REVIEWS

Differentiating between nonepileptic

and epileptic seizures
Orrin Devinsky, Deana Gazzola and W. Curt LaFrance Jr
Abstract | Psychogenic nonepileptic seizures (PNES) resemble epileptic seizures and are often misdiagnosed
and mistreated as the latter. Occasionally, epileptic seizures are misdiagnosed and mistreated as PNES. 70%
of PNES cases develop between the second and fourth decades of life, but this disease can also affect children
and the elderly. At least 10% of patients with PNES have concurrent epileptic seizures or have had epileptic
seizures before being diagnosed with PNES. Psychological stress exceeding an individual’s coping capacity
often precedes PNES. Clinicians can find differentiating between PNES and epileptic seizures challenging. Some
clinical features can help distinguish PNES from epileptic seizures, but other features associated with PNES
are nonspecific and occur during both types of seizures. Diagnostic errors often result from an overreliance on
specific clinical features. Note that no single feature is pathognomonic for PNES. When typical seizures can
be recorded, video-EEG is the diagnostic gold standard for PNES, and in such cases a diagnosis can be made
with high accuracy. When video-EEG reveals no epileptiform activity before, during or after the ictus, thorough
neurological and psychiatric histories can be used to confirm the diagnosis of PNES. In this article, we review
the clinical features that can help clinicians differentiate between PNES and epileptic seizures.
Devinsky, O. et al. Nat. Rev. Neurol. 7, 210–220 (2011); published online 8 March 2011; doi:10.1038/nrneurol.2011.24

Introduction
Psychogenic nonepileptic seizures (PNES) are paroxys-
mal behaviors that resemble epileptic seizures; however,
PNES are not associated with the changes in cortical
activity that characterize the latter.1 PNES and epileptic
seizures share many similar features: for example, both
of these disorders can be associated with convulsions
and/or alterations in behavior and consciousness. As a
result, differentiating between nonepileptic and epileptic
seizures can be difficult. Unlike epileptic seizures, PNES
have a psychological origin and are categorized in the
Diagnostic and Statistical Manual of Mental Disorders
4th edition as a type of conversion disorder.
Patients with PNES are often referred to neurology,
psychiatric or emergency departments and, in such
cases, can be given inappropriate treatments, including
New York University antiepileptic drugs (AEDs). AEDs do not cure PNES,
Epilepsy Center, and AED toxicity may worsen this disorder.2 Fortunately,
223 E34 Street New
York, NY 10016, USA
a study that monitored the discontinuation of AEDs in
(O. Devinsky). New York 78 patients with PNES revealed that the majority of
University Epilepsy
these patients experienced a reduction in the frequency
Center, 550 First
Avenue, HCC‑12, of PNES when taken off medication, indicating that
Room 1202, New York, withdrawal of AED treatment from patients with this
NY 10016, USA
(D. Gazzola). Rhode condition is safe.3
Island Hospital, The cost of mistreating PNES as epilepsy is high for
Neuropsychiatry,
Behavioral Neurology,
both the patient and society. In the US alone, up to
593 Eddy Street, US$900 million dollars per year is unnecessarily spent
Potter 3 Providence, on diagnostic evaluations, repetition of laboratory tests,
RI 02903, USA
(W. C. LaFrance Jr). AEDs and emergency department utilization in relation
Correspondence to:
O. Devinsky Competing interests
devinsky@nyumc.org The authors declare no competing interests.
to PNES.4 Furthermore, patients with PNES may receive
potentially dangerous invasive diagnostic studies, toxic
parenteral medications and unnecessary intubation as a
result of an incorrect diagnosis of epilepsy.5
Approximately 3 million people are diagnosed as having
epilepsy in the US, but 10–20% of these patients are actu-
ally thought to have PNES.6 The prevalence of PNES in the
US has been estimated to be 33 per 100,000 people,7 with
a mean incidence of three per 100,000 people per year.8
However, accurate surveillance of PNES is challenging
and the diagnosis of such seizures can be difficult. Thus,
at present, we lack good epidemiological data for this dis-
order and, as a result, the numbers cited above should be
considered rough estimates. PNES occur more frequently
in women (accounting for 80% of all cases) than in men
and the majority of patients (83%) are 15–35 years of age,9
although some studies suggest that this condition might
be more prevalent than was previously thought in men10
and in the elderly.11 PNES have been observed in diverse
ethnic groups.12–15
20–50% of individuals admitted to a seizure monitor-
ing unit (SMU) have PNES,16 and up to 40% of patients
with seizures who are seen in general neurology clinics
may also have this condition. 17 A history of epileptic
seizures has been reported in 7–32% of patients with
PNES,18,19 and a study that used stringent diagnostic cri-
teria for epileptiform activity reported that 10% of
patients diagnosed with PNES also had epileptic
seizures.20 Individuals who have family members with
epilepsy have a higher risk of developing PNES than
individuals whose family members do not have epilepsy,

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© 2011 Macmillan Publishers Limited. All rights reserved

possibly owing to imitation or ‘modeling’.21 A family
history of epilepsy was reported in up to 35% of patients
with childhood-onset PNES.22 The incidence of PNES
is similar to that of multiple sclerosis and Parkinson
disease in the US, indicating that PNES is a major
public-health problem and that an effective treatment
for this condition is urgently needed.23
Little international agreement exists on the most appro-
priate term for PNES. Most American neurologists and/
or epileptologists, including ourselves, use the term PNES
to describe this condition24 and avoid using the terms
‘pseudoseizures’ or ‘spells’, as some people deem these
latter two labels to have pejorative connotations. Some
epileptologists dislike the term ‘psychogenic nonepileptic
attack’ because of the potential allegorical meaning that
this term might represent for patients who have histories
of abuse and have suffered actual physical attacks.25–27
Nevertheless, the establishment of rapport is more impor-
tant than the terminology used when communicating a
diagnosis of PNES to a patient and their family.
