6-Diagnosis and Treatment of Nonepileptic Seizures.11

Review Article
Address correspondence
to Dr W. Curt LaFrance Jr,
Rhode Island Hospital, Brown
University, 593 Eddy Street,
Providence, RI 02903,
william_lafrance_jr@brown.
edu.
Relationship Disclosure:
Dr Chen reports no disclosure.
Dr LaFrance serves on the
Epilepsy Foundation
Professional Advisory Board;
has served as a clinic
development consultant for
the Cleveland Clinic, Emory
University, Spectrum Health,
and the University of Colorado
Denver; and has provided
expert medicolegal testimony.
Dr LaFrance receives royalties
from Cambridge University
Press and Oxford University
Press and has received research
support from the American
Epilepsy Society, the Epilepsy
Foundation, the Matthew Siravo
Memorial Foundation Inc, the
National Institutes of Health,
and Rhode Island Hospital.
Unlabeled Use of
Products/Investigational
Use Disclosure:
Drs Chen and LaFrance report
no disclosures.
* 2016 American Academy
of Neurology.
Supplemental digital content:

Videos accompanying this article 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 provided in the print version. Video
legends begin on page 128.
116
Diagnosis and Treatment

of Nonepileptic Seizures
David K. Chen, MD; W. Curt LaFrance Jr, MD, MPH, FAAN, FANPA, DFAPA
ABSTRACT
Purpose of Review: This article details the evaluation process involved in the diagnosis
of psychogenic nonepileptic seizures (PNES). The psychological underpinnings, prognostic factors, and recent treatment advances of PNES are also reviewed.
Recent Findings: The diagnosis of PNES is determined based on concordance of
the composite evidence available, including historical and physical examination
findings, seizure symptoms and signs, and ictal/interictal EEG. No single clinical data
point is definitively diagnostic of PNES. The diagnosis of PNES can be challenging
at times, such as when seizure documentation on video-EEG cannot be readily
obtained. Yet, delayed diagnosis of PNES portends poor outcome. A multicomponent approach to the diagnosis of PNES, with use of an aggregate of available evidence, may facilitate diagnosis and then care of patients with PNES. Emerging evidence
supports the effectiveness of cognitive-behavioralYbased therapy in the treatment of
these patients.
Summary: The diagnosis of PNES can be made reliably, and evidence-based treatment
now exists. Continued efforts remain necessary to enhance prompt recognition and
interdisciplinary management for patients with PNES.
Continuum (Minneap Minn) 2016;22(1):116131.
INTRODUCTION
Nonepileptic seizures are episodes of
altered movement, sensation, or experience distinguished from epileptic seizures by the lack of associated ictal
abnormal electrical brain discharges.
About one-quarter of patients referred
to specialist centers for apparent drugresistant epilepsy are found to be misdiagnosed.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), utilized greater health care resources, and
sustained more iatrogenic adverse effects than patients with epilepsy.4
Nonepileptic seizures are further categorized as physiologic or psychogenic
in origin. Physiologic nonepileptic events
result from systemic alterations or disease states that produce an ictus (eg,
convulsive syncope, cataplexy, or alcoholwithdrawal seizure) (Table 6-15). Treating

the underlying pathology of physiologic
nonepileptic events addresses the event.
In contrast, psychogenic nonepileptic
seizures (PNES) represent physical manifestations derived from psychological
underpinnings. In epilepsy specialty
centers, 88% of patients with nonepileptic seizures are deemed to have a psychogenic etiology for their events.6
This review therefore focuses primarily on the diagnosis and management
of PNES.
DIAGNOSIS OF PSYCHOGENIC
NONEPILEPTIC SEIZURES
The diagnosis of PNES can be challenging. When comprehensive neurologic
and psychiatric assessment and videoEEG are not available in one setting, an
iterative assessment process over time
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February 2016
TABLE 6-1 Physiologic Causes

of Nonepileptic
Seizuresa
b Syncope
Vasovagal
Cardiogenic
b Neurologic
Cerebrovascular
Migraine
Vertigo
Cataplexy
Parasomnias
Movement disorders
b Metabolic
Hypoglycemia
Electrolyte disturbances
Toxicity (eg, drugs and alcohol)
a
Modified with permission from Mellers JD,

