertension ataxia,
adrenergic crisis
Cannabis Active compound is Smoking Euphoria, relaxation, Conjunctival – Yes Abstinence
marijuana tetrahydocannabinol; heightened perceptual infection, dry
‘hashish’ G-protein receptor for awareness, Cannabis mouth, tachycardia,
cannabinoids recently psychosis – disputed respiratory tract
discovered; onset of effect entity irritation
is minutes to 1 hour; effect
lasts 6–12 hours
Barbiturates CNS depressants Oral, IM, IV Anxiolytic/respiratory Cellular signs, Restlessness, insomnia, Yes Withdrawal with
CNS, depression with respiratory anorexia, nausea, benzodiazepine
higher doses depression in seizures, delirium and anti-convul-
overdose sant cover
Benzo- CNS depressants; bind Oral, IV Anxiolytic; impaired Ataxia, nausea, Agitation, insomnia, Yes Gradual
diazepines to benzodiazepines-GABA concentration, respiratory tremor, withdrawal
receptor complex; also judgement; memory depression restlessness
see Chapter 21 disturbance
(Continued)
Table 10.1 Continued
Drugs Pharmacology Route of administration Psychic effects Physical effects Withdrawal effects Dependence Treatment
Belladonna, – – Euphoria Overdose: Mydriasis, dry mouth, – Yes Overdose:

alkaloids confusion, visual light sensitivity, physostigmine
homatropine hallucinations pyrexia 2 mg IV
atropine
scopolamine
hyoscyamine
Ecstasy Neurotoxic effect on Oral Euphoria, heightened Appetite loss, – ? Supportive
(MDMA-3,4 serotonin nerve terminals perceptual awareness, tachycardia, jaw measures,
methylene- (stimulates SHT release paranoid psychoses, tension, Bruxism, especially fluid
dioxymetham- and blocks SHT re-uptake), anxiety reactions have perspiration replacement
phetamine) especially in frontal cortex been reported fulminant hyperthermia,
and hippocampus disseminated
intravascular
coagulopathy
Gamma A naturally occurring fatty Oral Euphoria, disinhibition, Repiratory Similar to alcohol Yes Benzodiazepines,
hydroxybutyric acid found in all body drowsiness, confusion depression, withdrawal: sweating, phenobarbital,
acid (GHB) tissues that regulates bradycardia, anxiety, autonomic antipsychotics
GABA/dopamine/5-HT/ hypothermia, hyperactivity,
ACh decreased cardiac delirium
At high dose acts output, coma
as a CNS depressant/
anaesthetic
Volatile CNS depressants Inhalation – ‘bagging’ Initial euphoria, Irritation of eyes, – Yes, but rare Abstinence
substance disinhibition, throat, perioral rash,
abuse (VSA): later apathy, odour on breath, CNS
toluene acetone impaired judgement depression, ataxia,
benzene nystagmus,
trichloroethylene polyneuropathy,
halogenated arrhythmias, hepatorenal
hydrocarbons damage, aplastic anaemia
MANAGEMENT OF SUBSTANCE ABUSE 129
• Access and availability:

– There is convincing evidence in support of environmental influences.
– Ease of availability of ‘crack’ cocaine (inexpensive also) led to increased misuse
in high-risk groups: medical personnel, prostitutes.
MANAGEMENT OF SUBSTANCE ABUSE
PHARMACOLOGICAL TREATMENTS
• Methadone – long-acting synthetic opiate used in opiate addiction for mainten-
ance or detox.
– Maintenance therapy at doses of 20–70 mg, with regular urine monitoring for
abuse of other drugs.
– Moderate/high dosage of methadone required to maintain abstinence.
– There is a variable drop-out from maintenance programmes. Persistence is asso-
ciated with better outcome, less physical morbidity, slower progression of HIV
infection.
• Levomethadyl acetate (LAAM) – long-acting synthetic opiate agonist used in opi-
ate addiction.
– Potential for life-threatening arrhythmias due to QT prolongation limits its use
to opiate addicts who fail other treatments.
• Naltrexone – opiate antagonist used in detoxification and maintenance.
– Generally less acceptable to abuser than methadone. Compliance limits its use-
fulness.
• Buprenorphine – mixed opioid agonist–antagonist.
– As effective as methadone in opiate detoxification and maintenance.
– Also available combined with naloxone.
– Does not require special licensing to prescribe in the USA as with methadone/
LAAM.
• Clonidine – used in opiate withdrawal for autonomic suppression but does not
help withdrawal symptoms of insomnia or muscular aches.
• Benzodiazepines – used as an adjunct to opioid withdrawal for anxiety/
insomnia.
• Other agents not yet in routine clinical use/under investigation. Numerous agents
are currently being investigated for treating cocaine and marijuana use disorders
but their use is not supported by convincing evidence.
PSYCHOSOCIAL TREATMENTS
Aim to tackle underlying psychological/social/environmental factors perpetuating
SA. Increase awareness, and develop alternative coping mechanisms. Foster cognitive–
behavioural strategies to manage craving and eliminate reinforcing behaviours.
Biopsychosocial treatments combined with pharmacological therapy improve
treatment outcomes (Albanese and Shaffer, 2003).
PROGNOSIS FOR SUBSTANCE ABUSE
There is a high initial relapse after treatment. Follow-up shows high psychiatric mor-
bidity, continued use, high mortality (suicide, accidents, physical complications of
SA, AIDS).
Therapeutic communities are associated with better outcomes than methadone
treatment alone in opiate dependence.
Factors associated with poor outcome

• Early age of initial abuse.
• Long history of abuse.
• IV abuse.
• Early drop-out from maintenance programmes.
• Antisocial personality disorder.
PREVENTION OF ABUSE AND DISEASE
• Limit substance availability bycustoms surveillance, severe penalties for supplying/

using illicit drugs, specialized drug-crime police squads.
• Educate medical personnel.
• Educate the public.
• Access the wider drug-abusing population rather than focusing on short-term
treatment of some patients. This raises service and public health policy issues.
• Outreach programmes are essential.
SA AND HIV (ALSO SEE CHAPTER 13)

Twenty-five per cent of adults and adolescents in the USA with AIDS used injected
drugs (CDC, 2000). The horizontal spread via needle-sharing and sexual practices is
more severe in minority populations. Needle-exchange programmes result in lower
annual rates of HIV seroprevalence (Pollack, 2001).
PATHOLOGICAL GAMBLING
This is categorized in ICD-10 as Habit and Impulse Disorder, and in DSM-IV as an

Impulse Control Disorder NOS.
• There are frequent, repeated episodes of gambling that dominate the individual’s
life to the detriment of social, occupational, material and family commitments.
• The person may experience ‘craving’, a ‘rush’, ‘blackouts’, withdrawal syndrome.
• Males are affected more than females (4 per cent of Gamblers Anonymous mem-
bers are females). Females tend to present earlier.
• Addiction usually begins in childhood/early adolescence.
• Predisposing factors include family history of addiction disorders, parental rejec-
tion or criticism resulting in chronic low self-esteem.
• Progression from social gambler to pathological gambler may be precipitated/

exacerbated by death of a parent/relative, birth of a child, physical illness or per-
sonal threat to life, job demotion or promotion, or substance abuse.
PHASES OF ADDICTION
There are four phases: winning, losing, desperation, giving up. Stress-related physical
illness, depression, deliberate self-harm and criminal behaviour are common sequelae
of the final two phases.
Two-thirds of Gamblers Anonymous members have committed some illegal activ-
ity to support their gambling.
MANAGEMENT OF PATHOLOGICAL GAMBLING

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Suicide and non-fatal 11
deliberate self-harm
SUICIDE
DEFINITIONS
• Kessel – suicide and ‘deliberate self-poisoning/injury’. ‘Deliberate self-injury’ substi-
tuted for ‘attempted suicide’ because many patients ‘performed their acts in the
belief that they were comparatively safe’.
• Kreitman – suicide and parasuicide: ‘Parasuicide’ refers to ‘a behavioural analogue
of suicide but without considering a psychological orientation towards death being
in any way essential to the condition’.
• Morgan – non-fatal deliberate self-harm (DSH): ‘A deliberate non-fatal act,
whether physical, drug overdose or poisoning, done in the knowledge that it was
potentially harmful, and in the case of drug overdosage, that the amount taken was
excessive.’
• Beck – suicide: ‘A wilful self-inflicted life-threatening act which has resulted in death.’
• Durkheim: proposed three forms of suicide:
– Egoistic.
– Anomic.
– Altruistic.
EPIDEMIOLOGY OF SUICIDE
• Figures from the Centers for Disease Control and Prevention (2001):
– Suicide is the eleventh leading cause of death in the USA and the third major
cause of death in the 15–34 year age-group.
– Males complete suicide at a rate four times that of females.
– Whites commit suicide at twice the rate of blacks.
• In the UK, suicide is the second leading cause of death in the 15–34 year age-group.
• Methods of suicide: firearms 55.1 per cent, suffocation 20.2 per cent, poisoning
17.0 per cent, fall 2.1 per cent, cut/pierce 1.5 per cent, drowning 1.1 per cent.
PSYCHIATRIC ILLNESS AND SUICIDE 135
Table 11.1 Suicide rates per 100 000 population

1960 1999
England and Wales 11.2 15.1

Ireland 3.0 22.7
America 10.6 21.1
Hungary 25.0 60.1 (2001)
Mexico 1.9 6.4 (1995)
• Worldwide, almost one million suicides and over ten million suicide attempts
occur annually. See Table 11.1.
• Highest rates are in the spring, lowest in December.
FACTORS ASSOCIATED WITH INCREASE IN SUICIDE RATES

• Psychiatric illness.
• Unemployment.
• Social isolation.
• Poverty.
• Gun ownership.
VICTIM CHARACTERISTICS
• A psychiatric diagnosis is evident in over 90 per cent of victims; 60 per cent suffer
from a mood disorder. Alcohol and other substance use, schizophrenia, bipolar
disorder and personality disorder are commonly seen in suicide victims. Males
exceed females for all age-groups.
• Rates are highest in the divorced or widowed. Married have lowest rates.
• Urban dwellers exceed rural.
• Socioeconomic class – higher in lowest and highest groups, lower in middle
groups.
• Religion – strong religious affiliation is a protective factor.
• Occupation – higher-risk groups are doctors, lawyers, police officers, hotel and bar
trade owners.
• Unemployment – there is a strong statistical association, especially for males.
PSYCHIATRIC ILLNESS AND SUICIDE
EPIDEMIOLOGY AND ASSOCIATIONS
FIGURES FOR SUICIDE ATTEMPTS

See Hawton et al. (2003a):
• Affective disorder – 73.9 per cent.
• Alcoholism – 24.3 per cent.
• Drugs – 3.6 per cent.
136 SUICIDE AND NON-FATAL DELIBERATE SELF-HARM
• Neurotic/stress-related/somatoform disorder – 26.1 per cent.

• Schizophrenia – 4.5 per cent.
• Personality disorder (diagnosed 12–20 months later) – 45.9 per cent.
DEPRESSION
Fifteen per cent of patients hospitalized for mood disorder will kill themselves.
Greater risk of suicide is seen with psychotic depression. Risk factors include:
• General – male, older living alone.

• Specific – history of previous suicide attempt.
• Agitation, insomnia.
• Impaired memory, self-neglect.
• Hopelessness.
ALCOHOLISM
Fifteen per cent of alcoholics kill themselves. Risk factors are (Preuss et al., 2003):
• Separated or divorced.
• Drug dependence.
• Substance-induced psychiatric disorder.
• More severe course of alcoholism.
Of note, gender did not predict future suicide attempts in alcoholics.
SCHIZOPHRENIA (RAYMONT, 2001)

Suicide is the principal cause of premature death in schizophrenics. Between 9 and
13 per cent of schizophrenics commit suicide; 20–40 per cent attempt suicide. Their
characteristics are:
• Male, young, unemployed, socially isolated.
• Early in illness, immediately after discharge from first admission.
• High or low premorbid functioning.
• Numerous relapses, poor global functioning, hopelessness.
Fifty per cent had contact with mental health services within 7 days of suicide.
PERSONALITY DISORDER
Co-morbidity with other psychiatric disorders; risk highest in antisocial and border-
line personalities.
PHYSICAL ILLNESS
CNS disorders carry a high risk; AIDS, multiple sclerosis, epilepsy (especially TLE),
head injury, peptic ulcer disease, cancer.
The risk of suicide is reported to be higher in people with low cholesterol, particu-
larly for males. The relationship is poorly understood.
PSYCHIATRIC ILLNESS AND SUICIDE 137
SPECIAL POPULATIONS
Adolescents
• Rare before age 14 years; rate increasing in adolescents.
• Risk factors include psychiatric illnesses, substance use (especially alcohol), male
gender, disrupted family relations, availability of lethal means, involvement in legal
system, lack of religious involvement.
Elderly
• The rate is increasing in the elderly.
• Up to 74 per cent of elderly suicide victims visited a primary care provider within
1 month of death.
• Comprising only 13 per cent of the US population, those 65 years and older
accounted for 18 per cent of deaths by suicide in 2000.
• In 2000, death by suicide for white males over 84 years was 59 per 100 000, greater
than five times the national rate.
• 80–90 per cent of elderly suicides have depressive illness.
– Often the first episode of depression.
– Deliberate self-harm in elderly more closely associated with completed suicide.
– Denial of suicide more common.
– Physical illness is more associated, especially if debilitating physical illness.
General hospital inpatients

• Suicide rates are generally low, but still three to four times higher than among the
general population.
• At-risk groups are: patients admitted post DSH, patients with debilitating illness,
patients being investigated for physical complaints which are part of a depressive
disorder, women with postpartum psychiatric complications.
Prison inmates
• Rates are three to four times higher than in the general population.
• Remand prisoners are at particular risk; also prisoners convicted of murder/
violent/sexual crimes.
• One-half of suicides occur in the first 3 months of imprisonment; one-half have
have seen the doctor in the week prior to suicide.
• 90 per cent occur by hanging.
• One-third have a previous psychiatric history, almost one-half a history of DSH.
BIOLOGICAL FACTORS IN SUICIDE
NEUROCHEMISTRY
Research shows a general lack of serotonergic activity in the prefrontal cortex of sui-
cide victims, which would confer less behavioral inhibition and make them more
likely to act on suicidal thoughts.
• Lower CSF 5-HIAA levels are associated with more lethal suicide attempts.
• Decreased CSF 5-HIAA is the most consistent finding in patients with DSH.
• Post-mortem studies show a decreased number of 5-HT receptors in the prefrontal

cortex, hypothalamus, occipital cortex and brain stem.
• Suicide victims have abnormalities of the hypothalamic–pituitary–adrenal axis
and of noradrenergic systems.
GENETICS
• Twin studies – MZ:DZ ⫽ 11.3%:1.8% (Roy et al., 1991).
• Suicidal behaviour clusters in families. Familial clustering probably represents an
inherited genetic variation in the serotonin-related genes, which are the object of
ongoing research.
MANAGEMENT AND PREVENTION OF SUICIDE
1 Detect high-risk groups:

– Despite epidemiological and clinical associations that denote risk, prediction of
suicide is extremely difficult.
– Limit access to lethal means of suicide.
2 Active treatment of any mental illness:
– Psychopharmacology – use medications appropriate to diagnosis. Lithium and
clozapine are associated with reduced suicidal behaviour.
– Psychotherapy – dialectical behavior therapy reduces parasuicidal acts.
NON-FATAL DELIBERATE SELF-HARM
EPIDEMIOLOGY AND ASSOCIATIONS OF DSH
It is difficult to assess the true extent. Hospital-based information is likely to

underestimate.
• DSH is reported in 4 per cent of the general population.
• 14 per cent of college students report DSH.
• It is highly associated with personality disorder, especially borderline.
• A decline in the late 1970s has continued, especially among females.
RISK FACTORS
• Childhood trauma.
• Teenage to early adulthood.
• Female.
• Eating disorder.
• Marital status: divorced ⬎ single ⬎ widowed; least for married.
• Urban/rural: urban ⬎ rural; high rates in ‘inner city’ areas associated with over-
crowding, lack of facilities, less social cohesion.
• Social class: inverse relationship; strong association with unemployment both for
males (relative risk 12.1) and for females (13.6).
NON-FATAL DELIBERATE SELF-HARM 139
• Psychiatric illness:
– Most attempters have symptoms of psychological distress, but definite psychi-
atric illness found in under one-third.
– Most common diagnoses are ‘reactive’ depression, alcoholism, panic disorder (high
rates from ECA study now disputed), personality disorder (borderline, sociopathic).
• Most commit DSH as an impulsive act.
• 65 per cent followed some major life event.
• 50 per cent followed a serious argument with partner/friend.
REPETITION OF DSH AND EVENTUAL SUICIDE

One per cent involved in DSH commit suicide in the first year, 3–5 per cent within
5–10 years. The greatest risk is in the first 6 months. The risk remains high for 5 years,
but markedly decreases then if there has been no DSH during this period.
In general, the closer to demographic and clinical characteristics of completed suicide
the greater the risk with DSH. However, prediction for individual patients is very difficult:
• 10 per cent of DSH attempters ultimately commit suicide.
• 50 per cent of suicides had a history of DSH.
Predictors of repetition
• Number of previous episodes of DSH.
• Features of personality disorder.
• History of violence.
• Alcoholism.
• Unmarried, lowest social class.
• Females equivalent to males.
Factors of DSH indicating suicidal intent

• Isolation.
• Timing.
• Precautions to avoid intervention.
• Suicidal note.
• Anticipatory acts.
• ‘Subjective’ appraisal of state of mind.
• ‘Dangerousness’ of attempt.
MANAGEMENT OF DSH
Preceding the episode:

• 36 per cent had attended their GP within 1 week of DSH.
• 82 per cent had contact with some agency within 1 month of DSH.
• Efforts are needed to increase detection, to avoid prescription of agents to be used
for DSH, and effective recognition and treatment of psychiatric illness.
After the episode:
• ‘First-ever’ episodes respond best to therapy.
• There is a high default rate from clinic attenders.
Treatments
• Psychotherapy; dialectical behavior therapy, family therapy.
• Social support.
• Treat mood disorder, thought disorder, substance use disorder.
• Pharmacology – lithium reduces suicide risk; well–managed depression will
reduce risk.
• ECT may reduce suicidality in a manic or several depressed state.
For those with repeated DSH, the above interventions have been of limited effectiveness.
REPEATED SELF-MUTILATION
EPIDEMIOLOGY
• Types:
– Repeated minor lacerations (usually of the wrist) – the largest group.
– Psychotic patients.
– Seriously suicidal.
• Incidence:
– 3–4 per cent in the general psychiatric population within 1 month.
– 15 per cent of the subnormal population within 1 month.
• Age and sex – younger; women more than men in hospital populations.
SYMPTOMS
• Mounting tension, sense of emptiness/loss.
• Depressive feeling described less commonly.
• Emotional relief on self-injury.
CORRELATES
• The ‘typical’ wrist-cutter is described as young, female, aged 16–24.
– May have nursing or other medical connections.
– Low self-esteem, expressing dislike of own body.
– May have associated anorexia/bulimia nervosa.
– Around 50 per cent have used alcohol or drugs to excess.
– Some research has shown increased incidence of menstrual irregularity.
– Poor verbalizer.
• Childhood – increased incidence of broken homes and hospitalization before
age 5.
• Precipitants – recent loss, rejection or impasse in relationships.
MANAGEMENT
Management is difficult. A carefully coordinated team response is needed to mutilat-
ing behaviour (minimize ‘gain’). Therapy explores areas of self-image/esteem. Tension
reduction might be achieved by relaxation techniques.
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Uncommon psychiatric 12
syndromes
DELUSIONAL MISIDENTIFICATION
CAPGRAS’ SYNDROME (‘DELUSION OF DOUBLES’)
CLINICAL FEATURES
This is the belief that a person known to the patient has been replaced by an exact double.
Usually the person implicated is a close relative, particularly spouse. This is not part of
organic confusion, but repeated misidentification of a specific person or people.
AETIOLOGY
It is usually part of a paranoid disorder, particularly schizophrenic, but may be affective
or as a primary delusional disorder. It could be the result of an ambivalent attitude to
the person implicated. It may occur in the presence of organic brain disease, particu-
larly frontal lobe dysfunction.
MANAGEMENT
Treat the underlying disorder; support the relative.
OTHER CONDITIONS
• Fregoli’s syndrome – ‘ordinary’ people in the patient’s environment are ‘persecutors

in disguise’; less common than Capgras’.
• Syndrome of intermetamorphosis: person A becomes person B, B becomes C, C
becomes A, etc.
• Syndrome of subjective doubles – rare, but when it occurs it usually co-exists with
Capgras’. The patient believes that doubles of him/herself exist.
• Lycanthropy – the belief that the patient has been transformed into an animal.
• Reduplicative paramnesia – the belief that two identical places exist. It is clearly
associated with diffuse brain injury.
SUBTYPES OF DELUSION DISORDER 145
• Autoscopy – hallucination of oneself in a ‘near-death experience’. Is this a psychiatric

disorder, a metaphysical experience or a neurophysiological dysfunction?
SUBTYPES OF DELUSION DISORDER
When unassociated with any other secondary psychiatric or organic disorder, the
primary condition is considered a subtype of delusional disorders (see Chapter 3).
DE CLÉRAMBAULT’S SYNDROME
CLINICAL FEATURES
This is the delusional belief that another person (the object), often of unattainably
higher social status, loves the patient (the subject) intensely. The subject is usually
female. There may be sudden onset of delusion. ‘Pure’ erotomania is an isolated phe-
nomenon. ‘Secondary’ erotomania is much more common and occurs in the setting of
paranoid, manic or other disorder. The subject may be importunate and disrupt the
object’s life and, after rejection, the love may turn to hatred.
AETIOLOGY
If the ‘pure’ form, it may be projection of denied, narcissistic self-love.
MANAGEMENT
Treat the underlying disorder if secondary. It can be very resistant to physical treat-
ments and psychotherapy if in the ‘pure’ form.
OTHELLO SYNDROME (‘MORBID JEALOUSY’)
CLINICAL FEATURES
This is the delusion of infidelity on the part of the sexual partner. Normal phenomena
are interpreted to fit in with this conviction. The patient may examine underwear, sex-
ual organs, etc., in an attempt to find proof. There is a desire to extract a confession,
which may lead to severe aggression and murder.
AETIOLOGY
It may be associated with alcoholism (in a jealous, insecure personality), organic psycho-
sis, schizophrenia (particularly paranoia) or with paranoid, obsessional personality.
It might be a projection of the patient’s own desires for infidelity or of repressed
homosexuality, or the result of other feelings of inadequacy.
MANAGEMENT
Treat the underlying condition. Antipsychotic medications may help. Geographical
separation from the partner is often advisable.
146 UNCOMMON PSYCHIATRIC SYNDROMES
MONOSYMPTOMATIC HYPOCHONDRIACAL PSYCHOSIS (MUNRO, 1980)
CLINICAL FEATURES
Hypochondriacal delusions may take various forms; e.g. skin infestation by insects
(Ekbom’s syndrome), internal parasitosis, delusion of lumps under the skin (leading
to excoriation), conviction of personal ugliness or emission of foul smell, delusional
body image disturbance, delusional pain.
Some are coenaesthopathic states with exaggeration or distortion of subjective experi-
ence and sensation.
The patient is convinced of the physical cause and gathers ‘evidence’ for this. Multiple
opinions are sought and bizarre treatments are suggested by the patient. Increasing
anger and paranoia may be expressed. The delusional system may remain ‘encapsulated’
for years, without general thought disorder or personality deterioration.
HYSTERIA – ALLIED SYNDROMES
COUVADE SYNDROME
CLINICAL FEATURES
The husband (usually) develops extreme anxiety and various physical symptoms, as of
pregnancy, when his wife is pregnant. He may have morning sickness, abdominal
pains, constipation, food cravings, etc. It tends to present in the third or ninth month
of the wife’s pregnancy. The name ‘couvade’ refers to the ancient ritual of the husband
retiring to bed and simulating labour pains during the wife’s labour.
AETIOLOGY
This may be a manifestation of understandable anxiety in an anxious father-to-be.
It could be expression of frustrated creativity, jealousy of attention paid to wife or
over-identification with wife.
MANAGEMENT
Simple reassurance is usually adequate.
GANSER’S SYNDROME (‘SYNDROME OF APPROXIMATE ANSWERS’)
This is classified in ICD-10 under ‘other dissociative disorders’; classified as dissocia-

tive disorder NOS in DSM-IV.
CLINICAL FEATURES
The patient gives approximate answers (absurdly wrong but almost correct, such as
‘a horse has five legs’), which are inconsistent. There may also be hysterical conver-
sion symptoms (e.g. ataxia), dissociative amnesia (altered level of consciousness) and
HYSTERIA – ALLIED SYNDROMES 147
occasionally pseudohallucinations. Onset is often sudden and related to stressful

(or criminal) circumstances.
AETIOLOGY
There is an hysterical twilight state. Occasionally, it is post-epileptic or associated with
depression. It may be similar to the ‘buffoonery state’ of acute or catatonic schizophrenia.
MANAGEMENT
The person usually recovers when the stressor is removed.
MULTIPLE PERSONALITY DISORDER (MERSKEY, 1992)
This rare condition is now termed dissociative identity disorder. The patient has two or
more distinct personalities. with dramatic changes from one personality to another.
There is amnesia for existence and events during the other personality.
There is a history of childhood sexual abuse in more than 70% of patients. Epilepsy
was noted in 25 per cent in one study. There is a wide range of psychopathology (Ross
et al., 1990).
DIFFERENTIAL DIAGNOSIS
Malingering; dissociative fugue; dissociative amnesia; schizophrenia.
MANAGEMENT AND PROGNOSIS

• Thorough assessment, often forensic.
• Hypnotherapy and individual psychotherapy are used.
• Reintegration is the goal of therapy.
• Medication is of limited value.
Prognosis is poor and related to the number, type and chronicity of personalities.
Earlier onset confers poor prognosis.
MÜNCHAUSEN SYNDROME
This is classified under ‘other disorder of adult personality and behaviour’ in ICD-10.
In DSM-IV it is factitious disorder.
Symptoms are generated intentionally under voluntary will, motivated to assume
the sick role, with absence of external incentives (economic gain, avoiding criminal
prosecution, etc.). DSM-IV emphasizes whether there are predominantly psychological
or physical symptoms, or both.
CLINICAL FEATURES
The patient gives plausible, often dramatic, history and symptoms of acute physical
illness in the absence of that illness. He/she may inflict self-injury or simulate symptoms
148 UNCOMMON PSYCHIATRIC SYNDROMES
in a bizarre way (e.g. insert needles into chest, swallow blood, etc.). A common com-
plaint is of abdominal symptoms. There is a history of multiple hospital admissions
and multiple operations. Lying is pathological with a lack of personal rapport.
Variants of the syndrome present with psychiatric symptoms or false bereavements. It
may present with factitious illness in a child or dependent (Münchausen by proxy).
AETIOLOGY
There is hysterial behaviour in severely disordered personality. The person is
masochistic, attention-seeking, and may seek analgesic drugs.
MANAGEMENT
Sufferers frequently abscond from psychiatric treatment. Occasionally there is a degree
of treatable depression. There is a need to limit behaviour – keep a hospital registry of
such patients.
FOLIE À DEUX (LASÉQUE AND FAIRET, 1877)
Induced or shared psychosis – ICD-10, DSM-IV.
CLINICAL FEATURES
Usually one member of a couple is psychotic and the other comes to share the delu-
sional beliefs. It may occur in families or groups (folie à plusieurs). Persecutory or
hypochondriacal delusions may become shared by the submissive member of an over-
involved pair. There may not be evidence of this dominance and submission, however,
and it may be difficult to decide which members are primarily psychotic. It most
frequently occurs in a mother and daughter relationship.
AETIOLOGY
Often there is over-identification with the psychotic person in a submissive, over-
dependent personality. The person may have low IQ.
MANAGEMENT
Treat the psychotic member, if identifiable. Supportive and family therapy is often indi-
cated. Psychosis will need treatment if is co-morbid and independent; i.e. folie simultanée.
DEPRESSION – ALLIED SYNDROME
COTARD’S SYNDROME (‘NIHILISTIC DELUSIONS’)
CLINICAL FEATURES
There are delusions of negation, to a varying degree. The patient may believe that
his/her body or self has disappeared and he/she no longer exists, even that the whole
universe no longer exists. This occurs more commonly in women. Often it is associated
with anxiety and irritability. It may be associated with mutism, delusions of self-
blame, hallucinations (e.g. of rotting smells), refusal to eat.
AETIOLOGY
It is frequently a depressive symptom, but may have a basis in organic brain disease
(acute or chronic). Depersonalization is frequently the underlying phenomenon.
Treat as per underlying condition.
Asher R (1951) The Mü nchausen syndrome Lancet i, 339.

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Organic psychiatry 13
Stage 1: Organic or functional?

• Functional causes:
– Depressive pseudodementia.
– Hysterical pseudodementia (including Ganser’s syndrome).
– Schizophrenic disturbance.
– Simulation (malingering).
Stage 2: Acute or chronic?

• Features of acute organic disorder (delirium):
– Acute onset.
– Impaired consciousness.
– Perceptual abnormalities.
– Fluctuating course.
• Features of chronic organic disorder (dementia):
– Insidious onset.
– Clear consciousness.
– Global impairment of cerebral functions.
– Steady, progressive course.
Stage 3: Focal or diffuse lesion?
Stage 4: Precise aetiology.
DEMENTIA
Dementia is a global, progressive deterioration of all mental functions (memory, lan-

guage, recognition, intellect, and personality) occurring in clear consciousness.
LOCALIZATION OF CEREBRAL FUNCTION 151
DIFFERENTIAL DIAGNOSIS OF DEMENTIA

Clinical
• Amnesic syndrome.
• Dysphasic syndromes.
• Parietal lobe syndrome.
• Frontal lobe syndrome.
• Subcortical dementias.
• Pseudodementia.
Aetiological
Primary/degenerative
• Alzheimer’s, Pick’s, Huntington’s, Creutzfeld–Jakob, frontal lobar, Lewy-body,
Parkinson’s, multiple sclerosis, Wilson’s disease.
Secondary
• Vascular – multi-infarct dementia, subarachnoid, subdural haematoma.
• Infective – abscess, encephalitis, neurosyphilis, AIDS, prion diseases,
encephalopathies.
• Traumatic – head injury, punch-drunk syndrome, haematoma.
• Neoplastic – primary/secondary degree neoplasia, paraneo-plastic syndrome
(especially CA bronchi).
• Inflammatory – encephalopathies, SLE, cranial arteritis.
• Metabolic – hepatic, renal, cardiac failure, anaemia, hypoglycaemia, vitamin defi-
ciencies, metal toxicity.
• Endocrine – hypothyroidism, hypo/hyper-parathyroid, Addison’s disease.
• Hydrocephalus – normal-pressure or obstructive.
LOCALIZATION OF CEREBRAL FUNCTION
DYSFUNCTION OF FRONTAL LOBES
Prefrontal and orbital cortex

Personality changes include ‘pseudopsychopathic’ – disinhibition, facetious humour,
euphoria (said to be related to orbitofrontal area). ‘Pseudodepressive’ changes include
apathy, loss of initiative, slowing of thought and motor activity (said to be related to
dorsolateral area).
There can also be inattention, distractability, perseveration of actions (as seen in card-
sorting tasks), difficulty in programming and planning behaviour (seen in Porteus
Maze tasks) and urinary incontinence.
Motor and premotor cortex

Features are contralateral spastic paresis, reduced fine motor control, gegenhalten,
grasp reflex, reduced verbal fluency, impaired spelling, motor Jacksonian and adversive
attacks.
Damage to Broca’s area (dominant premotor cortex) produces expressive dysphasia.
152 ORGANIC PSYCHIATRY
DYSFUNCTION OF PARIETAL LOBES
• Cortical sensory loss.

• Astereognosis.
• Sensory Jacksonian fits.
• Disorders of body schema:
– Sensory inattention.
– Constructional apraxia.
– Dressing apraxia.
– Topographical agnosia.
– Hemisomatognosia, autotopagnosia.
• Anosognosia (denial of the disorders).
• If posterior dominant parietal lobe – Gerstmann’s syndrome:
– Right–left disorientation.
– Finger agnosia.
– Dyscalculia.
– Dysgraphia.
DYSFUNCTION OF TEMPORAL LOBES
Auditory functions
• Impaired auditory sensation – verbal (dominant), musical (non-dominant), auditory
agnosia.
• Sensory dysphasia (Wernicke’s area – dominant).
Visual functions
• Contralateral, upper quadrant, homonymous hemianopia (optic radiation).
• Prosopagnosia (inability to recognize faces).
Memory
• Bilateral lesions – global amnesia with normal immediate recall (includes
Korsakoff ’s psychosis).
• Unilateral lesions – dominant: impaired verbal memory; non-dominant: impaired
non-verbal (spatial) memory.
Personality/psychosis
• Related to temporal lobe epilepsy.
• Dominant – ? schizophreniform.
• ? Emotional lability, aggressive behaviour.
• Reduced sexual activity usually.
• Klüver–Bucy syndrome – extensive bitemporal lesions.
NEUROPSYCHIATRIC ASSESSMENT 153
DYSFUNCTION OF OCCIPITAL LOBES
There are visual impairments: cortical blindness (bilateral), contralateral homonym-

ous hemianopia (unilateral), scotomata (focal), loss of visual perception, visual object
agnosia, alexia without agraphia.
DYSFUNCTION OF DIENCEPHALON AND BRAINSTEM

(‘THE BASAL SYNDROME’)
• Korsakoff-type amnesia.
• Hypersomnia.
• Emotional lability.
• Hypothalamus:
– Polydipsia and polyuria.
– Appetite disturbance.
– Elevation of temperature.
OCCLUSION OF SPECIFIC ARTERIES
Anterior cerebral
• Contralateral lower-limb paresis and sensory deficits.
• Clouding of consciousness.
Middle cerebral
• Clouding of consciousness.
• Contralateral hemiplegia, hemianaesthesia and hemianopia.
• Motor and sensory aphasia if dominant.
Posterior cerebral
• As for middle cerebral.
• Contralateral hemianalgesia and spontaneous pain (thalamus).
Posterior inferior cerebellar artery
• Ipsilateral – facial analgesia, Horner’s syndrome, ataxia, weakness of vocal cords
and tongue.
• Dissociated or contralateral analgesia.
Basilar artery Headache, vertigo, coma, flaccid quadriplegia or monoplegia, total
anaesthesia, hyperpyrexia, ipsilateral cranial nerve palsies and cerebellar signs.
NEUROPSYCHIATRIC ASSESSMENT
Assess
Attention, memory, language, visuospatial functions, calculation, abstract thinking,
handedness, facial asymmetry, abnormal movements, primitive reflexes (e.g. palmo-
mental/grasp/snout reflexes), ‘soft signs’.
‘Soft signs’: These include non-normative performance on a motor or sensory test

identical or akin to a test item of the traditional neurological examination, but not
associated with any localizable neurological disorder.
They are related to cognitive dysfunction, learning difficulties and psychiatric dis-
turbance, but are also frequently found in children without these problems. Include –
synkinetic (mirror) movements, poor coordination, impaired constructional ability,
speech impediments, hyperactive reflexes, impaired special senses. They are not always
reliably detected.
Best discriminators of dementia (especially from depression)

Clinical
• Tests of orientation.
• Recalling an address after 5 minutes.
• Sentence repetition (Babcock).
• Tests of general information.
• No evidence of depressed mood.
The quality of answers is of prime importance. Look for:
– Perseveration.
– Confabulation.
– Dysphasia – especially nominal dysphasia.
History
• No history of depression.
Investigations
• Psychometry – verbal performance discrepancy.
• Sulcal widening on CT scan (and ventricular dilatation to a lesser extent).
• EEG abnormalities.
Depression/pseudodementia (also see Chapter 17)

• 8 per cent diagnosed as dementing later found to be depressed.
• 2.5 per cent diagnosed as depressed later found to be dementing.
DELIRIUM
Between 10 per cent and 30 per cent of all medical/surgical inpatients have had delir-
ium. There is a higher prevalence in the elderly or seriously ill. Risk factors include
increasing age, underlying dementia or physical illness.
ICD-10 criteria for delirium

1 Impairment for consciousness and attention.
2 Global disturbance of cognition (perceptual-impaired disturbances, orientation,
memory, comprehension).
3 Psychomotor disturbances (hypo- or hyper-activity).
4 Disturbance of sleep–wake cycle.
5 Emotional disturbances (anxiety, fear, depression, apathy, perplexity).
THE DEMENTIAS 155
Aetiology
There are multifactorial aetiological mechanisms, but relative similarity of individual
clinical pictures. Aetiology is undetermined in 5–20 per cent of the elderly delirious.
Dementia coveys increased risk.
Most common causes are CVA, UTI, diabetes, ischaemic heart disease, metabolic
abnormalities, major organ failure, drug toxicity (prescribed or alcohol or illicit).
There is significant mortality – up to 76 per cent of elderly, hospitalized delirious
patients die during hospitalization.
Management
• Adequate investigation – history from staff, relatives.
• Baseline laboratory tests, EEG, CT/MRI.
• Treat underlying cause, if known.
• Treat any (other) reversible component; e.g. infection, anaemia, dehydration.
• Nurse in well-lit room, avoid under/overstimulation from environment.
• Agitation – use lowest effective dosage of atypical antipsychotics.
THE DEMENTIAS
Common dementias include (per cent of total cases):

• Alzheimer’s disease – 50–70 per cent.
• Vascular dementia – 5–15 per cent.
• Alzheimer’s ⫹ vascular dementia – 10–15 per cent.
• Lewy-body dementia – 5–15 per cent.
• Other – ⬍10 per cent.
ALZHEIMER’S DISEASE (AD)
This historically refers to presenile dementia before 65 years, but now also includes
dementia after age 65.
EPIDEMIOLOGY
About 3 per cent of the population aged over 65 years have AD, 50 per cent over
85 years. Age is the most important risk factor for AD, but AD is not just a form of
accelerated aging!
There is a higher prevalence in females (2:1), even when controlled for greater
longevity in females and increased CVA in males.
AETIOLOGY
See the diagram on page 156.
Genetics
• Trisomy 21 – There is an association between AD and Down syndrome. All develop
the typical histopathological lesions of AD (amyloid plaques, neurofibrillary tan-
gles before age 40 years).
Unknown, probably multifactorial

Proposed model (Blass, 1993):
Environmental factors Aging Genetic abnormalities
Cytoskeletal Mitochondrial Amyloidosis

abnormalities abnormalities
(neurofibrillary
tangle, etc.)
Impaired cellular homeostasis

in response to stress
Loss of synaptic Inflammatory reaction

connections
Clinical syndrome
• Chromosome 21 – Mutations are found in the gene encoding for ‘amyloid precursor
protein’ (APP), seen in familial AD.
• Chromosome 14 – Early-onset AD.
• Chromosome 19 – Sporadic, late-onset AD.
Risk factors
• Head trauma (some similarity in neuropathology findings in punch-drunk
syndrome).
• Low educational level.
Neuropathology
The ‘amyloid hypothesis’ Either increased amyloid ␤-peptide synthesis or decreased
amyloid clearance in the brain results in aggregation of these peptides to form amy-
loid plaques (AP). APs are seen particularly in the outer three layers of cortex, but all
layers are affected – hippocampus, parietal regions usually first affected. The deposi-
tion of these neuritic plaques precedes AD.
The extent of APs correlates with severity of clinical illness, and are hypothesized to
be the pathogenesis of AD.
Apolipoprotein E (APOE) APOE is a cell membrane protein that transports choles-
terol into the cell. Homozygotes for APOE 4 on chomosome 19 have a higher risk of
AD than heterozygotes. APOE 4 is thought to increase the risk for AD by either
increasing the sythesis of AP, or decreasing the clearance of amyloid ␤-peptides.
Neurofibrillary tangles (NFTs) NFTs are intracellular hyperphosphorylated ␶ pro-
teins that accumulate and form paired helical filaments. The extent of NFTs serves as
a marker of severity of illness.
Other abnormalities:
• Glial proliferation.
• Granulovascular degeneration – especially in hippocampus.
• Hirano inclusion bodies.
THE DEMENTIAS 157
• Selective neuronal cell loss – early in hippocampal regions, nucleus basalis of

Meynert; visuosensory and sensorimotor areas relatively spared until later. The
loss of synapses correlates best with degree of cognitive impairment.
Neurochemistry
Cholinergic loss Evidence includes:
• Reduced cholinergic neurotransmission in the cortex and hippocampus.
• Reduced cholinergic cells in nucleus basalis of Meynert, medial septum and diago-
nal band.
• Cholinergic deficit correlated with cognitive dysfunction.
• Correlations between cortical cholinergic reduction, basalis nucleus reduction and
cortical plaque density.
Noradrenergic loss There is cell loss in locus coeruleus, especially in early-onset AD;
correlates with depression in AD.
Serotonergic loss There is loss in cortical 5-HT2 receptors, especially in frontal and
temporal lobes. Cell loss and NFT accumulation also in nucleus raphe dorsalis.
Other neurotransmitters/neuropeptides:
• Decreased somatostatin.
• Decreased GABA.
• Decreased dopamine.
OTHER ABNORMALITIES
• Oxidative damage caused by accumulation of free radicals is implicated in AD – ?
related to abnormal phosphorylation of ‘tau’.
• There is deficiency of mitochondrial ␣-ketoglutarate dehydrogenase complex or
pyruvate dehydrogenate complex.
• Mitochondrial enzymatic systems – ? may explain decreased glucose utilization in
AD brain.
Immunology
Immunohistochemistry shows:
• Localized inflammatory reaction in AD.
• Complement in SPs.
• Neuroglial reaction to amyloid.
• Increased acute-phase reactants.
However, these are probably not primary events because there is little evidence for an
autoimmune or infectious process.
Classification of AD
See Table 13.1. Features of Klü ver–Bucy syndrome (hyperorality, hypersexuality,
placidity, increased touching) are seen in type I AD, reflecting bitemporal damage.
CLINICAL FEATURES
There is generally an insidious onset. Memory failure is usually the presenting feature,
often accompanied by lability of mood, anxiety, depression or apathy, with impaired
attention.
Table 13.1 Type I and type II Alzheimer’s

Type I Type II
Later onset – SDAT Early onset

Pathology ⫹ ⫹ ⫹ ⫹ (esp. frontal, temporal)
Neurochemistry ⫹ ⫹⫹⫹
Clinical features Females ⬎ males More rapid, fulminant
More aphasia, myoclonus, increased
genetic loading
Adapted from Roth (1986).
There may be abnormal, disinhibited behaviour, often an exaggeration of former

personality traits. Agitation is a feature, especially at night. ‘Sundowning’ is confusion
and wandering at night.
There are generally three phases:
• First phase – memory (2 years) predominantly affected.
• Second phase – general cognitive decline, development of expressive/receptive
dysphoria, logoclonia, seizures, delusions, hallucinations.
• Third, terminal phase – profound dementia, neurological signs ↑↑, primitive
reflexes ↑, double incontinence.
MANAGEMENT
See Chapter 17. There should be a thorough initial assessment. Clarify the diagnosis,
rule out any medical cause, treat all/any reversible component (e.g. hypoxia, mild
heart failure, anaemia).
Education Intensive family and psychosocial support is necessary.
Psychotherapy Reality orientation, reminescence therapy are useful.
Drug pharmacotherapy
• Acetylcholinesterase inhibitors target cognitive symptoms – memory and attention –
and may delay but not alter disease progression. Commonly used drugs include
donepezil, galantamine and rivastigmine. No clear evidence at present for superior
efficacy between these drugs, but there may be advanages in dosing and tolerabil-
ity. Drugs stabilize functioning in the first year and make subsequent decline
more gradual. Uncertainty as to how early to start treatment and how long to
continue.
• NMDA receptor antagonists (e.g. memantine) slow the rate of cognitive and func-
tional decline.
• Experimental treatments include NSAIDs, oestrogen, statins, heavy metal chelators
(may enhance amyloid clearance); amyloid vaccine is also under investigation.
• Vitamin E and selegiline may delay but not alter disease progression.
• Antipsychotics may be used to target behavioral symptoms and psychosis.
• Antidepressants can be given for depressive symptoms.
Future treatments Research is under way involving vaccination with antibodies to
amyloid ␤-peptide.
THE DEMENTIAS 159
PROGNOSIS
Severity of cognitive impairment is a crude index of survival time. Deterioration to
death is within 2–5 years of hospital admission.
MILD COGNITIVE IMPAIRMENT (MCI)
The cognitive ability of the elderly naturally declines with age. The term MCI refers to
a state between normal age-related cognitive decline and dementia. MCI is marked by
objective evidence of memory deficits but with intact general cognitive and activity
functioning.
A significant proportion of individuals diagnosed with MCI will progress to
Alzheimer’s disease – up to 36 per cent per year. More research is needed to ascertain
whether MCI represents an early stage of AD.
The rate of death for those diagnosed with MCI is about 1.7 times that of those
without the diagnosis.
VASCULAR DEMENTIA (VaD)
This is the most common form of dementia after Alzheimer’s disease.
EPIDEMIOLOGY
VaD represents 5–15 per cent of dementias. As with AD, prevalence increases with age.
AETIOLOGY
VaD is caused by either ischemic injury from embolic and or atherothrombotic vessel
occlusions. An autosomal dominant gene on chromosome 19 conveys small vessel dis-
ease which results in VaD in 50 per cent of carriers.
CLINICAL FEATURES
There is acute onset with patchy, stepwise deterioration. There is fluctuating cognitive
impairment with episodes of nocturnal confusion. Depression and ‘emotional incon-
tinence’ may be prominent.
Personality is often preserved until late, and insight is often intact.
Focal neurological deficits are common, and hypertension is present in most cases.
Frequently, there is evidence of arteriosclerosis elsewhere.
The Hatchinski index (using the above clinical features) may give a diagnostically
indicative score.
Binswanger’s chronic progressive subcortical encephalopathy with white matter
degeneration may be caused by arteriosclerosis.
TREATMENT AND PROGNOSIS

Treatment is similar to that for AD, but additional importance is placed on controlling
the risk factors for coronary artery disease and stroke.
There is a slightly longer time course than with AD. Death occurs in 4–5 years;
50 per cent of deaths result from ischaemic heart disease.
PICK’S DISEASE
EPIDEMIOLOGY
The peak age of onset is 40–60 years, and it is most common in men. It accounts for
about 5 per cent of dementias.
AETIOLOGY
A minority of cases are due to an autosomal dominant gene with variable penetrance.
Pathology
• Frontal and temporal lobes are particularly affected.
• ‘Knife-blade’ atrophy is seen due to neuronal loss.
• Pick’s cells are present. These are swollen cells with silver-staining inclusion bodies
(‘balloon cells’).
• Fibrous gliosis is present.
• SPs or NFTs are absent.
CLINICAL FEATURES
Personality deterioration occurs early, with a ‘frontal lobe’ syndrome of disinhibition.
Perseveration and dysphasia are characteristic.
There is a less generalized cognitive decline than in AD. Hyperalgesia is experienced
late in illness in some patients.
PROGNOSIS
There is a slower time-course than in Alzheimer’s disease, being 2–10 years to death.
The average is 5 years from diagnosis.
HUNTINGTON’S CHOREA
EPIDEMIOLOGY
The prevalence is 2–10 cases per 100 000 population. The age at onset is usually 25–50
years.
AETIOLOGY
• There is a single autosomal dominant gene on chromosome 4 with almost
100 per cent penetrance. The gene is located on proximal arm of chromosome 4
(Gusella et al., 1993).
• There is selective loss of GABA neurones, particularly in basal ganglia.
• GABA and glutamic acid decarboxylase have been shown to be reduced, resulting
in dopamine hypersensitivity.
• Glutamate excitotoxicity a possible mechanism?
Pathology
There is atrophy of caudate and putamen in particular, but also of cortex (especially
frontal).
THE DEMENTIAS 161
CLINICAL FEATURES
• May present with chorea or with mental changes. Often they develop independ-
ently. Psychiatric illness may precede chorea.
• Personality change is often realized retrospectively. Characteristically the person
becomes irritable, distractable, apathetic and depressed.
• Psychotic disorders, particularly a paranoid psychosis, may develop.
• Insidious onset of global dementia may develop.
• Chorea, initially of face and upper limbs, may develop. There may also be intention
tremor, ataxic gait, dysarthria and rigidity.
• In children, rigidity, tremor and fits are more common and there is more rapid
deterioration.
• There is a high rate of suicide among (unaffected) relatives.
• CT/MRI – show dilated ventricles, caudate atrophy.
• PET/SPECT – show frontal and basal ganglia hypometabolism.
• EEG – ‘flat’.
PROGNOSIS
In adults, death occurs within 13–16 years; within 8 years in children.
CREUTZFELDT–JAKOB DISEASE (CJD)
EPIDEMIOLOGY
CJD is rare and occurs equally in males and females. Onset is usually within the range
50 to 70 years of age for the sporadic form; the average is 30 years with the variant
form (vCJD) – thought to be an animal crossover from eating beef from cows infected
with bovine spongiform encephalopathy.
Sporadic CJD accounts for 80–85 per cent of cases; inherited form, 5 per cent;
iatrogenic form, 5 per cent; other forms, 5–10 per cent.
AETIOLOGY
It is a prion disorder – neurodegenerative infective protein pathogens which are
encoded on human chromosome 20. It also appears as an inherited autosomal dom-
inant form.
Disease may be transmitted iatrogenically from infected CNS stereotactic needles,
or corneal transplant.
Pathology
There is spongiform, neuronal degeneration with astrocytic glial proliferation.
CLINICAL FEATURES
• Personality change, apathy, depression, anxiety, fatigue, withdrawal, slowness,
memory loss, organic psychosis.
• Seizures, myoclonic jerks, cortical blindness.
• CT/MRI – cortical atrophy, worse frontally.
• Abnormal EEG in 90 per cent – periodic triphasic complexes seen in CJD but
not vCJD.
PROGNOSIS
CJD is rapidly progressive over 6 months to 2 years.
FRONTAL LOBE DEMENTIA
This is a ‘spongiform’ disease predominantly affecting frontal lobe, producing charac-

teristic frontal lobe syndrome. The EEG is normal. There is a family history in
50 per cent of cases.
LEWY-BODY DEMENTIA
This is a recently described dementia which may be the second most common. It is
characterized by confusional states, fluctuating cognitive impairment, psychotic
symptoms (hallucinations, delusions, depression), mild/variable short-term memory
loss, some mild extrapyramidal features or extreme sensitivity to EPS effects with neu-
roleptic treatment.
The pathological hallmark is the Lewy-body (LB) – intracellular inclusion bodies of
ubiquitin, ␶ protein, and other proteins.
LBs are classically seen in Parkinson’s disease, especially in substantia nigra.
They are also seen cortically and subcortically in LB dementia, especially in
hippocampus.
HYDROCEPHALUS
Types
1 Non-obstructive and communicating – secondary to brain atrophy
2 Obstructive and non-communicating – secondary to obstruction of CSF flow within
the ventricular system.
3 Obstructive and communicating (‘normal pressure hydrocephalus’) – secondary to
obstruction of CSF flow in the subarachnoid space or failure of normal absorp-
tion. Fifty per cent of cases may be due to subarachnoid haemorrhage, meningitis,
head injury.
CLINICAL FEATURES
• Memory impairment.
• Slowness and apathy.
• Unsteady gait.
• Incontinence.