In this article, we review our knowledge of the risk
factors and pathogenesis of PNES, and provide an over-
view of the diagnostic evaluation of this disorder. We high-
light the gaps in our knowledge regarding the biological
mechanisms that underlie PNES, and the diverse nature
of these seizures and other non-epileptic events that make
differentiating between non-epileptic events and epileptic
seizures difficult.
Risk factors and pathogenesis
Epilepsy has a bimodal age curve, 28 with the highest
incidence of this disorder occurring in infants and the
elderly. By contrast, PNES have an inverse unimodal
curve:29 70% of cases occur during the second to fourth
decades of life, with only up to 20% of cases occurring
after the age of 40 years. Thus, risk factors for epilepsy
and PNES are age dependent.
In infancy, risk factors for epilepsy include genetic
metabolic disorders and infections, while in the elderly,
common risk factors for this condition include stroke,
neurodegenerative disorders and tumors.30 PNES has
been described as a heterogeneous disorder;31 however,
the majority of cases are caused by traumatic experiences
or developmental factors.32 Risk factors for PNES in chil-
dren include difficulties in school (present in 46% of all
cases of childhood PNES), family discord (42%), and
interpersonal conflicts such as bullying (25%); physical
(12%) and sexual (5%) abuse are infrequently associated
with PNES in children.22,33 Depression is frequently asso-
ciated with this condition in adolescents, while cognitive
dysfunction and comorbid epilepsy are commonly asso-
ciated with PNES in prepubescent individuals.21Adult
women who develop PNES aged <55 years often report
having a prior history of sexual abuse,33,34 while male
patients with such seizures often report having a predis-
posing factor for epilepsy.35 Patients with PNES are more
likely to be obese than patients with epileptic seizures,36
and male veterans with PNES are more likely to have
chronic pain, anxiety and post-traumatic stress dis­order
than men with epileptic seizures.37 The symptoms of
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Key points
■■ Psychogenic nonepileptic seizures (PNES) are often misdiagnosed and
mistreated as epilepsy
■■ The majority of patients with PNES have a history of developmental insults
or trauma that may cause psychological stress exceeding an individual’s
coping capacity
■■ No single clinical feature is pathognomonic for PNES; thus, diagnostic humility
is essential when considering PNES as a patient’s diagnosis
■■ Specific clinical features can help distinguish PNES from epileptic seizures and,
in most cases of PNES, a definite diagnosis can be made with video-EEG—the
diagnostic gold standard
■■ Consideration of a patient’s neurological and psychiatric histories alongside the
results of video-EEG can further improve diagnostic accuracy for PNES
PNES in young and older adults share similar character-
istics, although older adults with PNES are more likely
to exhibit severe physical-health problems and to have
reported having health-related traumatic experiences
than younger patients.34
The pathogenesis of conversion disorders such as
PNES remains unknown, but the majority of patients
with these disorders have a history of developmental
insults or trauma that may cause psychological stress
exceeding an individual’s coping capacity. For example,
the stressful stimulus might follow physical trauma
resulting from head injury or surgery.38 In some cases,
the stressor or mechanism underlying the conversion
disorder might not be identified at presentation, but
they are usually revealed after the development of a
therapeutic alliance. Janet hypothesized that traumatic
memories and emotions could dissociate, or split off,
from awareness, and that these unconscious “psycho-
logical automatisms” could influence a person’s behavior
without any conscious awareness.39 Freud believed that
an unconscious conflict (for example, a repressed inces-
tuous urge or an inappropriate fantasy) was symbolically
converted into somatic symptoms, and he hypothesized
that this process might reduce an individual’s anxiety
and shield their conscious self from a painful emotion.40
Freud’s model suggests that conversion disorders are
associated with both primary gain, whereby an inter-
nal conflict or need is suppressed, and secondary gain,
whereby the patient gains support or services and is able
to avoid unpleasant situations.
Patients with PNES may have abnormalities on
structural brain images (for example, encephalomala-
cia or a tumor),41 but such seizures are not associated
with a specific type of lesion or with lesions in specific
areas of the brain. Functional MRI (fMRI) has iden-
tified brain areas that are associated with conversion
disorders other than PNES. Compared with healthy
controls, patients with conversion disorders show
increased functional connectivity between the right
amygdala and the right supplementary motor area
during processing of positive and negative emotional
stimuli.42 This ‘hyperlink’ between brain areas associ-
ated with emotion and motor preparation might partly
underlie the pathology of some conversion disorders.
Another study has shown that patients with conversion
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disorder-associated tremor have decreased activity in
the right temporoparietal junction compared with
patients with physiological tremor.43 This brain area
compares internal predictions with actual events, and
the failure to match proprio­ceptive feedback with inter-
nal predictions might explain why conversion disorder-
associated tremor is not perceived as self-generated.43
Furthermore, studies of conversion disorder-associated
weakness, in which the lack of strength occurs as a con-
sequence of psychological rather than physical factors,
have identified abnormalities in striatothalamocortical
circuits,44 frontal regions45 and midline frontoparietal
regions.46 To date, fMRI has not been used to identify
brain areas that are associated with PNES.
