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Epilepsy: mimics,
Correspondence to
Professor Phil E M Smith,
Department of Neurology, The
Epilepsy Unit, University Hospital
of Wales, Cardiff CF14 4XW, UK;
smithpe@cf.ac.uk
Received 10 April 2012
Accepted 5 August 2012
borderland and chameleons
Phil E M Smith
Abstract
Epilepsy mimics such as syncope and
psychogenic attacks, can present like epilepsy,
and can be erroneously managed as epilepsy.
There are also several conditions at the
borderland that closely relate to epilepsy yet are
probably separate from it, eg. migralepsy and
parasomnia. Finally, there are times when
epileptic seizures resemble one of the epilepsy
mimics. This is epilepsy in disguise—the epilepsy
chameleons. Seizures with typically unusual
manifestations, such as occipital or parietal lobe
seizures, or those occurring in situations where
another cause seems more likely, eg, in a person
with alcoholism, may well be overlooked as
epilepsy and initially escape diagnosis. This
review explores the mimics of adult epilepsy, the
epilepsy borderland, and focuses particularly on
epilepsy chameleons.
Introduction
The wide differential diagnosis of epi-
sodic altered consciousness presents a
major diagnostic problem.1 Epilepsy
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mimics, notably syncope and psycho-
genic attacks, can present like epilepsy,
and may be managed erroneously as
epilepsy (often for the long term),
yet clearly are distinct from it.
Furthermore, there are several condi-
tions closely relating to epilepsy that
are probably separate from epilepsy,
for example, migralepsy and parasom-
nia: these are at the borderland of epi-
lepsy. Finally, there are situations when
epileptic seizures resemble one of the
epilepsy mimics. This is epilepsy in
disguise—an epilepsy chameleon.2
Figure 1 shows the diagrammatic rela-
tionship between epilepsy, its border-
land, its mimics and its chameleons.
Note that epilepsy mimics are part of
other conditions’ chameleons list, for
example, of transient ischaemic
attacks, dementia, multiple sclerosis.
Similarly, all epilepsy chameleons
appear on the lists of other conditions’
mimics (figure 2).
In practice, the labelling of episodic
loss of consciousness errs more
towards diagnosing epilepsy when it
is not, rather than failing to diagnose
epilepsy when it is. Thus, epilepsy
mimics are more problematic in prac-
tice than are epilepsy chameleons.
Nevertheless, our patients need us to
recognise and treat their epilepsy
promptly when it occurs, even if it
comes in disguise.
This review briefly explores mimics
of adult epilepsy, the epilepsy border-
land, and focuses particularly on epi-
lepsy chameleons. The main focus
here is in on adults: paediatric presen-
tations are more complex, with greater
propensity for misdiagnosis of parox-
ysmal events at either of the epilepsy
spectrum.
299
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Figure 1 Epilepsy: mimics, borderland and chameleons.
Epilepsy mimics
Syncope and psychogenic non-epileptic seizures
comprise the main mimics of epilepsy; others are
rare. The diagnosis of epilepsy is often incorrect,
perhaps up to 20% of cases. The main reason is that
epilepsy diagnosis relies largely on the history (and
witness account) rather than upon tests. Without a
consistent diagnostic test (such as there is for dia-
betes), clinicians must accept that epilepsy manage-
ment is often founded upon likelihood rather
than certainty. Although the inter-ictal EEG provides
additional information, it is rarely (in adults) suffi-
cient alone to make the diagnosis. Also, without a
Figure 2 One condition’s mimic is another condition’s
chameleon.
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test to monitor seizure frequency and severity—
equivalent to the ‘HbA1c’ in diabetes, there is no
alternative but to accept a patient’s report that there
have been, for example, three seizures in 6 months.
Some points in the history may be very
helpful in suggesting epilepsy: how the patient
tells the story;3 seizures clustering rather than
evenly spread out; and individual seizures being
stereotyped in character. Conversely, investiga-
tions may sometimes only muddy the water:
mimics are more often mislabelled as epilepsy
if undue weight is put upon a ‘positive’ EEG,
for example, photosensitivity or ‘epileptiform’
changes. The inter-ictal EEG is a great friend in
context, but a threat to well-being if seemingly
positive results are accorded power to overturn
a history-derived diagnosis. The three Cs of
EEG interpretation are ‘context, context and
context’.