Ventriculo-atrial shunt to lower the intraventricular pressure may help. The prognosis
is best in idiopathic disease, especially when the duration of illness is short.
VITAMIN DEFICIENCIES 163
SUBCORTICAL DEMENTIA
Initially described in progressive supranuclear palsy (Steele–Richardson–Olszewski

syndrome), this is now recognized in other dementing processes (e.g. Parkinson’s disease,
Huntington’s chorea).
CLINICAL FEATURES
• Forgetfulness.
• Slowing of thought processes – delayed answers (‘bradyphrenia’).
• Personality change – apathy, irritability, depression.
• Decreased ability to manipulate acquired knowledge.

• No specific treatment.
• Very gradual deterioration.
PUNCH-DRUNK SYNDROME
This is usually the result of repeated mild head injuries (e.g. in boxers). There is cere-
bral atrophy with brain stem and hippocampal–limbic damage.
CLINICAL FEATURES
• Cerebellar lesions – ataxia, festinant gait.
• Pyramidal lesions – spasticity.
• Extrapyramidal lesions – tremor.
• Intellectual and personality deterioration.
VITAMIN DEFICIENCIES
NICOTINIC ACID DEFICIENCY (PELLAGRA)
• ‘Dermatitis, dementia and diarrhoea.’

• May be florid confusion with hallucinations.
• May appear ‘hysterical’.
THIAMINE (B1) DEFICIENCY
Wernicke’s encephalopathy
• Acute onset of:
– Ophthalmoplegia and nystagmus.
– Clouding of consciousness.
– Ataxia.
– Peripheral neuropathy.
In 84 per cent of cases this results in Korsakoff ’s psychosis.
AETIOLOGY
• Korsakoff ’s psychosis:
– Thiamine deficiency.
– Head injury.
– Carbon monoxide (CO) poisoning.
– Tumour.
– Anaesthetic accident.
• Thiamine deficiency:
– Alcoholism.
– Starvation.
– Hyperemesis.
Pathology
• Parenchymal loss.
• Proliferation of blood vessels.
• Petechial haemorrhages.
Table 13.2 Psychiatric aspects of endocrine disorders

Condition Clinical features
Cushing’s syndrome Psychiatric features in 50 per cent

Depression
Acute anxiety
Paranoid features
Euphoria – particularly when on steroids
Hyperthyroidism Restlessness and agitation
May present as ‘agitated depression’ or ‘anxiety neurosis’
Rarely delirium
Very rarely functional psychosis
Hypothyroidism Fatigue
Apathy
Psychomotor retardation, rarely organic psychosis
‘Myxoedematous madness’ (Asher, 1949)
Slowing of cognitive functions
Addison’s disease Psychiatric features are frequently present
Depression
Apathy
Mild cognitive impairment
Impotence
Phaeochromocytoma Paroxysms of anxiety, tachycardia, sweating, headache,
hypotension
Hypopituitarism Depression
Apathy
Irritability
Cognitive impairment
Rarely delirium and coma
Hyperparathyroidism Fatigue
Depression
Occasionally cognitive impairment
Hypoparathyroidism Delirium
Agitation and depression
Epilepsy
DRUGS AND TOXINS 165
• Affecting walls of third ventricle, mamillary bodies, thalamus (medial–dorsal

nucleus).
CLINICAL FEATURES
• Very poor retention of recent memories, sometimes with confabulation.
• Retrograde amnesia.
• Apathy or euphoria.
VITAMIN B12 DEFICIENCY
Clinical features are:

• Depression and apathy.
• Dementia.
• Subacute combined degeneration of the cord.
• Pernicious anaemia.
ENDOCRINE DISORDERS (PSYCHIATRIC ASPECTS)
See Table 13.2.
DRUGS AND TOXINS
Table 13.3 Drugs causing toxic confusion
Anticholinergics Amphetamines
Isoniazid Hallucinogens
Cycloserine Corticosteroids
Mecamylamine Barbiturates
Bromides Digoxin
Almost all psychotropics in the elderly
Table 13.4 Toxins
Alcohol – see Chapter 9

Metals:
Lead
– Gastrointestinal disturbance
– Peripheral motor neuropathy
– Acute and chronic organic psychosis
Mercury
– Coarse tremor
– Erythism (nervous, timid, irritable)
Manganese
– Headaches
– Emotional lability
– Impotence
– Parkinsonism
– Delirium
INFECTIONS
NEUROSYPHILIS SHOWING CSF CHANGES
• Many are asymptomatic. There is up to 10 per cent occurrence rate in untreated

cases of syphilis. Increasing incidence is seen in individuals with HIV infection.
• Meningovascular:
– Usually 1–5 years after primary infection.
– Inflammation and exudate from leptomeninges.
– Arteritis.
– Headache, malaise.
– Lethargy, irritability.
– Delirium and/or dementia.
– Cranial nerve disturbance – optic nerve, 8th nerve.
• Tabes dorsalis:
– Atrophy of dorsal roots and posterior columns.
– Lightning pains.
– Degenerative joint disease.
– Ataxia due to proprioceptive loss.
– Paraesthesias of limbs.
– Argyll–Robertson pupils.
– 20 per cent of general paresis cases have tabes.
• General paresis (GPI):
– Spirochaetes found in the brain.
– Thickened dura, atrophied brain.
– Inflammatory changes – perivascular lymphocytes and plasma cells.
– Degenerative changes with cortical thinning.
– Neurological proliferation with ‘rod cells’.
– Insidious onset, though 50 per cent present abruptly.
• Personality changes – irritable, emotionally labile, frontal lobe changes, impaired
insight.
• Cognitive changes – poor concentration, dementia.
CLASSIC PICTURES
• Simple dementing – 20–40 per cent.
• Depressive – 25 per cent.
• Grandiose – 10 per cent.
• Also seen:
– Manic elation.
– Paranoid schizophreniform.
– Neuraesthenia.
Treatment
Penicillin is the only proven effective treatment.
INFECTIONS 167
HERPES SIMPLEX ENCEPHALITIS
Onset is rapid. There are severe inflammatory changes which may be necrotizing and
haemorrhagic. Infection especially affects medial temporal and orbital regions.
The viral aetiology of this disorder may also imply latent infection in other psychi-
atric disorders.
CLINICAL FEATURES
• Pyrexia.
• Focal signs (temporal lobe).
• Delirium, often with marked hallucinations.
PROGNOSIS
In 15 per cent there are severe sequelae – dementia, focal deficits, amnesic syndrome.
Seventy per cent of cases are fatal.
OTHER INFECTIONS/PSYCHIATRIC SEQUELAE
• Typhus.
• Trypanosomiasis (sleeping sickness).
• Cerebral malaria (Plasmodium falciparum, malignant tertiary malaria).
• Encephalitis lethargy – delirium followed by fatigue, parkinsonism, personality
change.
• Acute disseminated encephalomyelitis.
NEUROPSYCHIATRY OF ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS)
AETIOLOGY
This is multifactorial
• Cytopathic effects of virus on CNS (e.g. AIDS dementia).
• Secondary to CNS infection.
• Secondary to systemic illness/metabolic derangement.
• Secondary/exacerbation of pre-existing mental co-morbid illness (e.g. substance
abuse, depression).
• Secondary to psychosocial stressors (stigma, withdrawal of social support, finan-
cial insecurity).
AIDS dementia complex (ADC)
This is the most common neuropsychiatric complication of human immunodefi-
ciency virus (HIV) infection and can occur before AIDS develops.
It is associated with initially poor concentration, mental and motor slowing, apathy –
subcortical dementia features; later, profound dementia, frontal release signs.
In the early stages it is difficult to detect cognitive impairment on neuropsycho-
logical testing.
MRI shows subcortical involvement, widespread changes in cortical grey and white
matter and possibly vacuolation in the spinal cord. Post-mortem studies have shown:
• An encephalitic process.
• HIV-infected multinucleated giant cells and endothelial cells.
• Decreased neuronal density.
Psychosis
This may be paranoid, schizophrenia-like, affective-like, organic psychosis (CNS
involvement, opportunistic infection, CNS lymphoma, zidovudine or other
medication-related).
Affective disorder
There were reports of major depression and of mania which appeared secondary
to HIV infection; this responded to zidovudine treatment. Many symptoms of
depression overlap with clinical features of AIDS itself. Depression also is a grief
reaction.
Suicide is 66 times more common than in the general population (Marzuk et al., 1988).
Adjustment disorders
The most prominent adjustment disorders are anxiety and depression. Worries con-
cern illness progression, impact on family and friends, social status, and work.
MANAGEMENT
• Full evaluation:
– Immunology (CD4 count is best marker in illness progression).
– Neuropsychological tests.
– Neuroimaging.
– CSF, biochemistry.
– Full psychiatric and psychosocial evaluation.
• Psychosocial:
– Education.
– Supportive psychotherapy.
– Counselling.
– Information for patient and family about illness before cognitive deficits appear.
– Mobilize family and financial support.
• Medical:
– Treat infection, metabolic derangements, dehydration, drug toxicity.
• Pharmacological:
– ‘Highly active anti-retroviral therapy’ (HAART) has improved survival follow-
ing diagnosis of ADC.
– Zidovudine (AZT) partially ameliorates cognitive deficits.
– Antidepressants – use lower doses, agents with less anticholinergic toxicity.
– Neuroleptics – atypical antipsychotics for hallucinations/delusions.
– Psychostimulants – methylphenidate is worthy of consideration with psy-
chomotor retardation.
– Lithium – used in some HIV-mania cases, also helpful in leucopenia secondary
to AZT.
– ECT – if no response to mood stabilizers or antidepressants.
METABOLIC DISORDERS (PSYCHIATRIC ASPECTS) 169
METABOLIC DISORDERS (PSYCHIATRIC ASPECTS)
HEPATIC FAILURE
This may present with psychiatric disturbance. Exacerbations and remissions are
typical. Non-specific EEG changes are often an early sign; triphasic waves are seen later.
CLINICAL FEATURES
• Delirium, confusion, irrational and uninhibited behaviour.
• Hypersomnia, coma.
• Labile mood.
• Neurological abnormalities.
URAEMIA
There may be a progressive but fluctuating course.
CLINICAL FEATURES
• Malaise, fatigue, drowsiness.
• Depression.
• Occasionally functional psychosis.
• Acute delirium in 30 per cent.
• Seizures in 30 per cent.
ELECTROLYTE DISTURBANCE
• Sodium depletion – weakness, giddiness, lassitude, nausea, muscle cramps.

• Potassium depletion – depression, malaise, sleep disturbance.
• Hyper- and hypo-calcaemia.
• Hypomagnesaemia.
ACUTE INTERMITTENT PORPHYRIA
There is dominant autosomal inheritance with variable penetrance. Metabolic error

of haem breakdown leads to porphobilinogen in the urine. It may be a response to
barbiturates, alcohol, methyldopa or oral contraceptives.
CLINICAL FEATURES
• Abdominal – colicky pain, vomiting, constipation.
• Neurological – peripheral neuropathy, bulbar palsies, epilepsy.
• Psychiatric:
– Delirium in 50 per cent, depression and emotional lability.
– Psychosis, especially paranoid.
– ‘Hysteria’ – may be diagnosed.
• Skin changes, renal involvements, arthritis.

• Cerebral SLE in 60 per cent.
• Transient, fluctuating mental disturbance.
• Acute organic reaction is commonest; chronic organic reaction is sometimes seen.
• Depressive psychosis is less often seen.
• Schizophreniform psychosis is rare.
• Neurotic reactions are frequent.
MULTIPLE SCLEROSIS
Psychiatric illness may antedate neurological symptoms.

• Depression – reactive, drug-related (steroids)? intrinsic?
• Schizophreniform psychosis.
• Mania/euphoria – related to cognitive impairment.
• Dementia.
SEQUELAE OF HEAD INJURY
Injury may be focal (haemorrhage, infarct, contusion) or diffuse (diffuse axonal injury;
DAI):
1 Primary (at time of impact).
2 Secondary (oedema, hypoxia, increased intracranial pressure).
Prognosis is worsened by:
• Long post-traumatic amnesia (see below).
• Penetrating injury.
• Intracranial bleeding.
Impaired consciousness
Long duration of impaired consciousness suggests a poor prognosis. If longer than
1 month:
• 40 per cent die without regaining consciousness.
• 20 per cent return to work.
Retrograde amnesia
Retrograde amnesia covers the period between injury and the last clear memory from
before the injury. Initially, the period is lengthy but it shrinks over time. The final
duration is often less than 1 minute. This is not a good prognostic indicator.
Post-traumatic amnesia (PTA) (anterograde amnesia)

Anterograde amnesia covers the period between injury and recovery of normal, continu-
ous memory after the injury. There may be ‘islands’ of memory before this full recovery.
PTA is a good prognostic indicator. Duration is related to:
• Neurological sequelae.
• Psychiatric sequelae.
• Time off work.
SEQUELAE OF HEAD INJURY 171
A duration of less than 12 hours suggests probable full recovery; more than
48 hours – probably some residual damage.
PSYCHIATRIC SEQUELAE OF HEAD INJURY
• Amount of brain damage – correlates closely with sequelae.
• Location of brain damage – especially left temporal lobe.
• Development of epilepsy – 5 per cent of closed injuries; 30 per cent of penetrating
injuries.
• Premorbid personality.
• Family history of psychiatric disorder.
• Past history of psychiatric disorder.
• Emotional factors and the ‘meaning’ of the injury to the patient.
• Insecure convalescent environment.
• Compensation and litigation factors.
CLASSIFICATION
Neuroses (‘post-concussional syndrome’)
Neuroses are the commonest psychiatric sequelae (11–22 per cent of severe injuries)
and are often underestimated.
• Mild depression.
• Fatigue – frequently self-limiting but may not disappear for 1 year.
• Anxiety, phobias, hypochondriasis.
• Irritability and sensitivity to noise.
• Somatic complaints – headache, dizziness, impotence.
• Hysterical symptoms.
• Loss of sexual interest.
Personality changes
These are common (6–18 per cent of severe injuries).
• Injuries with brain damage:
– As part of dementia.
– Due to frontal lobe damage.
– As reduced control over aggression.
• Injuries without brain damage:
– Usually an exaggeration of previous traits.
Psychoses
These occur in 5–8 per cent of severe injuries.
• Affective:
– Usually depressive psychosis.
– Associated with right hemisphere and frontal damage.
• Schizophreniform:
– Especially paranoid, may be with morbid jealousy.
– Rarely show ‘process’ schizophrenia.
• Associated with temporal lobe damage.
This occurs in 3 per cent of severe injuries. It is more likely with:
• Long post-traumatic amnesia.
• Left parietal or left temporal lobe damage.
• Penetrating injury.
• Haemorrhage or infection.
• Increasing age.
Recovery may progress over 10 or more years.
MEDICO-LEGAL ASPECTS OF HEAD INJURY
The ‘compensation issue’ is more likely to contribute to disability when:

• The patient feels someone else is at fault.
• It is an industrial injury.
• Financial compensation is possible.
• The patient has low social status and/or is male.
Attitudes towards ‘compensation neurosis’ have recently altered. Symptoms may
persist independently of compensation issues and disability is often underestimated.
Compensation will depend on:
1 Degree of disablement.
2 Likely prognosis for quality of life.
3 Relationship between injury and disability:
– Degree attributable to brain damage.
– Degree attributable to psychic trauma of the accident.
– Degree attributable to mere manipulation.
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Psychiatric aspects of epilepsy 14
and sleep disorders
EPILEPSY
Epilepsy is a term used to describe a persistent neurological condition characterized

by sudden, discrete and recurrent abnormalities in electrical activity (seizures) of the
brain resulting in behavioural, motor or sensory changes or changes in consciousness.
CLASSIFICATIONS
Classification may be according to:
• Symptoms and signs of the seizure.
• Anatomical and electrophysiological evidence of the source of the seizure.
• Aetiology or precipitant of seizures.
Classification of seizure type is more straightforward than classification of ‘the
epilepsies’.
International league against epilepsy classification

1 Partial (focal) seizures (beginning locally in one hemisphere)
a. Simple partial seizures (consciousness not impaired).
i. With motor signs (‘Jacksonian’).
ii. With somatosensory or special sensory symptoms.
iii. With autonomic symptoms.
iv. With psychic symptoms (e.g. perceptual or mood changes).
b. Complex partial seizures (with impaired consciousness).
i. Beginning as simple partial (‘aura’) and progressing to impaired consciousness.
ii. With impaired consciousness at onset – either alone or with automatisms
(‘psychomotor seizures’).
c. Partial seizures secondarily generalized (to tonic–clonic).
2 Generalized seizures (begin bilaterally symmetrical, no local onset)
a. Absence seizures (‘petit mal’).
Atypical absence seizures (‘petit mal variant’).
176 PSYCHIATRIC ASPECTS OF EPILEPSY AND SLEEP DISORDERS
b. Myoclonic seizures.
c. Clonic seizures.
d. Tonic seizures.
e. Tonic–clonic seizures (‘grand mal’).
f. Atonic seizures (‘drop attacks’).
3 Unclassified seizures.
EPIDEMIOLOGY
• Lifetime prevalence – About 10 per cent of the population will experience at least
one seizure in their lifetime. About 3–4 per cent will develop epilepsy.
• Prevalence of active epilepsy is 5 per 1000.
• It is more prevalent in males; M:F ⫽ 1.5:1.
• Highest incidence is in young children and the elderly.
• Estimated 29 per cent of people with epilepsy overall show conspicuous psycho-
logical problems (50 per cent if temporal lobe epilepsy).
Age at onset
• 0–10 years – 30 per cent.
Seizure type
• Partial – 60 per cent (mostly complex, 90 per cent arising in temporal lobes).
• Generalized – 35 per cent.
• Mixed – 13 per cent.
AETIOLOGY
• Post-traumatic – 7 per cent.
• Cerebrovascular – 9 per cent.
• Other – 9 per cent.
• Unknown – 75 per cent.
PROGNOSIS
Eighty per cent of those having a first seizure will have further seizures. Fifty per cent
of those will have 10 or fewer seizures, usually as a short burst over a few months. If
free for 5 years on medication, they have 30 per cent chance of having further fits
if medication is stopped.
There is an increased risk of death due to accidents, especially drowning. The risk of
unexplained sudden death is 20 times greater than that of the general population.
GENETIC COUNSELLING
The recurrent risk is 1 in 25 if one parent has had epilepsy, 1 in 10 if parent and grand-
parent do. Certain epilepsies have a strong genetic component (e.g. juvenile myoclonic
epilepsy).
EPILEPSY 177
FEATURES AND DIAGNOSIS
PREICTAL PHASE
• Prodromal features:
– Irritability, tension, insomnia, restlessness, occasionally suicidal depression.
– May occur days or hours before fit.
• Aura:
– Usually precedes a fit by only a few seconds, and lasts a few seconds – acute
perceptual change, depersonalization, acute mood change, etc.
– In itself a focal fit, reflecting abnormal electrical discharge.
– Indicates focal disturbance in cerebral cortex.
– Temporal lobe aura typically a rising epigastric feeling; déjàvu.
ICTAL PHASE: AUTOMATISMS

The commonest source is temporal lobe structures – may also be frontal parietal,
uncal or cingulate.
There is a state of clouded consciousness which occurs during or immediately after
a seizure. The individual retains control of posture and muscle tone but performs sim-
ple or complex movements and actions without being aware of what is happening.
The phase lasts 5 minutes or less in 80 per cent, rarely more than 1 hour.
• Early features – staring, slumping, ‘dazed’.
• Midpoint – Repetitive movements, blinking, smacking lips, chewing.
• Terminal (integrated) – wandering, paranoid ideas, confusion.
Diagnosis
• This is essentially on clinical grounds. An abnormal EEG may confirm, but a nor-
mal EEG in-between episodes does not exclude. Seek evidence from a witness –
sudden onset, impaired awareness.
• There is no retrograde amnesia.
• If an offence is committed, seek evidence that it was unpremeditated and there was
no attempt at concealment.
• Hysterical amnesia and fugue. (Often covert conflict with purposeful escape.
Amnesia of longer duration.)
• Malingering (marked variability and inconsistency).
• Stress reaction (inhibited individual exercising denial mechanisms).
• Alcohol, drug intoxication.
• Sleepwalking (stage IV; rarely repetitive or stereotyped; behaviour usually well
integrated).
ICTAL PHASE: FUGUES

• Prolonged states of altered behaviour, impaired consciousness, amnesia, tendency
to wander.
• Complex partial status may give similar appearance.
• Less common than automatisms.
ICTAL PHASE: TWILIGHT STATES

• Occurrence of subjective abnormal experience rather than objective motor
manifestations.
• Twilight states last from one to several hours (occasionally 1 week or more).
• Consciousness impaired with abnormal affective and perceptual experience.
• Psychomotor retardation with perseveration of speech and action.
• Foci most commonly temporal lobe.
POST-ICTAL PHASE
• Automatism (see above).
• Twilight states.
• Transient paranoid–hallucinatory states (post-ictal psychosis).
INTER-ICTAL PERIODS
Aggressive behaviour
There is a higher prevalence of epilepsy in the British prison population but violence
is not more common in epileptics than in other prisoners; automatism could not account
for the majority of crimes.
Possibilities are:
1 Organic brain disorder is responsible for both epilepsy and offence behaviour.
2 Organic brain disorder causes epilepsy with consequent social rejection and sense
of inferiority, leading to offensive behaviour.
3 Adverse social factors lead to both epilepsy and antisocial behaviour (e.g. battered
child).
4 A tendency to reckless and antisocial behaviour leads to offences and accidents
which could injure the brain and cause post-traumatic epilepsy.
Serious violence as an epileptic phenomenon is very rare; any violence is usually
short-lived, fragmentary, unsustained, purposeless.
‘Episodic dyscontrol syndrome’ This is controversial. There are episodes of senseless,
poorly remembered unprovoked violence. Temporal lobe EEG abnormalities may be
present. It may be helped by carbamazepine.
Depression and suicide

These are possibly more common in non-dominant temporal lobe lesions. Flor-
Henry (1969) proposed that schizophreniform psychosis is more commonly associ-
ated with left-sided temporal lobe epilepsy.
Onset may be severe and rapid and may show an inverse relation to fit frequency.
The risk of suicide is increased in epilepsy.
Schizophreniform psychosis and epilepsy

There is an increased incidence of schizophrenia-like syndrome (usually paranoid
type) among chronic epileptics compared to the general population. It usually develops
10–15 years after onset of epilepsy.
EPILEPSY 179
It is associated with:
• Increased incidence of neurological abnormalities.

• Negative family history for schizophrenia.
• ‘Warmer’ affect with less personality disintegration than schizophrenia.
• Temporal lobe epilepsies.
Suggested mechanisms
• Epiphenomena – ? There is a common brain disorder responsible for both schizo-
phrenic symptoms and epilepsy.
• Psychodynamic – ? Symptoms are a response to social rejection, etc., associated
with epilepsy, and to abnormal mental experiences produced by it.
• Pathophysiological – ? Schizophrenic symptoms are produced by physiological
changes consequent on abnormal electrical or neurotransmitter activity.
Dementia
A small proportion develop progressive decline in intellectual ability, with diffuse
cerebral atrophy. This may develop after many years’ functioning at adequate level.
It is also associated with deterioration in personality.
Dementia is more common where epilepsy is secondary to a known brain lesion,
and where epilepsy is early-onset, severe, chronic and temporal-lobe.
Exclude:
• Effect of drug intoxication.

• Apparent dementia, where worsening of personality traits, neurotic withdrawal,
chronic end-state of schizophreniform psychosis.
TREATMENT OF EPILEPSY
Drug treatments
Remember:
1 Every case is different.

2 Be aware of the family, social and personal context.
3 Assess and encourage compliance.
4 Use one drug whenever possible.
5 Phenytoin metabolism is saturable (zero-order kinetics), so monitor levels.
Specific drugs:
• Partial seizures – carbamazepine, phenytoin, valproate, gabapentin, lamotrigine,

tiagabine, topiramate, levetiracetam.
• Generalized seizures:
– Tonic–clonic – valproate, carbamazepine, phenytoin, lamotrigine.
– Tonic – valproate, felbamate, clonazepam.
– Absence – ethosuximide, valproate, lamotrigine.
– Myoclonic seizures – valproate, clonazepam.
Surgery
Consider temporal lobectomy for treatment-resistant epilepsy (after adequate trials)
with a definite EEG focus. This usually requires extensive workup – neurophysiology
and imaging. Up to 60–70 per cent are seizure-free after surgery.
With other brain regions, up to 50 per cent are seizure-free afterwards (e.g.
callosotomy).
Vagus nerve stimulation

This involves surgical implantation of an electrical nerve stimulator similar to a car-
diac pacemaker, with electrodes attached to the left vagus nerve in the neck. This
reduces seizures by 50 per cent in up to one-half of patients.
Ketogenic diet
By maintaining a ketoacidotic state, seizures may be suppressed by an unknown
mechanism. However, it is difficult to maintain a ketogenic state. It has only been
demonstrated to be effective in children.
Psychosocial
Be aware of the family, social and personal context.
• Family – Overprotection may foster dependency.
• Personal – Is there poor self-esteem, inadequate social skills and social repertoire?
• Societal – Be aware of negative attitudes, discrimination.
NON-EPILEPTIC ATTACK DISORDER (PSEUDOSEIZURES)
See also Chapter 16 (Psychophysiological, somatoform, dissociative and related disorders).

Pseudoseizures may occur in those who also have true epileptic seizures. There is a
variable attack pattern.
• Often very frequent.
• Usually with others present.
• Usually occur indoors, at home.
• Often an emotional precipitant.
• Often gradual onset, rigidity with random struggling; rarely pass urine or injure self;
often talk or scream during attack, which may last many minutes. May be ‘swoon’-like.
• EEG normal during attack.
• Serum prolactin not raised after attack.
SLEEP DISORDERS
See Table 14.1. The normal physiology/normal sleep EEG is covered in Chapter 15.
INSOMNIA
Insomnia is a symptom, not a disease. Thirty-five per cent of the population experi-
ence some insomnia; in 10–15 per cent it is clinically significant.
SLEEP DISORDERS 181
Table 14.1 Classification of sleep disorders
Dyssomnias
Primary insomnia
Primary hypersomnia
Sleep–wake schedule disorders
Jet lag
Sleep delay
Other
Disorders of excessive sleep
Breathing-related sleep disorder (obstructive sleep apnoea)
Narcolepsy
Parasomnias
Nightmares
Sleep terrors
Sleepwalking
REM sleep behaviour disorder
Other
Sleep disorder related to other mental disorder
Sleep disorder related to general medical condition
Risk factors are: female, elderly, anxious, depressed, multiple health problems, lower
social group.
It is most prevalent in the elderly because of changes in the sleep pattern: ↓ REM,
↓ REM latency, ↑ number and duration of awakenings, ↑ shift through sleep stages,
↑ daytime napping; also increased physical and psychiatric morbidity.
Forty per cent of insomniacs self-medicate with over-the-counter drugs or alcohol;
20 per cent take prescription sedatives/hypnotics.
MANAGEMENT
There should be a thorough initial evaluation to rule out secondary (physical/psychiatric)
or situational (stress-related/environmental) causes.
Sleep hygiene
Encourage: regular bedtimes and rise times; a bedtime ritual (e.g. short read); diet
(avoid hunger or overeating at night); avoid caffeine; avoid alcohol; no daytime naps;
regular exercise. The bedroom should be dark, quiet, at normal temperature. Avoid
‘clock watching’ – use bed to sleep.
Cognitive–behavioural therapy
This is useful as a means of treating, possibly curing, primary insomnia as well as
achieving discontinuation of hypnotic drug use.
Drug therapy for temporary relief

This should be cautious and ‘targeted’. Start with non-prescription hypnotics.
Antidepressants with sedating qualities may be used.
• Benzodiazepines (↓ REM and slow wave sleep, ↑ stage 2) – Short- or intermediate-
acting drugs cause less residual daytime sedation, but are more likely to cause
rebound insomnia with discontinuation (see Chapter 21). Abuse and dependency
are problematic.
• Non-benzodiazepines: zolpidem and zopiclone – Although associated with lower
abuse than benzodiazepines, those with a history of substance abuse or depend-
ence, or psychiatric illness may be at increased risk to abuse these agents.
SLEEP AND PSYCHIATRIC ILLNESSES
Sleep disturbance is a prominent symptom in many psychiatric disorders. There is no

single sleep parameter with absolute specificity for any psychiatric disorder, but most
prominent differences are seen with affective disorder.
• Depression – This reduces stages 3 and 4, reduces REM latency, and REM occurs
earlier in the night. It is unclear as to the specificity to depression and prediction of
treatment response. Sleep deprivation has been used as a treatment.
• Schizophrenia – There is reduced slow-wave sleep and REM.
• Anxiety – There is difficulty falling and staying asleep, increased stages 1 and 2,
reduced efficacy of sleep, no characteristic REM changes as in depression.
• Panic disorder – There is increased sleep latency; other findings as in generalized
anxiety.
• Alcoholism – There is increased ␦, REM sleep and ␣ activity.
• Alzheimer’s – ‘Sundowning’ (confusion, wandering), increased sleep, fragmenta-
tion, reduced sleep efficiency, Stages 3–4, and total REM.
NARCOLEPSY
Narcolepsy has a population prevalence of about 0.05 per cent. The ‘narcoleptic
tetrad’ is:
1 Hypersomnia.
2 Cataplexy (sudden loss of muscle tone) in 80 per cent of cases.
3 Sleep paralysis (marked loss of muscle tone on awakening).
4 Hypnagogic hallucinations (i.e. on going to sleep) or hypnopompic (on waking).
Only 25 per cent of patients have the complete tetrad.
Two-thirds have fallen asleep while driving, 80 per cent fallen asleep while at work.
AETIOLOGY
There is an abnormality on chromosome 6 (HLA DQB1 and DQA1 alleles) seen in over
85 per cent of patients. An association with human leukocyte antigen (HLA) allele sug-
gests an autoimmune link. Neurochemical studies show absence of hypocretin in CSF.
DIAGNOSIS
Use the multiple sleep latency test (MSLT) EEG during the day – rapid onset of REM
(⬍10 mins after onset of sleep), ⭓2 sleep-onset REM periods during MSLT is virtually
diagnostic; also HLA testing.
Table 14.2 Parasomnias

Type Incidence Onset Sleep stage Behaviour Recall Treatment
Nightmares Very frequent Late in REM Easily rousable, Usual Support

in children sleep awareness
Night terrors 3% children, First Non-REM, Terrified, screaming, None Reassurance and
commonest in 1–2 hours stage 4 thrashing, can’t be practical advice
ages 4–7; often of sleep easily aroused, for parents;
family history ‘trance-like’, may behavioural
last 10–20 minutes waking schedule
if persistent
Sleepwalking 1–15%, normally First Non-REM, May last minutes None Safety precautions;
8–15 years old, 1–2 hours stage 4 to 1 hour avoid sleep
but also in adults of sleep deprivation
From Shapiro (1993).
TREATMENT
• Allow only scheduled daytime naps.
• Use of stimulants – modafinil, dexamphetamine and methylphenidate. Cataplexy
may be effectively treated with clomipramine or an SSRI.
OTHER CONDITIONS
See also Table 14.2.

• Kleine–Levin syndrome – episodes of hypersomnia, pathological overeating. Also
hypersexuality, hallucinations, mood disturbances. Disorder of hypothalamus.
There is no specific treatment.
• Sleep apnoea (and pickwickian syndrome) – episodes of apnoea during sleep; dis-
turbed noisy sleep; very tired during day. Causation may be central or peripheral.
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EEG and brain imaging in 15
psychiatry
ELECTROENCEPHALOGRAPHY (EEG)
An EEG records regular and irregular oscillations of potentials between electrodes

placed on the scalp. Repetitive waves reflect summated synaptic potentials generated
by cortical pyramidal cells as response to rhythmic thalamic discharges.
Amplitudes range from 5 to 150 microvolts. Frequencies (when regular) range from
about 1 cycle/second (hertz) to ⭓40 Hz.
THE NORMAL EEG
Frequency ranges
• Delta – less than 4 Hz. May occur as regular waves or irregularly. Diffusely distrib-
uted over scalp in sleeping adults and in children but invariably abnormal in non-
sleeping adults.
• Theta – 4–7 Hz. Transient ␪ are components found in 15 per cent of the normal
population.
• Alpha – 8–13 Hz. Prominent over occipital region, accentuated by eye closure and
attenuated by attention. A consistent difference of 1 Hz or more between hemi-
spheres is pathological. Slowing seen in early phenytoin toxicity.
• Beta – 14 Hz and above. Principally frontocentral. May be enhanced by anxiety,
alcohol and some drugs (barbiturates, benzodiazepines).
• Mu – Arch-like 7–11 Hz waves over precentral areas, attenuated by contralateral
limb movements.
• Lambda – Single sharp waves in occipital region, usually associated with visual
‘scanning’.
• Vertex waves – Electronegative sharp waves over vertex, evoked by auditory stimulus.
DEVELOPMENT
Infants have slower and usually higher-amplitude rhythms. They are asynchronous at
first and easily disturbed. Mature rhythms develop at between 2 and 6 years.
186 EEG AND BRAIN IMAGING IN PSYCHIATRY
Adults usually show either alpha posteriorly and beta anteriorly but generalized
low-amplitude beta may be present – established by puberty. When the subject is
drowsy, alpha becomes intermittent and theta appears.
Alpha frequency tends to slow in old age, and delta activity is decreased; by 60 years,
Stage 4 represents 10 per cent of total sleep. There is decreased rapid eye movement
(REM) latency, with increased frequency and duration of nocturnal arousals.
NEUROTRANSMITTERS AND SLEEP EEG

• Histamine – active wakefulness, neurones in hypothalamus.
• Cholinergic – wakefulness, REM sleep.
• Adrenergic – decreased REM sleep (MAOIs, clonidine, propranalol).
• Serotonergic – increased non-REM sleep.
• Dopamine – increased REM sleep.
NORMAL SLEEP
• Stage 1 (lightest) – low-voltage, desynchronized activity and sometimes low
voltage-regular activity at 4–6 Hz. Undulating low-frequency deflections seen due
to rolling eye movements.
• Stage 2 – frequent spindle-shaped tracings at 13–15 Hz (sleep spindles) and high-
voltage K complexes (high-voltage slow waves plus short episode of fast activity
over vertex, response to sound).
• Stage 3 – high-voltage delta waves begin to appear.
• Stage 4 – delta waves occupy more than 60 per cent of record.
Features of normal sleep

Sleep is cyclical, with four or five periods of emergence from stages 3 and 4 to a period
lasting about 20 minutes – termed ‘paradoxical’ or ‘desynchronized’ (REM) sleep:
• Low-voltage asynchronous fast waves on cortical EEG.
• Rapid eye movements, conjugate.
• Irregular respiration.
• Slight tachycardia with increased blood pressure.
• Increased gastric motility.
• Increased cerebral blood flow.
• Absent tendon reflexes.
• Penile erection.
• Vivid and bizarre dreams.
• 15–30 per cent of sleep time spent in REM.
ABNORMAL EEG PATTERNS
Abnormalities include:
• Reduced amount and amplitude of normal frequencies (generalized or localized).
• Increased slow frequencies (generalized or localized).
ABNORMAL EEG PATTERNS 187
• Abnormal waveforms – spikes (duration less than 80 ms), sharp waves (duration
80–200 ms), spike and wave complexes.
Abnormal forms may occur spontaneously or may be provoked by photic stimula-
tion, sleeping, or hyperstimulation.
Diffuse abnormalities
• Rhythmic slowing.
• Occasionally periodic discharges.
Focal abnormalities
• Polymorphic, arrhythmic unreactive delta.
• Periodic lateralized epileptiform discharges.
Epilepsy
• Initial interictal EEG is abnormal in 75 per cent of suffers.
• With repeated recordings, 90–95 per cent will show abnormalities.
• 2 per cent of normal population have abnormalities considered to be epileptiform.
• Absence seizures:
– 3/second spike and wave in infancy.
– 4/second spike and wave in a juvenile.
• Primary generalized tonic–clonic seizures:
– Interictal – bursts of spike and wave.
– Ictal – 10-Hz fast activity during tonic phase, followed by lower-frequency spike
and wave complexes during clonic phase.
– Postictal – generalized slowing ␦ range.
• Myoclonic epilepsy:
– Polyspike and wave.
• Partial (focal) epilepsy:
– Interictal – focal spikes or sharp waves.
– Ictal – focal rhythmic discharge.
Periodic complexes
• Herpes simplex encephalitis (look for localized temporal complexes).
• Creutzfeldt–Jakob disease (occurs in late stages).
• Subacute sclerosing panencephalitis.
Triphasic waves
These indicate liver, renal, hypoxic or metabolic encephalopathies.
Frontal intermittent rhythmic delta activity (FIRDA)

• Metabolic encephalopathy.
• Brain stem dysfunction.
Alpha coma
There is widespread, non-reactive alpha-range activity. It occurs in generalized
encephalopathy.
Burst-suppression
There are high-voltage bursts, followed by periods of extreme suppression (flattening).
It occurs with bihemispheric insult and deep anaesthesia.
USES OF THE EEG IN PSYCHIATRY
DETECTION OF ORGANIC PSYCHOSIS

In general, there is first a decrease in frequency and responsiveness of ␣ rhythm, pro-
gressing to increased amounts of activity at slower frequencies in both ␪ and ␦ ranges.
Changes are usually diffuse and symmetrical, especially where there are extracerebral
causes. Focal lesions usually produce localized abnormality.
DIAGNOSIS OF SEIZURE AND SLEEP DISORDERS

This is especially important to help identify atypical forms of epilepsy associated with
psychotic experiences, sudden affective disturbance or behavioural change.
Notes
1 The EEG showing ictal activity during a major or focal seizure is diagnostic of
epilepsy. Absence of simultaneous EEG changes during the episodes therefore
almost excludes a genuine fit.
2 An abnormal interictal EEG does not clinch a diagnosis of epilepsy. Taken together
with a full and careful history, interictal spike and wave disturbances give support
to a diagnosis of liability to epilepsy.
3 A normal interictal EEG does not exclude a diagnosis of epilepsy, which must be
based on eyewitness accounts and history.
4 In temporal lobe epilepsy, a routine and a sleep EEG will reveal spike foci in about
90 per cent of patients.
STUPOR
Non-organic stupor due to depression, schizophrenia or hysteria shows a preservation
of alpha rhythm.
BRAIN IMAGING
See the diagram below.
Brain imaging in psychiatry
Structural Functional
CT MRI SPECT Xenon PET MEG MRI

inhalation
Blood flow Spectroscopy

BRAIN IMAGING 189
STRUCTURAL INVESTIGATIONS (PRINCIPLES)
COMPUTERIZED TOMOGRAPHY (CT)

CT X-rays generate an image in a single plane. There is poorer grey–white tissue con-
trast than with MRI, but CT is better for examining bony structures/tissue calcifica-
tion. CT is still clinically useful but increasingly being replaced by MRI (see below).
MAGNETIC RESONANCE IMAGING (MRI)

MRI images are generated from motion of tissue protons when excited within a mag-
netic field. MRI possesses superior anatomical resolution and multiplanar scanning
capacity than CT. It allows for three-dimensional reconstruction and volumetric
quantification.
MRI tissue-relaxation parameters (T1 and T2) may also give information on tissue
hydration status and iron or lipid metabolism.
Recent developments
• Voxel-based quantitative morphometry, for more sophisticated volume
measurements.
• Shape morphometrics, for examining shape rather than volume.
• Diffusion tensor imaging (DTI), which is MRI of myelin traits.
• Magnetoencephalography (MEG) a very recent technique using measurement of
alteration in cerebral magnetic fields to provide detailed information on cortical
activity. It may be combined with MRI and is good for studying deeper brain
structures.
MRI AND CT IN PSYCHIATRY
MRI AND SCHIZOPHRENIA

• Confirmed ventricular enlargement (lateral ventricles, 4th ventricle) and cortical
tissue loss or hypoplasia, as seen in CT studies or longitudinal studies, generally
suggests a non-progressive nature, favouring a neurodevelopmental basis (see
Chapter 3), but some patients show neuroprogression.
• There is an association with subtle anomalies (e.g. agenesis of corpus callosum,
cavum septum pellucidum) of neurodevelopmental origin. Reduction in size of
mesial temporal lobe and superior temporal gyrus (especially on the left) is correl-
ated with positive symptoms. Other findings include smaller frontal lobes, and
larger basal ganglia structures (probably medication-related).
• Improved (tissue segmentation) methodology has suggested more widespread grey
matter cortical loss and findings consistent with generalized subtle tissue loss.
• T1 and T2 findings are inconsistent.
• There are associations of brain abnormalities with many clinical indices: poorer
premorbid function, negative symptoms, obstetric complications, family history of
schizophrenia, treatment resistance.
MRI AND AFFECTIVE DISORDERS

• There is a high prevalence of white matter/hyperintensity lesions in bipolar
patients, particularly in elderly depressives.
• Some studies report reductions in size of caudate and putamen nuclei in depres-
sion; others find only temporal lobe (right hippocampus) reduction.
• Neuroimaging findings are less pronounced than in schizophrenia. Late-onset
depression has more brain changes than early-onset. Brain abnormalities on neu-
roimaging generally are associated with cognitive impairment, poorer outcome
and higher mortality.
MRI AND ALZHEIMER’S DISEASE (AD)

• Selective loss of hippocampal tissue may occur early in AD, and in mild cognitive
impairment (MCI). Presence of apolipoprotein E gene is associated with more
(and earlier) neuroimaging abnormalities.
• Both ventricular enlargement and cortical tissue loss show high prevalence in the
‘normal’ population after age 60.
• In Alzheimer’s disease, ventricular enlargement is marked and progressive and is of
both diagnostic and prognostic significance. Cortical tissue loss is less clearly
related.
• MRI or CT is useful to distinguish aetiology and type of dementia: ‘patchy’ atrophy
and multiple lucencies in multi-infarct dementia; atrophy of caudate and fron-
totemporal region in Huntington’s chorea; hypodensities in basal ganglia in
Wilson’s disease.
• There is severe, bilateral atrophy of anterior frontal (⫾ temporal) lobes in Pick’s
disease; cortical and subcortical atrophy in Parkinson’s disease.
• Ventricular enlargement and cerebral atrophy is seen in chronic alcoholics.
Cerebral atrophy is related to the extent of cognitive impairment.
• In some patients, abstinence is associated with reversibility of CT findings.
MRI AND SUBSTANCE ABUSE

• Reduction in cortical grey matter and T1 changes correlate with cognitive impair-
ments in alcoholics.
• MRI detects neuropathological changes in Wernicke–Korsakoff ’s syndrome
(WKS).
• Gadolinium-enhanced MRI indicates blood–brain barrier impermeability in WKS
reduces after 1 week of thiamine treatment.
• Some report white matter hyperintensities in opiate addicts.
MRI AND AUTISM

• Generally larger brains are reported.
• Reports of hypoplasia of the 4th ventricle, cerebellar vermis and parietal tissue loss.
MRI AND GILLES DE LA TOURETTE’S SYNDROME (GTS)

There are some reports of asymmetry and/or reduction in basal ganglia structures in GTS.
BRAIN IMAGING 191
FUNCTIONAL INVESTIGATIONS IN PSYCHIATRY
Single photon emission (computerized) tomography (SPET; SPECT) uses single

photon (␥-ray) emitting isotopes – e.g. xenon 133, technetium 99 – to examine regional
cerebral blood flow (rCBF) or receptor pharmacology.
SPECT AND SCHIZOPHRENIA

• A large number of studies have shown a pattern of functional underactivity, with
reduced rCBF predominantly in the frontal regions – the ‘hypofrontality hypothesis’.
• SPECT has also been used to examine neuroanatomical correlates of psychotic
symptoms and to determine the pattern of receptor binding of antipsychotics.
SPECT AND AFFECTIVE DISORDERS

• Some studies report hypofrontality less pronounced than that in schizophrenia,
with reversal during antidepressant therapy.
• Studies also show different pattern of sadness in normal subjects compared with
depressed patients.
SPECT AND ALZHEIMER’S DISEASE

• Decreased rCBF in posterior parietal and temporal regions correlates with neuro-
psychological deficits.
• Primary motor, sensory, and visual cortices are relatively unaffected until late in illness.
XENON INHALATION
• This is another index of rCBF. There is well-documented hypofrontality in schizo-
phrenia, with failure of activation during performance of the Wisconsin Card
Sorting Test (WCST).
• There have been similar reports in affective disorder, but this may be a less consis-
tent finding.
POSITRON EMISSION TOMOGRAPHY (PET)

Unstable isotopes (oxygen 15, fluorine 18, carbon 11), generated from a cyclotron,
emit ␥-rays when penetrating tissue. These are then detected and an image based on
complex kinetic models is reconstructed.
Recently, overlay of MRI images has been used to achieve greater structural reso-
lution. rCBF is measured indirectly via 15O utilization; local metabolism is measured
with 18F-deoxy-D-glucose (18FDG).
PET and schizophrenia

• Hypofrontality is studied in unmedicated and medicated states; related to negative
symptoms and treatment resistance.
• Activation studies to examine neuroanatomical specificity of psychotic symptoms,
and studies of dopamine receptor occupancy, have been carried out (see Chapter 3).
PET and other disorders

• PET studies in affective disorder and Alzheimer’s have shown similar findings to
their respective SPECT research.
• Decreased activity in the right parahippocampus has been demonstrated in panic
disorder. Hypermetabolism in orbitofrontal cortex and caudate nucleus has been
reported in OCD; it normalizes with treatment (see Chapter 5).
MR SPECTROSCOPY (MRS)
This uses similar principles to structural MRI, but the tuning of the head coil at
particular frequencies will allow information to be obtained on phosphorus and ATP
metabolism (31P-MRS), glutamate, N-acetyl asparate (1H proton MRS), or pharma-
cology (19F MRS for neuroleptics or fluoxetine; Li+ MRS for lithium concentration in
brain).
• Schizophrenic patients show decreased phosphomonoesterases and ATP meta-
bolism in dorsolateral prefrontal cortex.
• Alzheimer’s disease patients show increases in phosphomonoesterases, even early
in the illness.
FUNCTIONAL MRI (fMRI)

This is an adaptation of MRI using exogenous contrast agents (e.g. GdPTA) or the
endogenous contrast agent effect of deoxyhaemoglobin in blood. It can achieve high
spatial and temporal resolution images of brain activity. It is now the major technol-
ogy for functional imaging available in clinical scanners. Overlay with structural
images is possible.
fMRI is used in the study of perception (e.g. patients with schizophrenia hearing
voices have overactivity in temporal lobes), emotions (sadness, anger) and treatment
response (drugs may alter and normalize blood flow in pretreatment/post-treatment
comparisons).
CLINICAL APPLICATIONS OF NEUROIMAGING
• Unusual onset of psychosis/depression/personality change.