Postgrad Med J.5 pmj.bmj.com/content/
81/958/498.full. B 2005 British Medical
Journal Publishing Group.
may be necessary to establish the diagnosis of PNES.7 Habitual seizures of interest, especially in patients with multiple
independent event types, are sometimes
not captured during an initial video-EEG
monitoring study. Long-term video-EEG
monitoring is also not readily available
in some locations. Appreciating these
diagnostic challenges and the importance
of prompt recognition of this disorder,
this article first details relevant features
from clinical history, symptoms and
signs, and video-EEG evaluations that
support the PNES diagnosis and differentiate it from epilepsy.
Historical Features Differentiating
Psychogenic Nonepileptic
Seizures and Epileptic Seizures
At the outset, a number of peculiar features uncovered from a carefully elicited
Continuum (Minneap Minn) 2016;22(1):116131
history are useful in raising the suspicion

for PNES. The seizure burden of patients
with PNES is generally more pronounced
than that of those with epilepsy, in terms
of both seizure frequency8 and duration.9 While stimuli-specific reflex epilepsies exist, the endorsement of more
pedestrian triggers, such as certain lighting level conditions, body movements,
sounds, or foods, would be unusual for
epilepsy and should raise suspicion for
PNES, especially if the reported association is strikingly consistent. Of note, seizure exacerbation by emotional stressors
is not pathognomonic for PNES. Studies
have shown that similar stressors can
also provoke epileptic seizures.10
Over the lifetime of patients with
PNES, about half have been diagnosed
with depression, about half have comorbid posttraumatic stress disorder
(PTSD), and about two-thirds have
personality disorders.11 The presence
of psychogenic disorders is a strong risk
factor for other forms of comorbid or
future psychosomatic symptoms.12 Accordingly, about 70% of patients with
PNES endorse comorbid experiences
with medically unexplained symptoms,
such as intractable pain.13
Clinical Features Differentiating
Psychogenic Nonepileptic
Seizures and Epileptic Seizures
Key elements in the evaluation of PNES
include the recognition of ictal features
that are: (1) suggestive of a psychogenic
process and (2) not in favor of an epileptic source (Table 6-25,14). Each of
these two elements should be considered separately. An important caveat is
that the features described by the patient and witnesses poorly correspond
with the observed PNES documented
during video-EEG monitoring.15 Therefore, ictal features described by patients
or witnesses report alone should be interpreted with less diagnostic certainty
than those visually documented from
KEY POINTS
h About one-quarter of
patients referred to
specialist centers for
apparent drug-resistant
epilepsy (ie, failing to
respond to adequate
trials of two or more
antiepileptic drugs) are
found to have physiologic
or psychogenic
nonepileptic seizures
rather than epilepsy.
h After an average delay

of about 1 to 7 years to
establish the correct
diagnosis, patients with
will frequently have
taken higher doses of
antiepileptic drugs,
utilized greater health
care resources, and
sustained more
iatrogenic adverse
effects than patients
with epilepsy.
h In epilepsy specialty
centers, a predominant
majority (about 88%)
of patients with
are deemed to have a
psychogenic etiology
for their events
(ie, psychogenic
nonepileptic seizures).
h The diagnosis of
psychogenic nonepileptic
seizures can be
challenging, hence
contributing to the
frequent time delay
(an average of 1 to 7 years)
before patients with
seizures are
correctly diagnosed.
117
Nonepileptic Seizures
to Help Distinguish Psychogenic

TABLE 6-2 Clinical Signs and Examination Findings Used
Nonepileptic Seizures From Epileptic Seizuresa,b
Signs
Examination Findings
Psychogenic nonepileptic
seizures
Long duration, fluctuating course, asynchronous

movements, pelvic thrusting, side-to-side head
or body movement, ictal eye closure, ictal
crying/weeping, memory recall for period
of unresponsiveness
Resists eyelid opening, guarding

of hand dropping over face,
evidence of visual fixationc
Epileptic seizures
Occurrence from EEG-confirmed sleep, postictal

obtundation/confusion, stertorous
breathing postictally
Very severe tongue biting,