Diagnostic evaluation of PNES
Clinical features
Video-EEG simultaneously records a patient’s behavior
and brain electrical activity. The clinical features and
brainwave patterns that are identified using this tech-
nique can help the treating physician to differentiate
between PNES and epileptic seizures.47 In most cases of
PNES, a detailed clinical history in combination with
video-EEG monitoring, during which a typical patient
event has been recorded, is sufficient for a physician
to provide an accurate diagnosis. However, diagnostic
humility is essential when considering a diagnosis of
PNES, since no single clinical feature is pathognomonic
for this condition. Indeed, some clinical features asso-
ciated with PNES also occur in epileptic seizures,48,49
and some unusual ictal signs associated with frontal
lobe epilepsy (FLE) can mimic PNES.50 How a patient
verbally describes their symptoms can provide valuable
diagnostic information. Linguists can accurately dis-
tinguish PNES from epileptic seizures in 85% of cases
through assessment of how a patient interacts with an
interviewer and describes their episodes during a 30 min
videotaped interview.51 Below, we describe the clinical
features associated with epileptic seizures, PNES or both
of these conditions that can help physicians differentiate
between the two disorders.
Ictal course
Epileptic seizures are predominantly stereotypical in
nature. PNES can also be stereotypical, but often the
features, sequence and time course of such seizures lack
consistency.49,52 A patient’s physiological state during
seizure onset can also inform diagnosis. Epileptic sei-
zures can occur during wakefulness or sleep, whereas
PNES rarely arise during true physiological sleep.53
PNES can occur during ‘pseudosleep’, a state in which
the patient seems to be asleep but is in fact awake,54
and pseudosleep onset is specifically associated with
PNES.54,55 The evolution of a seizure can provide further
information that can aid diagnosis. Like frontal lobe and
absence epileptic seizures, PNES can begin abruptly,56
but PNES can also be associated with prolonged pre-
monitory symptoms, begin gradually, and have a waxing
and waning course.56,57 The duration of PNES can be
highly variable; however, such events are typically longer
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© 2011 Macmillan Publishers Limited. All rights reserved
than epileptic seizures.58 For example, classic temporal
lobe complex partial epileptic seizures last 10–140 s,59
whereas PNES have been documented to last 20–805 s.58
Moreover, PNES are more likely to terminate abruptly
than epileptic seizures,60 which are typically associated
with gradual increases in the interval between jerks at
the end of a convulsion.
Motor manifestations
Motor manifestations can help physicians differenti-
ate between PNES and epileptic seizures. Complex
movements such as writhing, flailing and whole-body
thrashing are commonly associated with PNES. In fact,
thrashing and writhing movements have been shown
to occur in 45% of patients with PNES but only 17% of
patients with partial epileptic seizures.56 Nevertheless,
evidence of flailing and thrashing alone cannot be used
to distinguish between PNES and epileptic seizures,47
since these complex movements can also occur as a
consequence of FLE seizures. Side-to-side head move-
ments or body turning (jacitation) can occur during
PNES, but are not evident during convulsive epileptic
seizures; however, these movements are not diagnostic
for PNES, as they can also occur during partial epileptic
seizures, especially FLE seizures.47,50 Asynchronous body
movements (alternate clonic movements, usually of the
arms) are not typically associated with convulsive epi-
leptic seizures but can occur during convulsive PNES.61
Furthermore, discontinuous motor patterns and pelvic
thrusting are much more likely to occur in PNES than
in epileptic seizures.61,47 Opisthotonic posturing, also
termed ‘arc en cercle’,62 has been shown in one study to be
present in up to 28% of patients with PNES,52 but insuf-
ficient data currently exists in the literature to support
screening for this symptom in discriminating between
PNES and epileptic seizures.47
FLE seizures often consist of asynchronous, complex,
and sometimes bizarre motor movements, with lateral
head and body turning; thus, distinguishing between
these seizures and PNES can be difficult. However, FLE
seizures, which are stereotypical and brief (5–45 s), can
cluster nocturally and are often associated with promi-
nent axial body movements that begin abruptly; these
latter features are rare in PNES.50 Patients may turn to the
prone position during FLE seizures, which is an unusual
occurrence during PNES.50
The absence of motor features during a seizure can
also provide important diagnostic information. During
PNES, patients may be unresponsive or stare and, in
such cases, motor changes or automatisms are typi-
cally absent.63 Furthermore, periods of prolonged body
flaccidity, which can be associated with eye blinking,
swallowing or slumping forward, are more common
in patients with PNES than patients with epileptic sei-
zures.63,64 Nevertheless, many complex partial seizures
that originate in the temporal lobe are also ‘bland’, and
are only associated with impairment of awareness and
behavioral arrest.50,63 Thus, one must be cautious when
using the absence of motor features to distinguish
between PNES and epileptic seizures.