• Cognitive decline/suspected dementia.
• Confusion/delirium of unknown origin.
• Head trauma.
• Alcoholism (advanced); to rule out complications.
• Neuropsychiatric conditions.
RESEARCH APPLICATIONS OF NEUROIMAGING
• Are there any structural or functional brain changes?

• Are they associated with particular symptoms, illness subtypes, course?
• Are they related to other aspects – e.g. genetics, familial risk, neurochemistry?
• Do they change or worsen over the course of illness?

• Can treatment(s) improve or alter these changes?
• Can we predict illness and/or discriminate between illnesses based upon imaging
findings?
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Psychophysiological, 16
somatoform, dissociative and
related disorders
CONCEPTS
These are disorders in which the onset and exacerbation of organic change are often
seen in association with emotional distress – e.g. asthma.
Before 1950, Alexander’s concept of psychosomatic medicine dominated: ‘a causal
link between a specific constellation of unconscious conflicts, of psychological methods
of coping with them … and the development of one of several organic diseases’.
Psychophysiological disorders (involvement of autonomic nervous system, smooth
muscles) were then separated from conversion disorders (sensorimotor, skeletal muscle).
Between 1951 and 1965, the postulated ‘psychosomatic specificity hypothesis’ was
tested against bronchial asthma, rheumatoid arthritis, ulcerative colitis, dermatitis, essen-
tial hypertension, peptic ulcer and thyrotoxicosis by the Chicago Institute for
Psychoanalysis. Investigations concluded that it is possible to differentiate between illness
on the basis of psychological patterns associated with them – but neither the specificity
nor the direction of causality is established. Four possible models of the relationship are
show in the diagram below.
1. No relationship
2. Soma Psyche
3. Soma Psyche
Psyche
4. Constitution
Soma
Lipowski (1988) defined psychosomatic medicine as:

1 A science of the relationships between psychological, biological and social vari-
ables in relation to human health and disease.
2 An approach to the practice of medicine advocating the inclusion of psychosocial
factors in the study, prevention, diagnosis and management of all diseases.
196 PSYCHOPHYSIOLOGICAL, SOMATOFORM, DISSOCIATIVE AND RELATED DISORDERS
3 Clinical activities at the interface of medicine and the behavioural sciences, gener-
ally termed ‘consultation–liaison psychiatry’.
RECENT CONCEPTS
Recent concepts shift away from searching for psychodynamic formulations associated
with specific organic pathology, rather to increased interest in social/environmental
events and their effects on psychophysiological functioning, and relationship with
onset, course and outcome of various diseases.
• Murray Parkes (1970) has demonstrated vulnerability to physical illness in the first
year after death of the spouse.
• Recent research demonstrates superior outcome in cancer therapy among patients
who are psychologically minded and have less anxiety/depression (Spiegel, 2001).
• There is a large literature supporting a major role for depression in predicting
morbidity and mortality in patients with ischemic heart disease (Blumenthal et al.,
2003; Jiang et al., 2003).
Liaison psychiatry There has been growth of this concept in the last 60 years, facili-
tated by broader concepts of disease and location of psychiatric units in general
hospitals (Kornfeld, 2002):
1 Diagnosis, prevention and management of mental illness in physically ill patients

undergoing treatment.
2 Advice and mutual exchange of ideas on psychological aspects of care of the phys-
ically ill.
3 Management of psychopathological reactions to physical illness and injury (e.g.
postoperative psychosis).
4 Prevention and management of deviant illness behaviour consequent upon, or
part of, physical illness.
5 Advice and help in management of family problems related to illness and the
individual.
6 Facilitation of adequate communication between patients and staff to avoid poten-
tial conflict and misunderstandings.
7 Education of staff in psychological aspects of illness.
8 Research. Recent emphasis includes:
– Development of consultation (liaison psychiatry as sub-specialty).
– Combined medical–psychiatric inpatient units in the general hospital.
PSYCHOLOGICAL REACTIONS TO PHYSICAL ILLNESS
Physical and psychiatric disorders may coexist because:
• Both may have increased incidence in ‘vulnerable’ people.

• Psychiatric disorder may lead to physical disorder (e.g. alcoholism).
• Physical disorder may lead to psychiatric disorder (e.g. altered cerebral metabolism).
• Psychiatric drugs may lead to physical complications.
SOMATOFORM DISORDERS 197
• Medical drugs may lead to psychiatric complications.

• Physical illness may uncover a latent predisposition to psychiatric disorder.
FACTORS INFLUENCING RESPONSE TO PHYSICAL ILLNESS

1 Patient factors – Obsessional patients react to any doubt in the diagnosis. Narcissistic
patients react to disfigurement.
2 The illness – The significance and meaning of the particular illness. Acute or
chronic course.
3 The social environment – Financial or promotional threat. Illness may be welcomed
if it resolves conflict (e.g. marital).
PATTERNS OF RESPONSE
• Therapeutic adaptation – to the symptoms.
• Anxiety – usually the first response.
• Depression – commonest psychiatric disorder in medical inpatients (see Chapter 4
for notes).
• Paranoid reaction – especially if deaf or blind. May blame relatives or doctors.
• Denial of illness – may be a helpful defence but may delay seeking help.
• Preoccupation with illness – ‘vigilant focusing’ on the symptoms.
• Prolongation of the sick role – for secondary gain.
SOMATOFORM DISORDERS
See Table 16.1.
SOMATIZATION DISORDER
There is repeated presentation of physical symptoms, with persistent requests for

medical investigations, despite repeated negative findings and reassurances by doctors
Table 16.1 ICD-10 and DSM-IV classification of somatoform disorders

ICD-10 DSM-IV
Neurotic, stress-related and somatoform disorders Somatoform disorders
F44 Dissociative (conversion) disorder Conversion disorder

F45 Somatoform disorders
Somatization disorder Somatization disorder
Undifferentiated somatoform disorder Undifferentiated somatoform disorder
Hypochondriacal disorder Hypochondriasis
Somatoform autonomic disorder Pain disorder
Persistent somatoform pain disorder
F48 Other neurotic disorders
Neurasthenia Body dysmorphic disorder
that the symptoms have no physical basis. If any physical disorders are present, they
are insufficient to explain the severity of symptoms or patient distress/preoccupation.
These people are extensive users of healthcare resources. For example, the manage-
ment cost of treating chronic pelvic pain accounts for 0.6 per cent of UK health
expenditure. Claims of gastrointestinal, dermatological, sexual or menstrual symp-
toms are most common.
Prevalence rates vary. ECA reports 0.03–0.4 per cent (Escobar et al., 1987); approx-
imately 10 per cent rate in medical outpatients. The male:female ratio is 1:20.
There is a familial component. Between 10 and 20 per cent of first-degree female
relatives are somatizers. First-degree male relatives are prone to substance abuse, anti-
social personality disorder.
It is associated with other psychiatric disorders: depression, substance abuse, anti-
social and histrionic personality disorder.
MANAGEMENT
• It is a chronic disorder with a fluctuating course.
• Establish the absence of an underlying physical cause.
• Limit ‘window-shopping’ for doctors.
• Supportive psychotherapy is helpful.
• Pharmacotherapy is indicated for secondary complications (e.g. anxiety, depres-
sion) but has limited use otherwise (especially benzodiazepines because of poten-
tial for abuse).
CONVERSION DISORDER
There is loss of motor or sensory function without an identifiable physical cause. Both
primary and secondary gain encourage the persistence of the symptoms.
‘Classic’ conversion symptoms are those that suggest neurological disease, such as
paralysis, aphonia, convulsions, coordination disturbances, etc. Vomiting as a conver-
sion symptom may represent revulsion or disgust. Pseudocyesis (false pregnancy) may
represent both a wish for, and fear of, pregnancy.
Conversion symptoms can complicate true organic disease: Slater (1965) followed up
85 patients diagnosed as hysterical, after 9 years. One-third were found to have developed
organic disease not initially detected, but probably having played a part in initial symp-
toms; 12 patients had died, of whom 3 had symptoms which could account for the previ-
ous ‘hysterical’ symptoms. Of 33 patients who had no significant organic disease, 13 had
developed significant psychiatric illness.
Conversion symptoms may be distinguished from organic symptoms by:
• Their variability.
• A typical nature, often reflecting a patient’s concept of the disability.
• Inconsistency (e.g. apparently paralysed muscles may show synergistic power).
EPIDEMIOLOGY
There is no definite information on age. Female:male ratio ⫽ 2–10:1. The condition
accounts for about 3–4 per cent all psychiatric consultations.
SOMATOFORM DISORDERS 199
The estimated annual incidence is 11–22 cases per 100 000. Lower socioeconomic
groups may be most affected (Stefansson).
AETIOLOGY
Genetics
There is an incidence among first-degree relatives of about 5 per cent (lower in
fathers, higher in mothers and daughters). This level most likely reflects family
learning. There is some evidence of monozygotic twin-pair concordance, but not
dizygotic.
Psychophysiological aspects
Evoked responses in patients with hysterical anaesthesias suggest two underlying
mechanisms:
• A lowering of peripheral receptor sensitivity.
• A central mechanism of inhibition along different pathways.
Psychoanalytic aspects
Repressed anxiety leads to hysterical symptoms, often having symbolic meaning and
secondary gain. ‘Direct coping’ with conflict is avoided. Unresolved oedipal conflicts
are often a prominent source of anxiety.
Psychological/social aspects
Both primary and secondary gain encourage the persistence of the symptoms.
Hysterical symptoms have been viewed (Pilowsky) as a form of non-verbal communi-
cation in the doctor–patient relationship. (May particularly apply to those less
effective in verbal communication, e.g. those perceiving themselves in a dependent
inferior role.)

The course is variable:
• Lewis – 40 per cent well and working 5 years later (Maudsley Hospital inpatients).
• Cater – 70 per cent well 4–6 years later (acute conversion reaction).
Good prognostic factors are acute onset, nature of conflict clear and resolvable. Poor
factors are intractable personality problems and poor motivation on the part of the
patient.
TREATMENT
• Explain and reassure as to nature of the symptom.
• Investigate as far as necessary to exclude organic cause, not merely as a method of
reassurance.
• Detect and treat associated emotional disorder, psychotherapy.
• Interviewing with sodium amytal administration is sometimes useful diagnos-
tically as well as therapeutically.
PAIN DISORDER
This is defined as the complaint of pain in the absence of adequate physical findings and
in association with evidence of the aetiological role of psychological factors. Common
sites are head and neck, abdomen, lower back and genitals.
Patients may be any age, peaking around middle age. It is more common in women.
The course is variable and depends on reinforcement factors, including
secondary gain.
CLINICAL FEATURES
• Inconsistent with anatomical distribution of the nervous system.
• Continuous over long periods by day.
• May prevent getting off to sleep but not cause wakening.
• May have symbolic significance; e.g. chest pain where father died of a heart attack.
• Insight into role of psychological factors is often restricted.
• Responds better to psychotropics than analgesics.
ASSESSMENT AND MANAGEMENT

• Exclude organic disease.
• Beware of ‘detecting’ psychological conflict in the absence of good evidence. Get a
history from other witnesses if possible.
• Resolve current social stressors where possible.
• Earlier psychiatric illness may resemble current symptoms in course and precipitants.
• Earlier personality? Vulnerable aspects? Hypochondriasis? Pain threshold?
• Ethnic factors – some ethnic groups (e.g. Asian) have tendency to somatize problems.
The possibility of litigation is extremely important because resolution of the pain
symptom is unlikely, and significant numbers of patients continue with chronic pain
after settlement.
Pain clinics often adopt a multidisciplinary approach with anaesthetist, physician
and psychiatrist.
Ensure adequate medical treatment where necessary. Antidepressants are better
than placebo. Use behavioural methods of treatment where appropriate.
HYPOCHONDRIASIS
The predominant disturbance is an unrealistic interpretation of physical signs or

sensations as abnormal, leading to preoccupation with the fear of having a serious dis-
ease. The unrealistic fear persists despite medical reassurance and causes impairment
in social or occupational functioning.
It may present as primary hypochondriacal disorder, as a part of other syndromes,
or as a form of personality disorder.
Depressive illness presents more commonly with hypochondriacal/somatic features
in non-European cultures. The condition may reach delusional intensity in depressive
and schizophrenic illness.
DISSOCIATIVE DISORDERS 201
It is more common in men, young and old, in lower socioeconomic classes and
those closely associated with disease.
MANAGEMENT
• Exclude organic pathology.
• If secondary to primary illness (e.g. depression), treat this. Hypochondriacal
symptoms may then fade.
• If primary:
– Follow firm policy regarding further investigations.
– Educate over role of psychological factors in symptoms. Avoid equation of psy-
chological with ‘faking’. Use cognitive and distraction techniques.
– Search for meaning of symptoms in the social/family setting, where appropriate.
– Exercise caution where symptoms serve a powerful defensive purpose.
– Some advocate a trial of tricyclics in all patients.
PROGNOSIS
The outcome is variable, but poor in more chronic and established cases. Those asso-
ciated with depressive illness or anxiety disorder have better prognosis.
BODY DYSMORPHIC DISORDER (BDD)
This typically begins in adolescence and is characterized by a preoccupation with an

imagined physical defect or excessive concern over a minor physical flaw. Cases are
often seen by non-psychiatrists, such as dermatologists and plastic surgeons.
Individuals may isolate themselves, seek surgical interventions, or go to extremes to
conceal their perceived physical defect. Preoccupation with the supposed defect causes
clinically significant impairment in social, occupational, or other essential areas of
functioning.
EPIDEMIOLOGY
The prevalence is between 0.7 and 2.3 per cent in the general population, 11.9 per cent
in a dermatology setting (Phillips et al., 2000). There is a wide range of sex ratios, but
probably M ⫽ F. Seventy-five per cent have never been married.
TREATMENT
The condition is often chronic and difficult to treat. BDD is thought by some to be a
type of obsessive–compulsive disorder and treatment is similar. When patients agree
to psychopharmacological treatment, improvement is seen with SSRI or SRI therapy.
Cognitive–behavioural therapy has also been shown to help.
DISSOCIATIVE DISORDERS
These are a spectrum of disorders involving a disturbance in the integration of con-

sciousness, memory, identity or perception for which there are no demonstrable
organic findings, and which seem to have a psychological advantage or symbolic

value. There is a strong presumption that the symptoms are a defence mechanism
linked to unresolved internal conflict or stress, but the reaction appears to be at an
unconscious level.
Other features which may or may not be associated are:
• Primary gain (conflict ‘resolved’, anxiety reduced).
• Secondary gain (attention of others).
• A choice of symptom modelled closely on recent experience in self or others.
• Manipulation of others and the environment.
• Personality type/disorder.
DISSOCIATIVE TYPES AND CLINICAL FEATURES

Dissociative amnesia
There is a sudden, temporary alteration in the function of memory usually associated
with a traumatic or stressful event. There is an inability to recall important informa-
tion, the extent of which is too great to be explained by ordinary forgetfulness.
Dissociative fugue
Like dissociative amnesia, there is a sudden alteration in memory, especially import-
ant personal information, which is also accompanied by unexpected travel away from
the person’s usual setting.
It is important to distinguish dissociative fugue from fugue states that may occur
after head injury, in epilepsy, during depressive illness and in the context of heavy
drinking (alcohol amnesic episodes). Often it is difficult to decide whether a fugue is
an act of malingering or genuinely beyond the patient’s control.
Dissociative identity disorder (DID)

This is characterized by the presence of at least two separate identities or personalities,
each of which may or may not know about the other and which can dominate indi-
vidual behaviour. Individuals may report gaps in memory and lost time.
Depersonalization disorder
This is characterized by periods of feeling detached from one’s own body, identity or
mental processes.
Dissociative disorder not otherwise specified

This covers dissociative symptoms not meeting the criteria for one of the above types.
MANAGEMENT
• Rule out any medical cause for the symptoms.
• In a supportive therapeutic relationship, memory usually returns with dissociative
amnesia and dissociative fugue. With DID, long-term therapy is usually needed.
• Most dissociative disorders are not responsive to medications. With depersonaliza-
tion disorder, SSRIs may be helpful.
CHRONIC FATIGUE SYNDROME (CSF) – NEURASTHENIA
This is severe, disabling fatigue of uncertain aetiology associated with a variable extent
of somatic and/or neuropsychiatric symptoms. Presentation is between ages 20 and
50 years, and females predominate.
The prevalence is 7.4 per 100 000. There is no clear association with socioeconomic
status.
AETIOLOGY
Patarca (2001) postulates immune dysfunction along with psychological vulnerability,
but the evidence is inconclusive. There are immunological abnormalities, especially
cell-mediated. T-lymphocyte mechanisms are common, but their significance is
unclear.
There is a high prevalence (⬎60 per cent) of antecedent/lifetime psychiatric illness,
especially minor depression, anxiety and somatization.
MANAGEMENT
• Cognitive–behavioural therapy has been beneficial (Whiting et al., 2001).
• There is no effective medical treatment. Medications are given for symptomatic
treatment – antidepressants, analgesics. Non-steroidal anti-inflammatory agents
are ineffective.
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hypochondriasis. Arch Gen Psychiatry 55, 737.
Blumenthal JA, Lett HS, Babyak MA et al. (2003) Depression as a risk factor for mortality after
coronary artery bypass surgery. Lancet 362, 604.
Breitbart W, Gibson C, Tremblay A (2002) The delirium experience: delirium recall and delirium-
related distress in hospitalized patients with cancer, their spouses/caregivers, and their
nurses. Psychosomatics 43, 183.
Carson AJ, Best S, Postma K et al. (2003) The outcome of neurology outpatients with medically
unexplained symptoms: a prospective cohort study. J. Neurol Neurosurg Psychiatry 74, 897.
Crimlisk HL, Bhatia K, Cope H et al. (1998) Slater revisited: 6-year follow-up study of patients
with medically unexplained motor symptoms. BMJ 316, 582.
Escobar JI, Burnam MA, Karno M et al. (1987) Somatization in the community. Arch. Gen.
Psychiatry 44, 713.
Hickie I, Davenport T, Issakidis C, Andrews G (2002) Neurasthenia: prevalence, disability and
health care characteristics in the Australian community. Br. J. Psychiatry 181, 56.
Hollander E, Neville D, Frenkel M et al. (1992) Body dysmorphic disorder: diagnostic issues and
related disorders. Am. J. Psychiatry 33, 156.
Horwitz BJ, Fisher RS (2001) Current concepts. The irritable bowel syndrome. New Engl. J. Med.
344, 1846.
Jiang W, Babyak MA, Ronzanski A et al. (2003) Depression and increased myocardial ischemic
activity in patients with ischemic heart disease. Am. Heart J. 146, 55.
Kornfeld DS (2002) Consultation–liaison psychiatry: contributions to medical practice. Am. J.
Lipowski ZJ (1988) Somatization: the concept and its clinical applications. Am. J. Psychiatry
145, 1358.
Martin JB (2002) The integration of neurology, psychiatry, and neuroscience in the 21st century.
Medical Journal of Australia (2002) Clinical practice guidelines. Chronic fatigue syndrome. Med.
J. Aust. 176, s23.
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drome of myalgic encephalomyelopathy (SME): what is its nature? Pain. Prac. 2, 35.
Musselman DL, Tomer A, Manatunga AK et al. (1996) Exaggerated platelet reactivity in major
depression. Am. J. Psychiatry 153, 1313.
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51, 549.
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J. Psychiatry 159,1908.
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effect of group psychotherapy on cardiovascular and immunoreactivity to acute stress in
breast cancer patients. Psychother. Psychosom. 70, 307.
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Psychogeriatrics 17
PSYCHIATRIC DISORDER
EPIDEMIOLOGY
• In 2000, 15.6 per cent of the population of the UK was over 65 years of age, and is
projected to be 20.4 per cent in 2025.
• In 2000, 12.4 per cent of the population of the USA was over 65 years of age, and is
projected to be 18.2 per cent in 2025.
• 45 per cent aged over 65 live alone in the USA.
• About a 25 per cent increase in the population over 75 years of age is expected by
the year 2025 in both the USA and the UK.
• Over one-quarter of the elderly have a mental disorder (16 per cent with a psychi-
atric disorder and 10 per cent with dementia). This number is expected to increase
as the proportion of population over 65 years increases (Jeste et al., 1999; see also
Table 17.1).
AFFECTIVE DISORDER
EPIDEMIOLOGY
• First admissions for affective disorders fall over 65 years, although inception rates
for depressive psychosis in elderly men remain high.
Table 17.1 Psychiatric disorders over 65 years of age

One-year prevalence (%) Lifetime prevalence (%)
Major depression 0.9 1.4

Dysthymia – 1.7
Bipolar I 0.1 0.1
Bipolar II 0.1 0.1
Panic disorder 0.4 male 0.1, female 0.7
Generalized anxiety disorder (GAD) 2.2 2.6–4.3
Obsessive–compulsive disorder (OCD) 0.9 1.2
Adapted from Jeste et al. (1999).

206 PSYCHOGERIATRICS
• 44 per cent of over-65s score ‘depressed’ on the Zung rating scale.

• Only 20 per cent of elderly depressives are referred to a psychiatrist within the first
6 months of illness.
• Other forms of neurotic disorder may gradually change to depressive neurosis in
late middle age, although obsessional and hysterical neurosis may well improve
with age.
• Frequency of depressive episodes in those with a history of depression tends to
increase with age. Also, episodes last longer.
An increased prevalence is seen if:
• Female.
• Past psychiatric history – depressive or neurotic disorder.
• ‘Personality deviation’.
• Social isolation.
• Presence of physical ill-health.
• Early loss of parent.
• Smoking.
• Lack of satisfaction with life, loneliness.
Genetic factors
There is much less evidence of familial incidence in late-onset (over 50) compared
with early-onset (before age 40) depression. The risk of affective illness in relatives
decreases with increasing age of the proband.
Organic factors
No aetiological connection with senile dementia has been confirmed, although
depressive features may be a reaction to early dementia.
Cerebrovascular disease may act as a precipitant of depression, but depressed
patients may show increased incidence of cerebrovascular disease at follow-up.
Depression may include a subgroup who have delayed auditory-evoked responses,
evidence of ventricular dilatation on CT scan, more white matter hyperintensities on
MRI, and a higher mortality rate than other depressives. In some cases depression may
be a symptom of ‘general systems failure’.
Causes of symptomatic depression include antihypertensive drugs, myxoedema,
and potassium deficiency (see Chapter 4).
Environmental factors
It is widely held that environmental factors (bereavements, retirement, deprivation)
are aetiological factors, yet there is little proof of causal relationships. A significant
excess of losses in late-onset depression compared with early-onset has not been
demonstrated.
In the year following the death of a spouse there is increased incidence of suicide,
death and psychiatric referral, but most elderly people adapt to the loss well: 16 per
cent are still depressed at 13 months (Zisook and Shuchter, 1993). Prolonged grief
AFFECTIVE DISORDER 207
reaction is seen more commonly in the socially isolated, the poor and those with little
experience of death in earlier life.
Personality factors
Unipolar neurotic depression may be related to obsessional premorbid personality.
Psychotic depression is less clearly related to this personality type.
CLINICAL FEATURES
Agitation is much more common than retardation. The condition is often accompan-
ied by:
• Histrionic, importunate behaviour.
• Hypochondriacal preoccupations or delusions.
• Delusions of guilt, poverty, nihilism, persecution.
• Pseudodementia – with a tendency to answer ‘Don’t know’ rather than confabulate.
Suicide is a particular danger in elderly depressed, socially isolated men (see Chapter 11).
There is little evidence for a distinction between ‘reactive’ and ‘endogenous’ groups.
Indeed, many with clear reactive features have marked ‘endogenous’ symptoms.
Depression in the elderly is divided into:
• Agitated depression – characterized by apparently shallow affect, bizarre delusions,
importunate behaviour, somatic interpretations of anxiety and a high risk of suicide.
• Senile melancholia – severe agitated depression with delusions of nihilism, guilt,
grandiosity and hypochondriasis.
• Organic depression – depressive disorder precipitated or exposed by cerebral dis-
ease in a predisposed person.
• Depressive pseudodementia – depressive illness with perplexity, loss of interest, loss
of concentration and low self-esteem, leading to approximate answers or lack of
answers and the appearance of impaired awareness and memory. It is character-
ized by relatively acute onset, prominent complaints of cognitive difficulty, com-
munication of distress, patchy deficits, inattention, mental slowing and absence of
focal signs. Abreaction or sleep deprivation may clarify the diagnosis.
• Masked depression – depression expressed as physical symptoms or worsening of
longstanding neurotic symptoms. There is little apparent depressive affect but
many somatic symptoms of depression (anorexia, sleep disturbance, poor concen-
tration, etc.).
This may be a useful descriptive classification but it does not carry aetiological
implications.
Apathetic depression is also seen, in which self-neglect, loss of interest and social
withdrawal are marked features.
Manic–depressive psychosis
• Very rarely presents initially at ages over 65 years (Young, 1992).
• 5 per cent of affective episodes in over-65s are diagnosed as mania or hypomania.
Mixed affective states are more common.
• Hypomania in the elderly is characterized by:
– Irritability.
– Garrulousness, anecdotal speech with little flight of ideas.
– Paranoid or sexual delusions or preoccupations.

– Claims to be happy but tense appearance, irritable and miserable, often without
any infectious gaiety – ‘miserable mania’.
• May present as ‘confusion’ and possibly delirium.
MANAGEMENT
Hospital admission is necessary if the patient is agitated and a suicide risk. Make a full
assessment of social factors, isolation, housing, family support. Investigate and treat
any intercurrent physical illness which may form a focus of distress as well as a pos-
sible aetiological factor.
Drug treatment
Response to SSRI antidepressants is often very effective for the depression. Lower
dosages and careful timing of doses may be indicated. Introduction of medication
should be careful and increase should be gradual. Explanation and reassurance are
especially necessary.
Delusional depression does not respond well to SSRI therapy and usually requires
additional antipsychotic therapy.
Electroconvulsive therapy (ECT)

ECT is likely to lead to a more rapid response. It is especially effective in delusional/
psychotic/resistant depression.
Social therapies
Rehabilitation measures are vital in all cases. Occupational therapy, home assessment,
improvement of social support and development of ‘second careers’ are all of great
importance. Support of the family and reassurance and discussion with them is neces-
sary. Slow discharge with increasing periods at home to build confidence is indicated.
Day hospital, day centre or residential home supervision may be indicated.
PROGNOSIS
Overall, there is a similar pattern to depression in younger patients.
• 88 per cent are discharged from hospital, but only 30 per cent remain symptom-
free for 6 years.
• 17 per cent remain chronically depressed; i.e. initial prognosis is good but relapse
rate is high.
• 30 per cent die within 6 years.
Poor prognosis indicators are:
• Onset after age 70.

• Organic brain disease.
• Serious physical illness.
• Senile habitus.
• Uninterrupted depression for more than 2 years.
MRI brain changes carry a higher mortality risk.
PARANOID SYNDROMES 209
PARANOID SYNDROMES
There is much debate concerning the relationship between pure paranoid psychosis
and schizophrenia. Paranoid psychoses developing in late life may be distinguishable
from paranoid schizophrenia and are often called ‘paraphrenias’.
EPIDEMIOLOGY
• 4 per cent of schizophrenic disorders in men and 14 per cent in women arise after
age 65.
• 5.6 per cent of all psychiatric first admissions after age 65 are for paranoid
psychosis.
• Prevalence – 0.2–0.3 per cent of the population aged over 65 are affected. It is more
common in females.
AETIOLOGY
Genetics
There is an increased risk of schizophrenia in relatives of late paraphrenics when com-
pared with the general population, but a reduced risk compared with early-onset
schizophrenia.
There is an increased incidence of personality disorder in families, but not of
manic–depressive psychosis.
Sensory defects
Between 30 and 40 per cent of paranoid psychotics have impaired hearing. There is an
increased prevalence of visual defects also.
Organic causes
Cerebral lesions, especially of temporal lobe and diencephalon, are more common
(e.g. cerebrovascular disease). Other physical disorders may present with para-
noia; e.g. Parkinson’s disease, Huntington’s chorea and other dementias, metabolic
disorders.
Personality features
• Sufferers are often withdrawn and suspicious, with sensitive premorbid personality –
paranoid or schizoid type.
• Occasionally there is a history of schizophreniform illness in earlier life with per-
sonality defect since then.
• Patients are socially isolated, usually unmarried. They frequently live in self-
created social isolation.
• They are said to have been cold, unloving parents.
Environmental factors
Factors which appear to be precipitants are often merely uncovering pre-existing
psychosis. The condition occasionally does seem to be precipitated by life events.
There may be a sudden paranoid reaction to stress in a sensitive personality.
CLINICAL FEATURES
• Usually, there is insidious onset of increasingly secluded, isolated and suspicious
personality with episodes of bizarre behaviour, abuse of neighbours, self-neglect,
complaints to police, suicide attempt, etc.
• Often, once recognized, a well-organized paranoid delusional system is found to be
present. This often concerns plots to kill the patient, who may feel hypnotized,
drugged, spied upon and show other passivity phenomena.
• Hallucinations may not be present or may be bizarre (e.g. taste or smell of poison,
gases, etc.).
• Mood is often congruous, may be angry and excited or fearful and depressed.
Seventy per cent of paranoid patients appear depressed.
• Personality is frequently well preserved.
• Depression – especially if associated with ideas of guilt and retribution.
• Organic cerebral disease – especially if associated with marked misinterpretations,
lack of systematized delusions and visual hallucinations.
PROGNOSIS
The natural course is of chronic illness with only minor fluctuations in intensity. The
person may become mute, withdrawn, flat, characterless.
With treatment the illness usually becomes less florid, though the delusional system
is often maintained, but may not interfere with life.
• Best prognosis – short duration of illness, good initial response.
• Worse prognosis – severe personality difficulties, deafness, cerebrovascular disease,
non-compliance with medication.
TREATMENT
• Investigate and treat any intercurrent physical illness which may be an aetiological
factor.
• Hospital admission may be necessary if the patient is disorganized, lacks capacity
of self-care, or is at risk for harm to self or others.
• Antipsychotics, atypicals have a lower side-effect burden and require lower
doses.
• Consider cognitive–behavioral therapy or supportive psychosocial therapy.
• Social/environmental assessment is required.
• Modify the environment where necessary.
• Provide education and support for the care-giver.
DEMENTIA
See Chapter 13, Organic psychiatry.

GENERAL ASPECTS OF PSYCHOGERIATRIC MANAGEMENT 211
GENERAL ASPECTS OF PSYCHOGERIATRIC MANAGEMENT
PRINCIPLES
1 Early correct and full diagnosis of medical and social aspects:

– Assess at home, take a full history from patient, relatives, friends, co-workers, etc.
– Assess the problem where it presents, and assess local resources.
– Fewer than 50 per cent of those visited at home are admitted to hospital.
2 Keep the patient at home as long as possible. This reduces confusion and the danger
of institutionalization and encourages utilization of local resources. Major risk
factors which predict institutionalization for the elderly are:
– Extreme old age.
– Living in retirement housing.
– Recent hospitalization.
– No spouse or partner.
Family support is the most important factor here, and families must themselves be
supported, with their problems explained and discussed. High rates of physical and
psychiatric illness occur among carers.
Maximize home support with community nurses, social workers, practical help
(meals on wheels, home helps, laundry service, attendance allowance) and ensure correct
accommodation (warden-controlled flats, residential home, etc.). However, when
dementia patients cannot be managed on their own at home, support in this circum-
stance paradoxically accelerates institutionalization (O’Connor et al., 1990).
Outpatient clinic support of patient and relatives may be very helpful. Day hospital,
day centre or luncheon club attendance is beneficial. The day hospital needs to have a
high staff/patient ratio and multidisciplinary input. However, cost-effectiveness is
somewhat disputed.
Admission to a short-stay psychogeriatric unit for full physical, psychological and
mental state assessment may be indicated.
TREATMENT POSSIBILITIES
Use of drugs
• Beware of overmedication or undertreatment.
• Assess the physical condition (heart, lungs, kidneys, liver) and presence of other
drugs (including alcohol).
• Treat with the lowest effective dose.
• Use a limited range of familiar drugs.
• Introduce medication slowly and carefully, to avoid side-effects and to increase
compliance. Assess with plasma drug levels if available.
• If at home, give small quantities with each prescription and supply large written
instructions.
• Explain the treatment to the patient and carers and involve relatives as appropriate.
Use of psychotherapy
• The person may need longer-term therapy, but with shorter individual sessions
than for younger age-groups.
• Cognitive–behavioural therapy is effective in the elderly.
• There is an increased need for support and encouragement, attention to self-
esteem and practical issues.
Inpatient issues
Aim for a high staff/patient ratio. Build and maintain morale and interest in the unit.
Treat patients with respect, and avoid institutionalization.
ORGANIZATION OF SERVICES FOR THE ELDERLY
• Define those to be helped and their numbers.

• Define the components of the multidisciplinary service:
– Domiciliary service – consultant, nurse, social worker.
– Outpatient service to be offered.
– Day centre liaison in district and other local authority facilities present.
– Day hospital service offering assessment, short-term treatment and rehabilitation.
– Inpatient beds for acute admission and assessment, in conjunction with geri-
atric service.
– Inpatient beds for long-stay patients – includes elderly, chronic hospitalized
patients (e.g. chronic schizophrenics), old people with functional mental dis-
orders and old people with dementia.
– Inpatient beds for terminal care if necessary.
• Define other responsibilities of service:
– Support own staff and members of the multidisciplinary team.
– Support families and workers in the community.
– Teaching – of staff, of students and of local community.
– Liaison with colleagues and other disciplines.
– Research, for personal and general improvement of services.
– Campaigning for more and proper resources.
Further comments on service delivery

There is a need for an integration of mental health services with primary care services
in order to improve access and utilization of mental health services among the elderly.
Increased support, advocacy, training and in-home help for informal care-givers of
those with Alzheimer’s may delay or prevent costly nursing home placements.
Administration on Aging (2001) Older Adults and Mental Health Issues and Opportunities.
Department of Health and Human Services, Rockville, MD.
Beekman ATF, Geerlings SW, Deeg DJH, Smit JH et al. (2002) The natural history of late-life
depression. Arch. Gen. Psychiatry 59, 605.
Benbow SM, Jolley D (2002) Home assessments in old age psychiatry. Adv. Psychiatr. Treat. 8, 316.
Blazer DG (2003) Depression in late life: review and commentary. J. Gerontol. A. Biol. Sci. Med.
Sci. 58, 249.
Bouman WP, Pinner G (2002) Use of atypical antipsychotic drugs in old age psychiatry. Adv.
Brodaty H, Sachdev P, Koschera A et al. (2003) Long-term outcome of late-onset schizophrenia:
5-year follow-up study. Br. J. Psychiatry 183, 213.
Brown GK, Bruce ML, Pearson JL et al. (2001) High risk management guidelines for elderly with
suicidal patients in primary care settings. Int. J. Geriatr. Psychiatry 16, 593.
Bruce ML, McAvay GJ, Raue PJ et al. (2002) Major depression in elderly home health care
patients. Am J. Psychiatry 159, 1367.
Burns A, Dening T, Baldwin R (2001) Care of older people: mental health problems. BMJ
322, 789.
Burns A, Lawlor B, Craig S (2002) Rating scales in old age psychiatry. Br. J. Psychiatry 180, 161.
Cohen-Mansfield J (2001) Nonpharmacologic interventions for inappropriate behaviors in
dementia. Am. J. Geriatr. Psychiatry 9, 361.
Dewey ME, Saz P (2001) Dementia, cognitive impairment and mortality in personas aged 65 and
over living in the community: a systematic review of the literature. Int. J. Geriatr. Psychiatry
16, 751.
Evans M, Mottram P (2000) Diagnosis of depression in elderly patients. Adv. Psychiatr. Treat.
6, 49.
Furniss L (2002) Use of medicines in nursing homes for older people. Adv. Psychiatr. Treat. 8, 198.
Geller B, Craney JL, Bolhofner K et al. (2002) Two-year prospective follow-up of children with a
prepubertal and early adolescent bipolar disorder phenotype. Am. J. Psychiatry 159, 927.
Hybels CF, Blazer DG (2003) Epidemiology of late-life mental disorders. Clin. Geriatr. Med. 19, 663.
Jeste DV, Alexopoulos GS, Bartels SJ et al. (1999) Consensus Statement on the Upcoming Crisis in
Geriatric Mental Health: research agenda for the next 2 decades. Arch. Gen. Psychiatry 56, 848.
Kawas CH, Brookmeyer R (2001) Aging and the public health effects of dementia. New Engl. J.
Med. 344, 1160.
Lawlor B (2002) Managing behavioural and psychological symptoms in dementia. Br. J.
Lenze EJ, Dew MA, Mazumdar S, Begley AE (2002) Combined pharmacotherapy and psychotherapy
as maintenance treatment for late-life depression: effects on social adjustment. Am. J. Psychiatry
159, 466.
Mather AS, Rodriguez C, Guthrie MF et al. (2002) Effects of exercise on depressive symptoms in
older adults with poorly responsive depressive disorder: randomised controlled trail. Br. J.
Nebes RD, Vora IJ, Meltzer CC et al. (2001) Relationships of deep white matter hyperintensities
and apolipoprotein E genotype to depressive symptoms in older adults without clinical
depression. Am. J. Psychiatry 158, 878.
O’Connor DW, Pollitt PA, Roth M et al. (1990) Problems reported by relatives in a community
sample of dementia. Br. J. Psychiatry 156, 835.
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Forensic psychiatry 18
ANTISOCIAL PERSONALITY DISORDER (ASP)
See Table 18.1.
HISTORICAL DEVELOPMENT
• Pinel (1801) – Manie sans délire:
– Disturbance of emotions and volition; reason intact.
• Rush (1812) – Moral derangement:
– Innate, constitutional moral depravity, amenable to medical treatment.
• Pritchard (1835) – Moral insanity:
– Intellectually unimpaired, but affective and moral faculties disturbed.
• Koch (1891) – Psychopathic inferiority:
– Constitutional predisposition to mental disturbances of all kinds.
Table 18.1 ICD-10 and DSM-IV diagnostic criteria

ICD-10 DSM-IV
Dissocial personality disorder Antisocial personality disorder

Gross disparity between behaviour and social norms; i.e.: (a) current age ⭓18
(a) callous unconcern for others (b) incidence of conduct disorder with onset ⬍15
(b) gross, persistent irresponsibility, disregard for social (c) pervasive pattern of disregard since 15 as
norms/rules/obligations shown by ⭓3 of:
(c) incapacity to sustain relationships 1. repeated unlawful behaviour
(d) low frustration tolerance and low threshold for aggression 2. irritability and aggressiveness
(e) inability to experience guilt/benefit from experience 3. consistent irresponsibility (work, finances)
(f) blames others/society for behaviour and its consequences 4. impulsivity/failure to plan ahead
5. deceitfulness
6. reckless disregard for safety (self or others)
7. lack of remorse
(d) antisocial behaviour is not exclusively during
the course of schizophrenia or manic episode
216 FORENSIC PSYCHIATRY
• Kraepelin (1909) – Psychopathic traits:

– Degenerative disorders of personality, separate from neuroses or psychosis (his
views changed in later years).
• Schneider (1927) – Psychopathic personalities:
– People who either suffer themselves or cause society to suffer (this introduced
the concept of deviance).
• Partridge (1930) – Sociopath:
– Emphasized primary effect on society rather than on the individual (the
American perspective).
• Henderson (1939) – Psychopathy:
– Three types described – creative, inadequate, aggressive.
– Separate from neuroses.
– Selfish, lack of empathy, impulsive, low stress threshold, do not learn from
mistakes.
• Scott (1960):
– Absence of other psychiatric illness/defect, antisocial behaviour, persistence
since early youth; requires a specialized form of handling by society.
• Cleckley (1966) – the mask of sanity:
– Considered sociopathy equivalent to antisocial personality disorder: pernicious,
insightless, affectless.
• Lewis (1974):
– Antisocial personality too general; may apply to ‘normal’ persons who ‘struggle
to make a dishonest living’; insufficient regard for the possible neuropsychiatric
basis of this behaviour.
EPIDEMIOLOGY
There is a 2–3 per cent lifetime prevalence in Western societies (Coid, 2003a). Males
are more affected than females (ratio 5:1), and urban dwellers more than rural.
Highest rates are in 25- to 44-year-olds.
AETIOLOGY
Organic causes
• Twin studies – MZ:DZ concordance ⫽ 60%:30%.
• Adoption studies confirm a genetic component.
• There is an excess of obstetric complications, minor physical anomalies,
neuropsychological impairments – a form of minimal brain damage or
dysmaturation?
• EEG abnormalities:
– Generalized slow-wave ␪ abnormalities (but normal in 50 per cent of aggressive
criminals) which may be localized to the temporal region.
– Posterior slow and sharp waves.
– Immature ‘EEG’.
• Corpus callosum abnormalities may reflect atypical neurodevelopmental
pressesses and help explain abnormal interhemispheric transfer seen in psycho-
pathic individuals (Raine et al., 2003).
• Low serotonin is found in impulse disorders/ASP.
VIOLENCE IN THE CONTEXT OF MENTAL ILLNESS 217
Sociocultural factors
• Lower socioeconomic status families, single/divorced parents.
• History of parental sociopathy.
• Physical/sexual abuse.
Psychodynamic factors
Interference with early bonding may result in defective socialization and immaturity
of emotional and moral development. Defective superego development may result in:
• Abnormal, stereotyped antisocial behaviour under stress.
• Excessive anxiety at any perceived threat, so that all anxiety is ignored and there is
a lack of anxiety to reinforce morality.
• Failure to acquire social behaviour at critical learning periods.
MANAGEMENT
Primary prevention
• Prenatal care can lessen intrauterine insults to the brain.
• Parenting classes can establish a nurturing environment in infancy as well as effect-
ive parenting styles.
• Early identification of at-risk children (i.e. conduct disorder) can lead to interven-
tion in the home or at school.
Active management
• Pharmacological – control of aggressive and sexual impulses; treatment of
co-morbid illness (depression, DSH, substance abuse).
• Psychological:
– Supportive psychotherapy; advice to help avoid stressful situations; environ-
mental manipulation.
– Cognitive–behavioural therapy to heighten awareness of consequences of
behaviour; reshape to appropriate behaviour.
Hospitalization
Psychiatric hospitalization is of little benefit. More appropriate is a specialized inpa-
tient or day care unit. A therapeutic prison (e.g. Grendon Underwood, UK) may be
effective for aggressive psychopaths.
Incarceration limits damage to society by the offender.
PROGNOSIS
The more numerous the risk factors in early life, the greater likelihood of antisocial
personality developing. ‘Protective factors’ may offset risk factors; i.e. positive social
orientation, good family support system, structure and rules in the household.
Patients may become less aggressive and antisocial in later life. They tend to become
depressed and self-blaming later. There is an increased incidence of alcoholism and
suicide.
VIOLENCE IN THE CONTEXT OF MENTAL ILLNESS
The relationship between violence and mental illness is poorly understood and
overestimated by the public and media. In societies, violent behaviour is the result of
Table 18.2 Swedish epidemiological study of violence

Likelihood above normal population rate
Criminal offence Violent offence
Males with major mental disorder (schizophrenia/affective disorder) 2.5 4

Females with major mental disorder 5 27
Males with mental retardation 3 5
Females with mental retardation 4 25
Adapted from Hodgins (1992).
excessive motivation towards violence together with insufficient self-control. Possibly

it therefore occurs in the under-controlled under any stress and in the over-controlled
under extreme stress (leading to extreme violence).
The peak age for violent offenders is 17–21 years. Fifty per cent of violent crimes
occur in or near public houses or in domestic disputes. In 26 per cent of cases, the victim
is regarded as having actively precipitated violence.
• Dangerousness (Scott) – ‘A dangerous concept’; an ‘unpredictable and untreatable
tendency to inflict or risk serious irreversible injury or destruction or to induce
others to do so’.
• Violence and psychiatric patients (Tardiff, 1992) – In societies where rates of crimes
by the general population and crimes by substance abusers are very high, the men-
tally disordered and intellectually handicapped account for a very small proportion
of offences.
• Swedish epidemiological study (Hodgins, 1992) – The likelihood (above the normal
population rate) of police registration for violent offenses is shown in Table 18.2.
• 10 per cent of patients in general psychiatric hospital have a history of violence. In
general:
– Schizophrenia is the most common diagnosis, then organic brain disorders,
mania, substance abuse and antisocial personality disorder.
– Schizophrenia – related to delusions, hallucinations; often co-morbid substance
abuse; violence occurs usually during relapse of illness. The ‘threat–control–
override syndrome’.
– Mania – less violent than in schizophrenia; early in treatment.
– Substance abuse – may be due to disinhibition effect or secondary to delirium or
personality-related; associated with alcohol, cocaine (especially crack) and PCP.
PATIENT ASSESSMENT
Assessment is difficult, but detailed evaluation is essential.

• Obtain collateral, old records, police reports, etc.
• Evaluate carefully the extent and timing of violent episodes: precipitating, perpetu-
ating factors, severity of injury or intended injury, history of previous violence.
Past history of violence is best predictor of subsequent violence.
• Blood and urine screen for alcohol and drug abuse.
• EEG, CT/MRI may be indicated.
FEATURES OF VIOLENT CRIMES 219
• May depend on type and quality of violence. Aggressive sex offenders and the
morbidly jealous are particularly liable to reoffend with violence. Threats of vio-
lence and frequent violence when drunk may indicate further danger. Repeated
violence implies further violence.
• May depend on environmental factors – if stress remains or if potential victims are
still available.
• Disinhibiting factors (e.g. alcohol, drugs, fatigue) which may occur must be
assessed.
• Lack of remorse may indicate increased dangerousness.
• Widespread aggressive behaviour appearing at an early age (arson, cruelty to ani-
mals) and continuing, especially if also present in the family, indicates recurrence.
• Fear engendered in the examiner may well indicate dangerousness.
• Regressive, infantile behaviour during and after an offence may indicate
dangerousness.
• Sadistic fantasy life is an ominous finding.
FEATURES OF VIOLENT CRIMES
Violent crimes account for 5 per cent of all indictable offences.
KILLING
DEFINITIONS
• Murder – unlawful killing with malice aforethought (‘mens rea’).

• Manslaughter – unlawful killing without malice aforethought. Found if there
is provocation, diminished responsibility, suicide pact or involuntary killing, or
negligence.
• Infanticide – unlawful killing of a child of less than a year by the mother, who must
show postnatal mental disorder.
• Homicide – encompasses murder, manslaughter and infanticide.
EPIDEMIOLOGY
• 500 per year in England and Wales.
• Murderers have a male:female ratio of 11:1.
• 75 per cent of victims have a previous relationship with their murderer.
• 50 per cent of victims are a relative or lover.
• In the USA, homicide is the 11th most common cause of death.
• Up to 30 per cent of homicide suspects kill themselves following murder (espe-
cially women).
• Alcohol is involved in up to 50 per cent of cases.
• 50 per cent of murderers are mentally abnormal – particularly with severe person-
ality disorder.
• Fewer than 1 per cent recommit murder.
Thus the most common combination of factors leading to murder are: an irritable
and violent husband, alcohol and family disharmony.
Sadistic murderers are described as: usually male, under 35, solitary, emotionally
blunted, reserved, with a rich fantasy life (fascism, black magic, sadistic pornography).
RAPE
DEFINITION
Rape is sexual intercourse (i.e. penetration) with a woman who does not consent, the man
knowing that she did not consent or being reckless as to whether or not she consented.
A CLASSIFICATION
• Aggressive aim – sexual assault is primarily destructive and sadistic. May be
displaced anger (e.g. to mother). May humiliate the victim.
• Sexual aim – aggression with the aim of achieving sexual intercourse. Part of
general hedonism.
• Explosive – forcible expression of sexual drives in an over-controlled man. May
have compulsive quality.
• Aggressive and sexual aim – resistance and humiliation are essential for sexual
satisfaction.
EPIDEMIOLOGY
Most rapists are aged under 25 years, single, have a record of non-sexual crime and are
not mentally disordered. There is an increased incidence in summer, in the first half of
night and at weekends.
Thirty per cent of victims are neighbours or acquaintances. Twenty per cent of vic-
tims have a criminal record (especially soliciting).
OUTCOMES
• 80 per cent of rapists are sentenced to prison.
• 85 per cent of aggressive rapists later commit non-sexual crimes and 20 per cent
recommit sexual offences.
• 28 per cent of non-aggressive rapists later commit non-sexual crimes and 3
per cent recommit sexual offences.
ARSON
DEFINITION
Arson is to damage or destroy any property by fire, without lawful excuse.
A CLASSIFICATION
• Motivated arson:
– No psychotic disorder; insurance fraud, bankruptcy, revenge, political, to cover
up another crime, vagrant.
– Suicidal.
– Result of boredom, desire to impress.