impaired corneal reflex, extensor
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
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
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.
118
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 diagnostic of PNES.15 Instead, the degree of
diagnostic confidence correlates with
concordant features favoring PNES. For
example, assessment of the characteristic 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 beginning 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 reflecting somatic expression of emotional distress (eg, weeping, moaning,
and coughing).16 The generalized tonicclonic epileptic features can inform diagnosis, 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 unchanging 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 correlates with wakefulness or light drowsiness.18 On the other hand, paroxysms
with clear-cut emergence from EEGdocumented sleep would have a high
likelihood of being physiologic in origin
(ie, epileptic seizures or parasomnias).
PNES have been classified into distinct groups according to the predominant clinical features. These groupings
include rhythmic motor, hypermotor,
complex motor, dialeptic (impaired
awareness), subjective, and mixed.19
While such categorization can contribute to pattern recognition useful in the
evaluation of PNES, it is presently uncertain whether such categorization is
useful to distinguish psychological underpinnings or inform prognosis. Furthermore, unlike stereotyped epileptic
seizures arising from a singular epileptogenic substrate, the ictal features of
patients with PNES can often change,
transforming into other clinical presentations or unrelated somatic symptoms.20
February 2016
Distinguishing Syncope From

Other Causes of Drop Attacks
The mean duration of vasovagal syncope (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 recurrent 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 proceeds through a stereotyped pattern,
beginning with theta slowing, then delta
slowing followed by suppression.22
The presence of convulsionlike motor 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 movement pattern in this study was multifocal arrhythmic jerks in both proximal
and distal muscles, usually lasting only a
few seconds.23 The motor symptoms of
syncope terminate when the patient assumes a horizontal position that facilitates cerebral perfusion, whereas those
of epileptic seizures would not be influenced 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 prolonged continuous monitoring of the
patient, allowing for simultaneous video
and EEG documentation of the habitual

seizures of interest. In the setting of an
unconscious patient, physiologic causes
can be excluded by concurrent presence
of an intact alpha rhythm on the EEG
(a neurophysiologic correlate of alertness). In other scenarios, the absence
of an epileptiform ictal EEG correlate
before, during, or after the seizure indicates that the captured event is likely
nonepileptic in origin but does not necessarily distinguish a psychogenic versus
physiologic etiology. Consideration of
a psychogenic etiology requires the
demonstration of PNESYconsistent
clinical event features in the context
of supportive historical and ictal/
peri-ictal physical examination findings (Table 6-2). A concordant impression from each of these data elements
with the video-EEG provides the diagnostic gold standard with high levels
of certainty as well as excellent interrater reliability.15
Nuances of video-EEG interpretation.
For some patients with PNES who
experience dense amnesia for the details
of their seizures, any recorded event
should be confirmed by an eyewitness
to be typical of the habitual seizures of
interest. Otherwise, the clinical relevance
of the recorded event remains uncertain.
If the patients historical features suggest more than one type of event, then
an occurrence of each type should be
recorded, as independent event types
may reflect distinct etiologies. If not, the
etiology of the nondocumented event
type should be diagnosed with a more
cautious level of certainty. Indeed, approximately 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 preserved consciousness and rather restricted
motor, autonomic, or sensory/psychic
KEY POINTS
h No feature in itself is
definitively diagnostic
of psychogenic
nonepileptic seizures.
h Assessing the
characteristics of the
temporal evolution of a
seizure can frequently
yield helpful clues in
differentiating
seizures from
epileptic seizures.
h The EEG during syncope

proceeds through a
stereotyped pattern,
beginning with theta
slowing, then delta
slowing followed
by suppression.
h In the setting of an
unconscious patient,
physiologic causes
can be excluded by
concurrent presence
of an intact alpha
rhythm on the EEG
(a neurophysiologic
correlate of alertness).
h Upon demonstrating
seizureYconsistent clinical
event features in the
context of supportive
historical and physical
examination findings,
video-EEG offers a
diagnostic gold standard
with high levels of
certainty and reliability.
119
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.
120
components (simple partial symptomatology) 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 epileptiform changes on scalp EEG.26 Some
frontal lobe epileptic seizures arise from
deep-seated foci (eg, orbitofrontal or interhemispheric regions) such that ictal
epileptiform discharges can conduct/
distribute over a widespread area bilaterally, demonstrate a contralateral maximum, or become obscured by copious
artifacts related to hypermotor activity.
Therefore, ictal EEG epileptiform correlates of some frontal lobe epileptic
seizures can be very subtle, falsely lateralizing, 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 experience spontaneous seizures, use of
suggestion techniques (ie, provocative
inductions) can improve the rate of seizure capture28 and shorten the duration
of video-EEG admission.29 The success
rate of induction is higher among patients who demonstrate preinduction
characteristics of hypermotor ictal symptomatology, prevalent self-reporting
of uncommon cognitive and affective
symptoms, and absence of prior induction exposure.30 Moreover, when confronted with enigmatic cases for which
frontal lobe epileptic seizures, simple
partial epileptic seizures, or other physiologic nonepileptic events have not
been conclusively excluded, the demonstration 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 intervention to the patient.31 Such concerns can be circumvented by performing
induction techniques that utilize routine
EEG activation procedures (hyperventilation and photic stimulation) without placebo. Asking the patient or
family if they know of a trigger that
can be reproduced in the unit is frequently helpful (eg, scrolling on a computer screen). Comparable success rates
have been demonstrated between PNES
activation procedures with placebo versus 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 habitual stressors of their indigenous milieu. Under such circumstances, outpatient
ambulatory EEG (sometimes with concurrent video recordings) can be useful.
Because of less-standardized recording
settings and greater susceptibility to artifacts, the qualities of the ambulatory
EEG and video data can be quite variable. For cases in which supportive clinical 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. Considering the common availability of mobile
devices that can record video, home
video documentation of some patients
infrequent seizures may be able to provide useful diagnostic data. Video data
alone (without EEG) have been shown to
provide reasonably robust sensitivity and
specificity in distinguishing epileptic seizures from PNES.33 A key interpretive
caution is that home video recordings
may frequently miss the moment of seizure onset and instead capture the middle or recovery phase of the seizure.
Moreover, the neurobehavioral manifestations during the postictal recovery phase of epileptic seizures can highly
resemble the ictal symptomatology of
some PNES.
February 2016
Levels of Certainty in the

Diagnosis of Psychogenic
In acknowledging that video-EEG is not
readily available to every patient worldwide and that it may not always capture
seizures characteristic of the patients
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 different settings may not have access to
video-EEG, so different levels of diagnostic certainty were delineated based
on the available data.
The clinical data utilized in this
staged approach include patients historical 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
available aforementioned data reflective of scenarios commonly encountered in clinical practice, a diagnosis of
PNES can be made with several levels
of diagnostic certainty, the highest level
being documented (Table 6-3). With
this approach, the task force aims to
provide greater clarity regarding the
evaluation process for PNES, facilitate prompt recognition of this disorder, and enhance care of patients
with PNES worldwide.
KEY POINT
h Psychogenic nonepileptic
seizures are a subtype of
conversion (somatoform)
disorder in which
psychological conflicts
are manifested with
symptoms resembling
epileptic seizures.
PSYCHOPATHOLOGY
PNES are most commonly conceptualized as a subtype of conversion disorder
in which psychological conflicts are manifested as symptoms resembling epileptic
seizures. The Diagnostic and Statistical Manual of Mental Disorders, Fifth
Edition (DSM-5)34 provides revised diagnostic 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

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

recording or in person, showing
semiology typical of psychogenic
nonepileptic seizures (PNES)

or sleep-deprived interictal EEG
Clinically established
By clinician experienced in diagnosis

of seizure disorders (on video or in
person), showing semiology typical
of PNES, while not on EEG

EEG or ambulatory ictal EEG,
capturing a typical ictusb
Documented
By clinician experienced in diagnosis

of seizure disorders, showing
semiology typical of PNES, while
on video EEG
No epileptiform activity immediately

before, during, or after ictus
captured on ictal video EEG with
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).
121
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 psychological factors to precede or exacerbate conversion symptoms, such
requirement has been relegated to a
note in DSM-5.34,35 The reason for this
change is that while psychological factors are important in the evolution of
conversion disorders, they are not always
immediately apparent from the history.
Some patients readiness to discuss psychological 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, evidence 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 disorder 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 diseases (Table 6-2). The criterion on excluding other pathophysiologic conditions
has been revised to a criterion that requires that the symptom in question is
not better explained by another disease. 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.
122
February 2016
but also allows for a conversion disorder diagnosis even if a potentially

related disease is present. The other
notable change for conversion disorder
in DSM-5 is that the former requirement for exclusion of feigning has been
abandoned. In clinical practice, such
requirement is problematic, as exclusion of malingering may be difficult
to validate with absolute certainty
without surveillance or forensic evaluation.40 Volitionally feigned symptoms,
as in the cases of malingering or factitious 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 developmental.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 reflects an automatic cutoff phenomenon
in response to spontaneous intrusion
into consciousness of such intolerable
memories.43 Developmental PNES derives from difficulties coping with complex life tasks and milestones along the
patients continuum of psychosocial development in an environment of emotional 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 developmental types of psychological etiologies may coexist. In essence, PNES
(and other conversion disorders) are a
disorder of communication, where
distress is expressed somatically, rather

than in a healthy verbal manner.
BORDER ZONES OF PSYCHOGENIC
(PSYCHIATRIC DIFFERENTIAL
DIAGNOSIS)
Border zones of PNES represent neurobehavioral paroxysms with psychological underpinnings but are not considered
to be conversion disorders, as described
above. Panic attacks can be the paroxysmal manifestation of panic disorder or
other conditions associated with anxiety.
Symptoms of tremulousness, shaking,
derealization, or depersonalization can
be quite prominent in some panic attacks, hence showing a notable parallel
to seizures. Careful exploration of the
overall presentation should uncover
other key features meeting DSM-5 criteria 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 discomfort, dizziness, and the aforementioned seizurelike symptoms. Similar to
panic attacks, behavioral manifestations
of PTSD frequently entail derealization,
depersonalization, or affective numbing,
all of which can resemble seizure activities. In fact, the DSM-5 designates a
PTSD subtype with prominent dissociative symptoms. Upon careful evaluation,
if the patients overall symptomatology
can be better explained by PTSD per
DSM-5 criteria, then the additional diagnosis 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 numbness) are not sufficiently reliable in themselves to meet the criteria for PNES.40
Most of these cases likely represent anxious misinterpretation of common nonspecific paroxysmal symptoms of everyday
123
KEY POINTS
h An important prognostic
factor of psychogenic
nonepileptic seizures is
the duration of illness, in
which the prognosis
worsens the longer the
patients illness has been
mistreated as epilepsy.
h In children with
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
life, including transient dizziness, limb

numbness, or head sensations that may
briefly disrupt attention. The misinterpretation of benign symptoms as being
more pathologic may be more common
in patients who have had personal experiences 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 behavior) that occur not infrequently in some
cognitively impaired patients.45
PROGNOSIS
When considering the overall population of patients with PNES, seizure
cessation is reported to occur in about
40% of patients over time. About onethird of patients experience seizure
reduction, while the remaining approximately one-third of patients undergo a
chronically intractable course.46 A comprehensive assessment of PNES outcomes should encompass not only
seizure burden, but also the state of
psychosocial comorbidities, functionality,
and overall quality of life.47 Upon pursuing a more complete outcome assessment of PNES as such, one study showed
the following observations: 44% of patients were not seizure free and remained 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 diagnosed epilepsy.48
Several patient-specific characteristics
are identified as influencing the disease
course of PNES. An important prognostic factor is duration of illness, in which
the prognosis worsens the longer the
patients illness has been mistreated as
epilepsy.49 Correspondingly, a staged
approach to PNES diagnosis may be