Sensory and autonomic manifestations
Isolated sensory manifestations are less common during
PNES than are changes in motor behavior or respon-
siveness. In fact, only 9% of patients with PNES have
been shown to experience isolated sensory manifesta-
tions during an episode.52 Interestingly, patients with
epileptic seizures and patients with PNES have reported
that auras are a feature of their episodes,64,65 and family
members of patients with either of these seizures often
report observing ‘a change in their eyes before the
seizure’. Autonomic changes, such as pupillary dilatation,
palpitations, flushing or pallor, can occur during either
epileptic seizures or PNES. One study showed that while
the pupillary light response during PNES was shown to
be normal in 88% of patients, 12% of the study group
exhibited sluggish pupillary light responses during such
seizures. Note that the corresponding baseline inter­
ictal pupillary light responses for these patients were not
presented.65 In contrast to the situation in PNES, altera-
tions in pupillary light responses and pupillary dilatation
often occur during epileptic seizures.66 Changes in heart
rate are more prominent during both convulsive and
nonconvulsive epileptic seizures than during PNES. 67
An increase in heart rate of ≥30% from baseline during
a seizure has been shown to predict epileptic seizures
in 97% of events.67 Urinary incontinence occurs more
often during epileptic seizures than during PNES. In one
study, urinary incontinence was associated with 23% of
convulsive epileptic seizures but only 6% of PNES.47,68
Nevertheless, urinary incontinence does not reliably
distinguish between these two types of seizures.47
Affective manifestations and vocalizations
Feelings of anxiety or moaning and crying during a
seizure (not restricted to periods of aura) are much more
common during PNES than during epileptic seizures.69–72
Furthermore, women are more likely to cry after PNES
than are men.35 During such seizures, a patient’s speech
tends to contain more emotion—and evoke more feelings
of sadness or pain—than epileptic ictal speech, which has
a monotone quality.50,64 Indeed, epileptic speech is often
‘empty’, and typically comprises meaningless phrases or
sounds that are repeated, whereas speech during PNES
is often intelligible (patients with PNES often respond
to questions during episodes).50,64 Gates and colleagues
showed that 44% of patients with PNES vocalized at event
onset but not after the seizure was well-established.58 In
this study, 60% of patients with convulsive epileptic sei-
zures vocalized only after the seizure was well established,
and these vocalizations were related to respiratory muscu-
lar contractions;58 the ‘ictal cry’ that is strongly associated
with epileptic seizure onset occurred in 24% of patients
with this type of seizure.58 Ictal stuttering occurs in ≈8%
of patients with PNES,73 but almost never occurs during
epileptic seizures; thus, evidence of ictal stuttering should
raise suspicions of PNES.
Facial features and injuries
Changes in facial features and musculature, especially eye
closure, may help the treating physician distinguish
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between PNES and epileptic seizures.47,74,75 At the onset of
a convulsive epileptic seizure, a patient’s eyes tend to be
open.75 By contrast, at the onset of convulsive PNES, the
eyes of patients are typically closed.74 Although eye closure
can be observed during epileptic seizures, eye closure
throughout the entire ictal episode is considered a charac-
teristic feature of PNES.76 Forced eye closure—resistance
to the eyes being pulled open by an examiner—during
psychogenic unresponsiveness is also a sign of PNES.77
During the tonic phase of a convulsive epileptic seizure, a
patient’s mouth is often agape, whereas during PNES, an
individual’s mouth is often clenched shut.75
Following a convulsion, a clinician should determine
whether a tongue bite is present and, if so, determine
its location. Tongue bites are often located laterally in
patients with epileptic seizures, whereas patients with
PNES may experience tip-of-the-tongue, lip or buccal
bites.74,78 Other physical injuries, such as ecchymoses
and fractures, can occur as a result of epileptic seizures
or PNES, but are most often associated with the former.
Burns from fire are relatively specific for epileptic sei-
zures,79 but ‘rug burns’ or excoriations along long-bone
surfaces are often seen in patients with PNES.80
Postictal findings
Complete and abrupt recovery is more often observed fol-
lowing PNES than epileptic seizures, but complete recov-
ery can also occur following FLE seizures.48,50 By contrast,
altered breathing patterns, focal neurological deficits and
somatic complaints are more common after epileptic sei-
zures than PNES.47,61,81 Stertorous breathing is frequently
noted following convulsive epileptic seizures, but is rarely
observed after convulsive PNES.82 Postictal headache has
been reported to occur in 38% of patients with epileptic
seizures versus 4% of patients with PNES, and postictal
fatigue has been reported to occur in 56% of patients with
epileptic seizures versus 13% of patients with PNES.81
Refractory interictal headache and other pain syndromes,
however, are more common in patients with PNES than
in patients with epileptic seizures.83 Postictal confusion
is associated with both types of seizures,79 but the ability
to recall events that occurred during a seizure supports a
diagnosis of PNES over a diagnosis of epilepsy.78,84
In summary, clinical features that characterize PNES or
epileptic seizures can vary, and physicians should not rely
on any single clinical feature to differentiate between the
two seizure types. Through the use of clinical findings plus
other supportive data, diagnostic accuracy for PNES can
be maximized. Table 1 summarizes the clinical features
that can help distinguish epileptic seizures from PNES.
EEG
The results of standard EEG can be misleading when one
is trying to distinguish epileptic seizures from PNES.
For example, 30% of patients with epilepsy have normal
electro­e ncephalograms at presentation. 85 Moreover,
>10% of healthy individuals have nonspecific abnor-
malities or benign variants (waveforms that are subtly
different from the more common, normal waveforms,
but are not pathological in nature) on EEG, while ≈0.5%
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Table 1 | Salient clinical features associated with epileptic seizures and PNES can cause artifacts in the delta, theta and alpha ranges
on EEG and, therefore, mimic epileptiform discharges.
Clinical features Feature predominantly Feature predominantly
associated with associated with PNES Unlike epileptic seizures, however, the frequency of
epileptic seizures motion artifacts associated with PNES rarely progress
Ictal course from fast to slow.91 PNES often have a ‘stuttering’ pattern
Stereotyped nature Yes No
of rhythmic motor activity, where ‘rest periods’ between
the periods of motor activity correspond to normal
Occurrence during sleep Yes No
background electrical activity on EEG.91 This ‘on-off-on’
Occurrence during pseudosleep No Yes pattern of motor activity (alternating periods of rest and
Waxing and waning pattern No Yes rhythmic motor movement) during a seizure is common
Long duration No Yes in patients with PNES,91 but is hardly ever seen during
Motor manifestations
epileptic seizures.