– Juvenile fire (firesetting, fireplay).
• Motivated by mental illness:
– Schizophrenia (approx 8 per cent of convicted arsonists), probably in response
to voices, delusions.
– Depression, possibly due to morbid delusion, or in manic excitement.
– Drug or alcohol-induced psychosis, diminished responsibility.
– Mental retardation.
– Dementia.
• Motiveless arson:
– Primary interest is the fire is the excitement, sexual arousal, desire to be the hero,
release of tension.
– Repeated offenders (‘firebugs’) fall into this category.
EPIDEMIOLOGY
Arson accounts for 0.1 per cent of all serious crime (one-third the incidence of
murder or rape). There is a peak incidence at 17 years in men, at 45 years in women
(85 per cent of offenders are men). There is an increased incidence of mental retardation
(up to 50 per cent) and alcoholism.
OUTCOMES
• Fewer than 4 per cent repeat arson.
• There is an increased likelihood of recurrence with:
– History of previous arson.
– Presence of psychosis, severe abnormality or dementia.
– Marked pleasure or sexual excitement associated.
– Awareness by arsonist of overwhelming urge to start fires to relieve tension.
NON-ACCIDENTAL INJURY TO CHILDREN
DEFINITIONS
• In 1962 Kempe introduced the term battered child syndrome to describe the signs
and symptoms characteristic of physical abuse.
• In 1972 Caffey introduced the term shaken baby syndrome to describe the signs and
symptoms of violent shaking of an infant that results in tearing of intracranial
veins with the degree of brain damage corresponding to the intensity of shaking.
• An overall definition is ‘the killing of, physical violence towards, persistent abuse of
or neglect of a child, by those in charge of the child’.
A CLASSIFICATION (SCOTT)
• Elimination – of an unwanted encumbrance.
• Euthanasia – mercy killing (e.g. of handicapped child).
• Psychotic – the result of delusions.
• Displaced anger – from elsewhere on to the child.
• Anger – arising from within the child–parent relationship.
EPIDEMIOLOGY
Possibly 0.5 per cent of children aged under 3 years are involved (considerable under-
reporting). Underweight and ill children are particularly likely to be battered.
• 1 in 1000 children aged under 4 years suffers major injury each year in England
and Wales.
• The death rate is 10 per cent in 2 years, and 25 per cent are intellectually damaged.
• 2–4 per cent of children are in subnormality hospitals.
• There is a 60 per cent chance of further battering.
• 19 per cent of siblings have also been battered.
CLINICAL FEATURES TO AROUSE SUSPICION

In the child
• Bruises, burns or lacerations of different ages.
• Multiple fractures (or any fracture in child under 2 years).
• Subperiosteal haematomas, epiphyseal separations.
• Subdural haematoma, retinal injury, rupture of abdominal viscera or any bizarre
injury.
• Failure to thrive of unknown aetiology.
• ‘Frozen watchfulness’ towards parents.
• ‘Reverse caring’ (child shows over-anxious concern for parents).
In parents
• Delayed reporting.
• Parents do not volunteer information.
• Contradictory stories.
• ‘Mechanical handling’ of child, lacking warmth and confidence.
Associated features
In child
• Illegitimacy.
• Early separation from parents.
In parents
• Lower social class.
• Young maternal age.
• Unmarried or father absent.
• Subnormality in mother.
• Very rarely (3 per cent) psychotic mother.
• Criminal record and/or personality disorder in father.
• Family is socially isolated.
• Parents often victims of battering themselves.
PREVENTION
1 A high level of awareness of the problem is needed in baby clinic, by GPs, etc.
2 There should be good communication between services, with easy availability of help.
3 Emergency action (e.g. Place of Safety order) should be rapidly available.
4 ‘At risk’ case registers must be held by local authorities.
5 Case conferences should be held, with designation of a ‘key worker’.

6 Supportive family therapy should be considered to correct unrealistic expectations
of having a child, reduce resentment and improve marital understanding.
PAEDOPHILIA
Paedophilia is the erotic attraction to children. There are three characteristic groups:
• Immature adolescents.
• Middle-aged men with marital difficulties.
• Elderly, socially isolated men.
Fifty per cent of perpetrators are relatives or friends. Once discovered, most do not
reoffend.
INCEST
There is a variable extent of sexual activity, from fondling to intercourse. In 75 per cent
cases it is between a father/stepfather and daughter.
Five per cent of the adult female population report being abused by their father.
Forty-four per cent of incest perpetrators have also committed extrafamilial offences.
Characteristics of the offender

• No specific traits.
• High rates of alcohol abuse.
• 30 per cent sexually and/or physically abused as a child.
• Often a pattern of poor marital relationships.
Characteristics of the abused
Females ⬎⬎ males.
CHILD SEXUAL ABUSE (CSA)
Child sexual abuse is a general term that includes incest. A range of definitions results
in wide reported prevalence rates: 12–36 per cent of females and 3–29 per cent of
males report some sexual abuse in childhood.
CSA may occur at any age, but the peak occurrence is after age 12 years. The mean
duration of abuse before detection is 2 years.
Boys tend to be abused at an earlier age, and the offender is more likely to be a
stranger. Absence of one or both parents and the presence of a stepfather in the home
conveys greater risk of CSA.
Poverty is associated with greater reporting of CSA but not necessarily greater
incidence.
Presentation of CSA by child

There are diverse manifestations, such as sexualized behaviour, self-mutilation, child-
hood substance abuse and depression.
EVALUATION
• Attempt to confirm CSA.
• Many cases of ‘suspected abuse’ demonstrate incomplete evidence, and the family
declines investigation.
• Use of anatomical dolls is controversial. There is overlap in play behaviour of non-
abused and abused children, so this is not a good diagnostic tool.
• If CSA is confirmed in a minor, or strongly suspected by a health professional,
social services must by law be informed in the UK and USA.
• Children as witnesses – Younger children are suggestible; overall, children are com-
petent witnesses; most do not lie.
• Multidisciplinary evaluation – Legal involvement must be early on to protect the
child from ongoing CSA.
MANAGEMENT
This must be multimodal:
• Cognitive–behavioural therapy.
• Social skills education, stress management.
• Family intervention therapy, if appropriate.
• Legal action and a programme to prevent further CSA.
OUTCOMES
There is a drop-out rate of 18 per cent for incest families in therapy. However, with
therapy, 60 per cent of families are safe from further abusive behaviours.
Long-term sequelae for the abused child
Emotional: Anxiety/fear, low self-esteem, anger, guilt.
Psychiatric:
• Depression, deliberate self-harm.
• Personality disturbance (borderline, multiple personality).
• Substance abuse.
• PTSD symptoms.
• Eating disorders.
• Somatization.
Behavioural:
• Early sexual activity.
• Promiscuity, teenage prostitution.
• Adult sexual dysfunctional disorders.
NON-VIOLENT OFFENDERS (SHOPLIFTING)
There are several groups of shoplifters:

• Professionals who steal as a livelihood.
• Shoplifters with severe psychiatric disorder.
• Reactive shoplifters – as a transient stress reaction.
LEGAL ASPECTS 225
• Young shoplifters – the majority.

• Those with abnormal learned behaviour – repetitive theft.
EPIDEMIOLOGY
Figures in the early 1970s showed that most offenders were women. Ninety per cent
did not reoffend when caught. Fifteen per cent of British-born offenders showed a
psychiatric disorder.
Recent changes
• There has been an increase in young shoplifters (ages 10–18) – now the majority.
• There has also been an increase in male shoplifters – now the majority.
• The incidence of psychiatric disorder is reduced – now estimated at 5 per cent.
• The offence may be regarded by some as an ‘accepted perk’ of shopping.
Approximately 5 per cent shoplift at each shop they visit.
LEGAL ASPECTS
PREPARING COURT REPORTS
Plan of report
– Name, address and age of person charged.
– Charge.
– When and where interviewed.
– All other sources of information (notes, other doctors, relatives, etc.).
– Short description of person charged.
– Concise, relevant family history.
– Concise, relevant personal history.
– Past medical, psychiatric and criminal history.
– Brief account of circumstances of offence and any relevant psychiatric disturb-
ances, sources of tension, etc.
– Findings at interview, including assessment of personality.
– Findings of further investigations (EEG, psychological testing, etc.).
– Opinion – All the above information is merely an explanation of the basis of the
opinion. Comment on fitness to plead, responsibility for offence, mitigating fac-
tors, prognosis.
– Recommendations – for treatment and further management, if appropriate.
– Psychiatrist’s name, qualifications, professional address and approval under the
Mental Health Act.
Aim at accuracy, understandability, relevance and impartiality.
PSYCHIATRIC DEFENCES (APPLIES TO UK ONLY)
Unfit to plead (at the time of trial)

This is decided by a jury. It results in admission to a special hospital until fit to plead,
as decided by the Home Secretary.
The person charged must be:

1 Unable to understand the charge or the significance of the plea; or
2 Unable to challenge a juror; or
3 Unable to instruct counsel; or
4 Unable to examine a witness; or
5 Unable to follow the progress of the trial.
Not guilty by reason of insanity (‘special verdict’)

McNaughten rules: ‘Labouring under such a defect of reason, from disease of the
mind, as not to know the nature and quality of the act he was doing, or if he did know
it, that he did not know that what he was doing was wrong.’
This is less used in murder cases since abolition of the death penalty by the
Homicide Act (1957).
If the ‘special verdict’ is found, the defendant is detained in hospital and his/her
time of release is decided by the Home Secretary.
Diminished responsibility
This defence can be used only if the charge is murder. If found, it reduces the charge of
murder (carrying a mandatory life sentence) to manslaughter (sentencing at the dis-
cretion of the judge).
The defendant must be suffering from ‘such abnormality of mind … as substantially
to impair his mental responsibility for his acts’. ‘Abnormality of mind’ is a state of mind
so different from that of ordinary human beings that the reasonable person would term
it abnormal. It could include severe personality disorder, extreme intoxication, etc.
Possible results at sentencing
• The law takes its normal course – prison, fine, etc.
• Conditional or absolute discharge – possibly with voluntary psychiatric treatment.
• Probation order, under Powers of Criminal Courts Act 1973. An approved psych-
iatrist (s.12 of the Mental Health Act) takes on the responsibility for treatment, as
an inpatient or outpatient. The offender must agree to this.
• Detention in hospital under s.60 of the Mental Health Act, with or without s.65.
• Offenders aged under 17 years may be committed to the care of the local authority.
CRIMINAL RESPONSIBILITY (APPLIES TO UK ONLY)
AGE
• A child under 10 years is held to be incapable of forming a guilty intent (mens rea).
• A child of 10–13 years is so capable if he/she is able to discern good from evil.
• A child of 14 years and over is presumed to be fully responsible for his/her actions.
INTENT
Some offences require that specific guilty intent (mens rea) be proved present as well
as the unlawful act (actus reus) – e.g. murder, arson, rape, assault with intent to cause
grevious bodily harm.
Other offences do not require proof of guilty intent – e.g. manslaughter, indecent
assault, assault occasioning actual bodily harm.
LEGAL ASPECTS 227
Complicating factors
• Multiple intention.
• Unconscious intention.
• Changing intention during the crime.
• Overwhelming tension, stress or emotion.
• Amnesia, including that due to alcohol.
• Alien intention (as in schizophrenic passivity).
• Self-induced intoxication
Simple drunkenness is no defence. A person may not, however, be held to have com-
mitted a crime requiring mens rea if that person was too drunk to form an intent. The
person may, however, be held to have committed a crime not requiring proof of mens rea.
TESTAMENTARY CAPACITY (APPLIES TO UK ONLY)
A person may make a will if he/she is ‘of sound disposing mind’ and:
1 Knows the nature and extent of his/her property.
2 Knows the persons having a claim on it and the relative strengths of their claims.
3 Can express himself/herself clearly and without ambiguity.
COMPETENCE TO CONSENT TO TREATMENT (APPLIES TO UK ONLY)
INFORMED CONSENT
Informed consent, which may be verbal or written, includes:
1 Disclosure of information.
2 Competency.
3 Understanding.
4 Voluntariness.
5 Decision.
COMPETENCY
Does the patient understand:
1 The condition for which treatment is proposed?
2 The nature and purpose of the treatment?
3 The risks and benefits of undergoing the treatment?
4 The risks and benefits of not undergoing the treatment?
NEGLIGENCE
Negligence results in unintentional wrong to a person. To be found it requires the Four D’s:
1 A duty to a client.
2 A dereliction (breach) of duty.
3 The breach is a direct cause of the damage.
4 Actual damages result from the breach of duty.
Duty is accepted as the usual standard of care, as assessed by a responsible body of

medical opinion.
Common causes of action against psychiatrists include: suicide, injury to a third
party and treatment with medication (lethal overdose, side-effects, tardive dyskinesia,
benzodiazepine dependency).
TARASOFF DOCTRINE
In the USA, courts have decided that a psychiatrist who knows or should know of a
patient’s dangerousness to a third person must take all reasonable steps to protect (not
just inform) potential victims.
INVOLUNTARY COMMITMENT
There is wide variation across countries and mental health systems on terms and pro-
cedures for commitment. Common elements include:
• Commitment due to the presence of mental disorder which poses grave and immi-
nent risk to self or others.
• Certification by a health professional (not exclusively by a psychiatrist).
• Limitation on duration of involuntary hold.
• A review process (tribunal, court, etc.) prior to the end of the time limitation,
linked to patient appeal process.
Commitment must be for a defined mental disorder. Sexual deviancy, immorality,
excesses of drugs/alcohol, violence (without mental disorder ⫽ legal problem) are not
mental disorders and reasons per se for commitment. Commitment represents a deli-
cate balance between the protection of society and protecting personal autonomy.
In some systems, commitment procedures allow containment only for assessment,
there being a separate (secondary) procedure for involuntary treatment. Most systems
invoke both assessment and treatment.
Most commitment statutes are for inpatient hospitalization, but there is a growing
trend towards outpatient commitment. The patient is ordered to follow a ‘community
treatment order’, or else revocation of community tenure with rehospitalization. This
is difficult to enforce and monitor.
New initiatives
There is a broad move to enhance appropriate diversion of mentally ill offenders into
mental heath care rather than jails. In a jail diversion programme, for example, mental
health professionals might be called out to assist police at the time of disturbance of
the peace due to a patient’s psychotic behavior; the patient receives hospitalization
rather than jail.
Mental health courts are another initiative.
PSYCHIATRIC ADVANCED DIRECTIVES
Two types of directive are available to specify the wishes of an individual should
he/she no longer have the capacity to make decisions on his/her own behalf.
MANAGEMENT OF DANGEROUS MENTALLY DISTURBED PERSONS 229
• Living will – provides specific information about treatment concerns.

• Proxies or healthcare powers of attorney – designates an individual to act as a surro-
gate decision-maker.
MENTAL ILLNESS IN PRISONS
There is a high prevalence of psychiatric illnesses in prisoners (Fazel and Danesh,

2002):
• Males:
– 3.7 per cent psychotic disorder.
– 10 per cent major depression.
– 65 per cent personality disorder.
• Females:
– 4 per cent psychotic disorder.
– 12 per cent major depression.
– 42 per cent personality disorder.
The high prevalence of mental illness in prison has various causes, including:
• Small likelihood of early release.
• Small likelihood of being granted probation.
• High rates of revocation of probation.
MANAGEMENT OF DANGEROUS MENTALLY DISTURBED PERSONS
AT A POLITICAL LEVEL
Possible policies
1 Mental hospitals should provide secure facilities on an area or regional basis; i.e. a
return to traditional roles.
2 There should be better provision for the mentally disturbed within prisons. This
requires a change of policy: prisons are for punishment, hospitals for treatment.
Grendon Underwood, for people with severe personality disorders, is the only such
prison in England and Wales.
– Between 20 and 40 per cent of prisoners are found to be psychiatrically disturbed
(2 per cent are psychotic, 11 per cent have alcohol and drug addictions, 14 per cent
are mentally handicapped), and the suicide rate is three times higher than normal.
In Western societies the size of the prison population is inversely related to the
size of the mental hospital population.
4 There needs to be more provision of special hospitals (e.g. Broadmoor, UK). But
these may be expensive, institutionalized and have difficulty discharging patients
because other hospitals will not accept them. They are part of the Health Service
and are under the direct control of the Secretary of State for Health.
5 There can be provision of regional secure units and, more recently advocated,
development of smaller, more widely distributed units: 1500 medium secure units
and 750 long-term medical secure beds are recommended for England and Wales
(Reed Report; UK Government, 1992).
AT WARD LEVEL
Architectural considerations
• Adequate but unobtrusive security.
• Ease of arousal of alarm.
• Available space for exercise, expression of anger, etc.
Staff policies
• Develop a clear violence-prevention policy of which all staff are aware.
• Adequate training of staff in coping with violent behaviour.
• Adequate numbers of staff (1:1 ratio) in units with violent patients.
• Acceptance of responsibility of dealing with violence by all staff, teamwork.
• Effective communication of dangers.
• Rapid availability of more staff and of medical staff.
Management of the violent incident
• Raise the alarm.
• Free any victim, remove weapons as soon as possible.
• Assess diagnosis (e.g. alcohol, psychosis).
• Remain calm and non-critical.
• Use minimum necessary force; avoid force if possible.
• ‘Talk patient down’ – done by the most skilled staff member or member most
trusted by the patient. Involves listening, agreeing, reassuring.
• If force is necessary, ensure adequate numbers of staff.
• If sedation is needed (IV or IM), use carefully. Can be given even to informal
patients in an emergency.
• Ensure adequate reporting and ward discussions afterwards.
LONG-TERM MANAGEMENT
Psychotherapy
• Detainees need a place to call at times of stress.
• There should be attention to self-esteem and masculinity.
• Exploration of violent fantasies in a controlled setting can be beneficial.
• Increase the patient’s understanding of feelings behind violence.
• Counselling and behavioural techniques may help the patient to avoid stressful
situations.
Drug therapy Numerous drugs are claimed to be anti-aggressive (Corrigan et al.,
1993): lithium, antipsychotics, valproate, carbamazepine. Use of benzodiazepines may
result in paradoxical aggression due to disinhibition.
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Child psychiatry 19
OVERVIEW
EPIDEMIOLOGY
The Mental Health Evaluation and Community Consultation Unit at the University of
British Columbia (2002) reported on the prevalence of mental disorders in youth and
found a 15 per cent prevalence of any type of mental disorder. Of these, 6.5 per cent
had an anxiety disorder, 3.3 per cent conduct disorder, 3.3 per cent attention-
deficit/hyperactivity disorder (ADHD), 2.1 per cent depression.
DIFFICULTIES DIAGNOSING THE YOUNG

• There is only a limited life history.
• Children are in the process of developing.
• Symptoms overlap with other disorders.
• There tends to be co-morbidity of diagnoses.
• Multiple informants are needed – school, family, clinician.
• Reports of symptoms vary.
• Substance use and trauma must be ruled out.
TREATMENT CONSIDERATIONS
Psychopharmacology
• Research on psychopharmacology in the young is limited.
• There is frequent ‘off label’ use of prescribed medications, frequently treat target
symptoms.
• Appropriate consent for treatment is needed.
• Extended-release medications avoid school dosing.
• Children require lower dosing of dopamine antagonists.
• There is highly efficient hepatic metabolism in the young.
Other considerations
• Need for family involvement in assessment and treatment.
• Role of peer influence.
• School teachers/counsellors are important.
234 CHILD PSYCHIATRY
Table 19.1 Main groups of childhood psychiatric disorders as classified in ICD-10 and DSM-IV
ICD-10 DSM-IV
F80 Specific developmental disorders of Learning disorders

speech and language Communication disorder
F81 Specific developmental disorders of scholastic skills
F82 Specific developmental disorders of motor function Motor skills disorder
F83 Mixed specific developmental disorder
F84 Pervasive developmental disorder Pervasive developmental disorder
F90 Hyperkinetic disorders Disruptive behaviour and attention-deficit
disorders
F91 Conduct disorders
F92 Mixed disorders of conduct and emotion
F93 Emotional disorders with onset specific to childhood Other disorders of infancy, childhood or adolescence
F94 Disorder of social functioning with onset Feeding and eating disorders of infancy or early
specific to childhood and adolescence childhood
F95 Tic disorders Tic disorders
F98 Other behavioural/emotional disorders with Elimination disorder
onset usually in childhood/adolescence
CLASSIFICATIONS OF CHILDHOOD PSYCHIATRIC DISORDERS
See Table 19.1.
MATERNAL DEPRIVATION
Bowlby has expounded the theory that a warm, intimate and continuous mother–child
relationship is essential for subsequent mental health of the child. There are two
components:
1 Bonding describes the relationship formed between mother and baby, usually
over the first few days of life. This process may be impaired by illness, separation,
ambivalence towards the pregnancy, etc.
2 Attachment describes the relationship of child to mother. This is presumed not to
be formed until after the first 6 months.
‘Maternal deprivation’ is a loose term covering those experiences in which the

attachment process with mother is disrupted through death or other distortions. It is
important to discriminate between basic variables combined under the term ‘mater-
nal deprivation’, such as:
• Lack of opportunity to form attachments is different from their being broken.

• Physical separation is different from deprivation of maternal care (which could be
provided by someone else).
• Separation by death differs from separation through a broken home.
PERVASIVE DEVELOPMENTAL DISORDER (‘AUTISM’) 235
Rutter (1972) distinguishes between them thus:

• Short-term separation (e.g. hospitalization). Consequences are the ‘distress syndrome’:
– Protest (tears, etc.).
• Despair (apathy and misery).
• Detachment (apparent contentment, indifference on mother’s return).
• Long-term maternal deprivation. Consequences are:
– Antisocial behaviour.
– Poor development of IQ and language.
– ‘Affectionless psychopathy’.
– Poor physical growth (‘deprivation dwarfism’).
– Depression.
PERVASIVE DEVELOPMENTAL DISORDER (‘AUTISM’)
CLINICAL FEATURES
• Onset before 30 months of age.
• Major deficits in language development (echolalia, pronomial reversal, perseveration).
• Disturbance of normal social interaction.
• Bizarre responses to environment; e.g. resistance to change, irrational attachment
to various objects, rituals and routines.
• Absence of delusions, hallucinations, loosening of associations as in schizophrenia.
Associated features
• Unpredictable fears, screaming or laughter.
• Abnormal movements (stereotypies, etc.).
• Hyperkinesis.
• Self-destructive behaviour.
• Difficulties learning manipulative tasks.
• Isolated skills (e.g. rote memory).
• Up to two-thirds have IQs in the MR range.
EPIDEMIOLOGY
• By definition, onset is before age 30 months.
• Boy:girl ratio ⫽ 3.8:1.
• There is a normal socioeconomic distribution.
• There are 34 cases per 10 000 in the USA (Yeargin-Allsopp et al., 2003).
• There are 62.6 cases per 10 000 in the UK (Chakrabarti and Frombonne, 2001).
AETIOLOGY
Genetics
• Concordance rate – MZ:DZ twins ratio ⫽ 36:0.
• There is a 3 per cent prevalence among siblings of autistics.
• About 5 per cent of autistic patients have fragile X syndrome.
Non-genetic factors
Autism is (uncommonly) associated with PKU, congenital rubella, tuberous sclerosis,
Rett’s syndrome. There is a high prevalence of mental retardation and cognitive
impairments, even in ‘mild’ autistics. One-third of autistics develop seizures during
adolescence.
Neurochemistry
• Increased CSF HVA associated with autistic stereotypies.
• Increased 5-HIAA associated with symptom severity.
Other factors
There is an excess of perinatal complications, minor physical anomalies, abnormal
dermatoglyphics – suggesting a neurodevelopmental basis. Some MRI findings (cere-
bellar hypoplasia, polymicrogyria) are consistent with this, although there has been
overall inconsistency in neuroimaging findings to date.
Psychosocial factors
Emotional factors are not causative. The hypothesis of ‘refrigerator parents’ is now
discounted.
Exclude: deafness, childhood schizophrenia, mental retardation with behavioural
symptoms, disintegrative psychosis, developmental language disorder, CNS disorders
(tuberous sclerosis, etc.).

The condition is chronic. IQ and development of language skills are related to
prognosis:
• Severely handicapped – about 66 per cent.

• Fair adjustment – about 17 per cent.
• Adequate social adjustment – about 17 per cent.
MANAGEMENT
There is no ‘specific’ treatment. Modalities cover:
• Counselling and support for parents; self-help groups.

• Educational placement.
• Behaviour modification – social behaviour, language skills, etc.
• Drug treatments.
No drug is specifically recommended. Atypical antipsychotics probably decrease
behavioural symptoms. Antiepileptics have been shown experimentally to help some
autistic patients.
MOOD DISORDERS IN CHILDREN/ADOLESCENTS 237
OTHER DEVELOPMENTAL DISORDERS
ASPERGER’S DISORDER
Asperger’s disorder begins in the third year of life. Males are affected more than
females (6:1 ratio).
There are not the cognitive or verbal deficits as seen in autism. There is abnormal
social reciprocity – the child often appears odd or eccentric. He/she often exhibits
restricted obsessional, ritualistic or idiosyncratic interests/activities.
This disorder is said to have a better social prognosis than autism, but their separate
status is disputed by some.
CHILDHOOD-ONSET SCHIZOPHRENIA
Twenty-five per cent of schizophrenia has an onset before age 15 years. There are
prominent brain changes on MRI.
Medication treatment is complicated by the greater sensitivity to antipsychotic
medication side-effects, so lower doses are indicated. The prognosis is poor.
DISINTEGRATIVE PSYCHOSIS
There is severe and sustained impairment in social relationships, speech and language.
Onset is after 24 months.
MOOD DISORDERS IN CHILDREN/ADOLESCENTS
See also Chapter 4.

There is major concern about the diagnosis and possibly increasing incidence of bipo-
lar illness and depression in children.
BIPOLAR DISORDER
This is often a controversial diagnosis in adolescents, and especially so in young chil-

dren. The diagnosis is made difficult by the variability in presentation, overlap of
symptoms with other disorders, the low incidence rate, medication-induced mania
(SSRIs, steroids), and substance abuse.
• Severe or psychotic depression may precede mania.
• Psychosis is often part of mania in the young.
• Mixed states and rapid (sometimes ultra rapid) cycling are common.
There are serious lifelong implications with poorer prognosis if the parents have
psychiatric disorders: increased rates of substance use, suicide attempts/completions,
legal difficulties and academic difficulties.
MANAGEMENT
As with adults, manage with mood stabilizers, atypical antipsychotics, or a combination of
atypical antipsychotics with a mood stabilizer. However, treatment resistance is common.
DEPRESSION AND SUICIDE
Depressive symptoms are common in emotionally disturbed children, but earlier stud-
ies suggested that typical depressive disorder of adulthood was uncommon. Rutter et al.
(1970) found depressive disorders in only 1–2 children per 1000 of 10- to 11-year-olds.
A broader view suggests that masked depression (presenting as behaviour disorders)
and depressive equivalents (presenting with somatic symptoms) are much more com-
mon. However, these concepts are so over-inclusive that nearly all childhood disorders
could be included.
There are high rates (40 per cent) of co-morbidity, especially of anxiety disorder
and conduct disorder.
• Depression, irritability and social withdrawal are prominent features.
• Childhood depression is usually self-limiting, but may become chronic and
presage recurrent depression in adulthood.
• Suicide is extremely rare before puberty, but the incidence rises during adolescence.
DIAGNOSIS, MANAGEMENT AND PROGNOSIS

Use of self-report schedules (e.g. CDI) or semi-structured interviews (e.g. K-SADS)
may aid diagnosis.
Antidepressants may be started with low doses but, with close monitoring, adult
dosage may be required to achieve a therapeutic blood level. Non-specific social and
psychological treatments and cognitive approaches are also helpful but need further
research evaluation.
Early-onset bipolar disorder carries a poor prognosis.
Typical characteristics of a suicidal child

• Above-average intelligence.
• Disturbed family.
• Recent involvement in antisocial behaviour and non-attendance at school.
• Close experience of similar behaviour in peers.
• An apparently depressed mental state with marked guilt.
• Recent humiliation or imminent disciplinary action.
• Feels alienated socially.
Actual suicide in children and early adolescents is rarely impulsive, and frequently
warnings are given.
ANXIETY DISORDERS IN CHILDREN – OVERVIEW
See also Chapter 5.

SCHOOL REFUSAL 239
Anxiety in a child may be developmentally appropriate (e.g. stranger anxiety, separ-

ation anxiety) and becomes a disorder only when it occurs beyond developmental
norms, and causes distress and impairment.
Anxiety disorder may be difficult to diagnose in the young due to ‘normalization’ of
behavior, and minimalization of impairment. The young rarely present with a subject-
ive report of ‘feeling anxious’. Instead, somatic complaints are common.
Treatment is similar to that in adults: cognitive–behavioural therapy, SSRIs, etc.
SCHOOL REFUSAL
School refusal is a persistent reluctance or refusal to go to school in order to stay with

a major attachment figure. See the diagram and Table 19.2.
Not at home (truancy)

Domestic reasons
Child not at school
Kept at home
At home Emotional disturbance

in parent
School refusal
Separation Fear of General social Specific fears

anxiety travel withdrawal at school
The term ‘school phobia’ is now rarely used. Some classify school refusal under
‘separation anxiety disorders’ (ICD-10). Probably it is not an entity – possibly in some
cases it is a variant of childhood depression.
Other features
• Anxiety symptoms are seen more often than depressive symptoms.
• Onset is more often gradual than sudden.
• The child may be timid and fearful outside, demanding and wilful at home.
• Academic attainments good or superior.
EPIDEMIOLOGY
Age at presentation is most commonly 11 years but is distributed over a wide range.
Boys and girls are equally affected. They tend to be in a higher social class. They
account for 3 per cent of all child psychiatric referrals.
Table 19.2 Features distinguishing truancy and school refusal

Truancy School refusal
Other antisocial features Lacks antisocial traits, passive good child

Family history of psychopathy Parents have neurotic traits/agoraphobia
Poor school performance Average/above-average student of childhood
AETIOLOGY
There are three broad categories:
1 Separation anxiety, mainly in younger children.

2 True phobia of aspects of school or travel.
3 General social withdrawal, e.g. in older children with high standards and fragile
self-esteem.
Important features are:
• Mothers are frequently overprotective.

• Fathers are passive.
• There is a history of psychiatric illness in 20 per cent of mothers (especially anxiety
disorder).
• It is often precipitated by the move from junior to senior school or a change of class.

The treatment of school refusers also involves parents and teachers. A graded return to
school is most beneficial. Follow-up has shown good, moderate and poor outcomes
in equal proportions.
A good prognosis is associated with:
• Younger age.
• Stability of the home.
• ‘Psychological sophistication’ of the parents.
Probably one-third of school refusers later present as adult ‘neurotics’. Twenty per
cent of agoraphobics interviewed had had ‘school phobia’, but this is the same as in
neurotics in general.
INAPPROPRIATE SOILING
ENURESIS
Enuresis is repeated involuntary voiding of urine by day or at night, after an age at

which continence is expected. It is not due to a physical disorder, or a physiological
effect of a medication. By definition, the age of onset is at least 5 years (for nocturnal).
• Primary – if not preceded by period of urinary continence for at least 1 year.
• Secondary – if preceded by 1 year of continence.
ASSOCIATED FEATURES
The majority do not have a coexisting mental disorder, but psychiatric disorder is
twice as common in this group as the general population (especially among girls).
With functional encopresis, sleepwalking and night terrors may also be present.
Typically, disturbance occurs during the first third of the night, during non-REM sleep.
INAPPROPRIATE SOILING 241
Urinary-tract-infection (UTI) Five per cent of enuretics (usually girls) have signifi-
cant bacteriuria. Fifteen per cent of children with UTI are consequently enuretic.
EPIDEMIOLOGY
• Primary after age 4 years, secondary between ages 5 and 8.
• Boys are more affected than girls (3:1 ratio, but varies with age).
• Lower social classes are over-represented.
• At age 7 – about 7 per cent for boys, 3 per cent for girls.
• At age 15 and older – 2 per cent for boys, almost non-existent for girls.
AETIOLOGY
Any hypothesis must explain the following facts:
• Greater concordance in MZ than DZ twins.
• Higher incidence in relatives.
• Higher incidence in social classes IV and V.
• Larger families.
• Institutional upbringing.
• Male predominance.
• Below-average IQ.
• Stress events in early childhood (illness and hospitalization, maternal death).
• Small functional bladder capacity.
• No association with any specific syndrome, except encopresis.
Possible mechanisms
• Enuresis is secondary to a psychiatric disorder; or
• The same factors (e.g. stress) produce both psychiatric disorder and enuresis; or
• Psychiatric disorder is secondary to negative parental reactions to enuresis.

• Reassure and advise. Exclude UTI, diabetes, neurological/urological disorders.
• A star chart is effective for about one-third of children.
• A bell and pad is effective in 80–90 per cent, if done correctly and persisted with
over time.
• Tricyclics (imipramine, amitriptyline) are helpful, but there is a high relapse rate
on stopping the drug.
• Treat any psychiatric disturbance if present.
Most children become continent by adolescence; but in some the disorder continues
into adulthood.
ENCOPRESIS
Encopresis is the repeated voluntary or involuntary passage of faeces of normal, or

near-normal, consistency in inappropriate places. By definition it starts after age 4 years.
• Primary – after age 4 years.

• Secondary – if preceded by faecal continence for at least 1 year.
Encopresis is associated with inadequate, inconsistent toilet training and psychosocial
stress (e.g. family and school). Management includes reducing tensions in the family,
and behaviour modification to reinforce appropriate defecation as well as continence.
MANAGEMENT
• Exclude physical reasons for soiling, such as retention, constipation with overflow
leakage (possibly due to anal fissure, Hirschsprung’s disease) and/or diarrhoea.
• Reassure the child and support the parents, with explanations.
• Start retraining if necessary.
NIGHT-TIME INCIDENTS
SLEEPWALKING
See also Chapter 14.
Sleepwalking is repeated episodes of arising from bed during sleep, walking about for
several minutes and remaining unresponsive to the efforts of others to influence sleep-
walking, or to communicate. The child can be awoken only with great difficulty, and is
amnesic on waking.
It usually occurs between 30 and 180 minutes after onset of sleep (EEG: delta activity,
stages 3 and 4).
Between 1 and 4 per cent of children experience the disorder at some time. Isolated
episodes are even more frequent. Adolescence usually sees the disorder disappear.
NIGHT TERRORS
See also Chapter 14.
Night terrors are repeated episodes of abrupt awakening lasting 1–10 minutes, occur-
ring between 30 and 180 minutes after onset of sleep (typically occurs during stages 3
and 4). They usually begin with a panicky scream. There are then signs of autonomic
arousal – tachycardia, rapid breathing, dilated pupils, etc. There is confusion, dis-
orientation and perseveration of movements. The person is relatively unresponsive
to others.
SPECIFIC READING RETARDATION (SRR)
SRR applies to children whose reading ability falls significantly below the average for
their age, schooling and IQ. It must be distinguished from ‘reading backwardness due
ATTENTION-DEFICIT/HYPERACTIVITY DISORDER (ADHD) 243
to low IQ’. There is a prevalence of 4–10 per cent (higher in inner-urban areas), with a
male predominance of 3–4:1.
It is a broader concept than dyslexia, which implies localized cerebral immaturity.
ASSOCIATED FEATURES
• Large family size.
• Low socioeconomic status.
• Poor concentration and attention.
• Increased prevalence in epileptic children, but overall no overt prevalence of neuro-
logical abnormalities.
Conduct disorder
One-third of 10-year-olds with SRR in an Isle of Wight study were diagnosed as ‘con-
duct disorder’. There was a family history of reading difficulties, spelling difficulties,
speech delay, clumsiness and poor left–right differentiation.
AETIOLOGY AND OUTCOME

Developmental, neurological, constitutional, family and emotional factors all con-
tribute. The prognosis is poor, even with remedial education.
ATTENTION-DEFICIT/HYPERACTIVITY DISORDER (ADHD)
This is the leading neurobehavioural disorder among the young. Some will improve
with maturity, others persist into adulthood. Criteria include:
• There is inattention and/or hyperactivity–impulsivity.
• Behaviour occurs in at least two settings, e.g. home and school.
• It causes impairment in social, academic, or occupational functioning.
• Symptoms are evident before age 7 years.
• Behaviour is not due to other another disorder.
ADHD is classified into three subtypes:
1 Predominantly inattentive.
2 Predominantly hyperactive–impulsive.
3 Combined.
ASSOCIATED FEATURES
• Dyssocial behaviour, difficulty disciplining, temper episodes.
• Family discord.
• Injuries.
• Low self-esteem.
• Low frustration threshold.
• Learning difficulties common.
• Under-achiever at school even when IQ is taken into account.
• Soft neurological signs (motor coordination, perceptual and attention tests), EEG
abnormalities (dysmaturation EEG) have been described.
There is much overlap. Chief differentials are:
• Pervasive developmental disorder.

• Conduct disorder and oppositional defiant disorder (ODD).
• Inattention/overactivity associated with anxiety/depressive disorders of childhood.
• Extreme end of normal childhood behaviour.
EPIDEMIOLOGY
Onset is typically before age 3 years, though it may not present before school age. Boys
outnumber girls (3:1 ratio). Prevalence estimates in school-aged children range from
3 to 7 per cent.
AETIOLOGY
The aetiology is probably multifactorial. The heterogeneity view suggests a group of
syndromes which have a common clinical phenotype.
Genetics
It seems to be biological, although adoptive parents of hyperactive children show
increased rates of alcoholism and sociopathy. Biological fathers were likely to have been
overactive.
Recent risk analysis studies suggest a shared familial vulnerability for ADHD and
affective disorders.
Other factors
• Neurological soft signs, EEG, clinical evidence of maturational lags (e.g. associated
learning disabilities) may suggest in utero damage.
• fMRI studies indicate subnormal acitivation in prefrontal brain regions as well as
decreased putaminal blood flow (Yitzchak and Pavlakis, 2001).
• Noradrenergic dysfunction has been demonstrated.
• Other neurotransmitters are implicated.
It has been hypothesized that such children have under-aroused CNS with insuffi-
cient cortical inhibitory control. Hence, stimulants are said to stimulate the reticular
activating system (RAS) and increase cortical inhibition.

These are variable. Three patterns of course and outcome are proposed:
1 All symptoms persist into adolescence and adult life, especially attention deficit; or
2 There is attenuation of symptoms with maturity; or
3 The condition is self-limiting, with disappearance of symptoms at puberty.
‘SYMPTOMATIC’ DISORDERS 245
MANAGEMENT
The main focus for treatment is to maximize functioning.
• Psychostimulation – Methylphenidate and dextroamphetamine (short-, intermediate-

and long-acting variations) are first-line treatments (American Academy of
Pediatrics, 2002).
• Antidepressants – Imipramine, desipramine and bupropion, and the non-
psychostimulant selective norepinephrine reuptake inhibitor atomoxetine, are second-
line medications (ibid.).
• Behavioural regimens in classroom and home have proven to be effective.
• Remedial education.
• Counselling – of child and/or family.
• Dietary measures are expensive, lack scientific basis and are usually ineffective.
‘SYMPTOMATIC’ DISORDERS
TICS
Tics are rapid, sudden purposeless movements of a functionally related group of

muscles, frequently occurring in the same part of the body. They can be suppressed
voluntarily, but only at the expense of mounting tension and anxiety.
Most commonly the tics are facial (blink, grimace). Vocal tics appear as grunts and
coprolalia in Gilles de la Tourette syndrome.
Tics increase with anxiety and disappear during sleep. They may be attenuated dur-
ing periods of sustained attention.
• Choreiform movements – uncoordinated, irregular, non-repetitive.
• Athetiod movements – slow, writhing and irregular, frequently in fingers and toes.
• Myoclonic movements – brief, shock-like muscle contractions that may affect part
or whole of a muscle (not muscle groups).
• Dystonic movements – slower, more sustained movements.
• Dyskinesias – especially those such as tardive dyskinesia, which are oral, buccal,
lingual masticatory movements in the face and choreoathetiod movements in the
limbs.
• Hemiballismic movements – coarse, intermittent and unilateral movements of
the limbs.
• Spasmodic torticollis.
ASSOCIATED FEATURES
• Development disorders.
• Other psychiatric disorders.
• IQ normally distributed.
EPIDEMIOLOGY
Age at onset is nearly always during childhood and adolescence and may be as early as
2 years. Boys are more affected than girls (3:1 ratio). Between 10 and 20 per cent of
children are reported as having transient tic-like movements at some stage. There is a
normal social class distribution (?).
AETIOLOGY
There is association with other developmental disorders. Stress, temperamental fea-
tures and psychiatric disorder may act as precipitants.

The prognosis is generally good. At 8-year-old follow-up, one study suggested 40 per
cent completely recovered and 53 per cent improved, though with overall increased
rate of emotional symptomatology.
There is a poor prognosis for established Gilles de la Tourette syndrome.
MANAGEMENT
• Relaxation exercises, with massed practice, have been proposed. Evidence for their
effectiveness is unclear.
• Minor tranquillizers and haloperidol are sometimes effective.
• Individual and family counselling, including reassurance, is aimed at minimizing
stress.
GILLES DE LA TOURETTE SYNDROME (GTS)
This is a disorder characterized by multiple motor and at least one vocal tic. Onset is
before age 21 years. The site, frequency and pattern of tics change over time.
There is substantial overlap between GTS and obsessional disorders. About 40 per
cent of GTS patients exhibit obsessive–compulsive behaviours. First-degree relatives
of GTS patients have high rates for diagnosis of oppositional defiant disorder (ODD).
EPIDEMIOLOGY
The exact prevalence is unknown but a figure of 0.5 per 1000 has been suggested.
There are no known associations with race or social class. Males are more affected
than females (4:1 ratio).
AETIOLOGY
Genetics
A major autosomal dominant gene is likely. Linkage studies show preliminary evi-
dence: 18 per cent of first-degree relatives have GTS.
Non-genetic factors
• EEG abnormalities (non-specific) are seen in 10–40 per cent of GTS cases.
• PET and SPECT show hypermetabolism in frontal and basal ganglia regions.
CONDUCT DISORDER 247
• Dopaminergic abnormalities are implicated from:

– Decreased HVA in CSF in some studies.
– Efficacy of antipsychotics.
– Adverse effects of stimulants.
– A similar syndrome to GTS seen with neuroleptic use.
Dopamine D1/D2 imbalance has been suggested. Noradrenergic and cholinergic
systems are also implicated, but with less evidence. Recent interest has been shown in
serotonergic systems in GTS.
CLINICAL FEATURES
• Age at onset is 2–15 years, with mean 7 years.
• Vocal tics have mean age at onset of 11 years.
• Motor tics are most commonly facial. Others are squatting, jumping, gait
abnormalities.
• Vocal tics may be coughing, barking, throat-clearing grunting.
• Coprolalia (shouting obscenities) is seen in 30 per cent of GTS cases; mean onset
13–14 years.
• Echolalia is seen in 20–40 per cent.
• 40 per cent of GTS patients show associated disturbances, including attention deficits,
aggressive, antisocial or inappropriate sexual behaviour, and deliberate self-harm.

There have been no long-term follow-up studies. It appears to be a lifelong disorder,
but with some tendency for features to wax and wane. There is marked psychosocial
impairment.
CONDUCT DISORDER
Conduct disorder is characterized by persistent and excessive behaviour which attracts

social disapproval. It may be stealing, disobedience, lying, truancy, setting fire or
aggressive behaviour or promiscuity. The behaviour must be associated with disturb-
ances of personal functioning or subjective happiness to be labelled ‘conduct disorder’,
and to distinguish it from ‘delinquency’.
Classification has been problematic because antisocial behaviour is a heterogeneous
construct and is seen in conduct disorder, ADHD (less commonly) and ODD.
ODD is the presence of markedly defiant/disobedient behaviour but with absence
of more severe aggressive acts. It is debated whether this is a milder form of conduct
disorder.
Subclassification
1 Socialized – behaviour is viewed as normal within the context of the child’s subcul-
tural group (e.g. truancy and gang membership).
2 Unsocialized – behaviour is antisocial by any standards. This is more frequently

associated with abnormalities in personality, and absence of adequate social bonds.
3 Mixed disorder – antisocial behaviour accompanied by marked emotional
disturbance.
EPIDEMIOLOGY
Onset is usually before puberty for the unsocialized type, and pubertal or postpuber-
tal for the socialized type. There is a 5 per cent point prevalence in middle childhood.
It was the most common psychiatric disorder in an Isle of Wight study.
It is far more common in boys than girls (ratios range from 4:1 to 12:1). Lower
social classes appear to be most affected.
AETIOLOGY
Possible important factors:
• Unsocialized type – parental rejection, inconsistent management with harsh dis-
cipline, early institutionalization, frequent change of parent figures (e.g. fostering)
and being illegitimate.
• Socialized type – large family size, membership of a gang, absent father.
• Generally – disorder more common in children of alcoholic parents and parents
with antisocial personality disorder.
• Child factors – male, biological vulnerability, difficult temperament (see Chapter 6),
early behavioural problems, school failure.
• One-third show severe retardation of reading.

A proportion in the socialized group achieve adequate adjustment as adults. A large
proportion in the unsocialized group develop antisocial personality disorder as adults.
MANAGEMENT
Management is aimed at reversing significant aetiological factors:
• Conjoint family therapy; behavioural training for parents.
• Remedial teaching.
• Individual counselling or group counselling.
• Alternative peer-group provision (e.g. adventure clubs, etc.).
CHILDHOOD/TEENAGE SUBSTANCE ABUSE
See also Chapters 9 and 10.
Intoxication can lead to injuries and death, and impairment in social, educational and
psychological development and wellbeing.
There is variability over time in the popularity of different substances. Surveys show
that half of 12- to 15-year-olds have consumed alcohol. By age 15, almost two-thirds
had tried cigarettes and about one-quarter had tried marijuana. Over half of
12th-graders indicated they had used an illicit drug.
The most commonly used substances from greatest to least are as follows: (Kaul and
Coupey, 2002): marijuana; amphetamines; inhalants; hallucinogens; ecstasy; barbit-
urates; tranquilizers; cocaine; heroin.
RISK FACTORS
• Behavior and mood disorders at an early age.
• Previous diagnosis of ADHD, conduct disorder, personality disorder.
• A history of sexual or physical abuse.
• Inherited genetic factors.
• Association with drug-using peers.
• No after-school supervision.
• Broken family.
• Poverty.
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Mental retardation 20
OVERVIEW
DEFINITIONS
World Health Organization
• Impairment – any loss or abnormality of psychological, physiological or anatom-
ical structure or functions.
• Disability – any reduction or lack (resulting from impairment) of ability to
perform an activity in the manner or within the range considered normal for a
human being.
• Handicap – a disadvantage for the individual, resulting from impairment or dis-
ability, that limits the fulfilment of a role that is normal (depending on age, sex,
culture) for that individual. May be in dimensions of physical independence,
mobility, occupations, social integration, economic self-sufficiency, orientation
or other.
ICD-10
Mental retardation (MR) A condition of arrested or incomplete development of the
mind, which is especially characterized by impairment of skills manifested during the
developmental period, which contribute to the overall level of intelligence; i.e. cogni-
tive, language motor and social abilities.
DSM-IV-TR
A Subaverage intellectual functioning, IQ ⬍70

B Concurrent deficits in ⬎2 skills areas: communications, self-care, home living, social/interpersonal skills,
use of community resources, self-direction, academic skills, leisure, work, health and safety
C Onset before age 18 years
Coding See Table 20.1. The criteria are those of social competence. Precise classification
by IQ is not always possible. IQ of less than 50–55 usually denotes major impairment,
254 MENTAL RETARDATION
Table 20.1 Coding of mental retardation (MR)

IQ range (ICD-10 and DSM-IV-TR)
Mild MR 55–60 to 70
Moderate MR 35–40 to 50–55
Severe MR 20–25 to 35–40
Profound MR ⬍20–25
but 10–20 per cent become economically independent. An IQ of between 50 and 70

may denote impairment if accompanied by social incompetence.
EPIDEMIOLOGY
• Severe impairment has a prevalence of 3·5 per 1000 population. Between 2 and
3 per cent of the population have an IQ less than 70.
• It is more common in males, who have a larger variance in IQ.
• Of inpatient populations:
– 10 per cent have severe psychiatric disorders.
– 20 per cent have defects of vision or hearing.
– 20 per cent have severe speech defects.
AETIOLOGY
Severe impairment
• Nearly all cases have gross cerebral pathology at post mortem.
• Between 33 and 85 per cent have an organic aetiology diagnosed during life.
• 33 per cent are due to Down syndrome.
• 19 per cent are due to other inherited conditions or associated congenital
malformations.
• 18 per cent are due to perinatal injury.
• 14 per cent are due to infections.
• 4 per cent are due to biochemical disorders (inborn error of metabolism).
• 15 per cent are of unknown aetiology.
Mental impairment
• Fewer than 33 per cent have an organic aetiology diagnosed during life.
• Mental impairment shows a ninefold increase in the lower social class.
• A proven organic aetiology is more likely if the handicapped child is from a higher
social class.
Social factors (i.e. ‘subcultural problems’, poor education, poor home environment,
poor diet, etc.) therefore play a much larger part in the aetiology of impairment than
of severe impairment.
The lower end of the normal distribution curve of IQ (excluding the excess caused
by organic disease) will account for a proportion of the handicapped group.
CHROMOSOMAL ABNORMALITIES 255
CHROMOSOMAL ABNORMALITIES
TRISOMIES
TRISOMY 13–15: PATAU’S SYNDROME

There is severe handicap and facial abnormalities. Those affected rarely live longer
than 6 months.
TRISOMY 17–18: EDWARDS’ SYNDROME

There is severe handicap, with facial and skeletal abnormalities. Those affected rarely
live longer than 3 months. It is most common in females.
TRISOMY 21 (22): DOWN SYNDROME

Five per cent of cases result from translocation. The incidence is 1·8 per 1000 live
births (1 per 50 if mother older than 45). It is most common in males.
Features Low birthweight; small round head, epicanthic folds of eyelids, Brushfield
spots on iris, cataracts, strabismus, small nose and ears, high arched palate, protruding
tongue, short neck, short limbs, hypotonic muscles, umbilical hernia common, single
palmar crease in one-third, pathogenic dermatoglyphic patterns, significant deafness
in two-thirds. Severe handicap is usual but not invariable.
Associated conditions There is increased incidence of: congenital heart disease; gas-
trointestinal atresia; Hirschsprung’s disease; respiratory infections; Alzheimer’s dementia
(found in 95 per cent of those over 40 years); epilepsy (12 per cent aged over 40 years).
Recurrence likelihood
• Regular trisomy – 1 per cent.
• Translocation 21/21 – 100 per cent.
• Other translocations – 5–20 per cent.
DELETIONS
Deletion of short arm of 5: ‘cri du chat’ syndrome Most common in females. There is
a characteristic cry, facial abnormalities, severe handicap, spasticity. Compatible with
adult life.
Deletion of short arm of 4: Wolf syndrome There is severe handicap, facial abnormalities,
epilepsy.
Partial deletion of long arm of 18 There is severe handicap, small size, facial
abnormalities.
Partial deletion of long arm of 21 This is described as ‘antimongolism’.
SEX CHROMOSOME ABNORMALITIES

Increasing numbers of X chromosomes lead to increased degree of handicap, in males
and females.
• XXX – 1 in 1000 females.
– Slight mental handicap, no physical abnormalities.
• XXY (Klinefelter’s syndrome) – 1 in 500 men.