beneficial in prompting earlier discussion 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 significant delay, considering the aforementioned diagnostic challenges and
limited video-EEG availability in some
locations. Factors that may prognosticate better outcomes among adults
include higher level of education; younger age at both time of seizure onset
and time of diagnosis; seizures with
less- dramatic symptomatology; fewer
additional psychosomatic symptoms;
and neuropsychological measures supporting lower dissociative, inhibitive,
emotional dysregulating, and compulsive 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 increases with age, becoming the most
common type of nonepileptic seizure in
adolescents.52 Conversely, comorbid
epilepsy (mixed disorder) is more prevalent in younger children with PNES
than in older children or adolescents
with PNES.52 Compared to adults with
PNES, differences in psychiatric comorbidities include lower rates of mood
disorders (32%) and PTSD (10%) and a
higher rate of significant family stressors
(44%) for children with PNES.53 Importantly, serious psychosocial issues (eg,
physical or sexual abuses) can be ongoing 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, perhaps contributed to in part by a generally briefer duration of illness or that
dysfunctional patterns have become
less engrained.55
MANAGEMENT OF PSYCHOGENIC
Management of patients with PNES begins with a comprehensive evaluation
(ie, seizure history, psychosocial assessment, video-EEG), which includes a developmental history and review of past
trauma and abuse in the intake neurologic 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
who continue to use the outdated pejorative terminology of pseudoseizures,

with connotations of being false or fake,
create a distance between patients and
clinicians. Legitimization and confirmation of PNES through these efforts can
enhance the patients acceptance of
the subsequent diagnostic explanation
(Case 6-2). In turn, the patients acceptance of the PNES diagnosis has
been shown to be associated with seizure improvement.57
Hence, the neurologists explanation
of this diagnosis is vital, and should be
communicated to the patient via a tactful, empathetic, positive, nonpejorative,
and unequivocal approach.58 Provision
of supplementary written information
may help consolidate (and further legitimize) the PNES diagnosis.59 Communication with family and the referring
physician regarding this diagnosis can
also augment the uniformity of diagnostic
KEY POINT
h The neurologists
explanation of the
diagnosis of psychogenic
is vital and should be
communicated to the
patient via a tactful,
empathetic, and
unequivocal approach.
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 its 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 patients 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 patients 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 patients 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.
125
KEY POINTS
h Medications do not fully

treat psychogenic
Moreover, antiepileptic
drugs may
make psychogenic
worse. Selective
serotonin reuptake
inhibitors (SSRIs) help the
comorbidities (eg,
depression and anxiety)
but do not
stop psychogenic
h Targeted psychotherapy
appears to be the
mainstay of treatment
for psychogenic
To date, two pilot
randomized controlled
trials for psychogenic
have shown clinically
meaningful results using
either traditional
cognitive-behavioral
therapy or a
seizure-treatment
workbook based
on a multimodality
cognitive-behavioral
therapyYinformed
psychotherapy for
seizures and for epilepsy.
126
insight across the patients milieu. Not

providing the diagnosis with patient or
providers has been shown to be associated with no improvement or even
worsening of symptoms.60 Likewise,
merely sharing the diagnosis (without
further dedicated therapeutic efforts) is
frequently insufficient, as other somatic
and affective symptoms often develop
if the core issues are not addressed.13
Letting the patient and family know that
they are not alone in that many people
have the same disorder; that treatment
involves addressing predisposing, precipitating, and perpetuating factors; and
that effective treatment is available provides hope to patients and empowers
treating clinicians to engage.50
The mainstay of effective treatment
for PNES is psychotherapy directed at
the known pathologies in the population.
Pharmacologic interventions are used to
address common comorbidities (eg, selective serotonin reuptake inhibitors
[SSRIs] for depression and anxiety).
However, psychotropics may reduce
seizures but do not lead to seizure
cessation in PNES.3,61 Among psychotherapeutic approaches for patients with
PNES, cognitive-behavioral therapy has
the most substantial body of controlled
efficacy data. To date, two pilot randomized controlled trials for PNES have
shown clinically meaningful results. One
study used conventional cognitivebehavioral therapy,62 while the other
study used a multimodality cognitivebehavioral therapyYinformed psychotherapy3 based on a workbook used
by therapists and patients to treat
both epileptic seizures and PNES
(Table 6-4).63 Some patients may continue to maintain some ambivalence regarding 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
more open-mindedness toward acceptance 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 Affairs 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 misdiagnosed 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 patients acceptance
for mental health treatment referrals.
Once the transition to mental health
care is complete, then discussion can
commence regarding the patients discharge from the neurologists practice.
If a specific AED has no alternative
beneficial indication (eg, mood stabilization 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 outcomes.57 Patients with normal videoEEG 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 abnormalities 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
Therapeutic
approach
Outcomes
Goldstein et al, 201061
LaFrance et al, 20143
Based on traditional cognitive-behavioral therapy