Syncope
Syncope is the most common cause of sudden
loss of consciousness: most syncope is managed
either in primary care or is referred to a cardiolo-
gist. Myoclonic jerks are well known to accom-
pany syncope ( particularly following Lempert
et al’s4 memorable study). Those giving wit-
nessed accounts, often surprised and frightened
by the attack, will commonly overestimate how
long such jerks last. When patients with syncope
present to a neurologist it is usually because they
were thought first to have had a seizure. As a
result, neurologists see syncope mainly from the
severe end of a spectrum. These patients must be
considered carefully as a significant proportion
will have a cardiac (especially arrhythmogenic)
cause, which carries a high risk of sudden cardiac
death. On this basis discussions about the risk of
sudden unexplained death are perhaps more rele-
vant when the diagnosis is ‘unexplained loss of
consciousness’ than when the diagnosis is of
epilepsy.
Reflex syncope
Most transient loss of consciousness is reflex
(vasovagal) syncope, attributable to an overactive
autonomic nervous system in a young healthy
person. The classical tetrad (four Ps) of posture
(onset when upright), prodrome (blurring or
blacking of vision, nausea, light headedness and
sweating), provoking factors (sight of blood, pain
and bathroom) and prompt recovery are helpful
pointers, though none is diagnostic alone. Note
that nausea at the onset reflects vagal over-

Figure 3 Cardioinhibitory syncope during head-up tilt-table testing. The patient had been previously treated for epilepsy. At 20 min
into the tilt-table test, there was progressive bradycardia, culminating in cardiac arrest, with symptom reproduction; sinus rhythm
resumed on being lain flat.
activity, and so offers some reassurance as to the
benign nature of the blackout. Conversely,
absence of nausea leaves cardiac syncope as an
option. Reflex syncope can take other forms,
sometimes very severe with cardioinhibition and
convulsion (figure 3), sufficient convincingly to
mimic epilepsy. Other reflex syncopes have
unusual provoking stimuli; for example, mictur-
ition, coughing, swallowing, laughing or orgasm.
Carotid sinus syncope, unusually for a reflex
syncope, becomes more common with age: one
theory is that the rigidity of the ageing carotid
increases the carotid sinus movement resulting
from a physical stimulus.
Orthostatic syncope
Presyncope and syncope that quickly follow
standing suggest autonomic failure. The cause
may be autonomic neuropathy (eg, elderly and
diabetes mellitus) or vasodilator medications (eg,
for hypertension). The characteristic feature on
head-up tilt-table testing is a gradual fall in blood
pressure from the outset, without the usual com-
pensatory rise in pulse rate. Thus, in patients
with suspected orthostatic hypotension, lying
and standing blood pressure measurement is
helpful and worth spending a few minutes on
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(lying for 3 min, then measuring blood pressure
and pulse at 0, 3 and 5 min).
Cardiac syncope
Cardiac syncope often presents to neurologists as
a first suspected seizure. Textbooks may highlight
cardiac syncope as occurring on exertion; in
practice it more commonly presents as a sudden
unheralded loss of consciousness with subsequent
prompt and full recovery—the patient may
recover sufficiently to send away the ambulance
—or with convulsive seizures in sleep. Since
every such syncope represents an episode of
cardiac arrest, their recognition is urgent.