– The most common of the sex chromosome abnormalities.
– Tall, slightly reduced IQ, lack of male secondary sexual characteristics. Barr body
is present (⫽chromatin positive) because of extra X. Any more X chromosomes
(e.g. XXXY) have an extra Barr body each per X chromosome.
• XYY – 1 in 700 men.
– Tall, not notably handicapped, possibly show more criminal behaviour of non-
violent sort than normal controls.
• XO
– Dull normal IQ, short stature, webbed neck in 50 per cent. Lack of secondary
sexual characteristics, gonadal dysgenesis, coarctation of aorta in 35 per cent.
FRAGILE X SYNDROME
Fragile X syndrome is the second most common known cause of MR in males; it is
thought to account for 6 per cent of severe MR, 10 per cent of mild MR in males.
• Diagnosis is confirmed on fragility test of X chromosome in folate-deficient

medium.
• Chromosome analysis for fragile site (Q 27–28) on X chromosome (Young, 1993;
Warren and Nelson, 1994).
• There is an association with autism; about 20 per cent of autistics have fragile X
abnormality (Turk, 1992).
• There is a suggested clinical association with attention deficit disorders.
Clinical features
These include MR, floppy ears, prognathism, macro-orchidism, hypertelorism,
blue eyes, single palmar crease. Female carriers have physical stigma and somewhat
reduced IQ.
GENETIC ABNORMALITIES
• Tuberous sclerosis – Autosomal dominant with variable penetrance. Variable

handicap (mild to severe), epilepsy and skin changes – adenoma sebaceum
after 4 years old, café-au-lait spots, shagreen patches. Sclerotic brain nodules,
lung cysts.
• Apert’s syndrome – Autosomal dominant with poor penetrance. Mental handicap,
tower skull, protruberant eyes, abnormalities of fingers and toes.
• Craniofacial dysostosis – Autosomal dominant with poor penetrance. Low inci-
dence of handicap, tower skull.
• First arch syndromes – Autosomal dominant.
– Berry–Franceschetti syndrome of mandibulofacial dysostosis, with sheep-like
face, deafness and variable degree of handicap.
– Hallerman–Streiff syndrome of mandibulo-oculofacial dyscephaly with severe
subnormality and facial abnormalities.
INBORN ERRORS OF METABOLISM 257
• Hypertelorism – May be autosomal dominant or recessive. Severe handicap is

usual, with wide-set eyes and broad bridge to the nose.
• True microcephaly – Autosomal recessive. 1 in 1000 live births, males more common.
Severe handicap with a normal size face but very small cranial vault, short stature,
epilepsy common.
• Velo–cario–facial syndrome (VCFS) – Most commonly (85 per cent cases) 22q11
microdeletion. High prevalence of psychiatric disorders, especially psychosis and
mood disorders.
• Virchow–Seckel dwarf – Autosomal recessive. Small stature, facial and skeletal
abnormalities, mild or moderate handicap.
• Ataxia telangiectasia: Louis–Bar syndrome – Autosomal recessive. Gradual mental
deterioration after age 3 years with development of facial telangiectasia, café-au-lait
spots and cerebellar and extrapyramidal signs. Deficiency of IgA leads to infections
and lymphocytic neoplasia.
• Laurence–Moon–Biedl syndrome – Autosomal recessive. Severe handicap, obesity,
hypogenitalism, polydactyly, retinitis pigmentosa.
• Marinesco–Sjögren syndrome – Autosomal recessive. Severe handicap, microcephaly,
cataracts, cerebellar signs, skeletal abnormalities.
X-LINKED DISORDERS ASSOCIATED WITH SUBNORMALITY

• X-linked hydrocephalus – with aqueduct of Sylvius stenosis.
• X-linked spastic paraplegia.
• Menkes’ ‘kinky hair’ syndrome.
• Lesch–Nyhan syndrome.
• Lowe’s syndrome.
• Pseudo-pseudohypoparathyroidism (Albright’s syndrome).
• Diffuse cerebral sclerosis.
• Mucopolysaccharidosis type 2 (Hunter’s syndrome)
• Nephrogenic diabetes insipidus.
• Hyperammonia syndrome.
POSSIBLY GENETIC DISORDERS

• de Lange syndrome with handicap – Characteristic facial and skeletal abnormalities,
dwarfism and excessive body hair.
• Sturge–Weber syndrome (‘port wine syndrome’) – Facial angiomatous naevus with
corresponding intracranial abnormality leading to contralateral hemiparesis,
handicap and epilepsy.
• Prader–Willi syndrome – Gross obesity, hypogonadism, mild to severe handicap
and outbursts of anger. Possibly hypothalamic disorder.
• Autism – see Chapter 19.
INBORN ERRORS OF METABOLISM
Most are autosomal recessive except Hunter’s and Lesch–Nyhan syndromes and
nephrogenic diabetes insipidus, which are X-linked.
DISORDERS OF PROTEIN METABOLISM
OVERFLOW AMINOACIDURIAS
• Phenylketonuria – This is the most common inborn metabolic error (1 per 12 000
live births). Phenylalanine hydroxylase deficiency leads to build-up of phenylalan-
ine in blood and phenylpyruvate in urine. All newborn babies in the UK are tested
(Guthrie test) at 6–14 days for phenylalanine, which promotes the growth of Bacillus
subtilis in a quantitative fashion. Subjects tend to be fair-haired, blue-eyed and prone
to eczema. They may be epileptic and severely handicapped if untreated. Treat with
a phenylalanine-free diet.
• Homocystinuria – There is a deficiency of cystathionine synthetase leading to
raised homocystine and methionine. Clinically there is fair hair and skin, eye and
skeletal abnormalities, poor peripheral circulation, liver degeneration, epilepsy
and mental deterioration. Treat with a methionine-free diet.
• Argininosuccinic acidura – There is deficiency of argininosuccinase leading to
raised argininosuccinic acid and ammonia. Subjects have short brittle hair, epilepsy,
chorea and variable handicap.
• Maple syrup disease – There is a deficiency of ketoacid decarboxylase leading to
abnormalities of branched chain amino acids. There is epilepsy, spasticity, paralysis
and very early death if untreated. Treat with a diet low in leucine, isoleucine and valine.
RENAL AMINOACIDURIA (HARTNUP’S DISEASE)

There is deficiency of transport of amino acids across gut and renal membranes, lead-
ing particularly to low tryptophan absorption and abnormal amino acids in urine.
There is handicap, confusion, ataxia, photosensitive skin and pellagra. Some improve-
ment is shown with a high-protein diet and nicotinamide.
DISORDERS OF CARBOHYDRATE METABOLISM
• Galactosaemia – There is deficiency of phosphogalactose-uridyl transferase. There

is vomiting, lethargy, jaundice in the neonatal period leading to handicap and early
death if untreated. Treat early with a galactose-free diet.
• Idiopathic hypoglycaemia – Leucine ingestion leads to hypoglycaemia and raised
insulin levels. Epilepsy and handicap occur unless treated early with a leucine-
free diet.
DISORDERS OF LIPID METABOLISM AND CONNECTIVE TISSUE
• Tay–Sachs disease – There is deficiency of hexosaminidase A, leading to excess gan-

glioside. It occurs especially in Ashkenazi Jews. There is optic atrophy with ‘cherry-
red spot’ on the macula, epilepsy, spasticity, mental deterioration and early death.
There is no treatment, but it can be detected antenatally with amniocentesis.
• Niemann–Pick disease – There is deficiency of sphingomyelinase. Clinically it is like
Tay–Sachs, but also enlarged liver and spleen owing to Niemann–Pick cells.
NON-GENETIC CAUSES OF MENTAL RETARDATION 259
• Gaucher’s disease – There is deficiency of cerebroside-beta-glucosidase leading to

Gaucher cell (cerebroside) accumulations in many tissues. Mental deterioration is
rapid. There is no treatment, but it can be detected at amniocentesis.
• Refsum’s disease – There is deficiency of phytanic acid oxidase with loss of myelin.
Onset is in childhood, with mental deterioration, visual and auditory loss, cerebel-
lar signs and weakness. Treat with a phytanic-acid-free diet and vitamin A.
MUCOPOLYSACCHARIDOSES
• Type 1: Hurler’s syndrome – gargoylism, progressive mental and physical deterior-

ation with corneal clouding.
• Type 2: Hunter’s syndrome (X-linked recessive) – gargoylism, deterioration is slower
than Hurler’s and there is no corneal clouding.
• Type 3: Sanfilippo’s syndrome – mild physical signs but severe mental deterioration.
OTHER METABOLIC DISORDERS
• Hypothyroidism (cretinism) – Deficiency of thyroxine leads to lethargy, large

tongue and feeding problems, puffy skin, protuberant abdomen (often with
umbilical hernia), mental handicap. Treat with thyroxine as early as possible.
• Infantile hyperuricaemia: Lesch–Nyhan syndrome (X-linked recessive) –
Disturbance of purine metabolism leads to hyperuricaemia. There is development
of spasticity, choreoathetosis, self-mutilation and severe mental handicap. Early
death can be expected. It is partially treatable with allopurinol. It can be detected
by amniocentesis.
• Nephrogenic diabetes insipidus (X-linked recessive) – Renal tubules do not respond
to antidiuretic hormone; thus dehydration, epilepsy and handicap ensue. Treat
with large fluid intake, ethacrynic acid and potassium chlorate.
• Rett’s syndrome – Affects females only, with onset at 7–24 months. There is loss of
acquired hand skills and speech; stereotypies; lack of social interaction; later devel-
opment of ataxia, apraxia, kyphoscoliosis and seizures; MR is usually severe.
NON-GENETIC CAUSES OF MENTAL RETARDATION
• Nutritional/toxic:
– Placental insufficiency.
– Malnutrition.
– Infantile hypoglycaemia.
– Fetal alcohol syndrome (20–50 per cent risk with alcoholic mother).
– Lead encephalopathy.
• Anoxia:
– Perinatal.
– In infancy.
• Maternal infection:
– Rubella at up to 16 weeks of pregnancy. Leads to microcephaly, eye, ear and head
abnormalities and subnormality.
– Cytomegalovirus.
– Syphilis.
– Toxoplasmosis.
– Listeria.
• Child infection:
– Encephalitis.
– Meningitis.
• Trauma:
– Non-accidental injury – possibly one of the most important causes of mental
handicap.
– Accidental injury.
– Birth trauma.
• Rhesus factor incompatibility.
PSYCHIATRIC DISORDER IN THE MENTALLY HANDICAPPED
FACTORS CONNECTING PSYCHIATRIC DISORDER AND HANDICAP

• Reaction of the individual to the stigma of subnormality.
• Reaction of others (family, fellow employees, etc.) to the handicap.
• Psychiatric disorder as a consequence of the psychological abnormalities associ-
ated with handicap (e.g. lack of social skills, impaired attention).
• Possible genetic aetiology for both psychiatric disorder and handicap.
• Organic brain disease as a cause of both.
• Iatrogenic consequences of either (e.g. drugs, institutionalization).
• Psychiatric disorder may lead to lowered IQ in later years.
• Persons with handicap as well as psychiatric disorder are more likely to come to the
attention of services.
• Prevalence of mental illness in 165 MR adults (Holden and Gitlesen, 2003):
– Depression – 30.0 per cent.
– Anxiety – 21.3 per cent.
– Hypomania – 8.4 per cent.
– Psychosis – 15.5 per cent.
The prevalence of psychiatric disorder is greater in MR patients with challenging
behaviour – i.e. aggression, self-injury, destruction of property, sexual acting out.
INDIVIDUAL SYNDROMES
Schizophrenia
Between 3 and 6 per cent of handicapped inpatients suffer with schizophrenia. They
are characterized by childish behaviour and stereotypies, poverty of thought, perplex-
ity and ‘confusion’, loss of drive and ill-formed hallucinations and delusions.
SERVICES REQUIRED 261
Manic depressive psychosis

Between 1 and 6 per cent of handicapped inpatients or outpatients suffer. Depression is
characterized by agitation or withdrawal, apathy, somatic complaints and compulsive
behaviour. Mania presents as episodic excitation and overactivity.
Neurotic disorders
Hysterical symptoms tend to be more common than in the normal population.
Bereavement and adjustment reactions are underestimated.
Epilepsy
Epilepsy is found in 30 per cent of the severely handicapped. Hypsarrhythmia,
Lennox–Gastaut syndrome and West’s syndrome are associated. Incidence generally
reduces with age but may develop later in autism, Down’ syndrome and progressive
disorders (e.g. lipidoses).
SERVICES REQUIRED
OVERALL GUIDELINES
1 Developmental principle – Mentally handicapped people will continue to grow and

develop given an appropriate environment.
2 Principles of rights – The mentally handicapped are worthy of all the dignity and
rights of any citizens.
3 The dignity of risk – The concept of learning through risk-taking and avoiding
overprotection.
4 Principle of normalization – The availability of everyday, normal conditions of life.
5 Principle of generic environments and services – wherever possible.
Services should be community based, comprehensive, continuous, coordinated,
dignified and of high quality.
The responsibilities of the multidisciplinary team are:
• Official – to develop and maintain the best standards of care.
• Legal – clarification and recording of individual legal responsibilities.
• Interpersonal – support and communication between members.
ASSESSMENT SERVICES
Mental handicap is often impossible to assess at ages of less than 6 months.

Medical assessment includes neurological and general examination, details of any
family history, pathological screening of blood count and film, thyroid function tests,
amino acid chromatography of blood and urine, calcium levels, lead levels, blood
sugar, serological tests for syphilis, skull radiograph, electroencephalogram and chro-
mosomal analysis.
Developmental assessment includes tests of general IQ and tests of special functions

as well as assessment of developmental milestones.
General assessment must be made of the child and his/her family and social circum-
stances. This is to be done by the multidisciplinary team: psychiatrist, psychologist,
general practitioner, social workers, physiotherapist, paediatrician, teacher, occupa-
tional therapist.
All assessments must be repeated and the assessment is under constant review as
the child grows and his/her needs and abilities change.
EDUCATIONAL SERVICES
These are the responsibility of the local education authority, no matter how handi-
capped the child is, if under 19 years.
There is considerable debate about whether handicapped children are best
taught in special schools or in ordinary schools, integrated with normal children
(‘mainstreaming’).
Structured, active teaching with precise measurable goals is most effective, based on
careful developmental assessment.
Behaviour modification techniques are particularly useful for severely handicapped
people. Prolonged face-to-face care and teaching are important and more time needs
to be spent with the child. Education may need to go on for longer (e.g. into early 20s).
After this, sheltered workshops are often needed. Adult training and social education
centres provide continuing assessment and training for adults.
RESIDENTIAL SERVICES
Inpatient units are likely to continue to be needed for:

• Severe behavioural problems (including violence).
• Severe epilepsy.
• Severe physical handicaps.
• Major psychiatric illness.
In a population of 100 000 there will be about 100 severely handicapped children
(aged under 16): 70 per cent live at home, 20 per cent live in hospital care and 10 per
cent need residential care. There will also be 375 severely handicapped adults: 12 per
cent living at home and 88 per cent living in hospitals or hostels. The emphasis is now
on the use of ordinary housing (staffed homes, group homes).
Fifty per cent of the adult severely handicapped are regarded as employable.
MANAGEMENT PRINCIPLES
MEDICAL
Medical management is rarely useful, as in phenylketonuria and cretinism. Severe
physical handicaps may required medical or surgical treatment.
PREVENTION OF MENTAL RETARDATION 263
PSYCHIATRIC
Psychotropic medication may be required for agitation, depression, etc. Individual
and family psychotherapy may be appropriate. Behaviour therapy may be useful.
Behavioural modification involves detailed analysis of unwanted behaviour and the
supplying of immediate appropriate rewards for required behaviour.
ROLE OF THE PSYCHIATRIST

The psychiatrist must be:
• Trained in taking extensive histories.
• Able to negotiate with parents, staff, etc., to affect attitudes.
• Able to take a long-term view, tolerant of limited success.
• Skilled at understanding threatening events and suffering.
• Skilled at assessing subtle loss of intellectual skills.
• Able to support other staff.
• Concerned with maximizing personal growth.
• Able to use psychotropic medication appropriately.
The psychiatrist may have therapeutic areas (e.g. a ward) for admission.
GUIDANCE FOR PARENTS

The parents will need to be supplied with factual information about the disorder,
cause, prognosis and management. They will also need reassurance, discussion and
advice concerning the prognosis, likely disabilities and ways of helping with the child.
Genetic counselling may be appropriate. Practical help (e.g. house alteration) will be
needed. Occasionally family therapy will be appropriate.
PREVENTION OF MENTAL RETARDATION
PRIMARY PREVENTION
• Avoid development of the condition.
• Give genetic counselling.
• Manipulate the environment.
SECONDARY PREVENTION
Detect and treat the condition early.
TERTIARY PREVENTION
Avoid additional disability by good care and early intervention.
1 Genetic counselling:
– Unknown-cause severe handicap – 30 per cent recurrence risk.
– Balanced translocation – mother, 20 per cent risk; father, 5 per cent risk.
– Dominant – 50 per cent risk.

– Recessive – 25 per cent risk.
– X-linked – 50 per cent of sons affected; 50 per cent of daughters carriers.
– Neural tube malformation – 5 per cent risk if one child affected; 12 per cent
if two children affected.
2 Amniocentesis – Down’ syndrome, open neural tube defects (with alpha-fetoprotein)
and certain biochemical abnormalities are especially detected by this method.
Amniocentesis is offered if parents have an affected child, a positive family history
or the mother is over 35. Abortion is offered if the fetus is affected. Now selective
screening for amniocentesis.
3 Prenatal screening – PKU galactosaemia, Tay–Sachs disease.
4 Rhesus-negative screening – Kernicterus is prevented by the use of anti-D anti-
body, amniocentesis and exchange transfusion.
5 Neonatal blood sample screening for phenylketonuria and other metabolic
disorders.
6 Rubella immunization in all adolescent girls.
7 Maternal syphilis screening and treatment.
8 Improvement of obstetric care (avoidance of harmful drugs in pregnancy,
improved surveillance of pregnancy and delivery, improved neonatal care).
9 Folate supplement in pregnancy to prevent neural tube defects.
10 Prevention of malnutrition.
11 Improved social and educational standards.
12 Avoidance of maternal drug and alcohol abuse (fetal alcohol syndrome).
13 Detection and early treatment of psychiatric disturbance in MR.
14 Support for family.
15 Bereavement counselling for MR individuals after loss of parent, etc.
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tion? Pediatr. Neurol. 29, 11.
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rate of behaviour disorders among community based population aged between 16 and
64 years. J. Intellect. Disabil. Res. 45, 495.
Deb S, Thomas M, Bright C (2001b) Mental disorder in adults with intellectual disability. 2: The
rate of behaviour disorders among community based population aged between 16 and
64 years. J. Intellect. Disabil. Res. 45, 506.
Dekker MC, Koot HM (2003a) DSM-IV disorders in children with borderline to moderate intel-
lectual disability. I: Prevalence and impact. J. Am. Acad. Child Adolesc. Psychiatry 42, 915.
Dekker MC, Koot HM (2003b) DSM-IV disorders in children with borderline to moderate intel-
lectual disability. II: Child and family predictors. J. Am. Acad. Child Adolesc. Psychiatry 42, 923.
Dykens E (2001) Introduction to the special issue on behavioral phenotypes. Am. J. Ment. Retard.
406, 1.
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ation and challenging behaviour. Res. Dev. Disabil. 24, 323.
Ivanov D, Kirov G, Norton N et al. (2003) Chromosome 22q11 deletions, velo-cardio-facial syn-
drome and early-onset psychosis: molecular genetic study. Br. J. Psychiatry 183, 409.
Kahng SW, Iwata BA, Lewin AB (2000) Behavioral treatment of self-injury, 1964 to 2000. Am. J.
Ment. Retard. 107, 212.
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for offenders with developmental disabilities. Ment. Retard. 40, 41.
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predictors and adult outcome of disorder. J. Intellect. Disabil. Res. 45, 99.
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Disabil. Res. 45, 89.
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180, 405.
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with Mental Retardation. Washington, DC.
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Child Adolesc. Psychiatry 38, s5.
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Drug therapy 21
PHARMACOKINETICS AND PHARMACODYNAMICS
• Pharmacokinetics – What the body does to the drug. Time-course of drug absorption
(distribution, metabolism, excretion) and drug transport (to and from receptors).
• Pharmacodynamics – What the drug does to the body. Relationship between drug
concentration and efficacy (tolerability, drug effects at receptor level.)
ABSORPTION
Absorption depends on:
1 Nature of the drug – Particle size, diluents, coating materials, etc., affect rate of
absorption.
2 Gastric emptying and gut motility – Anticholinergic effects of many psychotropic
drugs slow absorption.
3 Gut mucosa – Malabsorption syndromes.
4 Liver enzymes – May be inhibited (e.g. by MAOIs) or induced (e.g. by barbitu-
rates). All drugs absorbed from the GI pass through the liver first and are partly
destroyed (about 15 per cent chlorpromazine reaches systemic circulation).
Compare IV, IM or sublingual preparations, which quickly reach the brain.
PROTEIN BINDING
Most drugs bind to plasma and tissue proteins. Only unbound drug is biologically
active. Binding may be influenced by:
1 Displacement by other drugs.
2 Change in concentration of plasma proteins.
METABOLISM
Metabolism is mostly in the liver, but also in lung, gut, kidney and placenta.
Metabolism in the liver is mostly through the cytochrome P450 hepatic microenzyme
system (e.g. CYP2D6, CYP3A3/4).
PHARMACOKINETICS AND PHARMACODYNAMICS 267
Liver metabolism produces derivatives of increasing polarity, which are less lipid-
soluble and so more readily excreted by the kidney. The rate of metabolism is an
important factor in influencing serum levels.
DRUG EXCRETION
This is mostly through the kidney by passive diffusion. Some drugs, particularly glu-
curonide conjugates, are excreted in bile.
OTHER FACTORS AFFECTING PHARMACOKINETICS

See Table 21.1.
• Age (increasing age reduces liver metabolism, affects cerebral circulation, reduces
renal clearance).
• Sex.
• Proportion of body fat.
IMPORTANT DRUG INTERACTIONS

Absorption The rate of gastric emptying is slowed by anticholinergic drug effects.
Colloidal antacids slow drug absorption.
Hepatic enzymes See Table 21.2.
Table 21.1 Pharmacokinetics in select populations

Renal clearance Hepatic metabolism Protein binding
Young ↑ ↑ ⫽
Old ↓ ⫽↓ ⫽
Pregnant ↑ ⫽ ↓↑ ⫽↓
Renal disease ↓ ↓ ↓
Liver disease ⫽↓ ↓ ⫽↓
Table 21.2 Enzyme inducers and inhibitors

Enzyme inducers (reduces drug level) Enzyme inhibitors (increases drug level)
Omeprazole MAOIs
Carbamazepine Fluoxetine, fluvoxamine, paroxetine
Phenytoin Nefazodone
Barbiturates ‘Azole’ antifungals (ketoconazole)
Co-trimoxazole
Macrolides
Cimetidine
Quinidine
Cigarettes
268 DRUG THERAPY
Genetic polymorphisms
• CYP2D6 – poor metabolizers, autosomal recessive, more in Asians.
– N-acetyltransferase – slow acetylators, autosomal recessive, more in Caucasians.
PHARMACOGENETICS
Pharmacogenetics is the study of genetically based, interindividual variability in
response to drugs and in susceptibility to drug-induced adverse effects. It focuses on
genetic polymorphisms influencing structure or function of proteins for which a
given gene codes. Examples include:
• Polymorphism of dopamine D3 receptor gene exists – homozygotes (serine–serine;
glycine–glycine) versus heterozygotes (serine–glycine) – DRD3 glycine–glycine phe-
notype associated with higher risk of tardive dyskinesia with antipsychotic therapy
(Lerer et al., 2002).
• Genetic variation in serotonin transporter gene predicts response to antidepressant
(especially SSRIs; see page 275) therapy (Lever and Marciardi, 2002) – still at
research stage but likely to influence clinical practice in coming years.
PRESCRIBING IN PREGNANCY
RISKS TO FETUS
• Increased incidence of dysmorphogenesis, especially cardiac anomalies with
lithium.
• Possible increased risk with other psychotropics, but no clear evidence.
• Do not use any drug during pregnancy, especially in first 12 weeks, except when
risks of relapse outweigh other risks. If necessary, give a minimum dosage.
RISKS TO NEWBORN
• May be born ‘flat’.
• May show withdrawal symptoms if mother dependent on opiates or alcohol.
• May be limp or goitrous if mother takes lithium.
• Most drugs cross the placental barrier. This is probably unimportant in pheno-
thiazines, tricyclics, hypnotics and anticonvulsants. Avoid breast feeding with
lithium and high doses of diazepam.
ANTIPSYCHOTIC DRUGS
CLASSES OF ANTIPSYCHOTIC DRUGS

• Typical antipsychotic classes – see Table 21.3.
• Atypical antipsychotic classes – see Table 21.4.
• Differences between atypicals and typicals – see Table 21.5.
ANTIPSYCHOTIC DRUGS 269
Table 21.3 Typical antipsychotics

Typical antipsychotic classes Example Potency
Phenothiazine
– Aliphatic class Chlorpromazine 100
– Piperidine class Thioridazine 100
– Piperazine class Trifluoperazine 10
Butyrophenone Haloperidol 5
Thiozanthene Fluphenthixol ?
Diphenylbutylpiperidine Pimozide 1
Substituted benzamide Sulpiride ?
Potency ⫽ milligrams of drug equivalent to 100 mg chlorpromazine.
Table 21.4 Atypical antipsychotics

Atypical antipsychotic classes Example
Dibenzodiazepine Clozapine
Benzisoxazole Risperidone
Thienobenzodiazepine Olanzapine
Dibenzothiazepine Quetiapine
Benzisothiazolyl Ziprasidone
Phenylindol Aripiprazole
Phenylindol Sertindole
Dibenzothiepine Zotepine
Table 21.5 Differences between atypicals and typicals

Atypical Typical
Extra-pyramidal side-effects ⫹/– ⫹⫹⫹

Hyperprolactinaemia ⫹/– ⫹⫹⫹
Mesolimbic D2 binding ⫹⫹ ⫹⫹⫹
Improves negative symptoms ⫹⫹ ⫹
Improves cognitive symptoms ⫹ –
Improves depressive symptoms ⫹ ⫹/–
Lessens suicide ⫹ ⫹/–
EVIDENCE FOR DOPAMINE BLOCKADE AS MECHANISM OF ACTION

• Amphetamine, which promotes dopamine (DA) release, induces a schizophrenia-
like psychosis.
• Antipsychotics (typicals) block DA D2 receptors, the extent of which is a measure of
their potency.
• cis-Fluphenthixol isomer (which blocks D2 receptors), but not trans-fluphenthixol
(inert isomer), is an effective antipsychotic.
• Homovanillic acid is the metabolite of dopamine and its plasma level is correlated
with response to antipsychotic agents.
• PET studies confirm the need for antipsychotics to achieve above 60 per cent D2
receptor blockage to be clinically effective, yet EPS occurs at 74 per cent receptor
270 DRUG THERAPY
occupancy and above. Binding of atypical antipsychotics is more complex

(e.g. quetiapine rapidly dissociates from D2 receptors; aripiprazole is a D2 partial
agonist).
SCHEME OF RECEPTOR ANTAGONISTIC BINDING PROFILE OF ANTIPSYCHOTICS

See Table 21.6.
EXTRAPYRAMIDAL SIDE-EFFECTS (EPS) OF ANTIPSYCHOTICS

See Table 21.7.
Table 21.6 Scheme of receptor antagonistic binding profile of antipsychotics

Drug D2 5-HT2A H1 Alpha-1 ACh
Haloperidole ⫹⫹⫹ – –/⫹ ⫹ –/⫹

Thioridazine ⫹ ⫹ ⫹ ⫹⫹ ⫹⫹
Trifluperazine ⫹⫹ – –/⫹ ⫹/– ⫹⫹
Amisulpride ⫹ – – – –
Clozapine ⫹/– ⫹⫹ ⫹⫹⫹ ⫹ ⫹⫹
Risperidone ⫹ ⫹⫹⫹ – ⫹ –
Olanzapine ⫹ ⫹⫹ ⫹⫹ ⫹ ⫹⫹
Quetiapine ⫹/– ⫹/– – ⫹⫹ –
Sertindole ⫹ ⫹ – ⫹ –
Aripiprazoleaa ⫹ ⫹⫹ – – –
Ziprasidone ⫹ ⫹⫹⫹ – ⫹⫹ –
Zotepine ⫹ ⫹ – ⫹ –
D2 ⫽ dopamine D2 receptor; 5-HT2A ⫽ 5-hydroxytryptamine receptor, type 2A; H1 ⫽

histamine H1 receptor; Alpha-1 ⫽ alpha-1 adrenoceptor; ACh ⫽ acetylcholine receptor;
⫺ ⫽ no significant receptor binding antagonism; ⫹/⫺ ⫽ or ⫺/⫹ ⫽ minimal receptor
antagonism; ⫹ ⫽ receptor antagonism; ⫹⫹ ⫽ moderate antagonism; ⫹⫹⫹ ⫽ strong
antagonism. a displays partial agonist properties at dopamine and serotonin receptors.
Table 21.7 Extrapyramidal side-effects (EPS) of antipsychotics

EPS Mechanism Risk factors Treatment
Acute dystonia Acute hypodopaminergic Young, male, high dose, Immediate: Oral/IM
– oculogyric crisis in basal ganglia high potency, typical anticholinergic
– torticollis antipsychotics Subsequent: decrease
– dysarthria dosage, add anticholinergic,
– dysphagia or change to atypical.
Parkinsonism Basal ganglia D2 blockage Dose related, more with Reduce dose or add oral
– tremor typical antipsychotics anticholinergic, or change to
– cog-wheel rigidity atypical.
– bradykinesia
Akathisia Basal ganglia D2 blockage Low serum iron Reduce dose, or add
– subjective and Low iron also relevant? Dose related, more with benzodiazepines or
motor restlessness typical antipsychotics betablocker.
Change to atypical.
ANTIPSYCHOTIC DRUGS 271
Tardive dyskinesia (TD)

This involves abnormal involuntary movements primarily involving the mouth and
tongue (but can involve the trunk and limbs). It is thought to occur after long-term
use of antipsychotics when postsynaptic dopamine receptors become hypersensitive
to dopamine. There is a 5 per cent incidence per year in the young; higher rates are
seen in the elderly.
Risk factors Female; advanced age; organic brain disease; mood disorder; prominence
of negative symptoms; long duration and high doses of typical antipsychotics.
Management Change to an atypical antipsychotic. Clozapine has an indication for
TD. Vitamin E or amantidine may help.
Neuroleptic malignant syndrome (NMS)

This is an idiosyncratic reaction, primarily to typical antipsychotics, characterized
by pyrexia, muscle rigidity, altered consciousness, autonomic instability, elevated
CPK.
Incidence Eighty per cent are over 40 years of age; male:female ratio ⫽ 2:1.
Risk factors Rapid neuroleptic titration or depot injection; pre-existing dehydration;
pre-existing agitation; organic brain disease.
Aetiology Unclear, but occurs within days or years after blockade of central dopamine
receptors. Vulnerability is hypothesized to be related to a defect of intracellular cal-
cium regulation in the sympathetic nervous system (Gurrera, 2002).
Treatment Hospitalization. Stop antipsychotic administration; supportive treatment;
change to atypical antipsychotic 2 weeks after resolution of NMS.
NON-NEUROLOGICAL SIDE-EFFECTS OF ANTIPSYCHOTICS

See Table 21.8.
Table 21.8 Non-neurological side-effects of antipsychotics

Side-effect Treatment
Orthostatic hypotension Lower dose, change drug.

– antiadrenergic effect
Anticholinergic effects Lower dose, change to atypical.
– blurred vision, dry mouth, constipation
Hyperprolactinaemia Change to prolactin-sparing atypical.
– amenorrhroea, galactorrhoea, gynaecomastia
Sexual dysfunction Rule out medical cause, change medication.
– impotence, ejaculatory delay/failure, anorgasmia
Sedation Lower dose, change medication.
Seizures (clozapine lowers Sz threshold) Slow dose titration, reduce dose, add antiepileptic.
Weight gain Dietary assistance, exercise, antiobesity agents.
Diabetes mellitus Treat diabetes accordingly.
(hyperglycaemia is a potential side-effect Weight management may help.
of all atypicals)
Cardiac arrhythmias Change to lower-risk antipsychotic.
– increased risk with thioridazine
272 DRUG THERAPY
Table 21.9 Antipsychotic safety and tolerability

Item Typ Clz Ris Olz Qtp Zip
EPS ⫹ – ⫹⫹⫹ ⫾ ⫾ – ⫹⫹⫹a ⫾ – ⫹a ⫾ ⫾ – ⫹a

TD ⫹⫹⫹ ⫾ ⫾–⫹ ⫾(?) ⫾(?) ⫾(?)
Somnolence ⫾ – ⫹⫹⫹ ⫹⫹⫹ ⫾ ⫹ ⫹⫹ ⫾
Prolactin ⫹⫹⫹ ⫾ ⫹⫹⫹ ⫾ ⫾ ⫾
Weight ⫾ ⫹⫹⫹ ⫹ ⫹⫹⫹ ⫹⫹ ⫾
Dyslipidaemia ⫾ ⫹⫹⫹ ⫹ ⫹⫹⫹ ⫹⫹ ⫾
DM ⫾ ⫹⫹⫹ ⫹ ⫹⫹⫹ ⫹⫹ ⫾
QTc ⫾ ⫹⫹ ⫹ ⫹ ⫹ ⫹⫹
Orthostatic BP↓ ⫾ ⫹⫹⫹ ⫹⫹ ⫹ ⫹⫹ ⫾
Typ ⫽ typical antipsychotics; Clz ⫽ clozapine; Ris ⫽ risperidone; Olz ⫽ olanzapine; Qtp ⫽ quetiapine; Zip ⫽ ziprasidone;
a
⫽ dose-related; ⫾ ⫽ none to minimal; ⫹ ⫽ mild; ⫹⫹ ⫽ moderate; ⫹⫹⫹ ⫽ marked compared with placebo rate.
ANTIPSYCHOTIC SAFETY AND TOLERABILITY

See Table 21.9.
ANTIDEPRESSANT DRUGS
The pharmacological action of antidepressant drugs (a few hours) does not correlate
with mood effect (2–4 weeks). The exact mechanism of altering mood is uncertain,
but the therapeutic effect occurs after manipulation of central neurotransmitters.
Unlike the older TCAs and MAOIs, most of the newer antidepressants have high
therapeutic indexes. Ensure maximum dose and adequate length of trial before aban-
doning a particular agent/class.
Side-effects can be used as therapeutic effects.
SIDE-EFFECTS
General
All antidepressants – with the exception of mirtazapine, bupropion and nefazodone –
have sexual side-effects which include impotence, anorgasmia and delayed ejaculation.
There have been rare cases of priapism with trazodone.
Gastrointestinal upset is associated to some degree with almost all antidepressants
except mirtazapine, TCAs and MAOIs.
Serotonin syndrome
With overstimulation of central serotonin receptors, the patient my appear agitated,
confused, and exhibit myoclonus, diaphoresis, nausea, vomiting, diarrhoea, syncope,
tachycardia and elevated blood pressure.
Ventricular tachycardia, seizures, disseminated intravascular coagulation, renal fail-
ure, coma and hypotension are complications seen in severe cases.
Aetiology Caused by serotonergic medication use – additive effect.
Treatment Discontinue serotonergic agents. With supportive treatment the syndrome
will usually resolve within 24 hours.
ANTIDEPRESSANT DRUGS 273
Table 21.10 Characteristics of antidepressants

Antidepressant Re-uptake ACh Half-life Dosage
class inhibition blockade Activating Sedating (h) (mg/d)a
SSRIs
Fluoxetine S – ⫹⫹⫹ – 330 20–80
Paroxetine S ⫹ ⫹ ⫹ 21 20–50
Fluvoxamine S – ⫹ ⫹ 16 100–300
Sertraline S – ⫹⫹ ⫾ 26 50–200
Citalopram S – ⫾ ⫾ 35 10–60
Escitalopram S – ⫾ ⫾ 27–32 10–20
Other
Bupropion D, N, S – ⫹⫹⫹ – 20 150–450
Trazodone S ⫾ – ⫹⫹⫹ 6 300–800
Nefazodone N, Sb – ⫾ ⫹⫹ 3 100–600
Mirtazapine Nb, Sb – – ⫹⫹ 30 15–45
Venlafaxine D, N, S – ⫹⫹ ⫹ 5 75–350
TCAs 2nd
Desipramine N ⫹⫹ ⫾ ⫹⫹ 14–25 50–300
Nortriptyline N, S ⫹⫹ – ⫹⫹ 18–35 20–150
TCAs 3rd
Amitriptyline N, S ⫹⫹⫹ – ⫹⫹⫹ 9–25 50–300
Clomipramine N, S ⫹⫹⫹ – ⫹⫹⫹ 19–37 50–300
Doxepine N, S ⫹⫹⫹ – ⫹⫹⫹ 6–8 50–300
Imipramine N, S ⫹⫹⫹ – ⫹⫹ 8–16 50–300
MAOIs
Phenelzine ␮ ⫹⫹ ⫾ ⫹ ␮ 15–90
Tranylcypromine ␮ ⫹⫹ ⫹ – ␮ 20–90
D ⫽ dopamine; N ⫽ norepinephrine; S ⫽ serotonin; – ⫽ none; ⫾ ⫽ none to minimal; ⫹ ⫽ mild; ⫹⫹ ⫽ moderate;

⫹⫹⫹ ⫽ marked compared with placebo rate; a may be in divided doses, long-acting formulations have different maximums,
see package insert; b ⫽ receptor antagonist; ␮ ⫽ inhibits monamine oxidase with maximal effect occurring in 5–10 days.
CHARACTERISTICS OF A RANGE OF ANTIDEPRESSANTS
See Table 21.10.
SELECTIVE SEROTONIN RE-UPTAKE INHIBITORS (SSRIs)
These are the first-line medical treatment for depression. They have a more
favourable side-effect profile than TCAs and MAOIs and a negligible mortality risk in
overdose. A report of increased suicidal ideation/behaviour in children is under
investigation.
USES OF SSRIs
• Depression.
• OCD.
• Bulimia nervosa.
• PTSD.
274 DRUG THERAPY
• Social phobia.
• Generalized anxiety disorder.
• Panic disorder.
• Premenstrual dysphoric disorder.
Side-effects of SSRIs Nausea; loose stools; headache; insomnia (best given in morning
dosage regime); nervousness, agitation; sweating; weight gain; withdrawal syndrome
(associated with agents with short half-lives).
OTHER ANTIDEPRESSANT COMPOUNDS
Bupropion
Bupropion primarily inhibits the re-uptake of dopamine and norepinephrine, and sero-
tonin to a lesser extent. It has no sexual side-effects, so it is used as an adjunct to SSRIs
to counter those side-effects. It has been associated with weight loss. Otherwise, the side-
effects are similar to those of SSRIs.
• Lower rates of mania induction.

