Review Article

Diagnosis and Treatment

Address correspondence
to Dr W. Curt LaFrance Jr,
Rhode Island Hospital, Brown
University, 593 Eddy Street,
Providence, RI 02903,
william_lafrance_jr@brown.
edu.
of Nonepileptic Seizures
Relationship Disclosure: David K. Chen, MD; W. Curt LaFrance Jr, MD, MPH, FAAN, FANPA, DFAPA
Dr Chen reports no disclosure.
Dr LaFrance serves on the
Epilepsy Foundation
Professional Advisory Board; ABSTRACT
has served as a clinic
development consultant for Purpose of Review: This article details the evaluation process involved in the diagnosis
the Cleveland Clinic, Emory of psychogenic nonepileptic seizures (PNES). The psychological underpinnings, prog-
University, Spectrum Health, nostic factors, and recent treatment advances of PNES are also reviewed.
and the University of Colorado
Denver; and has provided Recent Findings: The diagnosis of PNES is determined based on concordance of
expert medicolegal testimony. the composite evidence available, including historical and physical examination
Dr LaFrance receives royalties findings, seizure symptoms and signs, and ictal/interictal EEG. No single clinical data
from Cambridge University
Press and Oxford University point is definitively diagnostic of PNES. The diagnosis of PNES can be challenging
Press and has received research at times, such as when seizure documentation on video-EEG cannot be readily
support from the American obtained. Yet, delayed diagnosis of PNES portends poor outcome. A multicompo-
Epilepsy Society, the Epilepsy
Foundation, the Matthew Siravo nent approach to the diagnosis of PNES, with use of an aggregate of available evi-
Memorial Foundation Inc, the dence, may facilitate diagnosis and then care of patients with PNES. Emerging evidence
National Institutes of Health, supports the effectiveness of cognitive-behavioralYbased therapy in the treatment of
and Rhode Island Hospital.
Unlabeled Use of
these patients.
Products/Investigational Summary: The diagnosis of PNES can be made reliably, and evidence-based treatment
Use Disclosure: now exists. Continued efforts remain necessary to enhance prompt recognition and
Drs Chen and LaFrance report
no disclosures.
interdisciplinary management for patients with PNES.
* 2016 American Academy
of Neurology. Continuum (Minneap Minn) 2016;22(1):116–131.

INTRODUCTION convulsive syncope, cataplexy, or alcohol-

Supplemental digital content:
Videos accompanying this ar-
ticle are cited in the text as
Supplemental Digital Content.
Videos may be accessed by
clicking on links provided in the
HTML, PDF, and app versions of
this article; the URLs are pro-
vided in the print version. Video
legends begin on page 128.
Nonepileptic seizures are episodes of
altered movement, sensation, or expe-
rience distinguished from epileptic sei-
zures by the lack of associated ictal
abnormal electrical brain discharges.
About one-quarter of patients referred
to specialist centers for apparent “drug-
resistant epilepsy” are found to be mis-
diagnosed.1 After an average delay of
about 1 to 7 years to establish the correct
diagnosis,2,3 patients with nonepileptic
seizures will frequently have taken higher
doses of antiepileptic drugs (AEDs), uti-
lized greater health care resources, and
sustained more iatrogenic adverse ef-
fects than patients with epilepsy.4
Nonepileptic seizures are further cat-
egorized as physiologic or psychogenic
in origin. Physiologic nonepileptic events
result from systemic alterations or dis-
ease states that produce an ictus (eg,
withdrawal seizure) (Table 6-15). Treating
the underlying pathology of physiologic
nonepileptic events addresses the event.
In contrast, psychogenic nonepileptic
seizures (PNES) represent physical mani-
festations derived from psychological
underpinnings. In epilepsy specialty
centers, 88% of patients with nonepilep-
tic seizures are deemed to have a psy-
chogenic etiology for their events.6
This review therefore focuses primar-
ily on the diagnosis and management
of PNES.
DIAGNOSIS OF PSYCHOGENIC
NONEPILEPTIC SEIZURES
The diagnosis of PNES can be challeng-
ing. When comprehensive neurologic
and psychiatric assessment and video-
EEG are not available in one setting, an
iterative assessment process over time