Jacitation No Yes
Video-EEG
Asynchronous movements No Yes Video-EEG recordings that capture a patient’s typical
Discontinuity No Yes events remain the diagnostic gold standard for PNES.92
Pelvic thrusting Yes (with FLES) Yes Such recordings can reliably distinguish between epi-
Prolonged body flaccidity No Yes
leptic seizures and nonepileptic seizures (NES) of either
psychogenic or physiological origin.93 When video-EEG
Sensory and autonomic manifestations
recordings identify clinical features associated with PNES
Normal pupillary response No Yes and background EEG is normal before, during and after
Elevated heart rate from Yes No an event, a diagnosis of PNES should be considered. By
preictal to ictal contrast, brain wave slowing and amplitude dampening
Affective manifestations and vocalizations on EEG indicate that a patient might have physiological
Ictal moaning and crying No Yes NES of a cardiac origin.94 To identify cardiac triggers,
Emotive speech No Yes
the electrocardiogram tracing recorded during stan-
dard video-EEG monitoring should be reviewed. Before
Ictal stuttering No Yes
making a diagnosis, all clinical and EEG features should
Facial features and injuries be carefully analyzed, and one should avoid reaching a
Eye closure during tonic phase No Yes diagnosis until the entire seizure (or seizures, if available)
of convulsion is witnessed. Nevertheless, inital observations might
Jaw clenching during tonic No Yes bias subsequent interpretation; for example, if the early
phase of convulsion clinical or EEG features strongly suggest a diagnosis of
Lateral tongue bites Yes No PNES, subsequent features may be interpreted with this
Postictal findings bias. Some NES may be initiated by epileptic seizures,17
Stertorous breathing Yes No making a dual diagnosis a possibility. The factors men-
tioned above can contribute to epileptologists provid-
Postictal nose rubbing Yes No
ing different interpretations of video-EEG recordings.
Postictal headache Yes No A study of inter-rater reliability (IRR) in the context
Postictal fatigue Yes Yes of differentiating between epileptic seizures and PNES
Ability to recall items No Yes showed that after viewing one event video and EEG,
memorized during ictus epileptologists had good IRR for epilepsy and moderate
Abbreviations: FLES, frontal lobe epileptic seizures; PNES, psychogenic nonepileptic seizures. IRR for PNES.95 In a follow up study, epilepto­logists were
provided with video-EEG data, clinical history, physical
exam results and imaging findings for each study partici-
of healthy individuals show epileptiform discharges.86 In pant and were asked to provide a final diagnosis for each
patients with psychiatric illnesses and individuals with patient. Analysis of the results revealed that agreement
PNES coexisting with epilepsy, the above values relat- between the epileptologists was excellent, kappa coef-
ing to benign variants and epileptiform discharges are ficient 0.94 (95% CI 0.77–1.00).96
higher.18,64,85,87 Approximately one-third of patients with To differentiate between epileptic seizures and PNES
PNES have also been shown to have epileptiform dis- successfully, a typical seizure must be recorded. Once
charges on standard EEG.88,89 In these studies, however, captured, the seizures should be verified by the patient
the electroencephalograms were mostly interpretated and/or their family. If a patient experiences multiple
by general neurologists; in instances where such record- types of seizures then, ideally, all of the different types of
ings were evaluated by board-certified electroencephalo­ episodes should be recorded.97 As noted above, a small
graphers, normal findings or benign variants were minority of patients with PNES (10%) also have epilep-
identified.88 Nevertheless, since PNES often occur in tic seizures. Thus, patients on long-term AED treatment
patients with other brain disorders, nonspecific inter- who have been diagnosed with PNES should only be dis-
ictal EEG abnormalities are common in this group.90 charged from a SMU and tapered off AEDs after careful
Rhythmic shaking movements associated with PNES consideration and when the patient has no history of

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other seizure types. If a patient who has epileptic seizures
and PNES is abruptly taken off AED therapy, they could
have withdrawal seizures that are more intense than their
usual seizures.98
Although video-EEG is the most accurate method
of differentiating between epileptic seizures and PNES,
this technique does have its limitations. For example, we
have observed that in patients with seizures, the inpatient
video-EEG unit may provoke feelings of stress, anticipa-
tion and a desire to reproduce symptoms, and that in
individuals without behavioral disorders, this setting
can evoke psychologically based symptoms that closely
resemble PNES.99
Sometimes video-EEG recordings are not fully diag-
nostic. Suboptimal electrode impedance and muscle and
movement artifacts can all obscure the EEG recording or
lead to false identification of epileptiform discharges. As
ictal scalp electroencephalograms are often unchanged
during both simple partial epileptic seizures and FLE sei-
zures, even when the events have sensory and/or motor
features, artifacts can make diagnosis of these seizures
difficult.100,101 Frontal lobe hypermotor seizures pose a
special diagnostic problem. These episodes can be asso-
ciated with clinical features characteristic of PNES, such
as screaming, pelvic thrusting, wild movements, partially
preserved consciousness and an absence of a postictal
state. Since movement artifacts often obscure the EEG
recording during frontal lobe hypermotor seizures,
these episodes can be falsely ‘confirmed’ as PNES.102
Generalized epileptiform discharges can occur during
acute withdrawal of benzodiazepines and barbiturates,103
and while potentially supportive of an epilepsy diagnosis,
such discharges alone should not be used to confirm a
diagnosis of epilepsy in these settings.
Video-EEG is associated with time and space limita-
tions. Capturing a typical event in patients with PNES
or patients with epileptic seizures in a SMU can be time
consuming, especially when a patient experiences seizures
infrequently. In other patients, even in those no longer
receiving AEDs, the inpatient setting, where the stresses
and activities of daily life are absent, may not be conducive
to seizure occurrence. When a patient’s typical episode
has not been captured during a reasonable amount of
time in a SMU, despite lowering of AEDs, sleep depri-
vation, photic stimulation, hyperventilation and induc-
tion procedures (for example, suggestion combined with
hyperventilation or intravenous administration of saline)
can be used to induce seizures in some patients.104 The
medical team, however, must balance the ethics of using
a potentially perceived ‘deceptive’ placebo and the poten-
tial for evoking non-typical events against the benefits of
an early diagnosis, as discussed below.105,106 In children,
simple suggestion and hypnosis can elicit PNES.107
For patients with frequent episodes or episodes that
can be reliably provoked by specific stimuli or factors,
outpatient video-EEG monitoring offers a cost-effective
alternative to inpatient monitoring. 6–8 hour video-EEG
recordings can capture PNES in more than half of these
patients in the outpatient setting;108 this result is consistent
with the finding that typical events are captured in ≈90%
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REVIEWS
of patients with PNES within the first 48 h of video-EEG
monitoring.89,109 Ambulatory EEG with video can be used
to record typical events in patients who experience epi-
sodes infrequently or in patients who experience events as
a result of environmental triggers in specific settings.
Home video recordings
The widespread availability of home video equipment has
enabled patients to record seizures at home and transmit
the recordings to health-care workers over the inter-
net. When reviewed by experts, home video and audio
recordings of an event can be very helpful for diagnosing
a subset of patients with seizures.56 Home video record-
ings are, however, more limited than hospital recordings;
they lack EEG, often fail to show the ictal onset and often
capture only a partial view of the patient. Important fea-
tures such as facial expression, limb position and move-
ment can be either not included or obscured by bedsheets
or family members. If home video is to be used to record
a typical event, caregivers should be instructed to capture
the face and limbs as well as the trunk, to test the patient’s
level of consciousness and ability to follow commands,
and to assess memory during and after the event. The
same caveats for inpatient long-term monitoring hold
true for home recordings: the types of episodes must
be defined and typical events must be identified by the
patient and/or their family.
Provocative testing
Use of provocative testing to obtain a seizure diagnosis is
a contentious issue in the epilepsy field. When recordings
of spontaneous seizures are difficult to obtain, provoca-
tive tests that induce a patient’s typical PNES can reduce
the time to diagnosis, thus potentially contributing to
the well-being of the patient and avoiding the hazards
of an inappropriate diagnosis of epilepsy.107 Provocative
tests that can induce seizures include body part compres-
sion, verbal suggestion, placement of a tuning fork or
moistened patches onto the skin, intravenous adminis-
tration of saline (or other placebo), and hypnosis—this
technique can also be used to induce seizures in pediat-
ric patients.108 The controversy surrounding these tech-
niques arises over potential ethical concerns, especially
when a placebo is used to induce seizures. Furthermore,
the potential compromise of the physician–patient
relationship—such as when a patient feels ‘tricked’ after
discovering the nature of the procedure—may limit
the utility of subsequent provocative tests. However,
after successful induction of seizures, if the procedure
is disclosed to the patient in a supportive manner, the
physician–patient relationship is usually not altered and
patients typically agree to further interventions.110
Provocative tests that can induce seizures seem to have
high sensitivity and specificity for PNES;104,111–114 however,
some authors have questioned their specifici­t y. 105,115
Intravenous infusion of a placebo may elicit typical
events in most patients with PNES, but atypical events or
epileptic seizures may occur as a result of this pro­cedure
in a minority of patients. Thus, the assumption that all
placebo-induced seizures are typical PNES could lead
REVIEWS
to incorrect diagnoses in some cases.111 Photic stimu-
lation and hyperventilation induce both epileptic and
nonepileptic seizures, and are part of the typical seizure
monitoring work-up.116 Unlike the intravenous infusion
of placebos, these stimuli are not associated with ethical
concerns and might be used over the provocative tests
mentioned above to circumvent such issues.
Neurophysiological assays
Some epileptic seizures are associated with changes in
serum protein levels. Serum prolactin levels have been
shown to rise to concentrations >500 IU/ml in ≥90% of
patients following a generalized convulsion, and in ≥60%
of patients following a complex partial seizure.84,117 Further
studies have indicated that elevated prolactin levels depend
on the involvement of limbic regions during the epileptic
episode.118 After analysis of the literature, the American
Academy of Neurology concluded that serum prolactin
levels measured 10–20 min postictally can help differenti-
ate convulsive or complex partial epileptic seizures from
PNES, but cannot distinguish between epileptic seizures
and syncope or between partial epileptic seizures and
PNES.119 Other serum proteins such as neuron-specific
enolase and creatine kinase are not sensitive markers of
epileptic seizures and cannot reliably discriminate between
these seizures and PNES.120
Noninvasive imaging
MRI studies using ≥1.5 T and epilepsy-specific sequences
have shown that patients with epilepsy (especially refrac-
tory epilepsy) frequently have imaging abnormalities.121
Patients with PNES can also have abnormalities on MRI:
in one study, up to 30% of patients with PNES were iden-
tified as having MRI abnormalities (most often non­
specified gliosis),122 while other studies have indicated
that imaging abnormalities—the most common being
postoperative defects—are present in 10% of these
patients.87 Thus, when lesions typically associated with
epilepsy—for example, mesial temporal sclerosis or cor-
tical dysplasia—are identified on MRI, they support but
cannot confirm a diagnosis of epilepsy. Patients with
PNES and patients with epileptic seizures can both have
normal brain MRI findings, suggesting that MRI may not
differentiate between these two types of seizures.
Single-photon emission CT (SPECT) is commonly
employed during presurgical evaluation of patients
with epilepsy, as it can help identify the ictal focus
through imaging cerebral blood flow.123 Nevertheless,
the capability of SPECT to differentiate between PNES
and epileptic seizures remains unknown. One study
found that ictal SPECT abnormalities were more fre-
quently observed during epileptic seizures than during
PNES,123 but another study found no significant differ-
ences in SPECT abnormalities during these two types of
seizure.124 Furthermore, patients with epileptic seizures
or PNES can have normal ictal and interictal SPECT
findings. 123,125–127 Subtraction of interictal from ictal
SPECT coregistered to MRI (SISCOM) has revealed that
no changes in SPECT abnormalities occur during epi-
sodes in 85% of patients with PNES. Negative findings
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© 2011 Macmillan Publishers Limited. All rights reserved
on SISCOM are, therefore, considered to support a
diagnosis of PNES;118 however, patients with epilep-
tic seizures may also have non-localizing findings on
SISCOM, especially when injections are performed late
after ictal onset.128 As a result, the logistic challenges,
expense, and the lack of specificity make SISCOM of
little value in diagnosing PNES.
Psychiatric evaluation
Psychiatric comorbidity is common in patients with epi-
lepsy and in individuals with PNES,129,130 but the types of
comorbid psychiatric disorders that are associated with
these seizure types differ, and these differences may help
physicians to provide an accurate diagnosis. A study
evaluating psychiatric diagnoses and stressors in patients
with seizures found an absence of relevant psychological
factors in only 5% of 185 patients with PNES.131 The types
of comorbid psychiatric disorders most often present
in patients with PNES are depression, anxiety, post-
traumatic stress disorder and personality disorders.132
In our experience, other comorbidities such as dissocia-
tive and somatoform disorders, borderline personality
disorder, obsessive–compulsive personality disorder,
gender identity disorder and eating disorders are all more
common in patients with PNES than in patients with
epilepsy; depression, anxiety and attention deficit dis-
order are the most common psychiatric disorders in the
latter.133 Psychiatric disorders significantly impact quality
of life in patients with epileptic seizures134 or PNES.135
Psychiatric evaluation can identify conflicts or trau-
matic experiences that might aid diagnosis of PNES and
that would not be routinely addressed in a neurological
evaluation or a typical neuropsychological battery. On
occasion, however, the consulting psychiatrist might
not provide enough information and might merely rule
out suicidality, mood disorder, anxiety, psychosis and
abuse as initiating events, which is not sufficient for a
complete assessment of possible comorbidities. In addi-
tion, when comorbidities or intrapsychic conflict cannot
be elicited, psychiatrists can sometimes recommend an
incorrect diagnosis of epilepsy in patients with PNES.
In such situations, a clinician familiar and comfortable
with somatoform disorders could identify PNES and
neuro­psychiatric aspects of epilepsy.
Performance of psychiatric consultations during
monitoring of seizures may provide answers to ques-
tions that may arise from the patients and their family
when the neurologist delivers a diagnosis of PNES.
Furthermore, psychiatric consultations facilitate the
appropriate in­p atient or outpatient follow-up after
discharge. Thus, a team approach to the diagnosis of
PNES may yield better outcomes than the practice of
‘diagnose and adios’ that is sometimes seen in neurol-
ogy, whereby many patients are lost in the borderland
between neurology and psychiatry.
A detailed review of the treatment options for PNES
is beyond the scope of this article, but pilot random-
ized controlled trials indicate that psychotherapies and
pharmaco­logical interventions could benefit patients
with PNES.136,137 In patients with persistent seizures,

whether they are epileptic seizures or PNES, it is impor-
tant to establish a sense of hope and to help them to cope
with their disorder. Psychiatric evaluation might be a first
step to helping patients with seizures cope with their con-
dition but, at present, psychiatric assessments in seizure
evaluations are underutilized; we feel that they should be
incorporated into all SMU admissions.
Other nonepileptic events
In this Review, we have focused on differentiating
between PNES and epileptic seizures. Nonepileptic, par-
oxysmal physiological (NEPP) events, however, can also
mimic epileptic seizures and are discussed below.
Paroxysmal events of infancy and childhood
NEPP events of infancy can be challenging to differenti-
ate from epileptic seizures. Tremors are the most com-
monly observed abnormal movements in neonates,138
and can mimic focal motor seizures. However, if a
patient’s movements cease with passive flexion of the
affected body part or by restraint of the affected limb, a
diagnosis of tremor is likely.138 Infant ‘jitteriness’, which
is seen in up to 44% of newborns139 and can sometimes
be confused with epileptic seizures, may reflect CNS dys-
function or metabolic derangements, or may be benign.
Exaggerated startle responses to auditory, tactile and
visual stimuli with associated muscle rigidity (hyper-
ekplexia) can trigger apneic spells and falls, which can
be confused with epileptic seizures.138 Self-stimulatory
behaviors (tics, head-banging and masturbation) can be
accompanied by irregular breathing, facial flushing and
diaphoresis, which can also be associated with epileptic
seizures.140 In such situations, video-EEG monitoring is
frequently required to exclude a diagnosis of epilepsy.
Syncope and non-neurological conditions
Many medical conditions are associated with symptoms
that overlap with features of epilepsy. One such condi-
tion, syncope, can be preceded by a nonspecific aura
(for example, visual impairment, nausea, light-headed-
ness or dizziness) and can be associated with convulsive
movements.141 Syncope can result from vasovagal mech-
anisms or other less benign cardiac etiologies such as
arrhythmias, prolonged QT syndrome, or structural
abnormalities (for example, valvular disease or tetrol-
ogy of Fallot).141 Thus, an accurate medical history is
essential for distinguishing between epileptic seizures
and syncope.142 Determination of a patient’s age, and the
circumstances under which an event occurs might aid
diagnosis. If a patient’s typical event occurs shortly after
standing up or is preceded by dia­phoresis, a cardiac eti-
ology or vasovagal syncope should be suspected. 143
Metabolic disorders that induce hypo­g lycemia or
hyponatremia can cause episodic weakness and dizzi-
ness, 144,145 and both of these symptoms may be mis­
interpreted as epileptic seizures. Gastroesophageal
reflux disease (GERD) can cause substernal discomfort
that mimics a rising epigastric sensation similar to what
is experienced in temporal lobe auras and, 146 conse-
quently, this condition may be misdiagnosed
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REVIEWS
as epilepsy; Sandifer syndrome—comprising GERD,
irritability and abnormal body movements in children—
is often mis­diagnosed as epilepsy.147 By contrast, some
patients with mesial temporal lobe epilepsy with
abdominal visceral auras are misdiagnosed with GERD;
in such situations, patients may fail to receive the correct
treatment and end up taking medications that are asso-
ciated with adverse events. The frequency of these
medical mis­diagnoses is not widely published.
Neurological disorders
Sleep disorders such as night terrors and sleepwalking
can mimic frontal or temporal lobe seizures. Sleep starts
(hypnic jerks or sleep myoclonus), which are normal
physiological phenomena, can also be confused with
epileptic seizures. The prevalence of these involuntary
twitches in the general population has been reported to
be 70% for the Western world, and they have been noted
in persons of all sexes and ages.148 Sleep starts are com-
monly reported by patients with this condition, or their
bed-partners, and can be easily diagnosed with video-
EEG.148 Neurological disorders such as multiple sclero-
sis, transient ischemic attack, benign positional vertigo
and migraine with aura can manifest with intermittent,
fleeting neurological symptoms that mimic features
associated with epileptic seizures.
Nonconversion psychiatric disorders
In some individuals, ingestion of illicit drugs can alter
arousal and may cause episodes of behavioral arrest,
which could be misinterpreted as epileptic seizures;
however, a comprehensive social history and urine
drug screen can exclude a diagnosis of epilepsy in most
of these cases. Some axis‑1 psychiatric illnesses (for
example, schizophrenia or psychotic depression) should
be considered when patients present with intermittent
positive sensory phenomena. Tactile, gustatory, audi-
tory and visual hallucinations can occur with epileptic
seizures149 and are usually stereotypical in nature. By con-
trast, psychotic hallucinations can vary markedly, espe-
cially in composition. Furthermore, visual hallucinations
associated with epileptic seizures are most often ‘elemen-
tary’, and patients with these seizures typically report
seeing basic shapes or colored lights; however, complex
visions can occur when the ictus involves extensive cor-
tical regions.149 Psychotic hallucinations, however, are
frequently complex in nature and may involve multiple
modalities. Importantly, hallucinations associated with
epileptic seizures are typically brief (<3 min in dura-
tion), whereas psychotic hallucinations are often more
prolonged (>5 min in duration) and are woven into a
patient’s delusional thought processes.149
By no means is the above discussion of NEPP events
comprehensive. Rather, the purpose of the discussion
was to remind the reader of the multitude of conditions,
both neurological and non-neurological, that should
be considered when evaluating paroxysmal events. The
importance of considering organ systems other than
the CNS in patients exhibiting paroxysmal events is
strongly encouraged.
REVIEWS

Conclusions between epileptic seizures and PNES. Correct diagno-

Video-EEG is the gold standard for diagnosing PNES,
and this technique can reliably differentiate between
PNES and epileptic seizures. A diagnosis of PNES is
supported when epileptiform activity is absent before,
during and after a clinical event with a seizure-like
nature. A normal EEG recording, however, does not
rule out epilepsy, as some epileptic seizures, such as
simple partial epileptic seizures and FLE seizures, can
have scalp-negative EEG findings. Identification of
physical symptoms, patient characteristics and psy-
chiatric histories that are often associated with PNES
provides useful adjunctive information to video-EEG
that may help the treating physician to differentiate
ses enable patients with epilepsy or PNES to receive the
appropriate treatment.150
Review criteria
We reviewed the PubMed database for articles published
in English between 1980 and 2010 using the following
search terms: “nonepileptic seizure”, “psychogenic
seizure”, “conversion seizures”, “nonepileptic attack
disorder” and “dissociative seizure”. Full-text papers were
selected and priority was given to randomized controlled
trials, case–control series and meta-analyses. More than
700 articles were reviewed for potential inclusion.

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Author contributions
O. Devinsky, D. Gazzola and W. C. LaFrance Jr
contributed equally to researching data for the article,
discussion of content, writing, and reviewing and/or
editing of the manuscript before submission.