• Higher rate of seizures than SSRIs, especially at higher doses, therefore contraindi-
cated in patients with seizure disorder and eating disorder because of lower seizure
threshold in these patients.
• Sustained-release form decreases incidence of seizures and also has an indication
for smoking cessation.
• Used in ADHD with positive results.
Trazodone
• Blocks 5-HT2 receptors at low dosage, stimulates at higher dosage, and is a weak
inhibitor of serotonin re-uptake.
• Low therapeutic index due to sedation.
• Low anticholinergic effect, and reported to be non-cardiotoxic (mixed agonist effects).
• Side-effects include sedation, orthostatic hypotension, dizziness, headache, dry mouth.
Nefazodone
Similar to trazodone – weak inhibitor of norepinephrine and serotonin reuptake and
blocks 5-HT2 serotonin receptors. Side-effects also similar to trazodone, with the
exception of less sedation/sexual side-effects.
Mirtazapine
• Antagonizes ␣2-adrenergic and serotonin 5-HT2 receptors.
• Moderate therapeutic index owing to sedation.
• Has significant antihistamine activity, which accounts for its sedating effects – more
so at lower doses.
• No sexual or SSRI-like side-effects.
• Side-effects include sedation, increased appetite and weight gain, dizziness, dry
mouth, constipation.
• Rare cases of blood dyscrasias reported, but all recovered after cessation of this drug.
ANTIDEPRESSANT DRUGS 275
Venlafaxine
• Inhibits re-uptake of serotonin at low doses and norepinephrine and dopamine at
high doses.
• Extended-release formulation is indicated for generalized anxiety disorder as well
as depression.
• Side-effect profile similar to SSRIs.
• Monitor for increased blood pressure (dose related).
TRICYCLICS: TERTIARY AMINES (AMITRIPTYLINE, IMIPRAMINE)
Tricyclics preferentially block uptake of 5-HT. Demethylated metabolites are second-

ary amines which preferentially block dopamine and noradrenaline.
Tricyclics have a lower therapeutic limit for serum levels; 90 per cent is plasma- or
protein-bound. Major tranquillizers prescribed concurrently inhibit metabolism, so
increase serum levels.
Tricyclics infrequently prescribed because of their side-effect profile. Some use in
chronic pain – superior to placebo in somatoform pain disorder. May have a
direct effect on nerve conduction, treat affective component or enhance effects of
analgesics.
SIDE-EFFECTS OF TRICYCLICS
• Anticholinergic (dry mouth, blurred vision, worsening glaucoma, urinary hesi-
tancy, constipation).
• Hypotension (central effect – anti-␣1-noradrenergic).
• Drowsiness, sedation (anti-histamine/ ⫾ anti-acetylcholine).
• Cardiovascular:
– Palpitations.
– Tachycardia.
– ECG changes (‘R on T phenomenon’), quidine-like effect; QT prolongation,
decreased ST interval; myocardial sensitization to catecholamines.
– Ventricular tachyarrhythmias.
– Cardiomyopathy or heart failure (decreased inotropic effect following depletion
of catecholamines from myocardium).
– Distal conduction defects in bundle of His following overdosage.
• Weight gain/increased appetite (serotonergic ?).
• Confusional reactions in the elderly – probably due to anticholinergic effects, espe-
cially where phenothiazine (weak anticholinergic) and a strong antiparkinson drug
are combined.
• Tremor.
• Convulsions (rare).
• Sexual dysfunction, impotence, anorgasmia (especially clomipramine), delayed
ejaculation.
• Withdrawal syndrome – symptoms of noradrenergic and cholinergic ‘overdrive’.
276 DRUG THERAPY
TRICYCLICS: CONTRADICTIONS AND PRECAUTIONS

Cardiovascular
• Acute myocardial infarction.
• Presence of intraventricular or bundle block.
• Presence of multifocal premature contractions.
• Unexplained blackouts.
Neurological
• Elderly patients treated for Parkinson’s disease with anticholinergic drugs.
• Epilepsy.
Other
• Prostatic hypertrophy.
• Narrow-angle glaucoma.
Pregnancy Evidence for dysmorphogenesis equivocal.
Drug interactions Competition for plasma- and protein-binding – phenytoin, aspirin,
phenylbutazone; alcohol; antihypertensives (not beta-blockers); sympathomimetics;
MAOIs; anticholinergics; neuroleptics (same catabolic pathway); oral contraceptives
(slow metabolism).
TRICYCLICS: SECONDARY AMINES

Nortriptyline and desipramine are secondary amines. Desipramine is the least seda-
tive. They preferentially block uptake of noradrenaline.
OTHER TRICYCLICS
• Dothiepin – derivative of amitriptyline, with fewer autonomic side-effects.
• Doxepin – derivative of amitriptyline, strongly anxiolytic, with less cardiotoxicity.
• Mianserin – blocks ␣2-adrenergic receptors; effectively no re-uptake blocking activity
or anticholinergic activity. Minimal cardiotoxicity. Rarely causes convulsions; risk of
leucopenia requires careful monitoring.
MONOAMINE OXIDASE INHIBITORS (MAOIs)
Monamine oxidase is an enzyme that degrades tyramine, serotonin, dopamine and nor-
epinephrine, and its inhibition causes an increase in these monamines.
MAO inhibition reaches a maximum in 5–10 days. Restoration of MAO stores takes
2 weeks after stopping MAOIs. Drug and dietary restrictions are necessary to avoid
hypertensive crises (see below).
MAOIs are thought to be effective in refractory and atypical depressive states –
especially those with mixed anxiety, phobic, obsessional features.
SIDE-EFFECTS OF MAOIs
• Anticholinergic.
• Postural hypotension.
• Tremor.
MOOD STABILIZERS USED IN BIPOLAR ILLNESS 277
• Ankle oedema.
• Paraesthesia in limbs.
• Confusional states and possible precipitation of mania.
• Hypertensive crisis:
– Headache and neck pain.
– Throbbing neck veins.
– Palpitations.
– Hyperpyrexia.
– Convulsions, coma, death.
– Reverse with phentolamine 5–10 mg IV; chlorpromazine (PO) also used.
• Insomnia.
• Nausea.
• Myoclonus.
• Tranylpromine has amphetamine-like properties.
MAOIs: CONTRAINDICATIONS AND PRECAUTIONS

1 Cardiac failure, hypertension, infective hepatitis, obstructive jaundice or cirrhosis.
2 Avoid food high in tyramine: meat or yeast extracts, pickled herring, cheeses, alco-
hol (including wines), broad bean pods, chicken liver.
3 Drugs:
– Sympathomimetic amines (may be present in proprietary cold-relieving agents
and anaesthetics).
– Antihypertensive drugs.
– Antihistamines.
– Sensitivity to insulin increased.
– Oral antidiabetic agents.
– Morphine and meperidine.
– Metabolism of many drugs by liver, including barbiturates, phenytoin.
MOOD STABILIZERS USED IN BIPOLAR ILLNESS
Mood stabilizers used for bipolar illness include lithium, antiepileptic drugs (AED)
and, more recently, atypical antipsychotics. These agents are used with varying success
to delay or treat the onset of mood episodes.
Lithium has long been known to exert suicide-protective effects in bipolar patients.
Recent studies also suggest that AED mood stabilizers are associated with reduced sui-
cide ideation and attempts (Yerevanian et al., 2003).
Atypical antipsychotics have been shown to be useful both alone and in combina-
tion with mood stabilizers in the treatment of acute mania. Benzodiazepines are also
useful in the treatment of acute mania.
LITHIUM
Lithium is prescribed in the form of its simple salts. It was introduced into medicine in
1859 as a treatment for gout, but later abandoned because of toxicity. It was reintroduced
278 DRUG THERAPY
as a treatment for mania by John Cade in 1949, in Australia. Its use was generally estab-
lished by 1965.
KINETICS OF LITHIUM
Absorption is rapid following an oral dose and complete within 6–8 hours. Plasma level
peaks in 30 minutes to 2 hours. It is distributed in total body water, shifting slowly to
cells. There is no protein-binding. The therapeutic index is low due to neurotoxicity.
There is no metabolism – the substance is excreted unchanged by the kidney. Between
one- and two-thirds of the oral dose appears in urine after 8–12 hours; the rest is
excreted slowly over days. Once lithium therapy is established, the clearance rate is
fairly constant.
Rates of lithium clearance between different persons may differ fourfold. It depends
on renal function: the amount of fluid passing through the kidney and its sodium con-
tent. Lithium tends to follow sodium in reabsorption at proximal tubules; hence:
• Increased sodium intake produces decreased reabsorption, with decreased reabsorp-
tion of lithium.
• A sodium-restricted diet produces increased reabsorption, and lithium levels may
become toxic.
• Thiazide diuretics decrease lithium clearance by 24 per cent, owing to compensatory
reabsorption of sodium in proximal tubules.
ACTIONS OF LITHIUM
The therapeutic action is not understood, but the following effects have been noted.
Neurotransmitters
• Synapses – Lithium is thought to increase presynaptic destruction of catecholamines,
inhibit release of neurotransmitter, decrease sensitivity of postsynaptic receptors.
• Ions – Lithium influences sodium and calcium ion transfer across cell membranes.
These ions affect neurotransmitter release and receptor activity.
• Cyclic AMP – Lithium inhibits prostaglandin E-stimulated cyclic AMP.
• Lithium stimulates sodium and magnesium-dependent ATPase.
Cations and water Lithium stimulates exit of sodium from cells, probably by stimu-
lating the pump mechanism, where intracellular Na is elevated (as in depression).
Lithium stimulates entry of sodium into cells where intracellular Na is low (as may be
the case in mania).
Cell membranes Lithium may interact with both calcium and magnesium and increase
cell membrane permeability.
Other actions
• Lithium restores diurnal rhythm of corticosteroids to normal in mania (but may
simply reflect changes in behaviour as mania ameliorates).
• In depressed patients, there is restoration of normal slow-wave EEG rhythms during
sleep, and decreases in stage 1 and REM sleep correlate with plasma levels.
• Changes in magnesium and calcium may be the secondary effects of altered
carbohydrate metabolism. Lithium influences this by releasing insulin and increas-
ing transport of glucose and muscle glycogen formation. This may be the cause of
weight gain.
PLASMA LEVEL AND STABILIZATION OF DOSE

Take a blood sample 12 hours after the last dose because of ‘peaking’ of level. Therapeutic
and toxic ranges refer to this ‘basal’ level. Give smaller doses more frequently rather
than large doses infrequently, because large interpeak troughs are associated with
renal side-effects. Slow-release preparations also smooth out peaks.
• Acute treatment: 0.9–1.4 mEq/L.
• Maintenance: 0.6–0.8 mEq/L (some researchers suggest as low as 0.4 mEq/L).
USES OF LITHIUM
1 Control of mania (3–4 days for therapeutic effect).
2 Prophylaxis of recurrent bipolar and unipolar disorder.
3 Schizoaffective disorder.
4 Augmentation of antidepressant therapy.
5 Treatment of impulsive and aggressive behaviour.
There are significant reductions in aggressive behaviour among prisoners and men-
tally retarded on lithium compared with placebo treatment.
SIDE-EFFECTS OF LITHIUM
Early
• Nausea, vomiting, diarrhoea (related to ‘peak’ serum levels).
• Tremor, especially on voluntary movement.
• Dryness of mouth, slight thirst.
• Fatigue, drowsiness.
• Stuffy nose, metallic taste in mouth.
At any time Toxicity – tremor, ataxia, incoordination, slurred speech, confusion,
disorientation convulsion, coma and death. Symptoms begin to appear with blood
levels ⬎2.0 mmol/L.
Longer-term
• Nephrogenic diabetes insipidus. Polyuria and polydipsia may occur at therapeutic
plasma concentrations. The distal tubule becomes resistant to the influence of
antidiuretic hormone (ADH), possibly owing to blockade of ADH-sensitive adenyl
cyclase. This is reversible but may take weeks.
– Treatment: Reduce/stop lithium; use indomethacin or amiloride.
• Hypothyroidism occurs in about 3 per cent of chronic lithium-takers, females more
than males. The lithium ion interferes with production of thyroid hormones and
the action of TSH. This is reversible but will recur on restarting lithium.
• Oedema.
• Weight gain (not accounted for by water retention).
• Neurological – choreoathetosis, ataxia, dysarthria, tardive dyskinesia (rare), neuro-
toxicity with neuroleptics or carbamazepine, NMS.
• Cardiac T-wave flattening on ECG.
• Arrhythmias – possibly caused by reduction of intracellular potassium.
• Poor memory short-term.
• Nephropathy – association unclear; 5–10 per cent develop nephropathy, but this
does not invariably cause ‘clinical’ renal insufficiency.
280 DRUG THERAPY
• Dermatological/alopecia.
• SLE/myasthenia gravis.
DRUG INTERACTIONS AND CAUTIONS

1 Avoid in association with:
– Low salt diet.
– Diarrhoea/vomiting.
– Pregnancy.
– Dehydration.
2 Use cautiously in association with:
– Major tranquillizers.
– Renal insufficiency.
– Diuretics.
– NSAIDs.
MONITORING
• Baseline – examination; routine lab tests including urea, electrolytes, creatinine,
urine tests, thyroxine and TSH; weight; ECG; pregnancy test, if female of child-
bearing age.
• During treatment:
– Lithium – 8-weekly once stabilized.
– Chemistry, T4, TSH, creatinine, urea, urine – 6–12 months.
– ECG examination – annually.
VALPROIC ACID
The therapeutic level for bipolar disorder is 50–100 micrograms for both maintenance
and acute mania. It is better tolerated than lithium. It is equal to lithium in the treat-
ment of acute mania, and more effective for rapid cycling and mixed states.
The mechanism of action is unknown, but it is shown to increase central GABA levels
by inhibiting its degradation/enhancing its synthesis.
Valproic acid has a moderate therapeutic index gastrointestinal symptoms and
neurotoxicity. It is metabolized in the liver.
USES OF VALPROIC ACID

• Acute mania.
• Maintenance therapy for bipolar illness.
• Preferred for rapid cycling and mixed episodes.
• Treatment-resistant bipolar illness.
• Epilepsy.
• Migraine prophylaxis.
SIDE EFFECTS OF VALPROIC ACID

Gastrointestinal (nausea, vomiting, diarrhoea); headache; ear ringing; weight gain;
hair loss; polycystic ovarian syndrome (due to weight gain?); neural tube/craniofacial
defects during pregnancy; pancreatitis, liver damage (rare).
CARBAMAZEPINE
Carbamazepine inhibits limbic kindling. The therapeutic level is 8–12 micrograms.

It has a low therapeutic index due to neurotoxicity.
Carbamazepine is metabolized in the liver, where it induces its own metabolism.
It is excreted in the kidney.
Caution is needed with use of oral contraceptives and some antibiotics. It is con-
traindicated with MAOIs.
USES OF CARBAMAZEPINE
• Acute mania.
• Prophylaxis of bipolar illness.
• Rapid cycling mania – more effective than lithium.
• Trigeminal neuralgia.
• Epilepsy.
• Alcohol withdrawal.
SIDE-EFFECTS OF CARBAMAZEPINE
Dizziness, sedation, ataxia, dry mouth; generalized erythematous rash (Steven Johnson
syndrome); leucopenia/agranulocytosis occurring in early stages of treatment; hypona-
tremia; neural tube/craniofacial defects during pregnancy.
LAMOTRIGINE
Lamotrigine is used for maintenance therapy in bipolar disorder. It delays the onset of
manic/hypomanic as well as depressive episodes in bipolar illness. It is not effective for
acute mania.
Lamotrigine is thought to work by stabilization of neurons via inhibition of sodium
and calcium channels in presynaptic cell membranes.
It does not require serum level monitoring like lithium, valproic acid and
carbamazepine.
Valproic acid increases lamotrigine levels while carbamazepine lowers levels. It is
not associated with weight gain.
USES OF LAMOTRIGINE
• Maintenance therapy for bipolar illness.
• Epilepsy.
SIDE-EFFECTS OF LAMOTRIGINE
Headache; nausea; insomnia; rash (higher risk with rapid titration, higher doses,
younger age).
OTHER AEDs USED AS MOOD STABILIZERS
Gabapentin, tiagabine, oxcarbazepine and topiramate are used for mood stabilization
with promising reports, but studies do not fully support their use in this manner.
282 DRUG THERAPY
SEDATIVES AND ANXIOLYTICS
BENZODIAZEPINES
See Table 21.11.
MODE OF ACTION
There is enhancement of GABA effects, probably via benzodiazepine (bz) receptors
localized on neurones throughout brain, but with highest density in cortical and lim-
bic areas.
The bz receptors are closely tied to GABA receptors, which explains the CNS
inhibitory actions of the benzodiazepines.
Benzodiazepines are safe in overdoses, producing drowsiness or stupor, and
rebound insomnia in the next few days.
USES OF BENZODIAZEPINES
• Anxiety disorders.
• Insomnia.
• Withdrawal symptoms.
• Psychosis induced by hallucinogens.
• Status epilepticus.
• Abreactive techniques.
• Premedication and minor operative procedures.
• Muscle relaxant.
• Acute agitation.
SIDE-EFFECTS OF BENZODIAZEPINES
• Sedation.
• Ataxia/motor impairment.
Table 21.11 Benzodiazepines

Select bz drugs Half-life (h) Active metabolite
Long-acting
Clorazepate 40–50 Nordiazepam
Chlordiazepoxide 24–30 Desmethylchlordiazepoxide
Clonazepam 30–40 None
Diazepam 20–100 Nordiazepam
Flurazepam 47–100 N-hydroxyethyl-flurazepam
Intermediate-acting
Estazolam 10–24 4-hydroxy estazolam (weak)
Lorazepam 13 None
Oxazepam 6–11 None
Temazepam 3.5–18.4 None
Short-acting
Alprazolam 11.2 None
Triazolam 1.5–5.5 None
SEDATIVES AND ANXIOLYTICS 283
• Cognitive blunting.
• Apnoea on IV administration.
• Slight respiratory depression (important in patients with obstructive airways disease).
• Dependency – psychological and physical, associated with chronic use.
• Amnesia in large doses.
• Confusion in the elderly.
WITHDRAWAL EFFECTS
On withdrawal (placebo-controlled) of long-term normal-dose benzodiazepine
treatment, there is:
• Rebound insomnia, REM rebound.
• Tremor, anxiety, restlessness.
• Weight loss, appetite disturbance, sweating.
Symptoms usually subside after several days, but may last months in some cases.
Withdrawal is possibly aided by substituting long-acting bz, gradual titration, and
supportive/counselling measures.
Convulsions have been reported on abrupt withdrawal of long-term, very-high-dose
treatment.
NON-BENZODIAZEPINE HYPNOTICS
See Table 21.12.

These agents have a chemical structure unrelated to the benzodiazepines but share
many of the same pharmacological effects. The mechanism of action is via selective
interaction with only one GABA–bz receptor complex, resulting in sedation.
Side effects are similar to benzodiazepines and abuse potential is present.
Table 21.12 Non-benzodiazepines

Non-bz hypnotics Half-life (hours) Active metabolite
Zaleplon 1 None
Zolpidem 2.6 None
Zopiclone 3.5–6.5 None
AZAPIRONES (BUSPIRONE)
Azapirones are unrelated to benzodiazepines and are anxioselective. Buspirone is a full

agonist of presynaptic dorsal raphe 5-HT1A receptors and partial agonist of 5-HT1A
receptors in the hippocampus and cortex. It is rapidly absorbed: peak plasma concen-
tration in 40–90 minutes; half-life 2–11 hours. It is metabolized in the liver.
It is relatively non-sedative and does not interact with bz or alcohol. Side-effects
are mild and can include light-headedness, headache, drowsiness. There is no liability
of abuse.
The anxiolytic effect may take 1–2 weeks to achieve.
284 DRUG THERAPY
BARBITURATES
Barbiturates are rarely used now because of the high risk of psychological and phys-
ical dependence. There is tolerance and liver enzyme induction, drug accumulation
causing confusional states (especially in the elderly). Respiratory depression is another
drawback, as is the withdrawal syndrome (see Chapter 10).
Barbiturates are used sometimes in abreaction, for narcosis in a severely disturbed
patient.
ADRENERGIC AGENTS
ALPHA AGONISTS
The mechanism of action involves stimulation of central ␣-adrenoreceptors which

results in reduced sympathetic outflow.
USES OF ALPHA AGONISTS

• Hypertension.
• Opioid withdrawal – suppresses autonomic activity.
• Adjunct in treatment of ADHD for highly activated children.
• Aggression in children.
• Akathisia.
• Tic disorder.
• PTSD.
SIDE-EFFECTS OF ALPHA AGONISTS

Sedation; dry mouth; hypotension; headache; constipation; dizziness; rebound
hypertension.
CAUTIONS AND CONTRAINDICATIONS

• History of cardiac or cardiovascular disorder.
• Combining with other drugs.
• History of medication non-compliance.
• Taper during discontinuation.
• Autonomic hyperarousal with sudden cessation.
BETA BLOCKERS
Depending on the particular agent, the mechanism of action attained by selectively or

non-selectively blocking of ␤-adrenergic receptors throughout the body.
USES OF BETA BLOCKERS

• Hypertension.
• Familial and other tremors.
STIMULANTS 285
• Control of autonomic aspects of anxiety.

• Impulsive aggression.
• Akathisia.
• Opiate withdrawal.
SIDE-EFFECTS OF BETA BLOCKERS

Bradycardia, light-headedness; tinnitus, rashes, purpura; insomnia, nausea.

• May precipitate heart failure.
• Diabetes – prevents early recognition of hypoglycaemia and interferes with metab-
olism of glycogen.
• Obstructive airways disease – may precipitate bronchospasm.
• Presence of second- and third-degree heart block.
• Exercise caution in patients with poor cardiac reserve.
DISULFIRAM FOR ALCOHOLISM
If disulfiram is taken with alcohol, the person experiences severe headache, nausea,
facial flushing and general malaise. Severe reaction can be treated by oxygen, dextrose
drip or parenteral antihistamine. Effectiveness is limited by compliance issues.
Disulfiram interferes with metabolism of other drugs, especially barbiturates,
phenytoin, warfarin and paraldehyde.
Citrated calcium carbimide has fewer side-effects and milder reaction.
SIDE-EFFECTS OF DISULFIRAM
Nausea, constipation, fatigue; breath odour, metallic taste in mouth; psychotic and
confusional states; reduction in libido; hypothyroidism.
CONTRAINDICATIONS
• Cardiac failure or ischaemic heart disease.
• Pregnancy.
• Psychosis (may exacerbate schizophrenic psychosis).
STIMULANTS
PSYCHOSTIMULANTS
Psychostimulants cause CNS excitement by increasing the activity of the cat-

echolamines dopamine and/or noradrenaline.
The prototype stimulants are dextroamphetamine and methylphenidate (milder).
There are also mixed salt amphetamine/dextroamphetamine formulations. All have
generally comparable efficacies. Intermediate- and long-acting variations are available
in order to avoid multiple daily dosing.
286 DRUG THERAPY
Pemoline has similar effects but is structurally different from the prototype stimu-
lants and sees only limited use because of excessive morbidity and mortality associated
with liver complications.
USES OF PSYCHOSTIMULANTS
• ADHD (first-line treatment).
• Narcolepsy.
• Obesity.
• Augmentation of antidepressants.
SIDE-EFFECTS OF PSYCHOSTIMULANTS
Insomnia; appetite suppression; growth suppression; unmasking of latent tic disorder;
hallucinations; agitation, excitement; tolerance and dependency; rebound depression
on stopping or after prolonged use; paranoid psychosis; hypertension.

• Cardiovascular disease.
• Tic disorder.
• History of substance abuse.
• Glaucoma.
NON-PSYCHOSTIMULANTS (ATOMOXETINE)
Used in ADHD, atomoxetine’s mechanism of action is thought to be selective inhib-

ition of presynaptic norepinephrine re-uptake.
It has the advantage of once-a-day (morning) dosing and full-day coverage.
Therapeutic effect is not seen until 2 weeks.
It has fewer side-effects than classic stimulants. It is not a controlled substance and
there is no abuse potential.
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Physical treatments 22
ELECTROCONVULSIVE THERAPY (ECT)
HISTORY
Camphor-induced convulsions were first used by W. Oliver in 1785 for melancholia.
The effect was slow and produced fits inconsistently. In the 1930s, Meduna used IV
injections of metrazol, based on a belief that there is an antagonism between schizo-
phrenia and epilepsy. Cerletti, on the basis of the same notion in 1938, administered
an electrically induced fit to a catatonic vagrant found wandering in a Rome railway
station.
Later, anaesthesia was introduced and convulsions modified using muscle-relaxing
agents.
PRESENT INDICATIONS
In depressive illness
• Poor response to adequate pharmacotherapy.
• Person unable to tolerate side-effects of pharmacotherapy (especially the elderly).
• Depressive stupor, not eating or drinking.
• Severe suicide risk.
• ‘Severe’ depression with delusions, psychomotor retardation.
• Severe post-partum depression.
The presence of delusions and severe psychomotor agitation or retardation are the
main ‘reliable’ clinical predictors of response to ECT.
Numerous studies of real ECT versus simulated ECT confirm the therapeutic efficacy
of ECT. It is more effective than antidepressant medications (UK ECT Review Group,
2003). Up to 90 per cent show improvement in depressive symptoms.
In mania
• Quicker response and ‘better social response’ in ECT-treated patients.
• Equally efficacious but more rapid response with ECT ⫹ neuroleptics.
• Use generally reserved for acute treatment-‘refractory’ mania.
290 PHYSICAL TREATMENTS
Schizophrenia
ECT is useful when schizophrenia is superimposed with catatonia or major depression.
SIDE-EFFECTS OF ECT
Early reported side-effects are:
• Headache.
• Slight and temporary confusion.
• Short-term memory loss, increasing with the number used.
• Tachycardia and hypertension immediately after ECT.
At 6 months after the course, there is no significant difference in memory between
those receiving ECT and those receiving simulated ECT.
MORTALITY
Deaths are estimated 4.5 per 100 000 ECT treatments – similar to rates for minor
anaesthesia. The majority of deaths have been caused by cardiovascular complications
(arrhythmias, sudden cardiac arrest secondary to vagal inhibition).
CAUTION AND CONTRAINDICATIONS

There is no absolute contraindication, other than raised intracranial pressure, and
risks of treatment must always be weighed against risks of illness.
• Cardiac infarct in preceding 3 months.
• Other cardiac disease including arrhythmias.
• History of cerebral infarction.
• Brain tumour.
• Pulmonary disease.
ADMINISTRATION OF ECT
Before administration
1 Full physical examination.
2 Discuss any significant organic pathology with the anaesthetist.
3 Ensure an empty stomach in patient, and full resuscitatory equipment for the
anaesthetist.
Application of anaesthetic
1 Induction – methohexitole (most commonly).
2 Atropine – reduces secretions, counters cholinergic effects of muscle relaxants.
3 Muscle relaxant – succinylcholine; rarely, prolonged paralysis produced due to
pseudocholinesterase deficiency.
4 Oxygenate – will also facilitate seizure activity.
Application of electrical stimulation

The modern approach is to use brief square-wave pulses of 1–2 ms duration. This has
similar efficacy to a sine-wave stimulus, but with less memory disturbance.
The voltage stimulus needs to be in excess of seizure threshold to achieve an effect,
but this is also related to cognitive deficits. The degree to which this stimulus exceeds
ELECTROCONVULSIVE THERAPY (ECT) 291
the seizure threshold is critical for efficacy in unilateral ECT in particular, and for the
speed of response in unilateral or bilateral ECT.
If there is no convulsion, repeat the stimulation up to a maximum of three times
(ensure good skin contact, oxygenation). Increasing the stimulation, decreasing con-
comitant benzodiazepines, and giving caffeine will help to maximize seizure activity
in a seizure-refractory patient.
• Unilateral – on non-dominant hemisphere, produces less cognitive impairment:
– Between frontotemporal and mastoid region.
– Lancaster position – between frontotemporal position and vertically to vertex.
• Bilateral – frontotemporal position.
Post-ictal
1 Oxygenate.
2 Nurse in prone position with airway in situ.
3 Reassure the patient during recovery of consciousness.
Do not prescribe ECT in set courses, although the average number is 6–8. Continue
applications twice to three times weekly (UK and US practices respectively) until
euthymic, up to a maximum of 10–12.
Transient elevation of mood on recovery after the first 1–2 treatments predicts good
response. If no response whatsoever by the sixth treatment, then prognosis is poor.
Daily application does not improve response, and seriously increases memory
disturbance.
Maintenance treatment is usually pharmacological; but some recent evidence
suggests reduced relapses with maintenance ECT.
EFFECTS OF ECT
Cardiovascular
• Brief asystole on passage of current.
• Bradycardia during the tonic phase, tachycardia during the clonic phase and occa-
sional arrhythmias in the post-ictal period.
• Brief blood pressure decrease during the early tonic phase followed by a rapid rise
above normal level. The rise persists through the clonic phase.
• Blood pressure rise apparently is centrally stimulated, independent of peripheral
convulsive activity. It is exacerbated by atropine. ?? Related to memory impairment.
Neurological
• Immediate loss of consciousness (if given without anaesthesia).
• Flattening of EEG, followed by slow waves, and waves reappear as consciousness
recovers, with gradual return to normal pattern over 30 minutes. Frontal areas are
slowest in resuming normal activity.
• Very rarely post-ictal automatisms.
Neuropathological (neuroendocrine)
• There are complex effects, and the overall mechanism of action is unclear.
• Increase in blood–brain barrier permeability and capillary leakage in CNS: transi-
tory cerebral oedema. Absence of MRI changes disputed.
• Depletion of CNS noradrenaline (NA) – subsequent increase and turnover of NA?

• Increased dopamine, serotonin turnover – increased receptor sensitivity?
• Release of oxytocin-associated neurophysin – extent is predictive of eventual
response.
• ? Increased sensitivity of dopamine and other receptor sites.
Sleep and other changes

• Decreased amount of time spent in REM sleep.
• Decrease in number of eye movements during REM sleep – ? change in reticular
activity.
• Water retention.
• Occasional menstrual irregularities.
• Transient increases in plasma sodium, potassium, chloride, calcium, lymphocytes
and neutrophils.
• Eosinopenia.
• Rise in plasma hydroxycorticosteroid levels.
• Transitory rise in plasma glucose and in insulin secretion.
UNILATERAL VERSUS BILATERAL ECT

Unilateral ECT to the non-dominant hemisphere produces less post-treatment confu-
sion and memory loss. However, there is no clear consensus of therapeutic efficacy of
unilateral versus bilateral ECT. ‘Dose’ of ECT is also important in studies comparing
unilateral versus bilateral, especially for side-effects. Bilateral treatment is quicker, and
better in the elderly.
• Royal College of Psychiatrists (1989) recommends bilateral but recognizes alterna-
tive of unilateral.
• American Psychiatric Association (APA, 1990) gives greater preference to unilateral.
ETHICAL AND LEGAL ASPECTS

Treatment with ECT requires informed written consent. The doctor must also sign to the
effect that a full explanation of ‘the procedure, benefits and dangers of ECT’ has been
given (Royal College of Psychiatrists, 1989). Preferably obtain consent from a relative
also. The patient may withhold consent at any time during the course of treatment.
There has been improved care in delivery of ECT in response to Royal College of
Psychiatrists guidelines (1989). However, there is still insufficient consultant partici-
pation and training of juniors (Pippard, 1992).
US guidelines are rigorous (APA, 1990). EEG monitoring is required, and specialist
training and periodic recertification is necessary.
Patient refusal
What happens if the patient refuses treatment or is unable to understand what is pro-
posed? The patient’s right to refuse treatment must be weighed against his/her right to
receive treatment, where the ability to make a rational decision about his/her well-
being is impaired.
PSYCHOSURGERY 293
Under s.58 of the Mental Health Act 1983, ECT is a treatment requiring consent or a
second opinion, in the case of detained patients. A second opinion must be sought if
the patient is unable to give informed consent, refuses or withdraws consent. The opin-
ion is given by a medical practitioner appointed by the Mental Health Commission.
OTHER FORMS OF PHYSICAL STIMULATION
VAGUS NERVE STIMULATION (VNS)
This affects concentrations of serotonin, norepinephrine, ␥-aminobutyric acid and

glutamate. VNS has been shown to significantly improve depressive symptoms in
treatment-resistant depression in about one-third of patients. Response is usually seen
after about 6 weeks of stimulation.
The greater the treatment-resistance (i.e. non-responders to ECT, higher number of
unsuccessful trails of antidepressants), the less likely is the patient to improve with VNS.
SIDE-EFFECTS OF VNS
• Mild voice hoarseness (related to the electric current intensity); headache; dyspha-
gia; neck pain; coughing; dyspnoea on exertion (related to the electric current
intensity).
• Overall, VNS is well tolerated and the side-effects not related to current intensity
resolve after time in the majority of patients.
• Unlike ECT, VNS has no associated cognitive side-effects.
DEEP BRAIN STIMULATION (DBS)
DBS is used for the treatment of tremor in Parkinson’s disease. Electrodes are
implanted into the subthalamic nucleus or thalamus. Stimulation is via a pacemaker-
like device inserted on the anterior chest wall. High-frequency electrical stimulation
deactivates basal ganglia regions.
TRANSCRACNIAL MAGNETIC STIMULATION (TMS)
This provides non-invasive electrical stimulation of the brain, is well tolerated and has
been shown to improve depressive symptoms in numerous studies. A recent study on
bipolar depression showed no separation from sham treatment (Nahas et al., 2003).
Research continues into the treatment parameters and patient populations for TMS.
PSYCHOSURGERY
DEFINITIONS
• WHO – The selective surgical removal or destruction … of nerve pathways … with
a view to influencing behaviour.
• US National Commission for the Protection of Human Subjects of Biomedical and

Behavioural Research – Brain surgery on (i) normal brain tissue of an individual
who does not suffer from any physical disease, for the purpose of changing or con-
trolling the behaviour or emotions of such individual; or (ii) diseased brain tissue of
an individual, if the primary object of the performance of such surgery is to control,
change or affect any behavioural or emotional disturbance of such individual.
HISTORY
• 1875 – Ferrier removed frontal lobes of monkeys and noticed marked changes in
animal’s ‘disposition’ and ‘character’ with no effect on motor or sensory abilities.
• 1936 – Moniz performed a localized division of prefrontal tracts in a series of 20
patients. There was a claimed reduction in severe and chronic agitation without
marked side-effects.
• 1942 – Freeman and Watts introduced the ‘standard’ cut leucotomy involving wider
severing of prefrontal connections. It was an imprecise, nearly ‘blind’ operation,
with serious side-effects: epilepsy, incontinence, marked apathy with flattened
affect, disinhibition, intellectual impairment and aggression. Mortality was 6 per cent.
– At least 10 000 were performed between 1942 and 1952 in the UK, usually for
chronic illness with disturbed behaviour, unresponsive to other treatments –
66 per cent schizophrenia, 33 per cent affective disorder.
– ‘Modified’ operations were later designed to ablate more specific brain targets
without producing side-effects associated with the cruder ‘standard’ procedure.
• 1949 – Scoville introduced orbital undercutting. A modified form was used exten-
sively in the UK by Knight, who restricted orbital undercut to medial half of lobe.
• 1950s – The advent of effective psychotropic drugs with fuller documentation of
side-effects led to rapid decline of psychosurgery.
• 1961 – Only 11 British hospitals reported performing more than 10 leucotomies.
MODERN PROCEDURES
Modern surgery is highly selective, most often using radioisotopes (yttrium implants),
ultrasound, or electrocautery under stereotactic guidance by MRI and CT.
• Procedures for anxiety/OCD – cingulotomy, subcaudate tractotomy, limbic leuko-
tomy, capsulotomy.
• Procedure for depression with anxiety – subcaudate tractotomy.
• Procedures for Parkinson’s disease – thalamotomy, pallidotomy.
• Also for Parkinson’s disease – transplantation of embryonic mesencephalic or
genetically engineered autologous cells into the basal ganglia which synthesize
tyrosine hydroxylase.
INDICATIONS FOR PSYCHOSURGERY

It is rarely appropriate and is the treatment of last resort, after:
• Failed, adequate pharmacological treatment.
• Failed ECT (in refractory depression).
• Failed behavioural therapies (in refractory OCD).
• Failed psychosocial interventions.
• Failed pharmacotherapy for Parkinson’s.
Chronic intractable OCD is currently the main indication. There must be compre-
hensive presurgical evaluation including further pharmacological trials if indicated.
Psychosurgery is contraindicated if there is substance abuse, organic brain damage,
co-morbid personality disorder, insufficient evaluation or prior treatment.
PROGNOSIS AND OUTCOME

The prognosis is good if cases are carefully selected. Pharmacological and behavioural
treatments are usually continued, so that the apparent efficacy may reflect the primary
effect of surgery and/or synergism with ongoing treatments. There have been insuffi-
cient controlled trials because they are ethically difficult to do.
• Improvement may be gradual for even the first 2 years.
• 50–70 per cent show improvement.
• Fewer than 3 per cent get worse.
• No mortality now (high mortality in the 1950s and 1960s).
• 1 per cent epilepsy rate – controllable with medication.
• 6 per cent apathy/amotivation.
• 6 per cent personality change.
ETHICAL AND LEGAL ASPECTS

Under the UK Mental Health Act 1983, psychosurgery is considered a ‘treatment
which gives rise to special concern’ – this applies to formal and informal patients. It
requires consent and a second opinion by an independent doctor (appointed by the
Mental Health Commission) who must consult the nurse and other team member
(neither doctor nor nurse) involved with treating the patient.
American Psychiatric Association Task Force on ECT (1990) The Practice of ECT: Recommendations
for Treatment, Training and Privileging. APA, Washington, DC. (Summary of recommendations
in Convulsive Therapy (1990) 6, 85–120.)
Bridges PK, Bartlett JR, Hale AS (1994) Psychosurgery: stereotactic subcaudate tractomy, an
indispensable treatment. Br. J. Psychiatry 165, 599.
Brodaty H, Berle D, Hickie I, Mason C (2001) ‘Side effects’ of ECT are mainly depressive phe-
nomena and are independent of age. J. Affec. Disord. 66, 237.
Conway CR, Chinbnall JT, Li X, George MS (2002) Changes in brain metabolism in response to
chronic vagus nerve stimulation in depression. Biol. Psychiatry 51, 85.
Cosgrove GR, Rauch SL (2003) Stereotactic cingulotomy. Neurosurg. Clin. North Am. 14, 225.
Dougherty DD, Baer L, Cosgrove GR et al. (2002) Prospective long-term follow-up of 44 patients
who received cingulotomy for treatment-refractory obsessive–compulsive disorder. Am. J.
Eranti SV, McLoughlin DM (2003) Electroconvulsive therapy: state of the art. Br. J. Psychiatry 182, 8.
George MS, Nahas Z, Bohning DE et al. (2002) Vagus nerve stimulation therapy: a research
update. Neurology 59 (Suppl. 4), s56.
George MS, Nahas Z, Lisanby SH et al. (2003) Transcranial magnetic stimulation. Neurosurg.
Gershon AA, Dannon PN, Grunhaus L (2003) Transcranial magnetic stimulation in the treatment
of depression. Am. J. Psychiatry 160, 835.
Gilbody S, Whitty P, Grimshaw J, Thomas R (2003) Educational and organizational interventions

to improve the management of depression in primary care: a systematic review. JAMA 289,
3145.
Greenberg BD, Murphy DL, Rasmussen SA (2000) Neuroanatomically based approaches to
obsessive–compulsive disorder: neurosurgery and transcranial magnetic stimulation.
Hoppe C, Helmstaedter C. Schermann J, Elger CE (2001) No evidence for cognitive side effects
after 6 months of vagus nerve stimulation in epilepsy patients. Epilepsy Behav. 2, 351.
Katona CL (2001) Psychotropics and drug interactions in the elderly patient. Int. J. Geriatr. Psych.
16 (Suppl. 1), s86.
Lomarev M, Denslow S, Nahas Z et al. (2002) Vagus nerve stimulation (VNS) synchronized
BOLD fMRI suggests that VNS in depressed adults has frequency and/or dose dependent
effects. J. Psychiatry Res. 36, 219.
Marangell LB, Rush AJ, George MS et al. (2002) Vagus nerve stimulation (VNS) for major
depressive episodes: one year outcome. Biol. Psychiatry 51, 280.
Mathews K, Eljamel MS (2003) Status of neurosurgery for mental disorder in Scotland: selective
literature review and overview of current clinical activity. Br. J. Psychiatry 182, 404.
Mathews K, Eljamel MS (2003) Vagus nerve stimulation and refractory depression: please can
you switch me on doctor? Br. J. Psychiatry 183, 181.
Nahas Z, Kozel FA, Li X et al. (2003) Left prefrontal transcranial magnetic stimulation (TMS)
treatment of depression in bipolar affective disorder: a pilot study of acute safety and efficacy.
Bipolar Disord. 5, 40.
Philpot M, Treloar A, Gormley N, Gustafson L (2002) Barriers to the use of electroconvulsive
therapy in the elderly: a European survey. Eur. Psych. 17, 41.
Pippard J (1992) Audit of electroconvulsive treatment in two National Health Service regions.
Raoul S, Faighel M, Rivier I et al. (2003) Staged lesions through implanted deep brain stimulating
electrodes: a new surgical procedure for treating tremor or dyskinesias. Mov. Disord. 18, 933.
Rasmussen KG, Rummans TA, Richardson JW (2002) Electroconvulsive therapy in the medically
ill. Psychiatr. Clin. North Am. 25, 177.
Rocchi L (2002) Effects of deep brain stimulation and levodopa on postural sway in Parkinson’s
disease. J. Neurol. Neurosurg. Psychiatry 73, 267.
Rose D, Fleischmann P, Wykes T et al. (2003) Patients’ perspectives on electroconvulsive therapy:
systematic review. BMJ 326, 1363.
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Gaskell, London.
Russel E (2001) Running an ECT department. Adv. Psychiatr. Treat. 7, 57.
Sackeim HA, Rush AJ, George MS et al. (2001) Vagus nerve stimulation (VNS) for treatment-
resistant depression: efficacy, side effects and predictors of outcome. Neuropsychopharmacology
25, 713.
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thalamotomy and thalamic stimulation. Neurology 59, 1232.
UK ECT Review Group (2003) Efficacy and safety of electroconvulsive therapy in depressive
disorders: a systematic review and meta-analysis. Lancet 361, 799.
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electroconvulsive therapy in depressed elderly. The Cochrane Library, issue 2.
Psychotherapy 23
GENERAL ASPECTS
Psychotherapy is the development of a trusting relationship, which allows free com-

munication and leads to understanding, integration and acceptance of self.
COMMON FEATURES OF PSYCHOTHERAPIES (JEROME FRANK)

1 An intense, emotionally charged relationship with a person or group.
2 A rationale or myth explaining the distress and methods of dealing with it.
3 Provision of new information about the future, the source of the problem and pos-
sible alternatives which hold a hope of relief.
4 Non-specific methods of boosting self-esteem.
5 Provision of success experiences.
6 Facilitation of emotional arousal.
7 Takes place in a locale designated as a place of healing.
DIFFERING LEVELS OF PSYCHOTHERAPY

Informal As between friends and relatives and in self-help groups.
Formal
• Supportive – to restore or maintain the status quo. Useful in:
– Those in crisis for whom change is not desired.
– The emotionally severely handicapped who are not expected to improve greatly.
• Dynamic – to effect change in the individual. Uses:
– Confrontation of defences.
– Clarification.
– Interpretations – new formulations of problems.
PSYCHOANALYSIS
DEFINITIONS AND KEY TERMS

• Psychoanalysis – both (i) a psychological theory of the mind and (ii) a psychothera-
peutic treatment method.
298 PSYCHOTHERAPY
• Libido – now used to mean overall mental ‘energy’ or drive.

• Love object – person or thing towards which the libido is directed (or ‘cathected’).
• Actual neurosis – caused by physical damming-up of sexual urges (e.g. neurasthenia).
• Psychoneurosis – caused by psychological damming-up of fundamental instinctive
urges in a conflict situation (e.g. hysteria).
• Dream work – the process which turns the hidden ‘latent dream thoughts’ into the
reported ‘manifest content of the dream’. It consists of:
– Condensation – the manifest content shows ‘over-determinism’.
– Displacement.
– Dramatization.
– Symbolization.
– Secondary elaboration.
• Parapraxes – apparent errors or omissions in everyday life which symbolize under-
lying attitudes. They may be:
– Symptomatic – the emotional urge is not repressed at all.
– Disturbed – incomplete repression is present.
– Completely inhibited – with complete repression.
• The ego – that part of the individual which is in direct touch with reality.
• Ego functions:
– Relationships with reality: adaptive; reality testing; maintenance of a sense of
reality.
– Regulation and control of drives (‘libido theory’).
– Relationships with other people (‘object relations theory’).
– Cognitive.
– Defensive.
– Synthetic – the ability to hold together as a person.
– Autonomous – derived from autonomous energies of the ego.
• Ego defence mechanisms – habitual, unconscious and sometimes pathological men-
tal processes which are employed to resolve conflict between instinctive needs,
internalized prohibitions and external reality.
– Repression – the basic ego defence mechanism; refusal to recognize internal
reality; prevents the perception of instincts and feelings, with unconscious
inhibition of the conflicting impulse.
– Denial – refusal consciously to recognize external reality.
– Projection – attribution of one’s own unacknowledged feelings to others. May be
of delusional strength.
– Distortion – grossly reshaping external reality to suit inner needs.
– Reaction formation – feeling or behaving in a way which is the opposite of
unacceptable instinctual impulses.
– Turning against the self – unacceptable aggression towards others is
expressed, indirectly, towards the self. Seen in passive aggressive individuals and
hypochondriasis.
– Displacement – redirection of feelings towards a less cared-for object.
– Projective identification – dissociation of unacceptable parts of the personality
and projection on to another, resulting in identification with the other.
– Acting out – direct expression of an unconscious impulse in order to avoid
awareness of the accompanying affect.
PSYCHOANALYSIS 299
– Intellectualization – thinking about rather than feeling instinctive desires.

– Sublimation – a healthy coping mechanism; indirect expression of instincts
without adverse consequences.
– Splitting – the positive and negative fantasized relationships remain alternatively
in consciousness, with the alternative dissociated.
– Isolation – the separation of an idea from its associated affect.
• Transference – a repetition of the past which is inappropriate to the present.
Transfer of unconscious memories into consciousness. So, in therapy, transference
is the shifting of an emotional attitude from a past object or person on to the
therapist.
• Countertransference – the therapist’s emotional attitudes towards the patient.
• Therapeutic or working alliance – the normal, adult relationship between therapist
and patient. The therapeutic alliance leads to the transference neurosis which leads
to the countertransference. The transference neurosis is interpreted to the patient;
the countertransference may or may not be.
• ‘Working through’ – repeatedly experiencing a conflict, in the transference situ-
ation, so that it may be resolved.
Mental states associated with ego defence

• Hysteria – denial, projection, identification.
• Obsessional conditions – isolation, magic undoing, reaction formation.
• Paranoia – projection and splitting.
• Depression – turning on the self.
• Phobias – displacement of affect.
Components of repression
• Dissociation from the self of the unconscious idea leads to –
• Failure of comprehension of the enacted idea, so there is then –
• Unresponsiveness to feedback, and acts are not regulated (leading to repetition
compulsion).
But there is still the:
• Abnormal motivational state – since unconscious motivation still drives the acts.
There is also:
• Repression of memory – but the data are preserved in the unconscious and normal
forgetting is prevented.
PSYCHOANALYTIC TECHNIQUES FOR UNDERSTANDING THE UNCONSCIOUS

• Free association – of words and thoughts.
• Interpretation of dreams.
• Exploration of parapraxes.
Suitability for dynamic psychotherapy
1 The patient’s problem must be understandable in psychological terms.
2 The patient must be willing and able to understand his/her problems in psycho-
logical terms. A test interpretation may be used to assess the patient’s response.
300 PSYCHOTHERAPY
Table 23.1 Stages of sexual development

Age Stage
0–1 years Oral Breast is the love object

Gratification is by oral means
Basic trust develops
1–3 years Anal Gratification is achieved by control over defecation
A sense of self develops
Transitional object leads to:

3–5 years Phallic (Oedipal) Genital gratification leads to Oedipal mother and father object
relationships
5–12 years Latency period
12–20 years Puberty Sexual drives reawoken by hormonal changes
20⫹ years Adult sexual development
3 The patient must have adequate ‘ego strength’ – the ability to cope with the ten-
sions arising from inner conflict.
4 The patient must be able to form and sustain a psychotherapeutic relationship.
SEXUAL DEVELOPMENT
See Table 23.1.
• Oedipal complex – after the Greek tragedy in which Oedipus unknowingly killed
his father and married his mother. Signifies rivalry between son and father for
mother’s affection. The son imagines he will be castrated as a punishment.
• Electra complex – equivalent rivalry between daughter and mother, arising out of
daughter’s fear that she has been castrated.
Castration anxiety in males resolves the Oedipal complex and leads to the latency
period. Castration anxiety in females begins the Electra complex.
• Primary process thinking is unconscious and is based on the pleasure principle (the
libidinal drive for satisfaction).
• Secondary process thinking is conscious and is based on the reality principle (which
takes into account the social pressures).
There are two basic theories: instinct (libido) theory versus object relations theory;
i.e. the need to reduce instinctual drives versus the importance of the subject’s need to
relate to objects.
IMPORTANT PSYCHOANALYTICAL THEORISTS
EARLY THEORISTS
Freud (1856–1939)
Development of his theories:
1 The cathartic model (‘psychic abscess’) – therapy releases the blocked emotions. See
Studies in Hysteria (Breuer and Freud, 1895).
IMPORTANT PSYCHOANALYTICAL THEORISTS 301
2 The topographical model – unconscious, preconscious and conscious levels of the

mind. See The Interpretation of Dreams (Freud, 1900) and The Psychopathology of
Everyday Life.
3 The structural model – id, ego and superego. The balance of these three makes up the
character structure. This model also includes Eros, the life instinct, and Thanatos, the
death instinct. See Mourning and Melancholia, Beyond the Pleasure Principle and
The Ego and the Id (Freud, 1923).
Adler (1870–1937): School of Individual Psychology

Adler propounded theories of:
• Organ inferiority and psychic compensation.

• Fictive goals.
• Drive for superiority – importance of power and social significance in psycho-
dynamics.
Adler’s work was integrated into schools of ego psychology.
Jung (1875–1961): School of Analytical Psychology

Jung propounded three levels of psyche:
• Conscious – includes the persona.

• Personal unconscious.
• Collective unconscious (racial, universal).
The persona is the outer crust of the personality, which is the opposite of the per-
sonal unconscious on dimensions of:
• Thinking/feeling.
• Sensuousness/intuition.
• Extrovert/introvert (related to direction of flow of mental energy).
Archetypes are generalized symbols and images within the collective unconscious.
They include:
• Animus – the unconscious, masculine side of the woman’s female persona.

• Anima – the unconscious, feminine side of the man’s male persona.
A complex is a group of interconnected ideas which arouse associated feelings and
effect behaviour.
Wilhelm Reich
• Neurosis results from sexual frustration.
• Body armour. Orgone energy accumulator.
• Recently developed into bioenergetics.
Otto Rank
• Neurosis originates in the trauma of birth.
302 PSYCHOTHERAPY
NEO-FREUDIANS (USA)
Neo-Freudians were influenced by Adler to shift emphasis from:

• Biological to social processes.
• Intrapsychic to interpersonal processes.
• Past history to ‘here and now’.
Horney
Horney attributed sexual difficulties (especially female difficulties) to social rather
than biological causes.
Fromm/Stack-Sullivan
The self consists of:
• The ‘reflected appraisals’ of others.
• The roles it has to play in society.
In therapy there is ‘consensual evaluation’ – therapist and patient interact to valid-
ate each other’s experience.
BRITISH SCHOOLS
These are particularly involved with child analysis.
Anna Freud
• Ego psychology and the importance of ego defence mechanisms.
• Psychotherapeutic relationship with the child is more educational.
Melanie Klein
• Worked with pre-oedipal children using play analysis. Ego and its defence mech-
anisms are present from birth and the superego before the age of 2 years.
• Paranoid position develops first. There is splitting of good and bad aspects. The
good aspects of mother are introjected but are threatened by the externalized bad
aspects – leads to rage, fear and hatred.
• Depressive position develops next. The realization that mother is both good and
bad leads to guilt and fear of destroying the loved one with the hatred.
Bowlby
Bowlby’s work on maternal depreviation pointed to the importance of separation anx-
iety, with stages of:
• Protest.
• Despair.
• Detachment.
IMPORTANT PSYCHOANALYTICAL THEORISTS 303
POST-FREUDIANS AND THE NEW PSYCHOTHERAPIES

(‘GROWTH THERAPIES’, ‘HUMAN POTENTIAL MOVEMENT’)
Winnicot (1896–1971)
• Development of object relations theory, with Fairbairn, Guntrip and others.
Satisfaction is sought in relationships, not only in sexual relief.
• Personality develops from internalized early relationships, particularly with the
mother (‘good-enough mother’). Transitional objects are intermediate between
oral eroticism and true object relationships.
Erikson
Erikson underlined the importance of psychosocial development and the adolescent
identity crisis.
Rogers (1951): client-centred therapy and the Encounter movement

The therapist, by use of (i) genuineness, (ii) unconditional positive regard and
(iii) accurate empathy shows his/her acceptance of the client’s real self, thus leading to
reduction of the client’s discrepancy between real self and ideal self.
In Encounter groups, non-directive acceptance leads to exposure of emotions, lead-
ing to ‘basic encounters’ in which there is emotional and intellectual contact between
individuals.
Perls: Gestalt therapy

The therapist emphasizes awareness of here-and-now needs and how they are blocked,
by the use of various techniques (e.g.‘hot seat’ work,‘doing a round’). The client may thus
experience himself/herself as an organized whole (‘Gestalten’). See Perls et al. (1973).
Berne (1964): transactional analysis

The therapist explores, with the client, the ‘games’ that he/she plays with others and
the ‘scripts’ which he/she has made for his/her life. Based on a view of the personality
as consisting of parent, adult and child ego states.
Frankl: existential logotherapy

The therapist seeks to bring spiritual realities to awareness and uses paradoxical inten-
tion. This is based on the view that the individual is searching for meaning and purpose.
Others
• Ellis – rational–emotive therapy.
• Assagioli – psychosynthesis.
• Moreno – psychodrama.
• Janov – primal therapy.
• Maslow – self-actualization.
THE INTERNATIONAL APPROACH
An international approach has developed from the ideas of Adler, Stack-Sullivan and
Bateson and also from studies of control systems in physics and physiology.
304 PSYCHOTHERAPY
• Cybernetics – theory of control and communication between the individual and

machine. This developed into –
• General systems theory (von Bertalanffy) – used particularly in family therapy, with
the concept of concentric and overlapping systems and subsystems of interacting
individuals.
System process
1 Within a system there is maintenance of homeostasis whenever possible. But there
may be –
2 Crisis due to external challenge. This may lead to –
3 Exploration of the problems. This may lead to –
4 Reorganization and a new homeostasis.
Family therapists Family therapists may be:
• Conductors – acting as authority figures to alter family systems by persuasion or
criticism.
• Reactor analysts – experiencing the family conflicts by entering into them, to attain
greater understanding.
• Systems purists – analysing the subsystems and family rules and feeding this back to
the family without becoming involved.
Crisis intervention developed from this model. At the time of crisis there is max-
imum possibility for a change of the system for the better.
Key names Haley, Minuchin, Ackerman, Satir, Laing.
Crisis intervention (Caplan)

Common features of the crisis intervention:
1 Fast provision of service.
2 Intensive short-term work, with rapid withdrawal of help.
3 Here-and-now therapy, specific goals, exploration of all possibilities.
4 A more active, confronting therapeutic style.
This may operate by phone service, walk-in centre, self-help centre or multidisci-
plinary domiciliary teams.
GROUP THERAPIES
Groups may be simply supportive self-help groups and social clubs.
ANALYTIC GROUPS
Analysis in the group

This is treatment of the individual within a group setting.
Analysis of the group (Tavistock Institute groups)

The leader is inactive and interprets purely the transference relationship of the whole
group to himself/herself. Two writers on this type of group are Bion and Ezriel.
GROUP THERAPIES 305
Bion Two methods of working:

• Work groups – consciously working on a task.
• Basic assumptions group – defensive group cultures block the work of the group.
These cultures are:
– Dependency – the assumption that solutions are provided by the leader.
– Fight–flight – the assumption of threat to the group.
– Pairing – the assumption that a new leader will arise.
Ezriel Common group tensions are based on three levels of relationship with the leader:
1 Required (superficial).
2 Avoided.
3 Calamitous (in fantasy).
Analysis through and of the group (Institute of Group Analysis: Foulkes)

Groups function at three levels:
1 Current adult relationships.
2 Individual multipersonal transference relationships.
3 Hared feelings and fantasies.
CURATIVE FACTORS IN GROUPS (YALOM, 1985)

• Interpersonal learning.
• Catharsis.
• Group cohesiveness.
• Insight.
• Development of socializing techniques.
• Existential awareness.
• Universality.
• Instillation of hope.
• Altruism.
• Corrective recapitulation of primary family group.
• Guidance.
• Imitative behaviour.
THERAPEUTIC COMMUNITIES
In these there is open communication and shared examination of problems.
• Main, of the Northfield Clinic, made first use of the term in 1946.
• Maxwell-Jones – Henderson Hospital.
• Rapoport – basic features are:
– Democratization – abolition of hierarchy.
– Permissiveness – tolerance of disturbed behaviour.
– Reality confrontation – regular feedback to individuals of the results of their
behaviour.
– Communalism – equal shares for all.
306 PSYCHOTHERAPY
BEHAVIOURAL TREATMENTS
There are two basic theories:
1 Pavlovian – classic conditioning: association of conditioned stimulus (CS) with

unconditional stimulus (UCS) to produce the response.
2 Skinnerian – operant conditioning: alteration of the frequency of a piece of spon-
taneous behaviour by reward or punishment.
These two strands were brought together by Mowrer: the double learning theory (see
diagram below).
UCS Response Avoidance Reduction of fear

(fear)
CS
Reward
Pavlovian Skinnerian
BEHAVIOURAL TREATMENTS
These involve:
• Learning theory principles.
• Precise observation of behaviour.
• Concentration on symptoms.
• An empirical approach.
• Directive treatment methods.
• Clear goals.
• Objective evaluation of results.
USES OF BEHAVIOURAL TREATMENTS

They have been shown to be useful in:
• Single phobias – desensitization and flooding.
• Obsessional states – response prevention.
• Marital problems – contract therapy.
• Sexual inadequacy – Masters and Johnson techniques.
• Sexual deviancy – aversion, covert sensitization.
• Chronic schizophrenia – token economy.
• Mental subnormality – ‘behaviour modification’.
• Enuresis – ‘pad and bell’.
SOME PRINCIPLES
Premack principle Any frequently performed piece of behaviour can be used as a
positive reinforcer of the desired behaviour.
COGNITIVE THERAPY 307
Intermittent reinforcement This is more resistant to extinction than continuous

reinforcement.
Shaping This involves successive approximations to the required behaviour, with
contingent positive reinforcement.
COGNITIVE THERAPY
See also Chapter 4.