The first priority is to risk stratify for sudden
death.5 The most common and important cause
is scar-related ventricular tachycardia: a previ-
ously scarred myocardium providing the source
of ventricular arrhythmia. Thus, the most
important ECG finding in the emergency room
in an older person with unexplained blackout is
not of acute myocardial infarction but is of prior
myocardial infarction, notably pathological Q
waves. For the younger patient, the neurologist
(who will request a 12-lead ECG for all patients
with undiagnosed blackouts) also needs to recog-
nise several ECG patterns, notably hypertrophic
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cardiomyopathy, long QT syndrome, arrhythmo-

genic right ventricular cardiomyopathy, Brugada Box 1 Mimics of epilepsy
syndrome and Wolf-Parkinson-White syndrome.6
▸ Syncope
▸ Reflex
Psychogenic non-epileptic seizures – Vasovagal, micturition, swallow, carotid sinus, orgasmic
Psychogenic non-epileptic seizures (PNES) are an and laughing
important cause of apparently treatment-resistant ▸ Cardiac
epilepsy and remain a major diagnostic challenge – Arrhythmogenic
in epileptology. The two main PNES groups – Elderly: scar-related ventricular tachycardia
– Young: long QT syndrome, short QT syndrome, arrhyth-
are panic disorder (also occurring as a reaction mogenic right ventricular cardiomyopathy
in people with epilepsy) and dissociative – Structural, aortic stenosis, hypertrophic cardiomyopathy
disorder (‘pseudoseizure’), often developing in ▸ Orthostatic
patients with no history of epilepsy. The main – Autonomic failure
markers distinguishing PNES from epileptic ▸ Psychogenic non-epileptic attack disorder
– Panic disorder (especially in people with epilepsy)
seizures are:
– Dissociative
• the way the patient tells the story (not focusing on – Factitious and malingering
the seizure symptoms, avoids using the word ▸ Sleep disorders
‘seizure’, etc);3 – Narcolepsy syndrome and cataplexy
• that they are prolonged (many minutes); – Parasomnias (see Borderland of epilepsy section)
▸ Paroxysmal symptoms of structural brain disease
• associated with hyperventilation and eyes closed;
– Multiple sclerosis
and that they present as treatment-resistant epilepsy – Tumour, eg, brainstem glioma
despite an often normal intellect and brain imaging. ▸ Vascular
Note that patients with PNES may bite their – Migraine (hemiparetic, occipital, ‘basilar artery’)
tongue (though usually the front not the side), – Shaking transient ischaemic attack (critical bilateral
may injure themselves (though usually cuts, carpet stenosis)
burns or wrist injury from falling on to an out- – Subclavian steal syndrome
– Moyamoya (combination of TIA and seizures)
stretched arm) and may report seizures from sleep – Not vertebrobasilar insufficiency
(the night time being a vulnerable time for panic ▸ Hypoglycaemia
symptoms and likely to be awake at the onset). – Behaviour disturbance
– Hemiparesis
Rarer epilepsy mimics ▸ Movement disorder
– Paroxysmal kinesigenic dystonia/dyskinesia
Some less common epilepsy mimics are outlined – Myoclonus following hypoxia
in box 1 and have been reviewed in detail ▸ Hydrocephalus
elsewhere.7 – Colloid cyst
– Chiari malformation
Borderland of epilepsy ▸ Drop attacks
– Postural instability
Gowers8 coined the term ‘the borderland of epi-
– Psychogenic
lepsy’ in 1907 to describe a group of conditions
closely related to epilepsy: ‘faints, vagal attacks,
vertigo, migraine and sleep symptoms’. Although
may not always be obvious, even in video-EEG-
reflex (vasovagal) syncope and most forms of
recorded episodes.
vertigo can now clearly be separated from epi-
lepsy, migralepsy, parasomnias and startle syn-
dromes remain firmly where Gowers first Non-REM parasomnias
positioned them—‘near it, but not of it’.9 The Parasomnias arising from non-REM sleep include
treatment of conditions at the borderland confusional arousals, periodic limb movements,
overlap with epilepsy (eg, clonazepam for rhythmic movement disorder, night terrors and
parasomnia and topiramate for migralepsy) but somnambulism: all easily confused with seizures.
the social implications are very different, for Table 1 shows the clinical features that help to
example, for driving eligibility and social stigma. distinguish parasomnias from epilepsy.
Medications such as clonazepam may help both
Parasomnias conditions. Patients with ‘familial parasomnia’
Parasomnias clearly overlap with frontal lobe epi- are perhaps particularly likely actually to have
leptic seizures, and their distinction from epilepsy frontal lobe epilepsy.

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Table 1 Frontal lobe seizures versus parasomnias: clinical
pointers
Frontal lobe seizures Parasomnias
From sleep or awake From sleep
Onset in childhood or Onset in childhood (can persist to adult)
adult
Stereotyped Variable
Short: up to 1 min Longer: several minutes
Frequent, eg, many per Infrequent, for example, once per night
night
Clustering Isolated
Any time in sleep Early in sleep (NREM parasomnia) late in
sleep (REM parasomnia)
No amnesia (often retain Amnesia (but may recall dream from
awareness) REM-sleep behaviour disorder)
REM parasomnias
REM sleep behaviour disorder results from dis-
sociation between REM sleep and axial atonia—
without this loss of tone the patients physically
act out their dreams. It is usually of elderly
onset, and associated with brainstem disease, and
may predict later onset of idiopathic Parkinson’s
disease. Injury may result to self and others.
Clonazepam is usually effective.
Migraine
There are two groups of migraine overlap
syndromes.
Migralepsy
Migraine and epilepsy have many clinical over-
laps. Patients with migraine (especially with aura)
may report transient atypical symptoms during
episodes, such as depersonalisation or even loss
of consciousness, which overlap with (occipital)
seizures. Conversely, people with epilepsy may
report migraine-type headache following sei-
zures. Antiepileptic medications often prove
effective prophylaxis for migraine.
Clinicians may use the term migralepsy10 to
describe cases where there is clear overlap. The
2004 International Classification for Headache
Disorders (ICHD-II) proposed two diagnostic cri-
teria for migralepsy: (A) migraine fulfilling criteria
for migraine with aura and (B) a seizure fulfilling
diagnostic criteria for one type of epileptic attack,
occurring less than 1 h after a migraine aura.
Migraine syncope
Migraine syncope typically manifests as migraine-
type symptoms followed by gradual onset (over
many minutes) into loss of consciousness.
Patients with CADASIL (cerebral autosomal-
dominant arteriopathy with subcortical infarcts
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and leukoencephalopathy) appear particularly
prone to developing migraine coma.
Startle syndromes
Startle syndromes are rare and occur usually in
babies and young children, manifesting as a phys-
ical startle response to a loud or intense stimulus.
Startle syndrome diagnosis depends on clinical
history, electromyographic studies and genetic
screening. There are three main groups.11
Hyperekplexia.
1. ‘Major’ hyperekplexia is a genetic disorder (with
mutations in the α1 subunit of the glycine receptor
gene, GLRA1), presenting in the neonatal period
with continuous stiffness and includes excessive
startle and startle-induced falls. Milder forms pre-
senting later may be mislabelled as stiff-person
syndrome.
2. ‘Minor’ hyperekplexia, of unknown cause, where
there is excessive startle without stiffness. It may
be mislabelled as non-organic.
Neuropsychiatric startle disorders
In these conditions, behavioural features accom-
pany excessive startling.
Startle-induced epilepsy
This is considered as an epilepsy ‘chameleon’
(see Chameleons section).
Other reflex phenomena
Some non-epileptic reflex phenomena may rarely
present to neurologists. Photic sneezing, is a
common familial trait where sneezing results
from exposure to bright (though not necessarily
flashing) lights.
Chameleons
Seizures that resemble mimics more than seizures
risk being mislabelled. There are several reasons,
discussed below, as to why an epileptic seizure
may be misdiagnosed. Perhaps the most important
distinguishing feature is that seizures are typically
the highly stereotyped whereas events that are not
seizures tend to show more variation. A corollary
of this is that a diagnosis may become clearer with
follow-up if further events occur—which may
demonstrate the highly stereotyped nature of
events.
Seizures with unusual phenotypes
Seizures arising from certain parts of the brain
may show ‘atypical’ features, misleading the clin-
ician into missing the epileptic aetiology. This is
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especially likely if seizures remain localised rather
than going onto secondarily generalisation. This
is more likely in patients with intellectual disabil-
ity where symptom description may be less clear.
Furthermore, EEG can be normal between and
even during events (common if a seizure focus is
deep-seated). There are examples of ‘atypical’
seizure types arising from all lobes of the brain.
Generalised-onset seizures
Idiopathic (genetic) generalised epilepsies mani-
festing only as minor seizures (absences or myo-
clonus)—at least until generalised tonic-clonic
seizures occur—may not be recognised as
epilepsy.
1. Absence seizures may be dismissed (by patients,
parents, teachers and doctors) as daydreaming and
poor concentration, with consequent detriment to
school performance.
2. Myoclonic jerks of limbs or head, even if provoked
by flashing lights, may initially be labelled as a
character trait, a tic or as psychogenic.
3. Eyelid myoclonia are easily mistaken for behav-
ioural habit spasms if associated altered awareness
is only minimal or not recognised.
Frontal lobe seizures
The large size of the frontal lobe underlies its
broad spectrum of seizure phenotype. Frontal
complex partial seizures arising from the supple-
mentary motor area on the medial surface of the
frontal lobe typically arise from sleep, often
many times per night, and may be surprisingly
brief and with some retained awareness.
1. Hypermotor seizures, limited to agitation, vocalisa-
tions and aggression may easily be mislabelled as
parasomnia; those with bizarre posturing, back
arching, limb cycling risk, hyperventilation,
retained awareness and extreme fear being labelled
as REM-sleep behaviour disorder or psychogenic
non-epileptic seizures. Moreover, the ictal EEG
may not show the expected midline spikes because
of the deep-seated, localised seizure focus that may
not show on scalp EEG.
2. Autosomal-dominant nocturnal frontal lobe epi-
lepsy does manifest as repeated localised posturing
without altered awareness and arising from sleep,
and was for years considered to be a parasomnia
or even as a primary movement disorder (it was
long classified as ‘paroxysmal nocturnal dystonia’),
its epileptic nature easily passing unnoticed.
Temporal lobe epilepsy
This is the most common form of focal-onset
adult epilepsy, with many manifestations, often
with the risk of overlooking their epileptic
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nature. Very minor symptoms, such as déjà vu,
epigastric aura or auditory aura, particularly if
there is retained awareness, are easily dismissed
(by patient and doctor) as a normal character
trait. In practice, such ‘aura’ symptoms are often
only diagnosed retrospectively after a tonic-clonic
seizure. There are several situations where mis-
diagnosis is more likely:
1. Ictal fear, accompanied by palpitation and tachy-
cardia, is easily labelled as panic disorder.
Occasionally, ictal fear may trigger a psychogenic
non-epileptic response as the main manifestation
of the event, only adding to the diagnostic
confusion.
2. Ictal bradycardia, accompanying temporal lobe sei-
zures, manifests as a brief aura (epigastric or déjà
vu) followed by syncope (with pallor and sweating)
as the dominant feature. Many such patients
acquire a permanent pacemaker before seeing a
neurologist.
3. Transient epileptic amnesia, with recurrent antero-
grade memory loss and repeated questioning,
lasting often many minutes or even an hour, may
easily be confused with transient global amnesia
(although this is typically a one-off, with duration
of several hours).
4. Ictal vomiting may be the dominant manifestation
of temporal lobe epilepsy and can be diagnosed
initially (and especially in the learning disabled) as
gastrointestinal upset.
5. Ictal spitting is an unusual seizure manifestation
that suggests a non-dominant (right-sided) tem-
poral lobe focus, and is often labelled as behav-
ioural or psychogenic.12
6. Laryngeal spasm typically arises from the insular
region, and is easily misdiagnosed as psychogenic.
Parietal lobe seizures
Parietal lobe seizures are rare, though they may
be under-recognised. The risk of misdiagnosis is
increased by the sometimes bizarre nature of the
symptoms, the lack of visible motor manifesta-
tions and the often normal EEG even during
events. The patient’s distress may be com-
pounded by the retained awareness during
unpleasant symptoms, the delay in diagnosis
and the implications of a psychogenic cause.
A common underlying cause is low-grade glioma,
or alternatively ullegyria (figure 4) from ‘border
zone’ infarction in infancy (and hence the
importance of a birth history in epilepsy clinics).
Ullegyria typically affects the underlying white
matter (vulnerable to hypotensive infarction)
more than the overlying grey matter ( partially
protected by the greater number of collaterals).
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Figure 4 Ullegyria. MR brain scan (coronal T1-weighted)

showing ullegyria, with atrophy more marked deep in sulci
rather than superficially on gyri.

The main manifestations of parietal lobe seizures

are:
1. Ictal pain, manifesting as an intermittent focal
pain syndrome.
2. Non-specific sensory symptoms, including tingling,
numbness and feelings of unilateral body tightness,
which may be labelled as migraine with sensory
symptoms.
3. Perception difficulty intermittently, is easily
labelled as non-specific or psychological.
Occipital epilepsy
Occipital seizure symptoms may seem bizarre
and are particularly likely to be overlooked or
misdiagnosed as something other than epilepsy.
They occur more commonly in children, and so
adult neurologists may be less used to hearing
and interpreting such histories. Occipital seizures
have several manifestations:
1. Positive visual auras may be misdiagnosed as
migraine. Migraine visual auras, however, are typic-
ally monochrome and linear, with zigzags shaped
like the aerial view of a town wall (‘teichopsia’ or for-
tification spectra), whereas occipital epilepsy auras
are typically coloured shapes or even formed objects.
However, 5–10% of occipital seizures have no visual
component, but spread rapidly to the temporal and
frontal lobes, obscuring their occipital origin.
2. Ictal blindness is not widely known as a seizure
manifestation, particularly among adult physicians.
When it continues for many minutes and with
retained awareness as often happens, may lead to a
Figure 5 (A) Monocular polyopia, as described by a patient
with a right-sided (non-dominant) occipital epilepsy. (B)
Palinopsia (visual perseveration) in a patient with cerebral
infiltration of non-Hodgkin’s lymphoma in whom the image of
a knee X-ray became temporarily incorporated into his vision
(reproduced from Lancet 2003;361:1098, with permission).
child or teenager being considered to have a psy-
chogenic problem.
3. Palinopsia ( palin=again) is where a visual stimulus
leads to abnormal visual persistence, with the illu-
sion either becoming incorporated into vision or
manifesting as multiple images (figure 5A,B). It is
not surprising that such a bizarre symptom should
commonly be dismissed as functional.
4. Blinking is a common accompaniment of occipital
epilepsy, but again with the retained awareness,
can seem to be psychological.
5. Migralepsy is considered above under Borderland
of epilepsy section.
Hypothalamic seizures
Seizures resulting from a hypothalamic hamar-
toma may manifest (usually in children) as epi-
sodes of unprovoked giggling or laughing
(gelastic seizures). The MRI changes are subtle,

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even in specialist hands, and will be missed
unless is specifically sought. However, only half
of gelastic seizures arise from the hypothalamus:
half arise from the insular region.
Brainstem and cerebellar seizures
Occasional infants with cerebellar gangliogliomas
and ‘hemifacial spasm’ have had a proven diag-
nosis of ‘cerebellar epilepsy’. Cerebellar epilepsy
has not been reported in adults.
Non-convulsive status epilepticus
Complex partial status epilepticus is an important
treatable cause of abrupt onset of confusion
and/or subacute dementia. It may develop de
novo, but usually accompanies an acute brain
insult, for example, viral encephalitis or venous
sinus thrombosis. There may be only very minor
motor manifestations and even the EEG changes
may be subtle: it is easily dismissed as being
part of the underlying disease, or mislabelled,
for example, as immune encephalitis such
as N-methyl D-aspartate (NMDA)-associated
encephalitis or Creutzfeldt-Jakob disease.