(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.
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 seizure-directed

techniques; attention refocusing; relaxation;
dealing with avoidance behaviors, negative
cognitions, and other factors key toward
engendering PNES.
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.
CBT group experienced fewer seizures than

the control group at the end of treatment.
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.
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.
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 interventions 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 diagnosed by the mental health provider
alone; the neurologist is integral in the
evaluation and diagnosis. Indeed, patients
with conversion disorder frequently present to neurologists first in search of a
neurologic explanation to their symptoms.67 As such, neurologists have acquired substantial experience in making
a positive conversion disorder diagnosis

based on identifying incongruent examination and laboratory findings in relation to known anatomy or physiology.
Neurologists can work collaboratively with
mental health providers to adequately
address the psychological underpinnings
of these challenging patients. This team
approach highlights the importance of
interdisciplinary dialogue and transition
in the care of patients with PNES. To
this end, better communication by neurologists can overcome past diverging interdisciplinary perspectives regarding
PNES, with psychiatrists frequently being uncertain about the accuracy of videoEEG.68 Further efforts are necessary to
augment this vital interdisciplinary partnership. Recent diagnostic and treatment
KEY POINT
h For the 10% of patients

with mixed epilepsy/
seizures, use the lowest
effective antiepileptic drug
dose for the epileptic
seizure and use mental
health treatments for
the psychogenic
127
studies have shown momentum in shifting PNES to a neuropsychiatric interdisciplinary (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 induced by photic stimulation and verbal
suggestion. The documented features
of suggestibility (intensifying ictal manifestations with increasing photic frequency), somatic expression of distress
(coughing, semifetal posture), and clinical unresponsiveness despite EEG
demonstration of an intact posterior
dominant rhythm (reflecting an awake
state) are all supportive of a psychogenic etiology to this captured nonepileptic seizure.
links.lww.com/CONT/A169
B 2016 American Academy of Neurology.
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Diagnosis and Treatment

convulsive syncope, cataplexy, or alcoholwithdrawal seizure) (Table 6-15). Treating

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

TABLE 6-1 Physiologic Causes

Modified with permission from Mellers JD,

history are useful in raising the suspicion

h After an average delay

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to Help Distinguish Psychogenic

Long duration, fluctuating course, asynchronous

Resists eyelid opening, guarding

Occurrence from EEG-confirmed sleep, postictal

Very severe tongue biting,

h Over the lifetime

h Patients and witnesses

video-EEG monitoring and, to a lesser

clonic PNES may demonstrate unchanging frequency and variable amplitude

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Distinguishing Syncope From

and EEG documentation of the habitual

h The EEG during syncope

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h Only 21% of simple

h When confronted with

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Levels of Certainty in the

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

No epileptiform activity in routine

By clinician who reviewed video

No epileptiform activity in routine

By clinician experienced in diagnosis

No epileptiform activity in routine

By clinician experienced in diagnosis

No epileptiform activity immediately

EEG = electroencephalogram; + = history characteristics consistent with PNES.

Continuum (Minneap Minn) 2016;22(1):116131

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Diagnostic and Statistical Manual of

surgeries/anesthesia37Y39) can provoke

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but also allows for a conversion disorder diagnosis even if a potentially

distress is expressed somatically, rather

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life, including transient dizziness, limb

approach to PNES diagnosis may be

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

including somatopsychic and adversity

who continue to use the outdated pejorative terminology of pseudoseizures,

Continuum (Minneap Minn) 2016;22(1):116131

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h Medications do not fully

insight across the patients milieu. Not

more open-mindedness toward acceptance of this diagnosis.64,65 Because

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TABLE 6-4 Cognitive-Behavioral Approaches Evaluated in Randomized Controlled Trials for

Goldstein et al, 201061

LaFrance et al, 20143

Based on traditional cognitive-behavioral therapy

Based on CBT-informed psychotherapy model

Main topics include seizure-directed

Main topics include healthy communication,

CBT group experienced fewer seizures than