Like behaviour therapy, cognitive therapy uses directive methods and deals with pre-
sent problems. Unlike behaviour therapy, it regards inner attitudinal factors as vitally
important and seeks to change these.
Maladaptive internal habits of thought and self-statements are identified and alter-
natives suggested and ‘tried out’ in fantasy (Meichenbaum).
Irrational beliefs may be exposed and strongly confronted with ‘reason’
(‘rational–emotive’ therapy of Ellis).
Beck in particular has introduced cognitive theory and therapy into the under-
standing and treatment of depression.
COGNITIVE THEORY OF DEPRESSION

Depression results from a network of negative attitudes to the self, the future and the
world. Such cognitive distortions (‘silent assumptions’) arise from early traumatic
experiences and show four basic types of error:
• Arbitrary inference – always drawing the worst conclusions from a situation.
• Selective abstraction – focusing on the worst aspects of a situation.
• Over-generalization – drawing general conclusions about personal worth from one
example.
• Minimization and magnification – performance is underestimated and errors are
overestimated.
Such errors confirm attitudes of self-blame and hopelessness.
As a description of thinking in a depressive episode, this has much validity; but as a
causal theory it is not proven. Between episodes these errors may not be present.
‘COGNITIVE RESTRUCTURING’
Depressive cognitions (‘automatic thoughts’) are identified from present or recent
experiences. The patient is then encouraged to challenge those assumptions and
express alternatives. The person keeps a record of automatic thoughts and possible
alternatives. Reality testing, graded test assignments, role rehearsal (trying out the new
cognitions and behaviour), activity scheduling with experience of success and social
skills training are all used to support the cognitive restructuring.
COGNITIVE–BEHAVIOURAL THERAPY (CBT)

This is now an established modality in depression (Chapter 4), anxiety disorders
(Chapter 5), eating disorders (Chapter 7), and in schizophrenia (Chapter 3) to treat
persistent symptoms and to improve compliance (‘compliance therapy’).
308 PSYCHOTHERAPY
VARIATIONS
Interpersonal therapy (IPT ) Initially developed for depression (see Chapter 4). The
focus is on grief, interpersonal role disputes, interpersonal skill, life role and
transitions; also useful in bulimia nervosa.
Dialectic behavioral therapy (DBT) A form of cognitive behavioural therapy used
for borderline personality disorder (see Chapter 6). The focus is on emotional regula-
tion, distress tolerance and validation.
Motivational enhancement therapy (MET) Used for substance abuse (see Chapters
9 and 10). The focus is on the client’s motivation to change and plan for change.
PSYCHOTHERAPY RESEARCH
• ‘Outcome’ research is assessment of results of psychotherapy.

• ‘Process’ research is examination of how results are achieved.
METHODOLOGICAL PROBLEMS
Methodological problems have proven almost insuperable. There are many possible
confounding variables:
• Patients – diagnosis, severity, age, IQ, culture, personality type, motivation, expect-
ation of therapy, attendance, current life circumstances, spontaneous recovery rates.
Appropriate controls are required.
• Therapists – precise techniques used, personality type, level of experience, length of
therapy. The interaction of patient and therapist variables.
• Outcome – assessed by whom (patient, therapist, observer) and how (self-report,
family report, video observation, MMPI, PSE, etc.)? Length of follow-up?
Multicentre trials particularly have failed either because of insufficient standardiza-
tion or because rigorous standardization has prevented progress (e.g. Maudsley/
Tavistock study of 1972).
Several large-scale ‘meta-analyses’ of outcome research have been published.
OUTCOMES
Given the above provisos, all forms of psychotherapy seem to give a general remission
rate of 65 per cent.
Bloch (1979) suggests seven factors are predictive of good progress in therapy:
1 A reasonable degree of personality integration and functioning.
2 Motivation for change.
3 Realistic expectations based on psychological mindedness (this can be improved
by preparatory interviews).
4 At least average intelligence.
5 Neuroses and mild personality disorders (not psychoses).
6 Strong affect is present (especially anxiety or depression).
7 Life circumstances are free of unresolvable crises.
PSYCHOTHERAPY RESEARCH 309
Compare this list with the traditional (YAVIS): young, attractive, verbal, intelligent,
successful.
Freud and others advocated a ‘trial interpretation’ to assess acceptance.
Sloane et al. (1975) conducted a comparative trial of (i) behaviour therapy, (ii) psy-
choanalysis and (iii) waiting list in anxiety states. Behaviour therapy showed 93 per
cent improved at the end of therapy. Short-term psychoanalysis showed 73 per cent
improved. On the waiting list, again, 73 per cent improved.
In 101 studies of outcome of psychotherapy up to 1970, 81 showed favourable out-
come and 20 did not.
Eysenck (1952) reported a spontaneous remission rate of 70 per cent in 2 years.
Analysts’ recovery rates were between 44 and 64 per cent in 2 years.
Malan (1977) proposed that ‘spontaneous remission’ after a first interview may be
due to:
• Insight gained.
• Realization of personal responsibility.
• Genuine reassurance.
• Joining with ‘significant other’.
THE PROCESS
Most studies show the personality, enthusiasm and involvement of the therapist and
the therapist–patient interaction to be far more important than the theoretical form
of therapy.
Therapist skills
A trained analyst may do no better than concerned, intelligent, thoughtful people (e.g.
college professors). Accurate empathy, unconditional positive regard and genuineness
(congruity) are said to be related to good outcome, but are unreliably measured
(Truax and Carkhuff, 1967).
Yalom (1985) found negative group therapy factors: ‘aggressive stimulator’ type of
leader, attack by the leader, rejection by the group. Exploitiveness and disinterest from
the therapist are negative factors.
Transference
Malan found early development of therapist/parent transference, encouraged by inter-
pretations relating to early parent relationships, to predict good outcome. Working
through termination of therapy is important.
Arousal
Sifneos and other proponents of brief psychotherapy regard emotional arousal as vital
to success. Jerome Frank has pointed to its relevance in all forms of psychotherapy.
Assessment by patients
Malan wrote that patients valued warmth and individual attention. Patients disliked
therapists who did not support or advise. No patient remembered an analytic-group
interpretation.
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Community-orientated 24
psychiatry
HISTORICAL REVIEW
Large institutions were initially a humanitarian response to appalling conditions of

private madhouses, prisons and workhouses where the community ‘cared’ for its men-
tally ill. Originally, the concept of an asylum was as a place of ‘sanctuary’. There was an
early optimistic phase of non-restraint – ‘moral’ treatment.
PROBLEMS WITH LARGE INSTITUTIONS

• They were isolated from the communities they served, with a self-sufficient sub-
culture of their own.
• There was selective intake of chronically ill, behaviourally disturbed and socially
unsupported individuals.
• Institutionalization (Wing and Brown, 1970):
– Social understimulation – encourages inactivity and social withdrawal.
– Restriction of independence – leads to lack of initiative and drive.
– Authoritarianism and pauperism – underline individuals’ status as bottom of
the social hierarchy.
– Loss of skills – little training in domestic, practical or social skills.
– Depersonalization – loss of sense of individual identity.
DECARCERATION
The modern concept of reorientation of care away from large institutions was based
on principles of community mental health care:
• Locally based, accessible services.
• A comprehensive and integrated range of therapeutic interventions and resources
for range of mental health needs.
• Services delivered by locally based community mental health teams (CMHT).
Multidisciplinary teamwork involves medical and nursing staff, behaviour ther-
apists, psychologists, occupational therapists and social workers.
• Mental health teams work closely with, or integrated with, primary care teams.
RECENT DEVELOPMENTS IN COMMUNITY CARE 313
RECENT DEVELOPMENTS IN COMMUNITY CARE
1 ‘Assertive outreach’ models incorporating intensive community follow-up and

home treatment programmes, continued ‘down-sizing’ of mental hospitals, and
expansion of daycare facilities.
2 Targeting of resources to patients with enduring psychiatric illness.
3 Fully operational key worker programmes – incorporated in the UK into the ‘Care
Programme Approach (CPA). A named keyworker is responsible for a range of
agreed treatment objectives. Also, development in the UK of care management: a
worker supervises care for particularly vulnerable individuals across a range of
resources.
4 Users and carers have a crucial role in the planning, development and management
of mental health services through patient advocacy groups.
5 Promotion of the recovery model:
– Focus on patients’ strengths, not their disabilities.
– Focus on patients’ life aspirations.
– Focus less on the medical.
– Hope, autonomy and desire are key elements.
– Recognize the value of peer support and peer treatment programmes in helping
patients recover.
6 Training in the Community Living Programme (Stein and Test) and the successor
Programme of Assertive Community Treatment (PACT). Developed in Madison,
Wisconsin – embraces most of the principles of modern community mental health
care noted above. The assertive community treatment (ACT) model is the most
effective. ACT components include:
– High staff:patient ratio.
– 24-hour availability.
– Outreach to patient, with frequent (daily, or 3–5 visits/week) contact.
– Functional outcomes (patient satisfaction, level of social/vocational activities,
continued community tenure without rehospitalization) more important than
symptom outcomes.
7 Home-based treatment projects. Most are a development of the Stein and Test
model. Muijen et al. (1992) showed that at 3-month follow-up, the experimental
home-treatment group had fewer admissions, shorter length of stay, improved
clinical and social outcome compared with control groups offered standard
treatment. Home treatment was preferred (but only marginally) by patients
and relatives. There were similar findings in other programmes (Sparkbrook, UK;
Sydney, Australia).
POLICY INITIATIVES
State hospital beds in the USA have been declining in number:

• 1955 – 339 per 100 000 population.
• 1992 – 41 per 100 000 population.
• 1998 – 24 per 100 000 population.
314 COMMUNITY-ORIENTATED PSYCHIATRY
An estimate of inpatient bed requirements per 100 000 population in the UK is:
• Acute – 25.
• Substance abuse – 3.
• Medium-stay – 8.
• Long-stay and rehabilitation – 20.
Resources (as a percentage of gross domestic product) have not changed dramatically:
• In the UK – 0.26 per cent in 1960, 0.33 per cent in 1985.

• In the USA – 0.33 per cent in 1960, 0.32 per cent in 1985.
Mental disorders are a major cause of morbidity. They account for 14 per cent
reported days off work and for 23 per cent of British National Health Services inpa-
tient costs.
There are national and international efforts to:
• Reduce the incidence of suicide.

• Detect and treat mental illness early in children.
• Change health behaviour and public awareness to decrease drug and alcohol
abuse.
• Better integrate mental health and physical medicine services.
• Provide more community-based residential alternatives to reduce excess of men-
tally ill (the ‘transtutionalized’) in nursing homes, jails, long-stay facilities, acute
inpatient beds, and reduce homelessness.
• Continue to combat the stigma of and discrimination against mental illness.
OTHER IMPORTANT ISSUES IN COMMUNITY PSYCHIATRY
• Continuity of care.
• Implementation of evidence-based mental health best practice.
• Cost containment and resource allocation (distinguishing clinical ‘effectiveness’
from efficacy).
• Providing integrated (mental health and addiction) services for persons with dual
diagnosis (co-occurring mental disorder and alcohol/drug addiction).
• Development and integration of recovery model services, including peer support
programs.
• Multidisciplinary teamwork with the consultant seen as a fundamental part of the
service.
• Need for more community psychiatric nurses and clinical psychologists.
• Need for greater integration of social workers and occupational therapists within
the multidisciplinary team.
HOMELESSNESS
Cohen and Thompson (1992) – Is it that the mentally ill are homeless or that the
homeless are mentally ill?
PSYCHIATRY AND GENERAL PRACTICE/PRIMARY CARE 315
There are high rates of psychiatric and physical morbidity. Marshall (1989)
reported that 29/46 hostel residents in Oxford showed psychosis. Susser et al. (1989)
reported that 17 per cent of new arrivals at New York shelters were psychotic and 58
per cent were substance abusers.
NEEDS ANALYSIS
Needs are multifaceted. Steps in care include:
1 Identification of those in need through outreach programmes.
2 Systematic evaluations – mental and physical health, support, familial needs.
3 Integration of care – treatment of psychosis, depression, substance abuse, physical
conditions.
4 Housing requirements.
5 Continued support and rehabilitative care.
6 Continued research and audit.
7 Refinement of local and national policy.
At present, care is poorly coordinated. In the USA, the case management system is
not focused towards the homeless; a bureaucratic process of health delivery ‘discour-
ages’ re-entry of the homeless into the health system (Bachrach, 1992).
Many homeless people deny any mental illness, are non-compliant with medication
and avoid mental health care. The US system protects personal rights, possibly aggra-
vating the plight of the homeless. An alternative view maintains that mental health sys-
tems cannot understand the real needs of these individuals without adopting their
perspective.
REHABILITATION ASSESSMENT
1 To determine the kinds of mental and physical disability present and their severity.
2 To discover potential talents that could be developed.
3 To specify short-term and longer-term objectives and design plans to achieve
them. In the UK, operation of care programme and care management approaches.
4 To seek appropriate forms of professional, voluntary and family help and involve-
ment of patient advocacy.
5 To monitor progress and tailor care plans as necessary.
6 Specifically to assess:
– Chronic symptoms and liability to relapse (psychiatrist, community psychiatric
nurse (CPN)).
– Behavioural analysis (nurses, occupational therapist (OT), psychologist).
– Self-care and domestic skills (OT).
– Occupational skills and work assessment (work rehabilitation programmes).
– Social skills training (develop interpersonal skills and ability to develop and
maintain relationships).
PSYCHIATRY AND GENERAL PRACTICE/PRIMARY CARE
Primary care physicians or general practitioners (GPs) are in a prime position to detect
and begin early treatment of psychiatric illness. Twenty-five per cent of GP attenders
316 COMMUNITY-ORIENTATED PSYCHIATRY
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Psychiatry 181, 17.
Specific psychiatric 25
problems of women
EPIDEMIOLOGY
GENERAL
There is an increasing focus on women’s healthcare needs. Systems of care arrange to
promote comprehensive care to women – women’s Health Centers of Excellence – in
which mental health services play a major role.
In most Western societies, psychiatric disorders are more common in women.
Suggested reasons for this include:
• Genetic differences.
• Societal pressures.
• Differences of rearing patterns.
• Cultural expectations.
In general practice, the prevalence of mental disorders in females is three times that
in males. The inception rate is twice as high in females, suggesting a worse prognosis
in females.
SPECIFIC DISORDERS
Neuroses
• Women have twice the risk of developing neurotic depression.
• Interpersonal problems are reported more commonly in women.
• Anxiety states and obsessional disorders are equally distributed, but anxiety states
are more commonly reported by women.
Affective disorders
• The risk of developing unipolar psychotic depression is increased in women up to
the age of 75 (male, 3.5 per cent; female, 5.8 per cent).
• The risk of developing bipolar affective psychosis is evenly distributed.
• Women tend to report more somatic and psychic anxiety and more general
somatic symptoms.
EPIDEMIOLOGY 319
• Men tend to report more hypochondriacal fears and are more likely to lack insight.
• The oral contraceptive pill is not associated with a higher risk of depression in
females.
Schizophrenia
• The lifetime risk is equal in males and females.
• There is increased incidence in females aged under 16 years compared with males
under 16 and in females over 35 compared with males over 35.
• There is an increased incidence in males aged 16–35 compared with females aged
16–35.
• Process schizophrenia may be more common in men, while schizoaffective dis-
orders may be more common in women.
Suicidal behaviour
• Completed suicide is more common in men (11 per 100 000 per year) compared
with women (6 per 100 000).
• Deliberate self-harm is more common in women.
• Repeated deliberate self-harm seems to be slightly more common in men.
• The use of violent means of self-harm (knives, guns, etc.) is more common
in men.
Anorexia nervosa
• More common in females (female:male ratio about 9:1).
• More severe and with worse prognosis in males.
Mental handicap
More common in males (male:female ratio ⫽ 4:3).
Senile dementia
More common in females, but this may be due to the greater longevity of women.
Criminal behaviour
• Of children taken into care under the age of 13, 50 per cent of the boys have com-
mitted offences compared with 13 per cent of the girls.
• Adult males are convicted nine times more commonly than women. This figure
relates to reportability and sentencing policies as well as actual prevalence of
crime.
• Males commit more violent crime, while women tend to be convicted of offences
related to prostitution.
Alcoholism
Alcoholism is eight times more common in men (in a survey of south-east London).
320 SPECIFIC PSYCHIATRIC PROBLEMS OF WOMEN
PREMENSTRUAL SYNDROME
DEFINITIONS
There is no universally agreed definition.
• Physical symptoms – feeling bloated, weight gain, tender breasts, headache, back-
ache, cramps.
• Psychological symptoms – tension, irritability, depression, tiredness, forgetfulness.
There is recurrence of symptoms between ovulation and menstruation. They sub-
side during menstruation and are absent between menstruation and ovulation.
During this period there is said to be an increase in violent crimes, suicide and parasui-
cide, illness behaviour, accidents and poor academic performance. Many of these studies
are methodically flawed. Mental hospital admissions for all forms of disorder are higher
during the premenstrual period, suggesting that patients with pre-existing disorder feel
worse at this time. The relationship (if any) to mental disorder is unclear (Halbreich, 1995).
EPIDEMIOLOGY
Prevalence ranges from 20 to 95 per cent in studies, demonstrating diagnostic
unreliability.
Premenstrual complaint is found more commonly in those with psychiatric ill-
health. This may be because psychiatric distress sensitizes the women to the additional
premenstrual changes (Clare, 1983).
AETIOLOGY
Various unproven theories include:
• A relative deficiency of progesterone, raised prolactin levels, fluid retention, exces-
sive aldosterone, pyridoxine deficiency, raised MAO activity and ‘psychological’
effect.
• Premenstrual decline in circulating ␤-endorphin.
TREATMENT
Selective serotonin re-uptake inhibitors have been shown to be effective in reducing the
symptoms of severe premenstrual syndrome (Dimmock et al., 2000). Progesterones
(e.g. dydrogesterone) show some improvement in symptoms. Supportive psychother-
apy, information giving and relaxation therapy may be beneficial.
PSYCHOLOGICAL PROBLEMS IN PREGNANCY
EPIDEMIOLOGY
Women are less likely to be admitted to a psychiatric ward or to commit suicide dur-
ing pregnancy than at other times. This is in spite of the major life event which preg-
nancy forms.
POSTPARTUM PSYCHIATRIC DISORDERS 321
Minor psychological symptoms are common, however. Two-thirds of women have

some psychological symptoms during pregnancy, especially in the first and last trimesters.
Anxiety is common, as is a tendency to irritability and minor lability of mood.
Ten per cent of pregnant women become significantly depressed during pregnancy.
This usually lasts less than 12 weeks and is more common in the first trimester. It is
associated with: previous history of depression, previous history of abortion, the preg-
nancy being unwanted, marital conflict and anxieties about the fetus. It is character-
ized by fatigue, irritability, increased neuroticism scores and denial of the pregnancy.
Depression in the last trimester may persist as a postnatal depression.
MANAGEMENT
• Increased support by medical, nursing and other services, as well as by family, may
reduce the need to contact psychiatric services. Clear and informed reassurance,
antenatal classes and discussion with other mothers should help.
• Interpersonal psychotherapy can be effective in the treatment of depression during
pregnancy (Spinelli and Endicott, 2003).
• Conjoint marital therapy or separate counselling of the husband may be indicated.
Drugs
Drug treatment with SSRIs or TCAs appears to be safe during pregnancy (Kohen,
2004).
Between 10 and 35 per cent of women take psychotropic drugs at some time during
their pregnancy. All psychotropics that can cross the blood–brain barrier (i.e. are
lipophilic) can cross the placenta. Higher blood levels may develop in the fetus than in
the mother. During the immediate antenatal period, psychotropics may lead to
oversedation of the neonate.
POSTPARTUM PSYCHIATRIC DISORDERS
PUERPERAL PSYCHOSIS
EPIDEMIOLOGY
Psychoses occur following 1.5 per 1000 deliveries. They are associated with primi-
gravida status. A history of manic–depressive psychosis predicts 20 per cent chance of
developing puerperal psychosis.
Lack of specification of puerperal psychosis in ICD-10 and DSM-IV reflects con-
tinued confusion regarding the nosological status of puerperal disorders.
AETIOLOGY
• Genetic factors appear to play a part, since a family history of major psychiatric dis-
order predisposes to puerperal psychosis.
• Biochemical causes have been postulated for the functional psychoses, relating the
precipitation of psychosis to the effects of sudden decreases of progesterone and
oestrogen on tryptophan metabolism.
• There has been little evidence of an excess of psychological stresses in the peri-
natal period in the psychotic mother, although death of the baby may be a clear
precipitant.
• Psychodynamic factors may well be important and will include the patient’s relation-
ship with her own mother, her feelings about the responsibility of motherhood, her
reaction to this assertion of her female role, her relationship with her husband and
his personality (over-passive or over-dominant).
The relationship between lack of effective ‘bonding’ between mother and baby (due
to early separation, emotionally or physically) and the development of psychosis is
unclear.
CLINICAL FEATURES
Puerperal psychoses are widely held not to be a distinct and unitary form of psychosis
but to be divided into affective psychoses (70 per cent), schizophrenia (25 per cent)
and organic psychoses (very rare now in the UK).
The affective psychoses are primarily depressive. The few organic psychoses are par-
ticularly due to cerebral thrombophlebitis.
The evidence for suggesting that puerperal psychoses are not a distinct entity is:
1 Family history of psychotic disorder is as commonly present as in non-puerperal
psychosis.
2 There is an increased incidence of psychosis before and after the pregnancy and
puerperal period also.
3 Manic depressives have 10 times the risk of developing a puerperal psychosis com-
pared with the normal population.
4 The clinical syndromes resemble psychoses occurring at other times.
However, suggestions remain that there is a distinct clinical picture of puerperal

psychosis. This consists of:
1 A prodromal period, about 2 days after parturition, of insomnia, irritability, rest-
lessness, refusal of food and depression.
2 This is rapidly followed by the acute onset of confusion, excitability, overactivity,
hallucinations, fatiguability, very labile mood and preoccupations and delusions
concerning the baby. Elation, grandiosity and schizophreniform symptoms are
common.
3 Onset is almost always in the first 2 weeks. In character and timing the psychoses
are very similar to postoperative psychosis.
PROGNOSIS
Seventy per cent recover fully, affective psychosis having a better prognosis than schizo-
phrenic. The risk of psychosis in future puerperal periods is 14–20 per cent. The risk
of psychosis at any future time is up to 50 per cent.
Poor prognosis is indicated by a positive family history, schizophrenia, neurotic
personality and the presence of severe marital problems.
POSTPARTUM PSYCHIATRIC DISORDERS 323
PUERPERAL DEPRESSION
EPIDEMIOLOGY
Ten per cent (range 3–16 per cent) of women develop a non-psychotic depressive dis-
order in the postpartum period. Onset is usually within the first postpartum month,
often on return home and usually between day 3 and day 14.
It is associated with increased age, childhood separation from the father, problems
in relationships with mother- and father-in-law, marital conflict, mixed feelings about
the baby, physical problems in the pregnancy and perinatal period, a tendency to more
neurotic and less extroverted personalities.
AETIOLOGY
Possible aetiological factors include a postulated hormonal effect on tryptophan
metabolism.
Social and situational changes make the woman particularly vulnerable at this time.
Having a baby is an important life event involving changes in financial, social and
marital status. Lack of support from the partner or family may increase vulnerability
to depression.
CLINICAL FEATURES
Typically, the woman is tearful and irritable. Associated symptoms may include feeling
tired, despondent and anxious, with worry about ability to cope with baby, fear for
own and baby’s health and feeling generally inadequate.
There is often poor appetite, decreased libido and difficulty in sleeping. These
patients often have difficulty concentrating and may complain of feeling confused,
although cognitive testing is normal.
PROGNOSIS
Most symptoms (90 per cent) last less than 1 month, even without treatment. In 4 per
cent of cases they last longer than a year.
POSTPARTUM ‘BLUES’
EPIDEMIOLOGY
Fifty per cent of women have a short-lived emotional disturbance commencing on the
third day and lasting for 1–2 days. It is more common in primigravidae and in those
who complain of premenstrual tension.
CLINICAL FEATURES
Common features are: episodic weeping, feeling depressed and irritable, feeling sep-
arate and distant from the baby, insomnia and poor concentration. This coincides
with sudden weight loss, decreased thirst and increased urinary sodium secretion.
The syndrome would appear to have a biochemical basis.
MANAGEMENT OF POSTPARTUM DISORDERS
Postpartum disorders are important to detect. There should be an early high index of
suspicion – don’t assume ‘baby blues’ – with use of rating scales (e.g. Edinburgh post-
natal depression scale). Postnatal depression may have enduring emotional and cogni-
tive sequelae for the infant. Young mothers particularly need support.
PSYCHOSIS
Admission to hospital is frequently required, owing to the potential danger to the baby
(of violence, neglect or mishandling) and to the difficulty of dealing with a behav-
iourally disturbed and psychotic mother at home.
Admission of both mother and baby together is always advisable, if possible (mother
and baby units). This allows for the development of bonding, reduction in the emo-
tional deprivation of the child and reduction in the guilt of the mother. It also allows for
the supervision of mother and baby, and their relationship. By gentle advice, encourage-
ment and reassurance the mother’s confidence can be built up. Breast-feeding can be
continued where possible and desired. The father should be free to visit and keep his
contact with his family.
Mothers admitted with their babies tend to stay in hospital for less time and are less
disturbed on discharge than mothers admitted without their babies.
Drugs and other physical treatments should be given as appropriate to the symptoms. If
the baby is breast-fed, major tranquillizers will be present in the milk and the baby should
be observed for over-sedation. If this occurs, the needs of the mother for sedation and
those of the baby for breast-feeding must be balanced. It may be necessary to stop breast-
feeding for a short period while the mother’s symptoms are brought under control.
Psychotherapy, usually of a supportive kind, is always required. Discussion will
centre on the mother’s relationship with the baby and her feelings about herself. Her
relationship with her partner and family may also be necessary to explore. Psychotherapy
will be aimed at reducing her guilt and feelings of inadequacy and hostility and at fos-
tering maternal feeling.
Couple therapy is often a critical component of recovery.
DEPRESSION
Since this is usually self-limiting, supportive measures of encouragement and reassurance
are usually all that are required. If the depression lasts for more than 1 month, an anti-
depressant may be indicated, as well as more active psychotherapy and marital therapy.
‘BLUES’
This does not require any more than simple reassurance and explanation, both to the
mother and to her partner.
TERMINATION OF PREGNANCY
About one in five pregnancies in the UK are terminated for therapeutic reasons. Sixty-
three per cent of females seeking abortion are single, 32 per cent are aged 20–24 years.
MENOPAUSE 325
After abortion, transient psychological distress (anxiety, grief reactions) is common,

but prominent or persistent psychiatric illness is uncommon (⬍10 per cent) (Zolese
and Blacker, 1992).
Risk factors:
• Past psychiatric history.
• Poor social support.
• Young age.
• Multiparous.
• Sociocultural setting which discourages abortion.
STILLBIRTH
Stillbirth is viewed variously as ‘an overlooked catastrophe’ or as a ‘non-event’. There is

a risk of pathological grieving because there is no surviving child. There may be guilt
and fear of failure as a woman.
STERILIZATION AND HYSTERECTOMY
Psychiatric symptoms are rare after tubal ligation – 71–99 per cent are completely satis-
fied with the operation. Between 2 and 5 per cent greatly regret having the operation,
especially if aged less than 26, with a small family size and under pressure to be sterilized.
The incidence of psychiatric symptoms in the 18 months after sterilization is about
1 per cent and is no higher than the general population rate.
Sterilization has been shown to improve the mental state, social adjustment, general
health and marital and sexual relationships of the woman.
Although it was originally reported that hysterectomy is associated with increased
psychiatric illness, especially depression, subsequent studies have discounted this
claim.
MENOPAUSE
The menopause used to be regarded as an important aetiological factor in so-called

‘involutional melancholia’. There is now no evidence that this is a distinct entity, but
merely one presentation of depression in late middle age and not consistently related
to the menopause.
Whether the hormonal changes of the menopause lead to psychiatric disorder is
much debated. It is methodologically difficult to separate the hormonal aspects from
the psychodynamic aspects of altered perception of the self and altered relationship
with the partner. At this time, also, many other life events are happening (e.g. children
are leaving home, parents are dying, husbands are retiring, etc.).
The risk of depressive illness does not seem to be higher at the menopause than at
other times.
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Transcultural psychiatry 26
CULTURAL CONTEXT
Two views are debated:
• Psychiatric universalist view – mental disorders show similar phenomenology in all

cultures.
• Cultural determinist view – mental disorders show essential differences in different
cultures.
Evidence exists for both views. Patterns of ‘pathological’ behaviour may mirror and
exaggerate the patterns of normal behaviour in a culture, but still fall into the same
very broad diagnostic categories in all countries – the ‘pathoplastic’ effect of culture.
Delusions and hallucinations are recognized as abnormal in almost all cultures (e.g.
Yoruba of Nigeria, West Indians, Asians). Inhabitants of developing countries tend to
discriminate differently between different emotional states from inhabitants of developed
countries.
Reaction to mental disorder by the local community varies greatly; greater acceptance
may reduce social incapacity.
SPECIFIC DISORDERS
SCHIZOPHRENIA
Schizophrenia was originally noted to have increased incidence in the USA compared
with the UK, as well as reduced incidence in developing countries. Neither view is correct
(see Chapter 3).
Use of the PSE in the International Pilot Study of Schizophrenia showed that
reliable diagnosis of schizophrenia could be made throughout the world by local
psychiatrists in nine different countries, including India, Colombia, Nigeria, the Soviet
Union, the USA and the UK. Prevalence was similar in all countries, although the USA
SPECIFIC DISORDERS 329
and Soviet Union had apparently higher prevalence of locally (but not PSE-) diag-
nosed ‘schizophrenia’.
Confusion, excitement, transient hallucinations and unsystematized (often para-
noid) delusions are more common in Africa. Catatonic symptoms are more common
in India.
Outcome is consistently shown to be better in developing countries, in terms of
reduced social disability and psychopathology, even when single acute episodes are
discounted. The reason is unknown (Jablensky et al., 1992).
DEPRESSION
Depression was originally thought to be almost absent in developing countries.

Depression is probably widespread, but with differing symptomatology, making diag-
nosis imprecise. Many cultures do not have a word equivalent to ‘depression’.
Africans tend to show more paranoia and hypochondriasis. South Asians tend to
show more hypochondriasis, agitation and somatic complaints (e.g. stomach pains,
sexual dysfunction in men). Patients in Christian cultures may exhibit guilt, self-
depreciation and suicidal tendencies.
NEUROSES
Hysterical dissociation is more common in developing countries. Acute, dramatic

trance states with disturbed behaviour and fearfulness are also more common.
‘CULTURE-BOUND’ DISORDERS
In these disorders there is a relatively unique pattern of symptoms, usually a variant of

a major psychosis or neurosis.
• Latah (Far East, North Africa) – dissociative state with echolalia and automatic
obedience. Hysterical reaction to stress, usually in women.
• Windigo (North American Indians) – delusional belief that subject has turned into
a cannibalistic monster; may attempt to act on this. Regarded as a form of depres-
sive psychosis.
• Koro (Malaya, South China) – anxiety associated with fear of penis retracting into
abdomen and resulting in death. Acute anxiety state.
• Amok (South East Asia) – depressive withdrawal followed by indiscriminate mur-
derous frenzy. May kill self or others. Hysterical dissociation or depressive.
• Susto (Central and South America) – anxiety and fear attributed to loss of soul.
Acute anxiety state, possibly due to individual’s inability to fulfil his/her expected
social role.
• Dhat syndrome – ‘semen loss’, erectile dysfunction, fatigue, insomnia. An Asian
psychosexual disorder associated most commonly with neurotic depression.
330 TRANSCULTURAL PSYCHIATRY
ORGANIC PSYCHOSYNDROMES
Infectious and nutritional problems lead to increased incidence of acute confusional

states. Such causes also alter the presentation of functional psychiatric disorders.
ASSESSMENT AND TREATMENT
See Harrison (1991).

• Interpreters – There is a need for skilful interpreters. Health services require a net-
work of experienced interpreters and all information literature should be available
in all locally common languages/dialects.
• Presentation – Allow for variations in the presentation of common disorders and
for cultural differences in the meaning of words and concepts. Use the family to
help wherever possible.
• Role of ‘ethnic’ health workers – In some cases mental health workers will offer invalu-
able insight into cultural differences and variations where they share similar ethnic
backgrounds to patients. They also raise team ‘awareness’ of cultural issues.
• Stereotypes – Beware of racial or ‘cultural’ stereotypes.
• Somatization – Recognize somatic manifestations of mental disorder.
AFFECTS OF MIGRATION
Do migrants have increased incidence of psychiatric disorder?

Ødegaard (1932) demonstrated an increased incidence of admission to mental hospi-
tals in Norwegian immigrants to the USA (over Americans and Norwegians in
Norway), especially due to schizophrenia. This stimulated debate between:
• Social selection – mentally ill people or those prone to develop mental disorder
tend to migrate.
• Social causation – environmental factors associated with migration tend to lead to
mental disorder.
Ødegaard favoured social selection for schizophrenia, because (i) there was no particu-
lar association with time of migration, and an apparent tendency for ‘schizoid’ personality
before migration; and (ii) the reasons for breakdown seemed unrelated to the migration.
American social scientists (e.g. Srole et al., 1962; Mid-Town Manhattan Study)
favoured social causation, particularly of neurotic disorders.
A third possibility is that the increased incidence is caused by confounding vari-
ables (e.g. increased age, unmarried status or lower social class in migrants).
However, not all migrants have an increased incidence of psychiatric disorder.
Astrup and Ødegaard (1960) demonstrated that internal migrants (i.e. those not leav-
ing the country) have a lower incidence of psychosis. Only migrants into the capital city
had a higher incidence than non-migrants. British immigrants to Victoria, Australia, in
1960 showed lower risk compared with those from southern and eastern Europe.
Thus each group of migrants and each disorder must be investigated separately.
FACTORS RELATING TO MIGRATION

Before (i.e. culture of origin)
• Prevalence of disorder in original community.
• Attitude towards migration (betterment or desertion).
• Characteristics of upbringing (is independence encouraged?).
After (i.e. society of resettlement)
• May refuse entry to psychiatrically ill.
• May be tolerant or rejecting (both could lead to increased incidence).
• Hostility and discrimination.
• Size and cohesiveness of new community.
• Language and cultural difficulties.
The incidence of schizophrenia in second-generation Afro-Caribbean migrants
in the UK has been found to increase six-fold (Harrison et al., 1988, 1997) compared
with the ‘indigenous’ population. This finding has been replicated by others, although
methodological pitfalls include greater ease of Afro-Caribbeans to ‘filter’ through the
health services, confounding effects of substance abuse, diagnostic and cultural misin-
terpretations and social bias (‘labelling’).
The increased rate of schizophrenia among Afro-Caribbean migrants may result
from biological factors (e.g. virus exposure, obstetric complications), or be related to
social adversity (Harrison and Eaton, 2002).
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Bhui K, Stansfeld S, Hull S et al. (2003) Ethnic variations in pathways to and use of specialist
mental health services in the UK: a systematic review. Br. J. Psychiatry 182, 105.
Boydell J, van Os J, McKenzie K et al. (2002) Incidence of schizophrenia in ethnic minorities.
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Am. 24, 391.
Fabrega H (2001) Cultural psychiatry: international perspectives. Epilogue. Psychiatr. Clin.
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Fabrega H (2001) Mental health and illness in traditional India and China. Psychiatr. Clin. North
Am. 24, 555.
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Harrison G, Owens D, Holton T et al. (1988) A prospective study of severe mental disorder in
Afro-Caribbean patients. Psychol. Med. 18, 643.
332 TRANSCULTURAL PSYCHIATRY
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Jablensky A, Sartorius N, Ernberg G et al. (1992) Schizophrenia: manifestations, incidence and
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Jaycox LH, Stein BD, Kataoka SH et al. (2002) Violence exposure, posttraumatic stress disorder,
and depressive symptoms among recent immigrant schoolchildren. J. Am. Acad. Child Adolesc.
Johns LC, Nazroo JY, Bebbington P et al. (2002) Occurrence of hallucinatory experiences in a
community sample and ethnic variations. Br. J. Psychiatry 180, 174.
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Moldavsky D (2003) The implication of transcultural psychiatry for clinical practice. Isr. J. Psychiatry
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Rohde LA (2002) ADHD in Brazil: the DSM-IV criteria in a culturally different population.
J. Am. Acad. Child Adolesc. Psychiatry 41, 1131.
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Skapinakis P, Lewis G, Mavreas V (2003) Cross-cultural differences in the epidemiology of unex-
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24, 539.
Psychiatry and the Internet 27
MENTAL HEALTH ISSUES
• Mental health is a very common focus of Internet searches by the public.

• The Internet is used increasingly for support and discussion groups, and for infor-
mation on diseases and latest medications.
• Psychiatry is beginning to explore e-mental health which may be useful for:
– Short-term therapies.
– Counselling.
– Prescription renewals.
The Internet is also inappropriately used (e.g. Internet addiction).
USEFUL WEBSITES
GOVERNMENTAL
• US National Library of Medicine, creator of MEDLINE/PubMed:
– www.nlm.nih.gov
• National Institute of Mental Health (NIMH), the leading Federal agency for
research on mental and behavioral disorders in the USA:
– www.nimh.nih.gov
• Substance Abuse and Mental Health Services Administration, part of the US
Department of Health and Human Services
– www.samhsa.gov
• National Institute for Clinical Excellence (for clinical guidelines in UK):
– www.nice.org.uk
NON-GOVERNMENTAL
Advocacy/support sites
• Bazelon Center for Mental Health Law:
– www.bazelon.org
• National Alliance for the Mentally Ill (NAMI):
– www.nami.org
334 PSYCHIATRY AND THE INTERNET
• National Mental Health Association (NMHA):

– www.nmha.org
• Rethink:
– www.rethink.org
• SANE:
– www.sane.org.uk
• Schizophrenia.com:
– www.schizophrenia.com
Other sites
• American Psychiatric Association:
– www.psych.org
• Expert Consensus Guidelines Series:
– www.psychguides.com
• Internet Mental Health:
– www.mentalhealth.com
• Mental Health InfoSource:
– www.mhsource.com
• Mental-Health-Matters.com:
– www.mental-health-matters.com
• Mental Help Net:
– www.mentalhelp.net
• Mental Wellness.com:
– www.mentalwellness.com
• Pharmacology Algorithm Project (Harvard):
– http://mhc.com/Algorithms
• PlanetPsych.com:
– www.planetpsych.com
• PSYweb.com:
– www.psyweb.com
• Refdesk.com Mental Health:
– www.refdesk.com/mental.html
• Royal College of Psychiatrists:
– www.rcpsych.ac.uk
GENERAL INTERNET SEARCH ENGINES