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 KEY POINTS
history are useful in raising the suspicion h About one-quarter of
TABLE 6-1 Physiologic Causes for PNES. The seizure burden of patients patients referred to
of Nonepileptic with PNES is generally more pronounced
Seizuresa specialist centers for
than that of those with epilepsy, in terms apparent drug-resistant
of both seizure frequency8 and du- epilepsy (ie, failing to
b Syncope
ration.9 While stimuli-specific reflex epi- respond to adequate
Vasovagal lepsies exist, the endorsement of more trials of two or more
Cardiogenic pedestrian triggers, such as certain light- antiepileptic drugs) are
ing level conditions, body movements, found to have physiologic
b Neurologic or psychogenic
sounds, or foods, would be unusual for
Cerebrovascular nonepileptic seizures
epilepsy and should raise suspicion for
rather than epilepsy.
Migraine PNES, especially if the reported associ-
ation is strikingly consistent. Of note, sei- h After an average delay
Vertigo of about 1 to 7 years to
zure exacerbation by emotional stressors
Cataplexy establish the correct
is not pathognomonic for PNES. Studies
diagnosis, patients with
Parasomnias have shown that similar stressors can
nonepileptic seizures
Movement disorders also provoke epileptic seizures.10 will frequently have
Over the lifetime of patients with taken higher doses of
b Metabolic
PNES, about half have been diagnosed antiepileptic drugs,
Hypoglycemia with depression, about half have co- utilized greater health
Electrolyte disturbances morbid posttraumatic stress disorder care resources, and
(PTSD), and about two-thirds have sustained more
Toxicity (eg, drugs and alcohol)
personality disorders.11 The presence iatrogenic adverse
a
Modified with permission from Mellers JD, of psychogenic disorders is a strong risk effects than patients
Postgrad Med J.5 pmj.bmj.com/content/ with epilepsy.
81/958/498.full. B 2005 British Medical factor for other forms of comorbid or
Journal Publishing Group. future psychosomatic symptoms.12 Ac- h In epilepsy specialty
cordingly, about 70% of patients with centers, a predominant
PNES endorse comorbid experiences majority (about 88%)
with medically unexplained symptoms, of patients with
may be necessary to establish the diag-
such as intractable pain.13 nonepileptic seizures
nosis of PNES.7 Habitual seizures of in-
are deemed to have a
terest, especially in patients with multiple psychogenic etiology
independent event types, are sometimes Clinical Features Differentiating
for their events
not captured during an initial video-EEG Psychogenic Nonepileptic
(ie, psychogenic
monitoring study. Long-term video-EEG Seizures and Epileptic Seizures
nonepileptic seizures).
monitoring is also not readily available Key elements in the evaluation of PNES
h The diagnosis of
in some locations. Appreciating these include the recognition of ictal features
psychogenic nonepileptic
diagnostic challenges and the importance that are: (1) suggestive of a psychogenic seizures can be
of prompt recognition of this disorder, process and (2) not in favor of an epi- challenging, hence
this article first details relevant features leptic source (Table 6-25,14). Each of contributing to the
from clinical history, symptoms and these two elements should be consid- frequent time delay
signs, and video-EEG evaluations that ered separately. An important caveat is (an average of 1 to 7 years)
support the PNES diagnosis and differ- that the features described by the pa- before patients with
entiate it from epilepsy. tient and witnesses poorly correspond psychogenic nonepileptic
with the observed PNES documented seizures are
Historical Features Differentiating during video-EEG monitoring.15 There- correctly diagnosed.
Psychogenic Nonepileptic fore, ictal features described by patients’
Seizures and Epileptic Seizures or witnesses’ report alone should be in-
At the outset, a number of peculiar fea- terpreted with less diagnostic certainty
tures uncovered from a carefully elicited than those visually documented from
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 Nonepileptic Seizures

TABLE 6-2 Clinical Signs and Examination Findings Used to Help Distinguish Psychogenic
Nonepileptic Seizures From Epileptic Seizuresa,b

Signs Examination Findings

Psychogenic nonepileptic Long duration, fluctuating course, asynchronous Resists eyelid opening, guarding
seizures movements, pelvic thrusting, side-to-side head of hand dropping over face,
or body movement, ictal eye closure, ictal evidence of visual fixationc
crying/weeping, memory recall for period
of unresponsiveness
Epileptic seizures Occurrence from EEG-confirmed sleep, postictal Very severe tongue biting,
obtundation/confusion, stertorous impaired corneal reflex, extensor
breathing postictally plantar response
EEG = electroencephalogram.
a
Data from Avbersek A, Sisodiya S, J Neurol Neurosurg Psychiatry,14 jnnp.bmj.com/content/81/7/719.abstract; Mellers JD, Postgrad
Med.5 pmj.bmj.com/content/81/958/498.full.
b
No single sign distinguishes psychogenic nonepileptic seizures from epileptic seizures.
c
Visual fixation can be elicited by placing a mirror in front of the patient or rolling the patient from one side to the other.

KEY POINTS
h Over the lifetime
of patients with
psychogenic nonepileptic
seizures, about half
have been diagnosed
with depression, about
half have comorbid
posttraumatic stress
disorder, and about
two-thirds have
personality disorders.
h The diagnosis of
psychogenic nonepileptic
seizures requires the
demonstration of ictal
features that favor a
psychogenic process; are
not consistent with
epilepsy; and occur
in the context of
supportive historical,
physical examination,
and ictal/interictal
video-EEG findings.
h Patients’ and witnesses’
descriptions of the
ictal features have
been known to
correlate poorly with
observed features
of video-EEGY
captured seizures.
video-EEG monitoring and, to a lesser
extent, home video recording.
In distinguishing PNES from epileptic
seizures, clinical features are generally
more specific than sensitive,14 and no
individual feature is definitively diag-
nostic of PNES.15 Instead, the degree of
diagnostic confidence correlates with
concordant features favoring PNES. For
example, assessment of the characteris-
tic seizure temporal evolution is often
helpful. Ictal vocalization in epileptic
seizures is usually restricted to the
beginning of the seizure, primitive in
nature (laryngeal sound), and highly
stereotyped. In PNES, the vocalization
may be present not only at the begin-
ning of the seizure but may persist or
even intensify through the course of the
ictus. Vocalization in PNES can be more
complex, with affective content re-
flecting somatic expression of emo-
tional distress (eg, weeping, moaning,
and coughing).16 The generalized tonic-
clonic epileptic features can inform di-
agnosis, where ictal features evolve
through an organized fashion such that
clonic frequency progressively declines
while amplitude increases through the
course of the convulsion. In contrast, the
convulsive activity in generalized tonic-
clonic PNES may demonstrate unchang-
ing frequency and variable amplitude
throughout the ictus.17 Some PNES
show poorly discernible ictal onset from
a setting of apparent sleep, during
which EEG activity discordantly corre-
lates with wakefulness or light drows-
iness.18 On the other hand, paroxysms
with clear-cut emergence from EEG-
documented sleep would have a high
likelihood of being physiologic in origin
(ie, epileptic seizures or parasomnias).
PNES have been classified into dis-
tinct groups according to the predom-
inant clinical features. These groupings
include rhythmic motor, hypermotor,
complex motor, dialeptic (impaired
awareness), subjective, and mixed.19
While such categorization can contrib-
ute to pattern recognition useful in the
evaluation of PNES, it is presently uncer-
tain whether such categorization is
useful to distinguish psychological un-
derpinnings or inform prognosis. Fur-
thermore, unlike stereotyped epileptic
seizures arising from a singular epilep-
togenic substrate, the ictal features of
patients with PNES can often change,
transforming into other clinical presen-
tations or unrelated somatic symptoms.20

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Distinguishing Syncope From
Other Causes of Drop Attacks
The mean duration of vasovagal syn-
cope (the most common mechanism for
syncope) from the moment of event
onset to recovery of full consciousness
has been shown to be 41.4 seconds.21
Therefore, paroxysms of swoons that
last longer than 1 minute should raise
suspicion for other etiologies. It has
been suggested that patients with re-
current “syncope of unknown origin”
despite a thorough evaluation (about
20% to 30% of patients with syncope)
should undergo video-EEG monitoring
as some of them may, in fact, have
PNES.22 Contrasting with the absence
of significant EEG background change
for PNES, the EEG during syncope pro-
ceeds through a stereotyped pattern,
beginning with theta slowing, then delta
slowing followed by suppression.22
The presence of convulsionlike mo-
tor accompaniments does not preclude
the consideration of syncope. In a study
involving video analysis of 42 episodes
of syncope, 38 (90%) of the episodes
were associated with motor symptoms.
The most commonly observed move-
ment pattern in this study was multi-
focal arrhythmic jerks in both proximal
and distal muscles, usually lasting only a
few seconds.23 The motor symptoms of
syncope terminate when the patient as-
sumes a horizontal position that facili-
tates cerebral perfusion, whereas those
of epileptic seizures would not be in-
fluenced by body position.
Confirming the Diagnosis of
Psychogenic Nonepileptic Seizures
Diagnostic tools used to help support
the diagnosis of PNES include inpatient
video-EEG monitoring, ambulatory EEG
recording, and home video recording of
habitual seizures.
Video-EEG. Video-EEG entails pro-
longed continuous monitoring of the
patient, allowing for simultaneous video
Continuum (Minneap Minn) 2016;22(1):116–131
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KEY POINTS
and EEG documentation of the habitual h No feature in itself is
seizures of interest. In the setting of an definitively diagnostic
unconscious patient, physiologic causes of psychogenic
can be excluded by concurrent presence nonepileptic seizures.
of an intact alpha rhythm on the EEG h Assessing the
(a neurophysiologic correlate of alert- characteristics of the
ness). In other scenarios, the absence temporal evolution of a
of an epileptiform ictal EEG correlate seizure can frequently
before, during, or after the seizure in- yield helpful clues in
dicates that the captured event is likely differentiating
nonepileptic in origin but does not nec- psychogenic nonepileptic
essarily distinguish a psychogenic versus seizures from
physiologic etiology. Consideration of epileptic seizures.
a psychogenic etiology requires the h The EEG during syncope
demonstration of PNESYconsistent proceeds through a
clinical event features in the context stereotyped pattern,
beginning with theta
of supportive historical and ictal/
peri-ictal physical examination find- slowing, then delta
slowing followed
ings (Table 6-2). A concordant impres-
by suppression.
sion from each of these data elements
with the video-EEG provides the diag- h In the setting of an
unconscious patient,
nostic gold standard with high levels
physiologic causes
of certainty as well as excellent inter-
can be excluded by
rater reliability.15
concurrent presence
Nuances of video-EEG interpretation. of an intact alpha
For some patients with PNES who rhythm on the EEG
experience dense amnesia for the details (a neurophysiologic
of their seizures, any recorded event correlate of alertness).
should be confirmed by an eyewitness h Upon demonstrating
to be typical of the habitual seizures of psychogenic nonepileptic
interest. Otherwise, the clinical relevance seizureYconsistent clinical
of the recorded event remains uncertain. event features in the
If the patient’s historical features sug- context of supportive
gest more than one type of event, then historical and physical
an occurrence of each type should be examination findings,
recorded, as independent event types video-EEG offers a
may reflect distinct etiologies. If not, the diagnostic gold standard
etiology of the nondocumented event with high levels of
certainty and reliability.
type should be diagnosed with a more
cautious level of certainty. Indeed, ap-
proximately 10% of patients with PNES
also have an independent diagnosis of
epilepsy.24 For patients with a learning
disability, further diagnostic caution is
warranted as the percentage of mixed
PNES with epilepsy cases can be up to
30%.25 Focal epileptic seizures with pre-
served consciousness and rather restricted
motor, autonomic, or sensory/psychic
www.ContinuumJournal.com 119
 Nonepileptic Seizures
KEY POINTS
h Only 21% of simple
partial epileptic seizures
have been shown to
correlate with ictal EEG
epileptiform changes,
while some frontal lobe
epileptic seizures can
demonstrate very subtle,
falsely lateralizing, or
undiscernible ictal EEG
epileptiform correlates.
h When confronted with
enigmatic paroxysms of
uncertain etiologies,
the demonstration
of inducibility (ie,
provocative induction)
would strongly (but not
entirely) support a
psychogenic etiology.
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components (simple partial symptom-
atology) may arise from only a small pool
of neuronal tissue. As such, only 21%
of simple partial epileptic seizures have
been shown to correlate with ictal epi-
leptiform changes on scalp EEG.26 Some
frontal lobe epileptic seizures arise from
deep-seated foci (eg, orbitofrontal or in-
terhemispheric regions) such that ictal
epileptiform discharges can conduct/
distribute over a widespread area bilat-
erally, demonstrate a contralateral max-
imum, or become obscured by copious
artifacts related to hypermotor activity.
Therefore, ictal EEG epileptiform cor-
relates of some frontal lobe epileptic
seizures can be very subtle, falsely lat-
eralizing, or undiscernible.
Within 2 days after admission for
video-EEG monitoring, the majority of
patients with PNES will have experienced
a spontaneous and characteristic seizure
of interest.27 For those who do not ex-
perience spontaneous seizures, use of
suggestion techniques (ie, provocative
inductions) can improve the rate of sei-
zure capture28 and shorten the duration
of video-EEG admission.29 The success
rate of induction is higher among pa-
tients who demonstrate preinduction
characteristics of hypermotor ictal symp-
tomatology, prevalent self-reporting
of uncommon cognitive and affective
symptoms, and absence of prior induc-
tion exposure.30 Moreover, when con-
fronted with enigmatic cases for which
frontal lobe epileptic seizures, simple
partial epileptic seizures, or other phys-
iologic nonepileptic events have not
been conclusively excluded, the dem-
onstration of inducibility would strongly
(but not entirely) support a psychogenic
etiology. Ethical concerns are raised by
the use of placebos during induction
(eg, saline injection or alcohol wipes),
which inherently reflect a deceptive in-
tervention to the patient.31 Such con-
cerns can be circumvented by performing
induction techniques that utilize routine
EEG activation procedures (hyperven-
tilation and photic stimulation) with-
out placebo. Asking the patient or
family if they know of a trigger that
can be reproduced in the unit is fre-
quently helpful (eg, scrolling on a com-
puter screen). Comparable success rates
have been demonstrated between PNES
activation procedures with placebo ver-
sus without placebo.32
Ambulatory EEG and home video
recordings. Some patients with PNES
may not experience seizures in a hospital
setting that secludes patients from ha-
bitual stressors of their indigenous mi-
lieu. Under such circumstances, outpatient
ambulatory EEG (sometimes with con-
current video recordings) can be useful.
Because of less-standardized recording
settings and greater susceptibility to arti-
facts, the qualities of the ambulatory
EEG and video data can be quite var-
iable. For cases in which supportive clin-
ical or historic contexts are not available,
ambulatory EEG should be interpreted
with caution.
The frequency of some patients’ PNES
may be too rare to be practically captured
during limited time frames of video-EEG
or ambulatory EEG recordings. Consid-
ering the common availability of mobile
devices that can record video, home
video documentation of some patients’
infrequent seizures may be able to pro-
vide useful diagnostic data. Video data
alone (without EEG) have been shown to
provide reasonably robust sensitivity and
specificity in distinguishing epileptic sei-
zures from PNES.33 A key interpretive
caution is that home video recordings
may frequently miss the moment of sei-
zure onset and instead capture the mid-
dle or recovery phase of the seizure.
Moreover, the neurobehavioral man-
ifestations during the postictal recov-
ery phase of epileptic seizures can highly
resemble the ictal symptomatology of
some PNES.
February 2016

Levels of Certainty in the
Diagnosis of Psychogenic
Nonepileptic Seizures
In acknowledging that video-EEG is not
readily available to every patient world-
wide and that it may not always capture
seizures characteristic of the patient’s
single or multiple independent event
types, the Nonepileptic Seizure Task
Force of the International League
Against Epilepsy (ILAE) delineated a
staged approach to PNES diagnosis.7
The ILAE task force recognized that dif-
ferent settings may not have access to
video-EEG, so different levels of diag-
nostic certainty were delineated based
on the available data.
The clinical data utilized in this
staged approach include patients’ his-
torical presentation, witness accounts,
and clinicians’ observation in person
or via review of video recordings during
ictus, interictal EEG, and video-EEG.
Based on varying combinations of the
KEY POINT
available aforementioned data reflec- h Psychogenic nonepileptic
tive of scenarios commonly encoun- seizures are a subtype of
tered in clinical practice, a diagnosis of conversion (somatoform)
PNES can be made with several levels disorder in which
of diagnostic certainty, the highest level psychological conflicts
being “documented” (Table 6-3). With are manifested with
this approach, the task force aims to symptoms resembling
provide greater clarity regarding the epileptic seizures.
evaluation process for PNES, facili-
tate prompt recognition of this dis-
order, and enhance care of patients
with PNES worldwide.
PSYCHOPATHOLOGY
PNES are most commonly conceptual-
ized as a subtype of conversion disorder
in which psychological conflicts are mani-
fested as symptoms resembling epileptic
seizures. The Diagnostic and Statisti-
cal Manual of Mental Disorders, Fifth
Edition (DSM-5)34 provides revised diag-
nostic criteria for conversion disorder
in accordance with updated insights
regarding this disorder. Whereas the

TABLE 6-3 Overview of Proposeda Diagnostic Levels of Certainty for Psychogenic

Nonepileptic Seizures

Diagnostic Level History Witnessed Event EEG

Possible + By witness or self-report/description No epileptiform activity in routine
or sleep-deprived interictal EEG
Probable + By clinician who reviewed video No epileptiform activity in routine
recording or in person, showing or sleep-deprived interictal EEG
semiology typical of psychogenic
nonepileptic seizures (PNES)
Clinically established + By clinician experienced in diagnosis No epileptiform activity in routine
of seizure disorders (on video or in EEG or ambulatory ictal EEG,
person), showing semiology typical capturing a typical ictusb
of PNES, while not on EEG
Documented + By clinician experienced in diagnosis No epileptiform activity immediately
of seizure disorders, showing before, during, or after ictus
semiology typical of PNES, while captured on ictal video EEG with
on video EEG typical PNES semiology
EEG = electroencephalogram; + = history characteristics consistent with PNES.
a
Modified with permission from LaFrance WC Jr, et al, Epilepsia.7 onlinelibrary.wiley.com/doi/10.1111/epi.12356/full. B 2013 International
League Against Epilepsy.
b
Captured ictus should not resemble types of epileptic seizures that may not show ictal epileptiform correlate on EEG (eg, simple partial
epileptic seizures).

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 Nonepileptic Seizures

KEY POINT
h Whereas DSM-IV
approached conversion
disorder as a diagnosis
of exclusion, the
updated DSM-5 guides
users to make a positive
conversion disorder
diagnosis based on
inclusion of clinical
features that are
incongruent to known
anatomy, physiology,
or disease.
Diagnostic and Statistical Manual of
Mental Disorders, Fourth Edition
(DSM-IV) required the presence of psy-
chological factors to precede or exac-
erbate conversion symptoms, such
requirement has been relegated to a
note in DSM-5.34,35 The reason for this
change is that while psychological fac-
tors are important in the evolution of
conversion disorders, they are not always
immediately apparent from the history.
Some patients’ readiness to discuss psy-
chological factors may depend on the
strength of the clinician-patient alliance.
Even when psychological factors are
readily identified, it may not be clear
that they are etiologically relevant to
the symptoms at hand.36 Moreover, evi-
dence exists that physical factors (such
as traumatic brain injuries, undergoing
surgeries/anesthesia37Y39) can provoke
conversion symptoms and may involve
processes that are physiologic as much
as psychological (Case 6-1).
DSM-IV approached conversion dis-
order as a diagnosis of exclusion from
other pathophysiologic conditions. To
circumvent this problem, DSM-5 guides
users to make a positive conversion
disorder diagnosis based on inclusion
of clinical findings that are incongruent
to known anatomy, physiology, or dis-
eases (Table 6-2). The criterion on exclud-
ing other pathophysiologic conditions
has been revised to a criterion that re-
quires that the symptom in question is
“not better explained by another dis-
ease.” This revision encourages clinical
investigation for an alternative medical/
neurologic explanation for the symptom,

Case 6-1
A 57-year-old man presented with a 10-year history of seizures involving
abrupt loss of awareness with falls, followed by postictal disorientation/
confusion. Considering his known left frontal encephalomalacia from a
stroke that also occurred about 10 years ago, he had been treated for
(presumed) epilepsy with antiepileptic drugs. Since some of his paroxysms
were preceded by coughing fits, posttussive syncope was within the
differential diagnosis. However, he continued to experience frequent
seizures, despite trials of three antiepileptic drugs and measures to treat
his obstructive airway disease. He was referred for video-EEG monitoring,
which confirmed the diagnosis of psychogenic nonepileptic seizures (PNES)
(Supplemental Digital Content 6-1, links.lww.com/CONT/A169). This seizure
was induced by routine activation procedures that included photic stimulation
and provocation with verbal suggestion, but no placebo. PNES was
supported by the documented features of suggestibility (increasing seizure
intensity with higher photic frequency), ictal eye closure at ictal onset,
side-to-side head movements, illness-affirming behaviors (retching cough,
semifetal posture), and incongruence of intact EEG alpha rhythm (a
neurophysiologic correlate of alertness) during dialeptic symptomatology
with clinical unresponsiveness.
Comment. While strokes are associated with epilepsy and epileptogenic
foci, this case illustrates that the emotional affliction from significant
health-related adverse events should not be overlooked. Moreover,
evidence exists that physical factors (such as brain injuries) can provoke
conversion symptoms and may involve processes that are physiologic as much
as psychological. This case also exemplifies the importance of considering a
wide differential diagnosis in patients with paroxysmal disorders, which
includes epilepsy, physiologic nonepileptic events, and PNES.

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but also allows for a conversion dis-
order diagnosis even if a potentially
related disease is present. The other
notable change for conversion disorder
in DSM-5 is that the former require-
ment for exclusion of feigning has been
abandoned. In clinical practice, such
requirement is problematic, as exclu-
sion of malingering may be difficult
to validate with absolute certainty
without surveillance or forensic evalu-
ation.40 Volitionally feigned symptoms,
as in the cases of malingering or fac-
titious disorders, are not PNES (ie, not
psychogenic), and are rare, present
mostly in at-risk groups.
Several etiologic models have been
proposed in the effort to explain the
inception and evolution of conversion
disorder manifesting as PNES.41 One
model stipulates two main types of
psychological difficulties that underlie
PNES: posttraumatic and developmen-
tal.42 Posttraumatic PNES develop in
response to psychological or physical
trauma(s) that the patient struggles
to adequately process or integrate. In
the face of “unspeakable dilemmas,”
some authors postulate that PNES re-
flects an automatic cutoff phenomenon
in response to spontaneous intrusion
into consciousness of such intolerable
memories.43 Developmental PNES de-
rives from difficulties coping with com-
plex life tasks and milestones along the
patient’s continuum of psychosocial de-
velopment in an environment of emo-
tional privation (eg, relational neglect).
Studies have shown that some patients
with PNES rely on avoidant coping
responses (denial and repression) to
perceived threats,44 hence hindering
appropriate maturation of psychosocial
development. For some patients with
PNES, both posttraumatic and devel-
opmental types of psychological etiol-
ogies may coexist. In essence, PNES
(and other conversion disorders) are a
disorder of communication, where
Continuum (Minneap Minn) 2016;22(1):116–131
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distress is expressed somatically, rather
than in a healthy verbal manner.
BORDER ZONES OF PSYCHOGENIC
NONEPILEPTIC SEIZURES
(PSYCHIATRIC DIFFERENTIAL
DIAGNOSIS)
Border zones of PNES represent neuro-
behavioral paroxysms with psychologi-
cal underpinnings but are not considered
to be conversion disorders, as described
above. Panic attacks can be the paroxys-
mal manifestation of panic disorder or
other conditions associated with anxiety.
Symptoms of tremulousness, shaking,
derealization, or depersonalization can
be quite prominent in some panic at-
tacks, hence showing a notable parallel
to seizures. Careful exploration of the
overall presentation should uncover
other key features meeting DSM-5 crit-
eria for panic attacks, in which intense
fear is accompanied by at least four of
the following symptoms: palpitations,
diaphoresis, shortness of breath, chest
discomfort, nausea and abdominal dis-
comfort, dizziness, and the aforemen-
tioned seizurelike symptoms. Similar to
panic attacks, behavioral manifestations
of PTSD frequently entail derealization,
depersonalization, or affective numbing,
all of which can resemble seizure activ-
ities. In fact, the DSM-5 designates a
PTSD subtype with prominent dissocia-
tive symptoms. Upon careful evaluation,
if the patient’s overall symptomatology
can be better explained by PTSD per
DSM-5 criteria, then the additional di-
agnosis of conversion disorder should
not be made. Some authors contend that
the presentation of exclusively subjective
sensory symptoms (albeit neurologic
symptoms, such as paresthesia or numb-
ness) are not sufficiently reliable in them-
selves to meet the criteria for PNES.40
Most of these cases likely represent anx-
ious misinterpretation of common non-
specific paroxysmal symptoms of everyday
www.ContinuumJournal.com 123
 Nonepileptic Seizures
KEY POINTS
h An important prognostic
factor of psychogenic
nonepileptic seizures is
the duration of illness, in
which the prognosis
worsens the longer the
patient’s illness has been
mistreated as epilepsy.
h In children with
psychogenic nonepileptic
seizures, serious
psychosocial issues (eg,
physical or sexual abuses)
can be ongoing at the
time of presentation and
should be explored in
every case.
124 www.ContinuumJournal.com
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
life, including transient dizziness, limb
numbness, or head sensations that may
briefly disrupt attention. The misinter-
pretation of benign symptoms as being
more pathologic may be more common
in patients who have had personal expe-
riences with seizures or who have other
neurologic/medical conditions. Another
scenario that falls within the border zones
of PNES is the purposeless and repetitive
behavioral mannerisms (learned behav-
ior) that occur not infrequently in some
cognitively impaired patients.45
PROGNOSIS
When considering the overall popula-
tion of patients with PNES, seizure
cessation is reported to occur in about
40% of patients over time. About one-
third of patients experience seizure
reduction, while the remaining approx-
imately one-third of patients undergo a
chronically intractable course.46 A com-
prehensive assessment of PNES out-
comes should encompass not only
seizure burden, but also the state of
psychosocial comorbidities, functionality,
and overall quality of life.47 Upon pursu-
ing a more complete outcome assess-
ment of PNES as such, one study showed
the following observations: 44% of pa-
tients were not seizure free and re-
mained dependent (poor outcome);
40% of patients were either seizure free
but dependent or not seizure free but
independent (intermediate outcome);
and 16% of patients were seizure free
and independent (good outcome).48
The above results suggest that patients
with PNES, in general, may have a poorer
course than those with newly diag-
nosed epilepsy.48
Several patient-specific characteristics
are identified as influencing the disease
course of PNES. An important prognos-
tic factor is duration of illness, in which
the prognosis worsens the longer the
patient’s illness has been mistreated as
epilepsy.49 Correspondingly, a staged
approach to PNES diagnosis may be
beneficial in prompting earlier discus-
sion regarding potential psychological
contributions to seizures, as soon as
minimum criteria for the diagnosis of
PNES have been met. Deferring such
discussions until video-EEGYdocumented
diagnostic certainty may lead to sig-
nificant delay, considering the afore-
mentioned diagnostic challenges and
limited video-EEG availability in some
locations. Factors that may prognosti-
cate better outcomes among adults
include higher level of education; youn-
ger age at both time of seizure onset
and time of diagnosis; seizures with
less- dramatic symptomatology; fewer
additional psychosomatic symptoms;
and neuropsychological measures sup-
porting lower dissociative, inhibitive,
emotional dysregulating, and compul-
sive tendencies.50,51
PSYCHOGENIC NONEPILEPTIC
SEIZURES IN CHILDREN
While much of the earlier discussions
regarding PNES in adults also apply to
children, some differences are notable
in light of varying psychosocial elements
across developmental stages in children.
PNES can emerge in children as young
as 5 years old, and their frequency in-
creases with age, becoming the most
common type of nonepileptic seizure in
adolescents.52 Conversely, comorbid
epilepsy (mixed disorder) is more prev-
alent in younger children with PNES
than in older children or adolescents
with PNES.52 Compared to adults with
PNES, differences in psychiatric comor-
bidities include lower rates of mood
disorders (32%) and PTSD (10%) and a
higher rate of significant family stressors
(44%) for children with PNES.53 Impor-
tantly, serious psychosocial issues (eg,
physical or sexual abuses) can be on-
going at the time of presentation and
should be explored in every case. Risk
factors for pediatric PNES are noted,
February 2016

including somatopsychic and adversity
components related to maladaptive
coping.54 The clinical outcome of PNES
is better in children than adults, per-
haps contributed to in part by a gen-
erally briefer duration of illness or that
dysfunctional patterns have become
less engrained.55
MANAGEMENT OF PSYCHOGENIC
NONEPILEPTIC SEIZURES
Management of patients with PNES be-
gins with a comprehensive evaluation
(ie, seizure history, psychosocial assess-
ment, video-EEG), which includes a de-
velopmental history and review of past
trauma and abuse in the intake neuro-
logic assessment.56 Many times, patients
have been dismissed in prior emergency
department and neurologic encounters,
so conveying to the patient that the
seizures in PNES are just as real as those
in epilepsy is essential. Neurologists
KEY POINT
who continue to use the outdated pe- h The neurologist’s
jorative terminology of “pseudoseizures,” explanation of the
with connotations of being false or fake, diagnosis of psychogenic
create a distance between patients and nonepileptic seizures
clinicians. Legitimization and confirma- is vital and should be
tion of PNES through these efforts can communicated to the
enhance the patient’s acceptance of patient via a tactful,
the subsequent diagnostic explanation empathetic, and
(Case 6-2). In turn, the patient’s ac- unequivocal approach.
ceptance of the PNES diagnosis has
been shown to be associated with sei-
zure improvement.57
Hence, the neurologist’s explanation
of this diagnosis is vital, and should be
communicated to the patient via a tact-
ful, empathetic, positive, nonpejorative,
and unequivocal approach.58 Provision
of supplementary written information
may help consolidate (and further legit-
imize) the PNES diagnosis.59 Commu-
nication with family and the referring
physician regarding this diagnosis can
also augment the uniformity of diagnostic

Case 6-2
A 27-year-old man presented with near-daily seizures that involved diffuse
shaking with varying degree of unconsciousness. Given his high seizure
frequency, a brief 23-hour inpatient video-EEG was able to capture his
habitual seizure, and he received the diagnosis of psychogenic nonepileptic
seizures (PNES). He then sought additional referrals, endorsing the
frustration that, “My family thinks it’s all in my head,” and “It has to come
from something else.” During a subsequent video-EEG monitoring course,
efforts were made to capture the full spectrum of the patient’s seizures.
The diagnosis of PNES was explained to the patient and family members,
emphasizing PNES as a real, albeit nonepileptic, type of seizure. This
explanation of the diagnosis took place across two inpatient visits to allow
the patient and his family the opportunity to process their understanding
and ask questions. An explanation letter (addressed to the patient) and PNES
brochures were encouraged to be shared with other clinicians or individuals
pertinent to the patient’s care.
Comment. For patients with PNES, establishing the correct diagnosis is the
first step of treatment. Optimal management begins with comprehensive
evaluation (ie, neurologic and psychiatric assessment, description of the
events and psychosocial history taking, video-EEG monitoring). The
clinician-patient rapport and legitimization of PNES established through
these efforts can enhance the patient’s acceptance of diagnosis. In this
sense, neurologists can be a factor not only in the diagnosis, but also in the
initial treatment of patients with PNES as they prepare patients for
collaborative care with a mental health professional.

Continuum (Minneap Minn) 2016;22(1):116–131 www.ContinuumJournal.com 125

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

 Nonepileptic Seizures
KEY POINTS
h Medications do not fully insight across the patient’s milieu. Not
treat psychogenic providing the diagnosis with patient or
nonepileptic seizures. providers has been shown to be associ-
Moreover, antiepileptic ated with no improvement or even
drugs may worsening of symptoms.60 Likewise,
make psychogenic merely sharing the diagnosis (without
nonepileptic seizures further dedicated therapeutic efforts) is
worse. Selective frequently insufficient, as other somatic
serotonin reuptake and affective symptoms often develop
inhibitors (SSRIs) help the if the core issues are not addressed.13
comorbidities (eg,
Letting the patient and family know that
depression and anxiety)
they are not alone in that many people
but do not
stop psychogenic
have the same disorder; that treatment
nonepileptic seizures. involves addressing predisposing, pre-
cipitating, and perpetuating factors; and
h Targeted psychotherapy
that effective treatment is available pro-
appears to be the
mainstay of treatment
vides hope to patients and empowers
for psychogenic treating clinicians to engage.50
nonepileptic seizures. The mainstay of effective treatment
To date, two pilot for PNES is psychotherapy directed at
randomized controlled the known pathologies in the population.
trials for psychogenic Pharmacologic interventions are used to
nonepileptic seizures address common comorbidities (eg, se-
have shown clinically lective serotonin reuptake inhibitors
meaningful results using [SSRIs] for depression and anxiety).
either traditional However, psychotropics may reduce
cognitive-behavioral
seizures but do not lead to seizure
therapy or a
cessation in PNES.3,61 Among psycho-
seizure-treatment
workbook based
therapeutic approaches for patients with
on a multimodality PNES, cognitive-behavioral therapy has
cognitive-behavioral the most substantial body of controlled
therapyYinformed efficacy data. To date, two pilot random-
psychotherapy for ized controlled trials for PNES have
psychogenic nonepileptic shown clinically meaningful results. One
seizures and for epilepsy. study used conventional cognitive-
behavioral therapy,62 while the other
study used a multimodality cognitive-
behavioral therapyYinformed psycho-
therapy3 based on a workbook used
by therapists and patients to treat
both epileptic seizures and PNES
(Table 6-4).63 Some patients may con-
tinue to maintain some ambivalence re-
garding the nature of the PNES diagnosis
and express reluctance toward in-depth
individual psychotherapies. In such cases,
group psychoeducational approaches
have been shown to consolidate patients’
understanding of PNES and promote
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Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
more open-mindedness toward accep-
tance of this diagnosis.64,65 Because
driving is an issue for patients with
seizures, barriers to treatment delivery
are being overcome with computer
video telemedicine, which is being used
in the US Department of Veterans Af-
fairs to provide live-remote therapy for
veterans with either epileptic seizures
or PNES.66
The working relationship between
the neurologist and patient should not
abruptly end after a diagnosis of PNES
has been established, for several reasons.
For some patients with PNES, especially
those who have been chronically mis-
diagnosed as having epileptic seizures,
a proper understanding of the diagnosis
may not be achievable with a “one-shot”
disclosure. Instead, iterative explanation
of the diagnosis via a supportive/
noncoercive tone across serial visits may
gradually foster the patient’s acceptance
for mental health treatment referrals.
Once the transition to mental health
care is complete, then discussion can
commence regarding the patient’s dis-
charge from the neurologist’s practice.
If a specific AED has no alternative
beneficial indication (eg, mood stabili-
zation or migraine prophylaxis), then a
timely taper of the drug is advisable.
Early, as opposed to delayed, AED
withdrawal portends greater beneficial
effects on a range of clinical out-
comes.57 Patients with normal video-
EEG findings should be followed by a
neurologist for at least 6 months after
discontinuing AEDs. This consideration
is because of the small but ever-present
possibility of coexisting epilepsy and
the fact that breakthrough epileptic
seizures can occur several months
after discontinuation of AEDs. Patients
with PNES who also have known
interictal or ictal epileptiform abnormal-
ities on their video-EEG should continue
to be followed by a neurologist. Patients
with mixed epilepsy/PNES should be
February 2016
TABLE 6-4 Cognitive-Behavioral Approaches Evaluated in Randomized Controlled Trials for
Psychogenic Nonepileptic Seizures

Goldstein et al, 201061 LaFrance et al, 20143

Therapeutic Based on traditional cognitive-behavioral therapy
approach (CBT) and fear escape-avoidance model:
Psychogenic nonepileptic seizures (PNES) as
dissociative responses to cues associated with
extremely distressing or life-threatening
experiences. These experiences are, in turn, linked
to unbearable feelings of fear and distress.
Main topics include seizure-directed
techniques; attention refocusing; relaxation;
dealing with avoidance behaviors, negative
cognitions, and other factors key toward
engendering PNES.
Outcomes CBT group experienced fewer seizures than
the control group at the end of treatment.
During the last 3 months of a 6-month follow-up
period, between-group differences in seizure
frequency were not significant, although the CBT
group was 3 times more likely to be seizure free.
Based on CBT-informed psychotherapy model
initially aimed to enhance self-control of
epileptic seizures: PNES as the somatic
manifestations of maladaptive core beliefs
(negative schemas) that have been derived
chronically from life experiences and traumas.
Main topics include healthy communication,
support seeking, and goal setting; conducting
a functional behavioral analysis; aura
identification; linking triggers, negative
states, and target symptoms; relaxation;
examining external stressors and internal
conflicts; promotion of ongoing health
and wellness.
When compared to before treatment,
CBT-informed psychotherapy workbook
group showed significant seizure reduction
and improvement in depression,
anxiety, quality of life, and global
functioning measures.
When compared to baseline, the treatment
as usual/standard medical care control group
showed no significant difference in seizure
frequency or any secondary outcome measures.

treated with the lowest effective AED
dose for the epilepsy, noting that AEDs
do not treat PNES, and behavioral in-
terventions should target the PNES.
Continued follow-up by the neurologist
during the transition to mental health
providers mitigates repeat workups with
other providers.
CONCLUSION
Conversion disorder is usually not diag-
nosed by the mental health provider
alone; the neurologist is integral in the
evaluation and diagnosis. Indeed, patients
with conversion disorder frequently pres-
ent to neurologists first in search of a
neurologic explanation to their symp-
toms.67 As such, neurologists have ac-
quired substantial experience in making
a positive conversion disorder diagnosis KEY POINT
based on identifying incongruent exam- h For the 10% of patients
ination and laboratory findings in rela- with mixed epilepsy/
psychogenic nonepileptic
tion to known anatomy or physiology.
seizures, use the lowest
Neurologists can work collaboratively with
effective antiepileptic drug
mental health providers to adequately dose for the epileptic
address the psychological underpinnings seizure and use mental
of these challenging patients. This team health treatments for
approach highlights the importance of the psychogenic
interdisciplinary dialogue and transition nonepileptic seizures.
in the care of patients with PNES. To
this end, better communication by neuro-
logists can overcome past diverging in-
terdisciplinary perspectives regarding
PNES, with psychiatrists frequently be-
ing uncertain about the accuracy of video-
EEG.68 Further efforts are necessary to
augment this vital interdisciplinary part-
nership. Recent diagnostic and treatment

Continuum (Minneap Minn) 2016;22(1):116–131 www.ContinuumJournal.com 127

Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

 Nonepileptic Seizures
studies have shown momentum in shift-
ing PNES to a neuropsychiatric inter-
disciplinary (shared-care) model with
a mind/brain perspective.66 As research
in PNES advances, cognizance of and,
hence, empathy for patients with this
challenging condition can advance,
in parallel.
VIDEO LEGEND
Supplemental Digital
Content 6-1
Psychogenic nonepileptic seizure in-
duced by photic stimulation and verbal
suggestion. The documented features
of suggestibility (intensifying ictal mani-
festations with increasing photic fre-
quency), somatic expression of distress
(coughing, semifetal posture), and clin-
ical unresponsiveness despite EEG
demonstration of an intact posterior
dominant rhythm (reflecting an awake
state) are all supportive of a psycho-
genic etiology to this captured nonepi-
leptic seizure.
links.lww.com/CONT/A169
B 2016 American Academy of Neurology.
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