Reflex epilepsies
Reflex seizures, including photosensitivity, com-
prise up to 9% of epileptic seizures.13 Various
sensory and emotional stimuli may provoke sei-
zures, notably light and music. Photosensitive
epilepsy is well known and hugely over-
diagnosed by patients—many of whom habitually
but unnecessarily avoid flashing lights—and so
true photosensitivity rarely escapes diagnosis.
Seizures as a reflex response to other phenom-
ena are less well known. Examples include
pattern-sensitive seizures (which, if occurring
without photosensitivity, may initially seem suffi-
ciently strange to be overlooked as epilepsy) and
reading epilepsy (lower lip tremor building over
many minutes of reading and culminating in a
generalised tonic-clonic seizure). Some provoking
factors for seizures might initially seem just too
bizarre to be true: eating, tooth brushing, hot
water (especially as a genetic trait in India), mic-
turition, and emotionally triggered seizures.14
Sexual activity may rarely triggers epileptic sei-
zures (orgasmic epilepsy): case reports suggest
that this occurs mainly in women and mostly
localises to the right hemisphere on inter-ictal
EEG. Startle-induced epilepsy is rare (considered
under Borderland of epilepsy section), and mani-
fests as seizures provoked by startle phenomena
in genetically susceptible children.
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Seizures where mimics are more likely
Special situations
Loss of consciousness in certain situations may
imply diagnoses other than epilepsy.
1. Seizures in the bathroom, a restaurant, and the
doctors’ surgery, prompt the likely diagnosis of
syncope ( provoked by posture, heat, sight of
blood, etc).
2. Seizures on a psychiatric ward or in patients with
strong psychiatric history prompt initial suspicion
of psychogenic non-epileptic attacks.
3. Seizures on a cardiac ward may be understandably
suspected first as having had cardiac syncope.
4. Seizures on an intensive care unit may sometimes
be first attributed to movement disorder associated
with either metabolic disturbance or hypoxic-
ischaemic encephalopathy.
Seizures accompanying existing conditions
Some clinical situations are so dominated by
associated features that epileptic seizures can be
overlooked.
1. Psychiatric history: Seizures in a person with
chronic anxiety, self-harm, drug addiction, dyscon-
trol (eg, following previous head injury) risk,
despite their increased risk of epilepsy, being
labelled as psychogenic episodes.
2. Learning disability: Seizures, particularly of
complex partial (dyscognitive) type in someone
with significant intellectual disability, may easily be
labelled as a behavioural disturbance only.
3. Neurodegenerative disease: Seizures in patients
with Alzheimer’s disease or Huntington’s disease
(eg, blank spells or automatism) may be ascribed
to movement disorder or behaviour disturbance.
Spontaneous seizures where acute symptomatic seizures
are more likely
1. Diabetes mellitus, with previous hypoglycaemic
episodes, may lead to subsequent sleep-related sei-
zures being too easily attributed to hypoglycaemia.
This mislabelling sometimes persists despite docu-
mented normal ictal plasma glucose levels.
2. Alcoholism, with previous alcohol withdrawal sei-
zures, may delay the diagnosis (and management
of ) epilepsy, with seizures being presumed due to
alcohol withdrawal.
3. Illicit drug use, for example of cocaine or intraven-
ous drugs, may prompt the clinician to think first
of psychogenic non-epileptic seizures or drug with-
drawal seizures, rather than epilepsy.
Seizures in rare conditions
Some rarely encountered conditions may present
with seizures but, because of other manifestations,

the seizures may be mislabelled and the under-
lying condition remain undiagnosed.
1. Autoimmune encephalitis: The facio-brachial dys-
tonic seizures characteristically preceding limbic
encephalitis due to voltage-gated potassium
channel-complex-antibody (VGKC-complex-Ab)
manifest as brief (a few seconds) and frequent
(eg, 50 per day) dystonic seizures, easily be mis-
labelled in the context of behavioural disturbance
and memory loss, especially as they are typically
resistant to antiepileptic medication (though
responsive to immunosuppression).15
2. Acute intermittent porphyria: Patients with seizures
caused by porphyria may have these mislabelled as
psychogenic non-epileptic seizures—understand-
able, given their psychiatric manifestations and
paradoxical worsening of symptoms on taking anti-
epileptic medications such as carbamazepine.
Where the tests do not help and even hinder
The gold standard for diagnosing epilepsy is to
record a seizure with video EEG. Again, the
stereotyped nature of seizures ( perhaps more
that for other types of event) may be a big
pointer to their diagnosis. Even here, however,
some seizures may escape diagnosis.
Normal EEG during seizures
Brief seizures arising from a deep midline focus
may not be detected on a surface EEG, especially
if there is a lot of movement artefact (see above,
especially frontal and parietal seizures).
Abnormal EEG obscuring seizures
Seizures occurring in conditions where the EEG
is already very abnormal, for example, acute viral
encephalitis or Creutzfeldt–Jakob disease, may be
overlooked on the EEG recording.
Conclusion
Many conditions mimic epileptic seizures (espe-
cially syncope and psychogenic non-epileptic sei-
zures), giving a well-known risk of misdiagnosing
and unnecessarily treating epilepsy where it does
not exist. The converse, where the underlying
cause is epilepsy but it is overlooked or misdiag-
nosed as something else (epilepsy chameleon), is
REVIEWS
less of a problem that often needs clarifying.
A further group of conditions lie at the border-
land between epilepsy and ‘not epilepsy’, the
so-called borderland of epilepsy, where better
understanding of the pathophysiolgy will eventu-
ally clarify the cause.
This paper was reviewed by Mark Manford, Cambridge, UK.
Competing interests None.
Provenance and peer review Commissioned: externally peer-
reviewed.
References
1. Smith PEM. The bare essentials: epilepsy. Pract Neurol
2008;8:195–202.
2. Edlow JA, Selim MH. Atypical presentations of acute
cerebrovascular syndromes. Lancet Neurol 2011;10:550–60.
3. Plug L, Sharrack B, Reuber M. Conversation analysis can help
to distinguish between epilepsy and non-epileptic seizure
disorders: a case comparison. Seizure 2009;18:43–50.
4. Lempert T, Bauer M, Schmidt D. Syncope: a videometric
analysis of 56 episodes of transient cerebral hypoxia. Ann
Neurol 1994;36:233–7.
5. Smith PE, O’Callaghan PA. Transient loss of consciousness
(‘blackouts’) in adults and young people. Pract Neurol
2011;11:108–10.
6. Marsh E, O’Callaghan P, Smith PEM. The humble
electrocardiogram. Prac Neurol 2008;8:46–59.
7. Smith PEM. If it’s not epilepsy…. J Neurol, Neurosurg
Psychiatry (Educ Suppl) 2001;70(Suppl 2):9–14.
8. Gowers WR. The border-land of epilepsy: faints, vagal attacks,
vertigo, migraine, sleep symptoms, and their treatment.
Philadelphia: P. Blakiston’s Son, 1907.
9. Crompton DE, Berkovic SF. The borderland of epilepsy:
clinical and molecular features of phenomena that mimic
epileptic seizures. Lancet Neurol 2009;8:370–81.
10. Sances G, Guaschino E, Perucca P, et al. Migralepsy: a call for
a revision of the definition. Epilepsia 2009;50:2487–96.
11. Bakker MJ, van Dijk JG, van den Maagdenberg AM, et al.
Startle syndromes. Lancet Neurol 2006;5:513–24.
12. Kellinghaus C, Loddenkemper T, Kotagal P. Ictal spitting:
clinical and electroencephalographic features. Epilepsia
2003;44:1064–9.
13. Seneviratne U. Reflex epilepsies; clinical and demographic
characteristics in a tropical country. J Clin Neurosci
2005;12:767–9.
14. Gilboa T. Emotional stress-induced seizures: another reflex
epilepsy? Epilepsia 2012;53:e29–32. doi: 10.1111/j.
1528-1167.2011.03342.x
15. Lee R, Buckley C, Irani SR, et al. Autoantibody testing in
encephalopathies. Pract Neurol 2012;12:4–13.
Practical Neurology 2012;12:299–307. doi:10.1136/practneurol-2012-000304 307