Search for ‘psychiatry’, ‘mental health’, etc.
• www.google.com
• www.yahoo.com
• www.excite.com
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of the art. Health Educ Res. 16, 671.
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depression and anxiety disorders in primary care. J. Med. Internet Res. 5, e23.
Greist JH, Marks IM, Baer L et al. (2002) Behaviour therapy for obsessive–compulsive disorder
guided by a computer or by a clinician compared with relaxation as a control. J. Clin.
Psychiatry 63, 138.
Marks IM, Mataix-Cols D, Kenwright M et al. (2003) Pragmatic evaluation of computer-aided
self-help for anxiety and depression. Br. J. Psychiatry 183, 57.
Prasad V, Owens D (2001) Using the internet as a source of self-help for people who self-harm.
Psychiatr. Bull. 25, 222.
Pratarelli ME, Browne BL (2002) Confirmatory factor analysis of internet use and addiction.
Cyberpsychol. Behav. 5, 53.
Proudfoot J, Goldberg D, Mann A et al. (2003) Computerised, interactive, multimedia CBT
reduced anxiety and depression in general practice: a RCT. Psychol. Med. 33, 217.
Shaw LH, Gant LM (2002) In defense of the Internet: the relationship between Internet commu-
nication and depression, loneliness, self-esteem, and perceived social support. Cyberpsychol.
Behav. 5, 157.
Slater MD, Zimmerman DE (2002) Characteristics of health-related websites identified by com-
mon Internet portals. JAMA 288, 316.
Stein DJ, Black DW, Shapira NA, Spitzer RL (2001) Hypersexual disorder and preoccupation
with Internet pornography. Am. J. Psychiatry 158, 1590.
Tantum D (2001) A guide to the Internet from psychotherapists. Psychiatr. Bull. 25, 29.
Theodosiou L, Green J (2003) Emerging challenges in using health information from the
Internet. Adv. Psychiatr. Treat. 9, 387.
Whang LS, Lee S, Chang G (2003) Internet over-user’s psycholoigical profiles: a behavior sam-
pling analysis on internet addiction. Cyberpsychol. Behav. 6, 143.
Index
Page numbers in bold refer to tables
abnormal motivational state 299 clinical features 45–6

absorption, drugs 266 cognitive/behavioural theories 51
acamprosate 119 course 52
accelerated tempo of thought 17 elderly patients see psychogeriatrics
acetylcholine 48 epidemiology 46
affective disorders 48 genetics 46–7
Alzheimer’s disease 157 HIV 168
acetylcholinesterase inhibitors, Alzheimer’s life event studies 51
disease 158 mixed affective states 54
acquired immunodeficiency syndrome neurochemistry 47–9
(AIDS) 167–8 neuroendocrine abnormalities 48
adjustment disorders 168 neuroimaging 49
aetiology of CNS effects 167–8 MRI 190
affective disorder 168 PET 192
management 168 SPECT 191
psychosis 168 neuropathology 49
see also HIV infection neuropeptides 49
acting out 298 neurotransmitter abnormalities 47–8
actual neurosis 298 organic causes 49–50, 49
actus reus 226 pharmacology 53–4
Addison’s disease 164 poor outcome predictors 52
adjustment disorders, AIDS 168 premorbid personality 51
adolescents primary/secondary 43
anorexia nervosa 87 prognosis
mood disorders 237–8 long-term 52
non-fatal deliberate self harm 138 short-term 52
suicide 137 psychodynamics 50
adrenergic agents 284–5 psychological theories 50–1
antagonists see beta blockers psychotherapy 52–3
sleep EGG 186 sociological theories 51
␣-adrenergic agonists 284 treatment 52–4
adrenogenital syndrome 100 unipolar/bipolar 43
affect 18 vulnerability factors 51
affective disorders 43–59 women 318–19
aetiology 46–51 see also depression; manic states
AIDS 168 affectless states 18
bereavement reactions 55 agoraphobia 63, 65
childhood experiences 50 AIDS dementia complex (ADC)
classifications 43–5 167–8
DSM-IV 44 akathisia 270
ICD-10 44 Albright’s syndrome 257
338 INDEX
alcohol dependence 109–22 epidemiology 155

aetiology 112–13 genetics 155–6
biochemical factors 113 immunology 157
family studies 112 management 158
psychological factors 113 mild cognitive impairment 159
sociocultural factors 113 neurochemistry 157
clinical features 113–14 neuroimaging
complications 114–18 CT 190
anaemia 117 MRI 190
cardiovascular 116 MR spectroscopy 192
CNS 114–16 PET 192
gastrointestinal 116 SPECT 191
haematological 117 neuropathology 156
neoplasms 117 prognosis 159
in pregnancy 117 risk factors 156
psychiatric 116 sundowning 158, 182
respiratory 116 aminoacidurias 258
detection 118, 118 amitriptyline 275–6
detoxification 119 amniocentesis 264
DSM-IV criteria 109 amok 329
economic effects 118 amphetamines 126
epidemiology 109–11, 110, 319 mechanism of action 269
co-morbidity 110, 110, 119 amyloid ␤-peptide 156, 158
ethic factors 110 amyloid plaques 156
sex 110 anakastic personality disorder 79
genetics 112 anatomical dolls 224
ICD-10 classification 109 animal phobias 64
management 118–20 anorexia nervosa (AN) 87–91
drug therapy 119, 285 aetiology 88–9
general guidelines 118–19 body image disturbance 88
psychosocial rehabilitation 120 clinical features 89, 90
molecular genetics 112 complications 89
prognosis 120 diagnostic criteria 90
relapse 113, 114 differential diagnosis 89
sleep disorders 182 epidemiology 87–8, 319
social effects 117–18 hypothalamic-pituitary -gonadal axis
suicide 136 89, 89
type I 112 laboratory abnormality 89
type II 112 management 89–90
vulnerability markers 112 predisposing factors 88
alcohol dependency syndrome 113–14 prognosis 90–1
alcoholic dementia 115 anorgasmia (frigidity) 97
alcoholic hallucinations 114 antidepressants side-effect 272
alcohol-related disabilities 114–18 behaviour therapy 102
alpha agonists 284 anoxia, mental retardation 259
Alzheimer’s disease 155–9 anterior cerebral artery occlusion
aetiology 155–7 153
classification 157, 158 anterograde amnesia, head injury
clinical features 157–8 170–1
Down’s syndrome 155 anti-aggressive drugs 230
drug treatment 158 anticonvulsants, epilepsy 179
INDEX 339
antidepressants 53, 272–7 generalized 61, 69

attention-deficit/hyperactivity disorder 245 genetics 62
characteristics 273 ICD-10 classification 60
childhood depression 238 personality development 77
pain disorder 200 predisposing factors 62
side-effects 272 pregnancy 321
SSRIs see selective serotonin re-uptake psychosurgery 294
inhibitors (SRRIs) sleep disorders 182
tricyclics see tricyclic antidepressants treatment 62–3
antiepileptics 179–80 ‘anxiety management’ training 62
autism 236 anxiolytics 282–4
antimongolism 255 anxious personality disorder 79
antipsychotic medication 268–72 apathetic depression 207
anorexia nervosa 90 apathy 19
atypical 269 Apert’s syndrome 256
atypical vs typical 269 apolipoprotein E (APOE) 156
autism 236 appearance disorders 13–15
classes 268–9, 269 approximate answers, syndrome of 146–7
delusional disorder 38 argininosuccinic acidura 258
dopamine blockade 269–70 arson 220–1
mania 53 classification 220–1
mechanism of action 269–70 definition 220
receptor antagonistic binding profile 270 epidemiology 221
safety/tolerance 272 arterial occlusion 153
schizophrenia 34–5 Asperger’s disorder 237
side-effects assertive community treatment (ACT) 313
extrapyramidal 270–1, 270 assertive outreach models 313
non-neurological 271 ataxia telangiectasia 257
typical 269 atomoxetine 286
antisocial personality disorder (ASP) 79, atropine 128
215–17 attachment, maternal-infant 234
aetiology 216–17 attention 20
diagnostic criteria 215 tests 20
epidemiology 216 attention-deficit/hyperactivity disorder
historical development 215–16 (ADHD) 243–5
hospitalization 217 aetiology 244
management 217 associated features 243–4
organic causes 216 atomoxetine 286
primary prevention 217 course 244
prognosis 217 differential diagnosis 244
psychodynamic factors 217 epidemiology 244
sociocultural factors 217 genetics 244
anxiety 18, 61 management 245
anxiety disorders 60–3 prognosis 244
assessments 5 subtypes 243
biological aspects 66–7 atypical depression see masked depression
children 62, 238–9 atypical grief 55
complications 62 autism 235–6
course 62 aetiology 235–6
DSM-IV criteria 60 clinical features 235
epidemiology 61 course 236
340 INDEX
autism (contd) beta blockers 284–5

differential diagnosis 236 anxiety disorders 63
epidemiology 235 contraindications 285
fragile X syndrome 256 side-effects 285
genetics 235 uses 284–5
management 236 bias 4
MRI 190 binge-eating disorder 91
neurochemistry 236 Binswanger’s chronic progressive subcortical
prognosis 236 encephalopathy 159
automatic obedience 14 bipolar disorder
autoscopy 145 children 237–8
avoidant personality disorder 79 DSM-IV criteria 44
azapirones 63, 283 ICD-10 classification 44
molecular genetics 47
barbiturates 127, 284 mood stabilizers 277–81
liver enzyme induction 266, 284 body dysmorphic disorder (BDD) 201
basal syndrome 153 bonding, maternal-infant 234
basilar artery occlusion 153 borderline personality disorder 79, 81
battered child syndrome 221 bovine spongiform encephalopathy 161
behavioural disorders 13–15 bradyphrenia 163
behaviour therapy 306–7 brain imaging see neuroimaging
anorexia nervosa 90 brainstem dysfunction 153
double learning theory 306 breast feeding 268, 324
intermittent reinforcement 307 Briquet’s syndrome 82
mental retardation 262 Broca’s area damage 151
obesity 87 bulimia nervosa 91–3
Pavlovian 306 aetiology 91–2
phobic disorders 65 clinical features 92, 92
premack principle 306–7 drug treatment 93
shaping 307 epidemiology 91
Skinnerian 306 management 92–3
uses 306 prognosis 93
see also cognitive-behavioural therapy buprenorphine 129
(CBT) bupropion 274
belladonna 128 busipirone 283
benzodiazepines 282–3, 282
alcohol dependence detoxification 119 cAMP signalling pathway, alcohol
anxiety disorders 63 dependence 112
insomnia 181–2 cannabis 127
mode of action 282 children/teenagers 249
phobic disorders 65 Capgras’ syndrome 144
psychopharmacology 127 carbamazepine 179, 281
side-effects 282–3 affective disorders 53
substance abuse 129 alcohol dependence 119
uses 282 side-effects 281
withdrawal effects 283 uses 281
bereavement reactions 55 carbohydrate craving 55
psychogeriatrics 206–7 carbohydrate metabolism disorders 258
stillbirth 324 cardiovascular problems
termination of pregnancy 324 alcohol dependence 116
Berry–Franceschetti syndrome 256 tricyclics side-effect 275
INDEX 341
Care Programme Approach (CPA) 313 coenaesthopathic states 146

case-note studies 4–6 cognitive-behavioural therapy (CBT) 307
castration anxiety 300 affective disorders 52
cataplexy 182 antisocial personality disorder 217
catego 25 anxiety disorders 62
caudate nucleus 71 bulimia nervosa 92
census 4 insomnia 181
cerebral artery occlusion 153 schizophrenia 35–6
character 77 cognitive impairment 172
childhood-onset schizophrenia 237 cognitive therapy 307–8
children 233–52 automatic thoughts 307
anxiety disorders 238–9 restructuring 307
assessments 6 theory of depression 307
depression 238 variations 308
diagnosis difficulties 233 coma 20
disorder classification 233 combat guilt 69
epidemiology 233 combat necrosis see post-traumatic stress
Huntington’ s chorea 161 disorder
inappropriate soiling 240–2 combination therapies 53
maternal deprivation 234–5 community mental health teams 312
mood disorders 237–8 community-orientated psychiatry
non-accidental injury see non-accidental 312–17
injury historical review 312
school refusal 239–40, 239 policy initiatives 313–14
substance abuse 248–9 recent developments 313–14
suicide 238 community treatment order 228
treatment considerations 233 compensation necrosis 172
child sexual abuse (CSA) 223–4 competency 227
behavioural outcomes 224 compliance therapy 36
evaluation 224 compulsions 70
management 224 compulsive phenomena 16
personality disorders 82 computerized tomography (CT)
presentation by child 223 affective disorder 206
psychiatric outcomes 224 Alzheimer’s disease 190
cholinergic neurogransmission, Alzheimer’s Creutzfeldt–Jakob disease 161
disease 157 Huntington’ s chorea 190
chromosomal abnormalities 255–6 schizophrenia 33, 189
alcohol dependence 112 structural investigations 189
deletions 255 concentration 20
narcolepsy 182 conduct disorder 243, 247–8
chronic fatigue syndrome (CSF) 202 aetiology 248
cirrhosis 117 course 248
clang associations 17, 18 epidemiology 248
clinical trial design 10 management 248
clonidine prognosis 248
alcohol dependence detoxification 119 subclassifications 247–8
substance abuse 129 connective tissue metabolism disorders
clozapine 258–9
schizophrenia 34 consciousness 20
suicide prevention 138 clouding 20
cocaine 126 control group 4, 10
342 INDEX
conversion disorder 198–9 deliberate self-harm (DSH), non fatal

aetiology 199 138–40
course 199 associations 138–9
epidemiology 198–9 definition 134
genetics 199 epidemiology 138–9
prognosis 199 management 139–40
psychoanalytic aspect 199 post episode 139
psychophysiological aspect 199 pre episode 139
social aspect 199 personality disorders 83
treatment 199 repetition 139
coprolalia 247 risk factors 138–9
corpus callosum abnormalities 216 suicide 139
corticotropin releasing factor (CRF) 49 delirium 154–5
Cotard’s syndrome 148–9 aetiology 155
countertransference 299 clinical features 150
court report preparation 225 ICD-10 criteria 154
Couvade syndrome 146 management 155
crack-cocaine 126 delirium tremens 114
craniofacial dysostosis 256 delusion(s) 16
cretinism (hypothyroidism) 259 delusional atmosphere 16
Creutzfeldt–Jakob disease (CJD) 161–2 delusional disorders 37–8
aetiology 161 differential diagnosis 38
clinical features 161 DSM-IV criteria 38
neuroimaging 161 hypochondriacal 146
prognosis 162 management 38
cri du chat syndrome 255 subtypes 145–6
crime, violent 219–24 types 16
criminal responsibility (UK only) 226–7 delusional misidentification 144–5
age 226 delusional mood 16
complicating factors 227 ‘delusions of doubles’ 144
intent 226–7 dementia 150–1
crisis intervention 304 alcoholic 115
CT see computerized tomography clinical features 150
culture-bound disorders 329 differential diagnosis 151
Cushing’s syndrome 164 epilepsy 179
cybernetics 304 neuropsychiatric assessment 154
cyclic AMP (cAMP) signalling pathway, types 155–63
alcohol dependence 112 dementia praecox 24
cyclothymia 44, 44 denial 19, 298
dependent personality disorder 79
dangerous patient management 229–30 depersonalization 19
long-term 230 depersonalization disorder 202
political level 229 depression 18–19
staff policies 230 aetiology 46–51
ward level 230 agitated 207
decarceration 312 arson 221
De Clérambault’s syndrome 145 assessments 5
decreased tempo of thought 17 children 238
deep brain stimulation (DBS) 293 clinical features 45–6
de Lange syndrome 257 cognition 45
delayed ejaculation 272 cultural aspects 329
INDEX 343
DSM-IV criteria 44 disability 253

ECT indications 289 disintegrative psychoses 237
elderly patients 207 dispersion measurements 8
epidemiology 46 displacement 298
epilepsy 50, 178 dissociative amnesia 202
hypochondriasis 200 dissociative disorders 201–2
ICD-10 44 clinical features 202
integrative models 51 management 202
masked (atypical) 55, 238 types 202
medication 50 dissociative fugue 202
MRI 190 dissociative identity disorder 147, 202
pregnancy 321 management 202
psychosurgery 294 distortion 298
psychotic/retarded/endogenous distress syndrome 235
43–5, 45 disulfiram 119, 285
sleep disorders 182 divalproex 119
suicide 136 donepezil 158
treatment-resistant 54 dopamine (DA)
unipolar 47 affective disorders 48
see also affective disorders alcohol dependence 113
depression-allied syndrome 148–9 antipsychotic medication 269–70
depressive pseudodementia 207 Gilles de la Tourette’s syndrome 247
derealization 19 schizophrenia 32
descriptive statistics 7–8 dothiepin 276
desipramine 276 ‘double’ depression 45
desultory thinking 18 Down syndrome
detoxification Alzheimer’s disease 155
alcohol dependence 119 associated conditions 255
methadone 129 features 255
naltrexone 129 recurrence likelihood 255
dexamethasone suppression test (DST) 48 doxepin 276
dextroamphetamine 285 dream work 298
attention-deficit/hyperactivity disorder drowsiness 20
245 drug excretion 267
Dhat syndrome 329 drug interactions 267–8, 276
diabetes mellitus 271 drug therapy 266–88
Diagnostic and Statistical Manual of Mental affective disorder 208
Disorders IV criteria see DSM-IV anti-aggressive 230
criteria anxiety disorders 62–3
dialectic behavioural therapy (DBT) 308 depression causing 50
diazepam epilepsy 179
agoraphobia 65 obsessive-compulsive disorder 71–2
breast feeding 268 pharmacodynamics 266–8
diencephalon dysfunction 153 pharmacoeconomics 286
diet pharmacogenetics 268
ketogenic 180 pharmacokinetics 266–8
obesity 87 phobic disorders 65
dietary chaos syndrome see bulimia pregnancy 268
nervosa sexual dysfunction 103
diffuse tensor imaging (DTI) 189 toxic confusion 165
diminished responsibility 226 see also specific drugs, and disorders
344 INDEX
DSM-IV criteria electroconvulsive therapy (ECT) 289–93

affective disorders 44 administration 290–1
alcohol dependence 109 anaesthetic application 290
anorexia nervosa 90 bilateral 291
antisocial personality disorder 215 electrical stimulation application 290–1
anxiety disorders 60 post-ictal 291
bipolar disorder 44 pre treatment 290
bulimia nervosa 92 unilateral 291
child psychiatric disorders 233 affective disorder 208
cyclothymia 44 consent 292
delusional disorder 38 contraindications 290
depressive disorders 44 effects 291–2
gambling, pathological 130 cardiovascular 291
mental retardation 253–4 neurological 291
Münchausen syndrome 147 neuropathological 291–2
obsessive-compulsive disorder 60 sleep 292
panic disorder 60 ethical/legal aspects 292–3
personality disorders 79 history 289–93
phobic anxiety disorders 60 indications 289–90
schizoaffective disorder 36 mortality 290
schizophrenia 26, 27, 28 patient refusal 292–3
sexual disorders 98 prescription 291
social anxiety disorder 60 schizoaffective disorder 37
somatoform disorders 197 schizophrenia 35
stress reaction 60 seizure threshold 290–1
substance abuse 123–4 side-effects 290
substance dependence 123 unilateral vs bilateral 292
duration of untreated psychosis (DUP) 32 electroencephalography (EEG) 185–8
dyskinesias 245 abnormal patterns 186–8
dysphasias 21 alpha coma 187
dysphoria 49 burst-suppression 188
dysthymia 45 diffuse abnormalities 187
dystonia 270 focal abnormalities 187
frontal intermittent rhythmic delta
eating disorders 86–96 activity (FIRDA) 187
assessments 5 periodic complexes 187
echolalia 14 triphasic waves 187
echopraxia 14 adults 185
ecstasy (MDMA) 128 antisocial personality disorder 216
ecstasy states 19 Creutzfeldt–Jakob disease 161
Edwards’ syndrome (trisomy 17–18) 255 developmental changes 185–6
ego 298 frequency ranges 185
ego defence mechanisms 298 infant 185
associated mental states 299 normal 185–6
ego functions 298 organic psychosis detection 188
eidetic images 15 psychiatric uses 188
ejaculatory impotence 97 seizure diagnosis 188
behaviour therapy 102 sleep 186
Ekbom’s syndrome 146 disorder diagnosis 188
elderly patients see psychogeriatrics neurotransmitters 186
Electra complex 300 stupor 188
INDEX 345
electrolyte disturbance 169 erectile dysfunction (impotence) 97

emotional blunting 19 antidepressants side-effect 272
emotional disorders 18–19 behaviour therapy 102
abnormal expression 19 organic causes 101
abnormal reactions 18–19 erotomania 145
predisposition 18 error 4, 6
emotional incongruity 19 euphoria 19, 49
emotional incontinence 19 evidence-based medicine (EBM) 11
emotional indifference 19 excretion, drug 267
emotional lability 19 exhibitionism 103–5
encephalitis lethargy 167 aetiology 104
encopresis 241–2 classification 104
management 242 epidemiology 104
endocrine disorders 164 management 104
alcohol dependence 117 prognosis 104–5
depression 50 expressive behaviour disorders 14
enuresis 240–1 expressive dysphasias 21
aetiology 241
associated features 240–1 family therapy 304
epidemiology 241 fetal alcohol spectrum disorder (FASD) 117
management 241 fetal alcohol syndrome (FAS) 117
prognosis 241 firebugs 221
epigenesis 78 first arch syndromes 256
epilepsy 175–80 flexibilitas cerea 15
aetiology 176 flooding (implosion) 65
classifications 175–6 folie à deux 148
depression 50 folie à plusieurs 148
diagnosis 177 folie simultanée 148
differential diagnosis 177 forensic psychiatry 215–32
EEG 187 competence to consent to treatment 227
epidemiology 176 court report preparation 225
genetic counselling 176 criminal responsibility (UK only) 226–7
ictal phase involuntary commitment 228
automatisms 177 legal aspects 225–8
fugues 177 negligence 227–8
twilight states 178 psychiatric defences 225–6
inter-ictal periods 178–9 testamentary capacity 227
aggressive behaviour 178 fragile X syndrome 256
dementia 179 Fregoli’s syndrome 144
depression 178 frigidity see anorgasmia
schizophreniform psychosis 178–9 frontal lobe dementia 162
suicide 178 frontal lobe dysfunction 151
mental retardation 261 frontal lobe syndrome 162
post-ictal phase 178 frontal lobe syndrome of disinhibition 160
preictal phase 177 functional MRI (fMRI) 192
aura 177 attention-deficit/hyperactivity disorder
prodromal features 177 244
prognosis 176
seizures 175–6 GABA neurotransmission, Huntington’s
treatment 179–80 cholera 160
episodic dyscontrol syndrome 178 gabapentin 179, 281
346 INDEX
galactosaemia 258 hashish 127

galantamine 158 Hatchinski index 159
gambling, pathological 130–1 head injury
addiction phases 131 diffuse 170
classification 130 focal 170
management 131 medico-legal aspects 172
gamma hydroxybutyric acid (GHB) 128 psychiatric sequelae 171–2
Ganser’s syndrome 146–7 aetiology 171
Gaucher’s disease 259 classification 171–2
general paresis (GPI) 166 sequelae 170–2
general practice care 315–16 hepatitis, alcoholic 117
genetic abnormalities, mental retardation hermaphroditism 100
256–7 heroin 126
genetic counselling herpes simplex encephalitis 167
epilepsy 176 high expressed emotion (HEE) 35
mental retardation 263–4 Hirano inclusion bodies 156
geriatric disorders see psychogeriatrics histamine, sleep EEG 186
Gerstmann’s syndrome 152 HIV infection
Gilles de la Tourette’s syndrome (GTS) affective disorder 168
246–7 AIDS dementia complex 167
aetiology 246–7 neurosyphilis 166
clinical features 247 substance abuse 130
course 247 see also acquired immunodeficiency
epidemiology 246 syndrome (AIDS)
genetics 246 home based treatment 313
MRI 190 homelessness 314–15
obsessive-compulsive disorder 70, 246 homicide 219
prognosis 247 homocystinuria 258
tics 247 homosexuality 106
glutamate neurotransmission homovanillic acid 269
Huntington’s cholera 160 hospital admission
schizophrenia 33 affective disorder 208
grand mal seizure 175 alcohol dependence 110
grief reaction puerperal psychosis 324
atypical 55 Hunter’s syndrome (mucopolysaccharidosis
chronic 55 type 2) 257, 259
psychogeriatrics 206–7 Huntington’ s chorea 160–1
typical 55 aetiology 160
group therapy 304–5 children 161
analytic groups 304–5 clinical features 161
therapeutic communities 305 CT 190
growth hormone 113 subcortical dementia 163
Hurler’s syndrome (mucopolysaccharidosis
Hallerman–Streiff syndrome 256 type 1) 259
hallucinations 15 hydrocephalus 162
alcoholic 114 5-HT see serotonin
narcolepsy 182 17 hydroxysteroid deficiency 100
hallucinogens 127 hyperparathyroidism 164
haloperidol 246 hyperprolactinemia 271
handicap 253 hypertelorism 257
Hartnup’s disease (renal aminoaciduria) 258 hypertensive crisis 277
INDEX 347
hyperthyroidism 164 affective disorders 49

hyperuricaemia, idiopathic 259 Alzheimer’s disease 157
hyperventilation syndrome 67 schizophrenia 33–4
hypochondriasis 200–1 impaired consciousness, head injury 170
management 201 impairment 253
prognosis 201 implosion (flooding) 65
hypofrontality hypothesis 191 impotence see erectile dysfunction
hypoglycaemia, idiopathic 258 impulsive type personality disorder 79
hypomanic states 45–6 inappropriate soiling 240–2
behavioural features 45 inborn errors of metabolism 257–9
elderly 207–8 incest 105, 223
seasonal affective disorder 55 offender characteristics 223
hypoparathyroidism 164 victim characteristics 223
hypopituitarism 164 indecent exposure 103
hypothyroidism 164, 279 infanticide 219
hypothyroidism (cretinism) 259 infection 166–8
hysterectomy 325 depression 50
hysteria-allied syndromes 146–8 mental retardation 260
inferential statistics 8–9
ICD-10 classification informed consent 227
affective disorders 44 insight 21–2
alcohol dependence 109 insomnia 180–2
anorexia nervosa 90 drug therapy 181–2
antisocial personality disorder 215 management 181–2
anxiety disorders 60 risk factors 181
bipolar affective disorder 44 institutionalization 312
bulimia nervosa 92 elderly 211
child psychiatric disorders 233 problems with 312
delirium 154 intellectual function disorders 20–1
depressive episode 44 intellectualization 299
manic episode 44 intermetamorphosis, syndrome of 144
mental retardation 253 International Classification of Diseases, 10th
obsessive-compulsive disorder 60 edn see ICD-10 classification
pathological gambling 130 internet 333–5
persistent mood disorders 44 search engines 334
personality disorders 79 interpersonal psychotherapy (IPT) 308
post-traumatic stress disorder 68 affective disorders 53
recurrent depressive disorders 44 intersexual disorders 100
schizophrenia 26, 26, 28 interventional strategies, schizophrenia 35,
sexual disorders 98 35
somatoform disorders 197 interviews 4–6, 5–6
stress reaction 60 involuntary commitment 228
substance abuse 123–4 involutional melancholia 325
substance dependence 123 isolation 299
illness
psychological reactions 196–7 Jacksonian seizure 175
response patterns 197 jail diversion programme 228
illness phobia 64
illusions 15 killing 219–20
imipramine 275–6 definition 219
immunology epidemiology 219–20
348 INDEX
Kleine–Levin syndrome 183 ‘made actions’ 17

Klinefelter’s syndrome (XXY genotype) magic mushrooms 127
100, 256 magnetic resonance imaging (MRI)
Klüver–Bucy syndrome 157 affective disorders 49, 190, 206
koro 329 AIDS dementia complex 168
Korsakoff ’s psychosis 115, 164 Alzheimer’s disease 190
autism 190, 236
la belle indifférence 19 childhood -onset schizophrenia 237
lamotrigine 179, 281 Creutzfeldt–Jakob disease 161
side-effects 281 depression 190
uses 281 Gilles de la Tourette’s syndrome 190
language function disorders 21 mild cognitive impairment 190
latah 329 Pick’s disease 190
Laurence–Moon–Biedl syndrome 257 psychiatric uses 189–90
lead toxicity 165 schizophrenia 33, 189
Lesch–Nyhan syndrome 259 structural investigations 189
leucotomy 294 substance abuse 190
levomethadyl acetate (LAAM) 129 Wernicke–Korsakoff syndrome 190
Lewy-body (LB) 162 magnetoencephalography (MEG) 189
Lewy-body dementia 162 manganese toxicity 165
liaison psychiatry 196 manic-depressive psychosis 207–8
libido 101, 298 manic states 45–6
lipid metabolism disorders 258–9 assessments 5
lithium 277–80 behavioural features 45
actions 278 cognition 45
affective disorders 53 ECT indications 289
breast feeding 268 ICD-10 classification 44
cautions 280 management 53
dose stabilization 279 mental retardation 261
drug interactions 280 rapid cycling 56
HIV-mania 168 violence 218
kinetics 278 manic stupor 54
mental retardation 230 mannerisms 14
monitoring 280 manslaughter 219
plasma level 279 maple syrup disease 258
pregnancy 268 Marchiafava–Bignami disease 116
schizoaffective disorder 37 Marinesco–Sjögren syndrome 257
side-effects 279–80 masked (atypical) depression 207
suicide prevention 138, 277 children 238
uses 279 Masters and Johnson technique 102, 103
liver damage 117 maternal deprivation 234–5
liver enzymes 266, 267 McNaughten rules 226
liver failure 169 MDMA (ecstasy) 128
living will 229 melancholia 43
logoclonia 14 memantine 158
lorazepam 119 memory 20–1
Louis–Bar syndrome 257 Alzheimer’s disease 157
love object 298 temporal lobe dysfunction 152
Lowe syndrome 257 tests 21
lycanthropy 144 Menkes ‘kinky hair’ syndrome 257
lysergic acid diethylamide (LSD) 127 menopause 325
INDEX 349
mens rea 226 contraindications 277

mental impairment 254 precautions 277
mental retardation 253–65 side-effects 276–7
aetiology 254 monosymptomatic hypochondriacal
assessment 6 psychosis 146
developmental 262 mood 18
general 262 mood disorders
medical 261 children 237–8
chromosomal abnormalities 255–6 children/adolescents 237–8
coding 253–4, 254 delusional 16
definitions 253–4 depression 45
educational services 262 hypomanic/manic states 45
epidemiology 254, 319 ICD-10 44
epilepsy 261 mood stabilizers 277–81
management principles 262–3 morbid jealousy 145
medical 262 morphine 126
parental guidance 263 motivational enhancement therapy (MET)
psychiatric 263 308
manic depressive psychosis 261 alcohol dependence 120
neurotic disorders 261 motivational state, abnormal 299
non-genetic causes 259–60 motor cortex dysfunction 151
prevention 263–4 motor disorders (general behaviour) 13–15
tertiary 263–4 mourning 55
psychiatric disorders 260–1 movement disorders, adaptive 14
residential services 262 MRI see magnetic resonance imaging
schizophrenia 260 MR spectroscopy 192
services required 261–2 mucopolysaccharidosis type 1 (Hurler’s
assessment 261–2 syndrome) 259
guidelines 261 mucopolysaccharidosis type 2 (Hunter’s
meperidine 126 syndrome) 257, 259
mercury toxicity 165 mucopolysaccharidosis type 3 (Sanflippo’s
mescaline psilocybin 127 syndrome) 259
metabolic disorders 169–70 multiple personality disorder see dissociative
depression 50 identity disorder
methadone 126, 129 multiple sclerosis 170
methylphenidate 245, 285 multiple sleep latency test (MSLT) 182
mianserin 276 Münchausen by proxy 148
microcephaly 257 Münchausen syndrome 147–8
middle cerebral artery occlusion 153 clinical features 147–8
mild cognitive impairment (MCI) 159 management 148
MRI 190 murder 219
mirtazapine 274 myopathy, alcoholic 116
miserable mania 208
mitgehen 14 naltrexone
mitmachen 14 alcohol dependence 119
mitral valve prolapse 66–7 substance abuse 129
modelling, phobic disorders 65 narcolepsy 182–3
monoamine oxidase inhibitors (MAOIs) aetiology 182
276–7 clinical features 182
affective disorders 53 diagnosis 182
anxiety disorders 63 treatment 183
350 INDEX
nefazodone 274 induced movements 14

negligence 227–8 posture disorders 15
nephrogenic diabetes insipidus 259 non-benzodiazepine hypnotics 283, 283
lithium side-effect 279 non-epileptic attack disorder 180
nephropathy 279 non-parametric statistics 8, 8
neurasthenia 202 non-psychostimulants 286
neurofibrillary tangles (NFTs) 156 non-violent offenders 224–5
neuroimaging 188–92 noradrenaline
clinical applications 192 affective disorders 48
functional investigations 191–2 Alzheimer’s disease 157
research applications 192–3 schizophrenia 33
schizophrenia 33 nortriptyline 276
structural investigations 189
see also individual techniques obesity 86–7
neurokinin 1 49 aetiology 86
neuroleptic malignant syndrome (NMS) management 87
271 obsessional phenomena 16
neuroleptics obsessions 70
schizoaffective disorder 37 obsessive-compulsive disorder (OCD)
schizophrenia 34–5 69–72, 70
neuropeptide Y (NPY) 112 aetiology 70–1
neuroses anankastic type personality 71
cultural aspects 329 assessments 5
head injury 171 body dysmorphic disorder 201
school refusal 240 course 72
women 318 DSM-IV criteria 60
neurosyphilis 166 epidemiology 70
neurotic depression 43–4 genetics 70
neurotic disorders 60–76 Gilles de la Tourette’s syndrome 246
anxiety disorders 60–3, 60 ICD-10 classification 60
mentally handicapped 261 neuroanatomy 71
neurotransmitters neurochemistry 71
anxious patients 66 PANDAs 71
lithium 278 PET 192
sleep EEG 186 phenomenology 70
nicotinic acid deficiency (pellagra) 163 prognosis 72
Niemann–Pick disease 258 psychosurgery 294, 295
nightmares 183 theories 71
post-traumatic stress disorder 68 treatment 71–2
night terrors 183, 242 obstruction 14
night-time incidents 242 occipital lobe dysfunction 153
nihilistic delusions 148–9 Oedipal complex 300
non-accidental injury, children 221–3 opioids 126
classification 221 alcohol dependence 113
clinical features oppositional defiant disorder (ODD) 246, 247
child 222 optic atrophy 116
parents 222 orbital cortex 151
prevention 222–3 orbital undercutting 295
definition 221 organic disorders 150–74
epidemiology 222 acute see delirium
non-adaptive movements 14 arterial occlusion 153
INDEX 351
brainstem dysfunction 153 pareidolia 15

cerebral function localization 151–3 parental absence 50
chronic see dementia parietal lobe dysfunction 152
cultural aspects 330 Parkinsonism 270
diencephalon dysfunction 153 Parkinson’s disease
differential diagnosis 150 deep brain stimulation 293
EEG 188 Lewy-bodies 162
frontal lobe dysfunction 151 psychosurgery 294
neuropsychiatric assessment 153–5 passivity phenomena 16–17
occipital lobe dysfunction 153 Patau’s syndrome (trisomy 13–15) 255
parietal lobe dysfunction 152 pediatric autoimmune neuropsychiatric
soft signs 154 disorders (PANDAs) 71
temporal lobe dysfunction 152 pellagra (nicotinic acid deficiency) 163
orlistat 87 pemoline 286
orofacial dyskinesia 14 pentazocine 126
Othello syndrome 145 perception disorders 15
outpatient clinics 211 performance anxiety 99, 101
oxazepam 119 perseveration 14, 21
oxcarbazepine 281 personality 77
development theories 77–8
paedophilia 105, 223 tests 5
pain disorder 200 personality changes
assessment 200 pseudodepressive 151
clinical features 200 pseudopsychopathic 151
management 200 personality disorders (PD) 78–83
palilalia 14 aetiological theories 80–2
pandysmaturation 32 assessments 5, 80, 83
panic disorder 61 behavioural psychology 81
clinical symptoms 61 biopsychosocial model 80
DSM-IV criteria 60 borderline 81
hyperventilation syndrome 67 childhood experiences 82
PET 192 classification 80
parametric statistics 8, 8 DSM-IV 79
paranoid personality disorder 79 ICD-10 79
paranoid syndromes 209–10 definitions 78–9
aetiology 209 epidemiology 80
clinical features 210 frontal lobe dysfunction 151
differential diagnosis 210 genetics 81–2
environmental factors 209 head injury 171
epidemiology 209 prognosis 83
genetics 209 psychodynamic theory 81
organic causes 209 self-image 81
personality features 209 suicide 136
prognosis 210 temperament 82
sensory defects 209 temporal lobe dysfunction 152
treatment 210 treatment 83
paraphilias 103–6 pervasive development disorder see autism
paraphrenias 209–10 PET see positron emission tomography
parapraxes 298 petit mal seizure 175
parasomnias 183 petit mal variant seizure 175
parasuicide 134 phaeochromocytoma 164
352 INDEX
pharmacodynamics 266–8 prognosis 69

pharmacogenetics 268 posture disorders 15
pharmacokinetics 266–8, 267 power of attorney 229
absorption 266 Prader–Willi syndrome 257
drug excretion 267 praecox feeling 24
drug interactions 267–8 pregnancy 320–1
metabolism 266–7 alcohol 117
phenomenology 13 drug prescribing 268
phenylcyclidine (PCP) 127 drug treatment 321
phenylketonuria 258 epidemiology 320–1
phenytoin 179 management 321
phobic disorders 63–5 psychotropics 321
animal phobias 64 termination 324–5
DSM-IV criteria 60 tricyclics 276
ICD-classification 60 premature ejaculation 97
illness phobia 64 behaviour therapy 102
social phobia 64 premenstrual syndrome 320
treatment 64–5 premorbid personality
physical treatments 289–96 affective disorders 51
Pick’s cells 160 obsessive-compulsive disorder 71
Pick’s disease 160, 190 premotor cortex dysfunction 151
pickwickian syndrome 183 pressure of speech 17
placebo effect 9 priapism 101
polymorphisms, genetic 268 prion disorder 161
porphyria, acute intermittent 169–70 prison inmates
port wine syndrome (Sturge–Weber mental illness 229
syndrome) 257 suicide 137
positron emission tomography (PET) 191–2 progesterones 320
affective disorders 49, 192 Programme of Assertive Community
Alzheimer’s disease 192 Treatment (PACT) 313
antipsychotic medication 269–70 projection 298
Gilles de la Tourette’s syndrome 246 projective identification 298
obsessive-compulsive disorder 71, 192 prolactin 47
panic disorder 192 propranolol 69
schizophrenia 33, 191 protein metabolism disorders 258
post-concussional syndrome 171 pseudocyesis (false pregnancy) 198
posterior cerebral artery occlusion 153 pseudohallucinations 15
posterior inferior cerebral artery occlusion 153 pseudohermaphroditism 100
postpartum ‘blues’ 323 pseudoseizures 180
management 324 psychiatric advance directives 228–9
postpartum psychiatric disorders 321–4 psychiatric defences (UK only) 225–6
management 324 diminished responsibility 226
post-traumatic amnesia (PTA) 170–1 not guilty by reason of insanity 226
post-traumatic stress disorder (PTSD) 67–9 special verdict 226
aetiology 68 unfit to plead 225–6
clinical features 68 psychic retardation 17
co-morbidity 68 psychoanalysis 297–300
drug treatment 69 definition 297–9
ICD-10 classification 68 theorists 300–4
management 69 British schools 302
prevention 69 early 300–1
INDEX 353
international approach 303–4 history 294

Neo-Freudians (USA) 302 indications 294–5
post-Freudians 303 obsessive-compulsive disorder 72
unconscious 299 outcome 295
psychogeriatrics 205–14 procedures 294
affective disorder 205–8 prognosis 295
aetiology 206–7 psychotherapy 297–311
clinical features 207–8 affective disorders 52–3
environmental factors 206–7 anorexia nervosa 90
epidemiology 205–6 anxiety disorders 62
genetics 206 common features 297
management 208 elderly patients 212
organic factors 206 levels 297
prognosis 208 mental retardation 230
assessments 6 obesity 87
epidemiology 205, 205 obsessive-compulsive disorder 71
home support 211 patient suitability 299–300
management 211–12 personality disorders 83
drug therapy 211 phobic disorders 65
inpatient issues 212 psychoanalysis 297–300
principles 211 research 308–9
psychotherapy 212 arousal 309
paranoid syndromes 209–10 methodological problems 308
services organization 212 outcomes 308–9
suicide 137 patient assessment 309
psychometric testing 6–7 process 309
psychoneurosis 298 standardizations 308
psychopathology, descriptive 13–23 therapist skills 309
psychophysiological disorders 195–7 schizophrenia 35–6
psychophysiological tests 7 sexual dysfunction 103
psychosis see also specific modalities
affective 171 puerperal depression 323
AIDS 168 management 324
head injury 171–2 puerperal psychosis 321–2
schizophreniform 172 aetiology 321–2
psychosocial treatment biochemical causes 321
epilepsy 180 bonding lack 322
schizophrenia 35 clinical features 322
psychosomatic specificity hypothesis 195 epidemiology 321
psychostimulants 285–6 genetics 321
attention-deficit/hyperactivity disorder management 324
245 prognosis 322
contraindications 286 psychodynamic factors 322
side-effects 286 punch-drunk syndrome 163
uses 286
psychosurgery 293–5 questionnaires 4–6
anxiety disorders 63
contraindications 295 rape 220
definitions 293–4 rapid cycling mania 56
epilepsy 180 reaction formation 298
ethical/legal issues 295 reactive depression 43–4
354 INDEX
reality testing 81 ECT indications 289

‘recovery’ approaches, schizophrenia 35 epidemiology 29–30, 319
recovery model 313 family dynamics 34
5␣-reductase deficiency 100 first-rank symptoms 25
reduplicative paramnesia 144 genetics 30–2, 30
Refsum’s disease 259 immunology 33–4
regional cerebral blood flow (rCBF) 191 life events 34
rehabilitation assessment 315 management 34–6
relationship behaviour, normal 97 mental retardation 260
reliability 3 migration 330–1
reliability paradox 3 neurochemistry 32–3
renal aminoaciduria (Hartnup’s disease) 258 neurodegenerative 29
repression 298, 299 neurodevelopment 29
research design 2–3 neuroimaging 33
research methodology 1–12 CT 33, 189
definitions 2–4 functional MRI 192
measurements 4–7 MRI 33, 189
planning 1–2 MR spectroscopy 192
sample selection 4, 10 PET 33, 191
statistics 7–9 SPECT 191
trial design 10 neuropathology 33
research protocol 1–2 poor outcome predictors 36
research publication review 10–11 positive/negative disorganization
retrograde amnesia 170 syndromes 28
Rett’s syndrome 259 prodromal studies 32
rhesus-negative screening 264 prognosis 36, 37
rivastigmine 158 psychophysiology 33–4
psychosis continuum 29
sample selection 4, 10 relapse rates 35, 35
Sanflippo’s syndrome spectrum 31, 31
(mucopolysaccharidosis type 3) 259 substance abuse 124
schizoaffective disorder 36–7 suicide 136
DSM-IV criteria 36 symptoms
management 37 positive/negative 28
prognosis 37, 37 ranking 25
women 319 thought disorders 17–18, 17
schizoid personality disorder 79 type I/type II syndromes 28
schizophrenia 24–42 violence 218
aetiology 30–4 women 319
arson 221 xenon inhalation 191
assessments 5 schizophrenia-like syndrome 178–9
childhood -onset 237 school refusal 239–40, 239
classification 25 aetiology 240
cognitive impairment 29 course 240
concepts 24–5 epidemiology 239
controversies 27–9 prognosis 240
cultural aspects 328–9 seasonal affective disorder (SAD) 55–6
deficit syndrome 29 treatment 56
diagnostic criteria 25–9 sedatives 282–4
DSM-IV 26, 27, 28 seizures 175–6
ICD-10 26, 26, 28 EEG 188
INDEX 355
selective serotonin re-uptake inhibitors shaken baby syndrome 221

(SRRIs) 273–4 shell-shock syndrome see post-traumatic
affective disorder 208 stress disorder
anxiety disorders 62–3 shoplifting 224–5
body dysmorphic disorder 201 epidemiology 225
bulimia nervosa 93 sibutramine 87
obsessive-compulsive disorder 71 single photon emission computerized
phobic disorders 65 tomography (SPECT)
pregnancy 321 affective disorders 191
premenstrual syndrome 320 Alzheimer’s disease 191
side-effects 274 Gilles de la Tourette’s syndrome 246
uses 273–4 schizophrenia 191
self-awareness disorders 19–20 sleep apnoea 183
self-mutilation, repeated 140 sleep deprivation, affective disorders 54
senile melancholia 207 sleep disorders 180–3
sensate focus technique 102 alcoholism 182
sensory deceptions 15 Alzheimer’s disease 158 # check ref #, 182
sensory distortions 15 anxiety 182
serotonin (5-HT) classification 180
affective disorders 47 depression 182
alcohol dependence 113 EEG diagnosis 188
Alzheimer’s disease 157 sleep EEG 186
bulimia nervosa 91 neurotransmitters 186
personality disorders 81 sleep hygiene, insomnia 181
schizophrenia 32 sleepwalking 183, 242
suicide 137–8 social phobia 64
serotonin syndrome 272 social therapy, affective disorder 208
sex chromosome abnormalities 255–6 sodium lactate infusion response 66
sexual abuse see child sexual abuse (CSA) somatization disorder 197–8
sexual behaviour, normal 96–7 somatoform disorders 197–201
epidemiology 96 classification 197
neurophysiology 97 conversion disorder 198–9
physiology 97 hypochondriasis 200–1
relationship behaviour 97 pain disorder 200
sexual development 300 somatization disorder 197–8
stages 300 specific reading retardation (SRR) 242–3
theories 300 associated features 243
sexual dysfunction 97–106 SPECT see single photon emission
aetiology 100–1 computerized tomography
assessment 99–100 spectatoring 101
behaviour therapy 102 speech changes
classifications 98–9, 98, 99 depression 45
definitions 97–8 hypomanic/manic states 45
drug treatment side effects 103, 271, 272, splitting 299
275 standard deviation 8
female 97 statistics 7–9
investigations 100 descriptive 7–8
male 97 inferential 8–9
prognosis 103 non-parametric 8, 9
psychotherapy 103 parametric 8, 9
treatment 101–3 Steele–Richardson–Olszewski 163
356 INDEX
sterilization 325 hypothalamic-pituitary -adrenal axis 138

sterotypies 14 illness 136
Steven Johnson syndrome 281 management 138
stillbirth 325 neurochemistry 137–8
stimulants 285–6 obsessive-compulsive disorder 70
stress reaction personality disorders 136
DSM-IV criteria 60 pregnancy 321
ICD-10 classification 60 prevention 138
stroke victims 49 prison inmates 137
stupor 20 psychiatric illness 135–8
EEG 188 schizophrenia 30, 136
manic 54 victim characteristics 135
Sturge–Weber syndrome (port wine women 319
syndrome) 257 sundowning 158, 182
subcortical dementia 163 surgery see psychosurgery
sublimation 299 survey 4
substance abuse (SA) susto 329
aetiological theories 125–9 symptomatic disorders 245–7
assessments 6 syndrome of approximate answers 146–7
behavioural theories 125 systemic desensitization 65
children/teenage 248–9
co-morbidity 124 tabes dorsalis 166
DSM-IV 123–4 tarasoff doctrine 228
epidemiology 124–5 tardive dyskinesia (TD) 271
genetics 125 Tay–Sachs disease 258
HIV 130 temporal lobe
ICD-10 123–4 language functions 21
management 129 schizophrenia 33
MRI 190 temporal lobe dysfunction 152
pattern of abuse 125 termination of pregnancy 324–5
physiological theories 125 testamentary capacity (UK only) 227
prevention 130 testicular feminization syndrome (Y
prognosis 130 genotype) 100
psychosocial treatments 129 therapeutic alliance 299
theories 125–9, 126–8 thiamine (B1) deficiency 163–5
violence 218 Wernicke’s encephalopathy 114–15
suicide 134–8 thought blocking 18
adolescents 137 thought broadcast 17
AIDS 168 disordered forms of thinking 17–18
alcoholism 136 thought disorders 16–18
biological factors 137–8 disordered content 16–17
children 238 schizophrenic 17–18, 17
definitions 134 thought insertion 17
deliberate self-harm 139 thought stopping 71
depression 136 thought withdrawal 17
drug prevention 277 thrombocytopenia 117
elderly 137, 207 tiagabine 281
epidemiology 134–7, 135 tics 14, 245–6
epilepsy 178 aetiology 246
genetics 138 associated features 245
hospital inpatients 137 course 246
INDEX 357
differential diagnosis 245 validity 3

epidemiology 246 valproate (valproic acid) 280
Gilles de la Tourette’s syndrome 247 affective disorders 53
management 246 epilepsy 179
prognosis 246 schizoaffective disorder 37
topiramate 281 side effects 280
toxic confusion 165 uses 280
toxins 165 variables 2
trait approach 80 variant Creutzfeldt–Jakob disease (vCJD)
transcranial magnetic stimulation (TMS) 161
293 vascular dementia (VaD) 159
transcultural psychiatry 328–32 velo-cario-facial syndrome (VCFS) 257
assessment 330 venlafaxine 63, 275
migration 330–1 ventriculo-atrial shunts 162
treatment 330 violence
transference 299 epidemiology 218, 218
research 309 management 230
transsexualism 106 mental illness 217–19
transvestism 105 patient assessment 218–19
trauma, mental retardation 260 repeated 219
traumatic neurosis see post-traumatic stress violent crime 219–24
disorder Virchow–Seckel dwarf 257
trazodone 274 visuospatial functions 21
treatment resistant depression, vagus nerve vitamin B12 deficiency 165
stimulation 293 vitamin deficiencies 163–5
tricyclic antidepressants 275–6 volatile substance abuse (VSA) 128
contraindications 276 vomiting, conversion disorder 198
drug interactions 276 vulnerability-stress models 34
enuresis 241
precautions 276 ‘waxy flexibility’ 15
pregnancy 321 websites 333–4
side-effects 275 governmental 333
trisomies 255–6 non-governmental 333–4
trisomy 13–15 (Patau’s syndrome) 255 Wechsler Adult Intelligence Scale 6
trisomy 17–18 (Edwards’ syndrome) 255 weight phobia 88
trisomy 21 see Down syndrome Wernicke–Korsakoff syndrome 114–15
tuberous sclerosis 256 detoxification 119
Turner’s syndrome (XO genotype) 100, 256 MRI 190
turning against the self 298 Wernicke’s encephalopathy 114–15
Twelve-Step Facilitation (TSF) 120 thiamine deficiency 114–15, 163
windigo 329
ultraviolet light therapy 56 Wisconsin Card Sorting Test (WCST), xenon
unfit to plead 225–6 inhalation 191
uraemia 169 withdrawal
urinary tract infection, enuresis 241 alcohol dependence 113, 114
tricyclics side-effect 275
vaginismus 97 Wolf syndrome 255
behaviour therapy 102 women, psychiatric problems 318–27
vagus nerve stimulation (VNS) 293 epidemiology 318–19
epilepsy 180 affective disorders 318–19
side effects 293 alcoholism 319
358 INDEX
women, psychiatric problems (contd) World Health Organization (WHO)

anorexia nervosa 319 mental retardation definition 253
criminal behaviour 319 psychosurgery definition 295
mental handicap 319 wrist-cutting, repeated 140
neuroses 318
schizoaffective disorder 319 xenon inhalation 191
schizophrenia 319 X-linked disorders 257
self harm 319 XO genotype (Turner’s syndrome) 100, 256
senile dementia 319 XXX genotype 255
suicidal behaviour 319 XXY genotype (Klinefelter’s syndrome) 100,
hysterectomy 325 256
pregnancy 320–1 XYY genotype 256
premenstrual syndrome 320
stillbirth 325 zidovudine (AZT) 168
working alliance 299 zolpidem 182
working through 299 zopiclone 182

Examination Notes in Psychiatry

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Examination Notes in Psychiatry

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Examination Notes in

PETER BUCKLEY MD MRCPsych

JONATHAN BIRD BSc MB ChB FRCPsych

GLYNN HARRISON MD FRCPsych

Distributed in the United States of America by

All rights reserved. No part of this publication may be reproduced or

British Library Cataloguing in Publication Data

Library of Congress Cataloging-in-Publication Data

ISBN-10: 0 340 81003 3

Commissioning Editor: Serena Bureau

Typeset in 9/11pt Minion by Charon Tec Pvt. Ltd, Chennai, India

1 Find a problem – from everyday practice, past research or theory.

• Statement of hypotheses to be tested

Designs may also be:

SAMPLE SELECTION (see also Chapter 21)

MEASUREMENT IN PSYCHIATRIC RESEARCH

QUESTIONNAIRES, INTERVIEWS AND CASE-NOTE STUDIES

Aims may be:

Table 1.1 Commonly used psychiatric instruments

Table 1.1 Continued

Minnesota Multiphasic Personality Self-rating questionnaire, validated on

Psychological tests must be:

These are the quantification of biological events as they relate to psychological

These simply summarize the data.

MEASURES OF CENTRAL TENDENCY

These assess the meaning of the data.

Table 1.2 Parametric and non-parametric tests

(Student’s) t-test Chi-squared (␹2)

THE PLACEBO EFFECT

A placebo is any therapeutic procedure (or that component of a therapeutic proced-

See Freeman and Tyrer (1992).

Analysis and presenting results

REVIEWING A RESEARCH PUBLICATION

• Title and abstract – should be interesting, informative.

EVIDENCE-BASED MEDICINE (EBM) AND PSYCHIATRY

REFERENCES AND FURTHER READING

Descriptive psychopathology attempts to portray in words, as subtly and accurately as

DISORDERS OF APPEARANCE AND BEHAVIOUR

Appearance (state of health, posture, cleanliness, clothing, self-care) is an important

MOTOR DISORDERS (OF GENERAL BEHAVIOUR)

The form of abnormal movements may be classified (after Hamilton, 1974) as

DISORDERS OF ADAPTIVE MOVEMENTS

Other mental images

OBSESSIONS AND COMPULSIVE PHENOMENA

DISORDERED FORM OF THINKING

DECREASED TEMPO – PSYCHIC RETARDATION

SCHIZOPHRENIC THOUGHT DISORDER

Table 2.1 Some descriptive terms

Bleuler (1951) Loosening of associations, condensation

Other features of schizophrenic thought disorder

ABNORMAL EMOTIONAL PREDISPOSITION

ABNORMAL EMOTIONAL REACTIONS

by disturbance of appetite, sleep, concentration, etc., or by depressive delusions.

ABNORMAL EXPRESSION OF EMOTION

Self-experience has four aspects, according to Jaspers (1959):

AWARENESS OF THE EXISTENCE OF ACTIVITY OF THE SELF

The alteration of awareness of one’s activities (moods, thoughts, acts) as belonging

DISORDERS OF INTELLECTUAL FUNCTIONS

ATTENTION AND CONCENTRATION

LANGUAGE FUNCTIONS (PARTICULARLY CENTERED IN THE TEMPORAL LOBE)

Language functioning is tested both by listening to spontaneous conversation and by

VISUOSPATIAL FUNCTIONS (PARTICULARLY CENTRED IN THE PARIETAL LOBE)

Insight according to Lewis (1934) is a ‘correct attitude to morbid change in oneself ’.

According to Amador et al. (1993), insight includes: