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27/8/2018 Psychogenic nonepileptic seizures - UpToDate
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Psychogenic nonepileptic seizures
Author: David K Chen, MD

Section Editor: Paul Garcia, MD
Deputy Editor: John F Dashe, MD, PhD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2018. | This topic last updated: Jul 17, 2018.
INTRODUCTION — Clinicians are regularly challenged to identify the nature of episodic neurologic symptoms.
Events associated with prominent motor activity or altered consciousness are often presumed to be epileptic
seizures. However, the event may actually represent one of a wide array of nonepileptic paroxysmal events, such
as syncope, parasomnias, movement disorders, and psychogenic nonepileptic seizures (PNES) (table 1).
PNES are characterized by sudden and time-limited disturbances of motor, sensory, autonomic, cognitive, and/or
emotional functions that can mimic epileptic seizures. However, in contrast to epileptic seizures, PNES are not
associated with abnormally excessive neuronal activity but are instead derived from psychologic underpinnings.
Historical terms for PNES, including pseudoseizures and hysterical seizures, are now discouraged.
It is important to consider PNES when evaluating patients with episodic symptoms, as missing this diagnosis can
be consequential. On average, patients with PNES receive a higher total dose burden of antiseizure drugs, utilize
greater health care resources, and sustain more iatrogenic adverse effects than patients with epilepsy [1]. They
also endure opportunity costs of delaying appropriate psychologic treatment, which has been associated with
worse outcomes [2]. Accurate diagnosis is best achieved by assimilating a wide variety of clues, including a
detailed history from the patient and observers, the physical examination, selected testing, and a psychiatric
evaluation.
The epidemiology, clinical features, diagnosis, and treatment of PNES are discussed here. Other nonepileptic
paroxysmal disorders are discussed separately. (See "Nonepileptic paroxysmal disorders in adolescents and
adults".)
EPIDEMIOLOGY — Incidence rates of PNES in the general population are not well established. Based on
several population-based studies, the estimated incidence rate ranges from 1.5 to 5 per 100,000 persons per
year [3-6]. The prevalence of PNES has been estimated to be between 2 to 33 per 100,000 persons [7].
Among patients referred to outpatient epilepsy centers, 5 to 25 percent are felt to have PNES, while 25 to 40
percent of patients evaluated in inpatient epilepsy monitoring units for intractable seizures are diagnosed with
PNES [5,8].
PNES most commonly present in the third decade of life [9-13]. However, most age groups can be affected,
including young children and older adults [14-17]. Age of onset may be influenced by preexisting conditions; in
one study, patients with learning disabilities had a relatively younger age of onset compared with those with a
history of physical or psychosocial trauma [18]. (See "Nonepileptic paroxysmal disorders in children" and
"Treatment of seizures and epilepsy in older adults".)
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PNES has a female predominance ranging from 66 to 99 percent in different series [6,10,11,13,16,19-23]. This is
consistent with gender ratios described in conversion disorder, one of the salient psychiatric conditions
underlying PNES [24,25]. The gender distribution of patients with PNES is more even when examining specific
subpopulations, such as children, individuals with intellectual disability, and older adults [26,27]. Race, marital
status, and years of education do not appear to influence the prevalence of PNES [12].
ETIOLOGY — Dissociative disorders and conversion disorders are felt to underlie most PNES [28]. In these
conditions, psychosocial conflicts are "converted" to physical symptoms rather than expressed through a healthy
verbal channel [23,29].
Diagnostic criteria for conversion disorder were revised in the Diagnostic and Statistical Manual of Mental
Disorders, Fifth Edition (DSM-5) in ways that are relevant to PNES [30]. Whereas conversion disorder was
previously approached as a diagnosis of exclusion, DSM-5 stipulates "rule-in" of conversion disorder diagnosis
based on inclusion of clinical findings that are incongruent to known anatomy, physiology, or diseases. The
previous requirement to exclude feigning has also been abandoned, since such exclusion can be difficult to
definitively establish without surveillance or forensic evaluation. Moreover, DSM-5 no longer requires the
presence of psychologic factors to precede or exacerbate conversion symptoms, as such factors may not always
be immediately apparent from the history. Some patients' readiness to discuss psychologic factors may depend
on the strength of the clinician-patient alliance. (See "Conversion disorder in adults: Terminology, diagnosis, and
differential diagnosis" and "Conversion disorder in adults: Clinical features, assessment, and comorbidity".)
Dissociative disorders and conversion disorders contrast with factitious disorder and malingering, in which
symptoms are, at least to some extent, voluntary and consciously produced. Factitious disorders and malingering
are rarely responsible for PNES. While the clinician should seek evidence for potential primary gain (affording
relief from emotional conflict or tension) and secondary gain (deriving advantages such as attention, relief from
responsibilities, or attaining disability benefits), it should never be preemptively assumed that patients with PNES
are "faking" their symptoms. (See "Factitious disorder imposed on self (Munchausen syndrome)".)
Psychosocial stressors that may precipitate the emergence of PNES in vulnerable patients include bereavement;
unwanted pregnancy; ongoing physical, verbal, or sexual abuse; lawsuits; job pressure; financial difficulties;
impending divorce; domestic conflicts; and assault [9,21,23,31,32]. In children, separation anxiety, school
avoidance, and parental discord or divorce may also play a role [14,33]. Sometimes the recent event seems
relatively minor, but may serve as the "last straw" in a series of events or may serve as a reminder of more
significant remote events [34]. Cultural variation and seizure modeling may also play a role [21,35,36].
One proposed model considers two main types of psychologic underpinnings of PNES: post-traumatic and
developmental [37].
● Post-traumatic – In response to indelibly threatening experiences that the patient struggles to adequately
process, post-traumatic PNES reflect a psychologic defense via a "cutoff phenomenon" upon spontaneous
intrusion of intolerable memories [38]. A history of sexual or physical abuse is prevalent in patients with
PNES; in various cohorts, this is reported in one-third to one-half of patients [9,18,21-23,39-41]. However, in
one case series, a past history of sexual abuse was equally prevalent (38 percent) among 37 patients with
PNES and 58 patients with epilepsy [42]. Patients with PNES who report a history of sexual abuse may be
more likely to have events that are clinically more severe and more likely to resemble epileptic seizures [43].
In another series, they were also more likely to exhibit self-harming behaviors and other medically
unexplained symptoms in addition to PNES [18].
● Developmental – Developmental PNES are derived from maladaptive coping in the face of complex life
tasks and milestones along the patient's continuum of psychosocial maturation. Dysfunctional family
relationships (poor communication or support, interpersonal conflict, trauma) are reported by many PNES
patients and/or family members [21,44-46]. A repressive style of coping may develop in response,
characterized by avoidance of perceived threats and reluctance to confront problems directly. In the
subconscious pursuit to avoid inner emotional difficulties, conscious attention will tend to be focused on
external physical symptoms [47].
Functional imaging has investigated neural circuit disturbances in patients with PNES. Several studies have
documented widespread functional connectivity alterations in emotion control, executive, attentional,
sensorimotor, and default mode networks [48-50].
CLINICAL FEATURES OF EVENTS — Recognizing PNES can be challenging even for experienced observers,
in part because of the broad diversity of presentations. Nonetheless, clues that raise suspicion for this diagnosis
are often apparent from the clinical history (table 2).
A history from patients with suspected PNES should elicit information relevant to any paroxysmal disorder,
including seizures:
● Precipitants and circumstances in which episodes occur
● Detailed description of the ictus as perceived by the patient and as witnessed by others, including prodromal
features, event frequency and duration, and factors that reduce event frequency or attenuate event intensity
● Postictal symptoms
● Response to treatment
Precipitants and setting — The setting in which an episode occurs can be helpful in distinguishing PNES and
epilepsy.
● Witnesses present – Most episodes of PNES occur in front of witnesses [17,51,52]. In one study, the
occurrence of an episode in the doctor's waiting or examination room was estimated to have a 75 percent
predictive value for PNES [51]. Similarly, in a study of patients undergoing electroencephalography (EEG)
monitoring, episodes that occurred at the time of electrode placement were found to be PNES, not epileptic
seizures [53].
● Relationship to sleep – PNES tend not to occur during sleep [53,54]. By contrast, epileptic seizures can
occur during sleep, and in some forms of epilepsy, nocturnal episodes are most frequent. Some of these
syndromes are associated with dramatic and bizarre movements that, although stereotyped, are sometimes
mistaken for PNES. (See "Sleep-related epilepsy syndromes", section on 'Clinical features'.)
Nocturnal seizures are frequently unwitnessed, and patients with PNES may report (erroneously) that
seizures occur during sleep [55-57]. Patients with PNES may appear to be asleep just before seizure onset,
but the EEG in these cases demonstrates wakefulness [56]. (See 'Video-EEG monitoring' below.)
● Stress – While it is intuitive that PNES would be more likely to be associated with stressful situations, stress
is also commonly cited as a seizure precipitant in patients with epilepsy [58,59]. In patients with PNES,
witness responders may be more likely than patients to associate emotional stress as a trigger for events
[60].
● Menstrual cycle – Increased seizure frequency during the perimenstrual time period suggests epileptic
seizures. In one series, perimenstrual exacerbation was associated with 13 of 27 patients with epileptic
seizures versus 1 of 38 patients with PNES [61]. (See "Initial treatment of epilepsy in adults", section on
'Catamenial epilepsy'.)
Ictal features — Unresponsive behavior with motor manifestations mimicking a generalized tonic-clonic seizure
or a focal seizure with impaired awareness is the most common manifestation of a PNES [10,11,16,21,52,62-64].
Events that mimic atonic, absence, or focal aware seizures are less common.
A variety of clinical behaviors may occur during PNES, some of which are useful in distinguishing them from
epileptic seizures (table 2). One systematic review found that long duration, fluctuating course, asynchronous
movements, pelvic thrusting, side-to-side head or body movements, ictal eye closure, ictal crying, memory recall,
and absent postictal confusion were the most reliable signs in distinguishing PNES from epileptic seizure;
occurrence out of true sleep favored epileptic seizure [54]. However, it is important to note that no single
semiologic feature is either sensitive or specific for PNES [6]. In addition, patients and eyewitnesses can report
clinical features that are discrepant from each other and from review of video-recorded events [60,65].
● Motor activity – A variety of convulsive-like motor activities can occur in PNES. While motor manifestations
of an epileptic seizure usually take the form of brief tonic posturing or a synchronized convulsion with a
defined progression of motor activity, movements in PNES are more often asynchronous, variable, and may
wax and wane over the course of the ictus [8,10,54,66]. Specific movements such as writhing, thrashing,
pelvic thrusts, opisthotonus (arched back), and jactitation (rolling from side to side) suggest PNES, but these
are not always present, particularly in children [10,17,52,63,66,67].
Some epileptic seizures, such as those of frontal lobe origin, can produce unusual-appearing motor activities
similar to those seen in PNES [8,54,55,68-73]. Stereotyped and consistent lateralization of motor features
usually, but not always, suggests epilepsy; some patients have PNES with consistent semiology and little
variation [54,55,64,74]. (See "Localization-related (focal) epilepsy: Causes and clinical features", section on
'Frontal lobe epilepsy' and "Sleep-related epilepsy syndromes", section on 'Sleep-related hypermotor
epilepsy (previously NFLE)'.)
● Tongue-biting and self-injury – Classic symptoms of epileptic seizures such as tongue-biting,

incontinence, and self-injury are more common in epileptic seizures, but they can occur in a third or more of
patients with PNES [9-11,23,54,62,75,76]. A tongue bitten on the side (versus the tip) and severe tongue-
biting (with laceration) are more specific for epileptic seizure [76,77]. Seizure-related burn injuries are also
highly specific for epileptic seizures [78].
● Level of awareness – Incomplete loss of consciousness during the episode, suggested either by
responsiveness to stimuli or by later recall of events during segments of ictal unresponsiveness, supports
PNES [10,65,79]. The presence of an alpha rhythm on the EEG (ie, neurophysiologic evidence of
wakefulness) during an episode in which the patient is clinically altered or amnestic also supports a
nonepileptic process. (See 'Video-EEG monitoring' below.)
● Vocalizations – Ictal features of emotional overlay, such as weeping, stuttering, and vocalizations with
affective content, are relatively uncommon in epileptic seizures and suggest PNES [17,54,80-83]. When
vocalization occurs in an epileptic seizure, it is usually isolated to the seizure onset and is frequently
characterized by a fragmented guttural utterance, caused by a tonic diaphragm forcing air against tonic or
clonic vocal cords [84]. By contrast, the ictal vocalization of PNES may exhibit affective content and not only
occur at seizure onset, but also persist or even intensify through the course of the seizure.
● Auras – A seizure aura is frequently reported in PNES (25 to 60 percent) and may be a more common
symptom than in epilepsy [21,23,52].
● Autonomic signs – Autonomic manifestations during an ictus (eg, tachycardia, cyanosis) suggest epileptic
seizure, and their absence, particularly during a major convulsion, suggests PNES [66,83,85].
● Eye closure – Eyes are usually open during the ictus of a convulsive epileptic seizure [54,65,67,77,86].
Forced eye closure in particular suggests PNES. Sensitivity and specificity of eye closure as a sign for
PNES varies according to how it is defined [66]. One study that calculated duration of time for eye closure
(rather than absolute presence or absence) found only moderate sensitivity but high specificity for PNES
[87]. Similarly, in another study, eye-opening at seizure onset was found to have a high sensitivity and lower
specificity for epileptic seizure as compared with PNES [65]. In both of these series, observer reports of ictal
eye closure were not reliable.
● Atonia – Ictal atonia is not a common PNES manifestation. However, when prolonged events of atonia
occur, they almost always represent PNES rather than epileptic seizure [63]. Completely limp or motionless
events are also uncommon for syncope, as approximately 90 percent of syncopal events have been shown
to be accompanied by motor symptoms [88].
● Duration – While the ictus of an epileptic seizure is typically very brief, often less than one minute, PNES
are rarely less than one minute and are usually much longer [10-12,17,54,55,64,67,72,89,90]. Prolonged
episodes (ie, psychogenic status epilepticus) are not rare. In one series, 78 percent of patients with PNES
reported at least one event longer than 30 minutes, and half of these patients had recurrent episodes of
psychogenic status epilepticus [91].
● Frequency – Patients with PNES generally report a higher seizure frequency than patients with epilepsy
[92]. Suspicion for PNES is raised by an apparently protracted seizure duration or daily convulsive events,
despite a normal exam during history-taking [91]. Demonstration of an apparently explosive attack burden
from the moment of the first event and onward can also be characteristic of PNES [93].
Postictal symptoms
● Return to baseline – Rapid alerting and reorientation are common after PNES but uncommon with epileptic
seizures, except for certain seizure types, such as absence or frontal lobe seizures [52,54,55,65,68].
However, in some case series, half or more of patients with PNES exhibited postictal confusion or
drowsiness [21,52].
● Respiratory changes – The postictal period after a generalized tonic-clonic seizure was found in one cohort
to be characterized by a breathing pattern of deep and prolonged inspiratory and expiratory phases
(stertorous breathing pattern), compared with shallow, rapid respirations in patients after a PNES [54,67,86].
Epileptic seizures arising from the frontal lobe, however, were associated with a postictal breathing pattern
similar to PNES. Another case series described a stertorous postictal breathing pattern after 6 of 27 epileptic
seizures but in none of the 15 observed PNES [66].
A key interpretive caution is that neurobehavioral manifestations during the postictal phase of epileptic seizures
can highly resemble the ictal features of PNES in some patients [94]. During history-taking, it is important to
clarify that the witness has observed the onset of the episode.
Response to treatment — Most patients with PNES have seizures for many years prior to diagnosis, and most
are treated unsuccessfully with antiseizure drugs [6,11,16,21,52,63,75]. A failure to make even small
improvements in seizure frequency despite vigorous antiseizure drug trials suggests the diagnosis of PNES.
Similarly, patients who present with prolonged PNES are often treated with drug protocols for status epilepticus
and fail to respond [1,95,96].
COMMON COMORBIDITIES
Psychopathology — While patients with PNES have a higher burden of psychiatric disease and symptoms than
control groups with epilepsy, these conditions are also common in patients with epilepsy and are not specific for
PNES [9,10,12,13,23,39,89,97-99]. The presence of these conditions is often not known at the time of
presentation with PNES and may instead be revealed later as part of the evaluation when sufficient rapport has
been established.
Psychiatric conditions associated with PNES include [21,23,29,32,62,97,98,100-104]:
● Depression
● Anxiety
● Somatic symptom and related disorders
● Post-traumatic stress disorder
● Dissociative disorders
● Personality disorders, especially borderline personality disorder, but also narcissistic, histrionic, and
antisocial personalities
By contrast, depression with major psychosis and schizophrenia are relatively uncommon in patients with PNES
[16].
Dissociative disorders and conversion disorders are felt to underlie most PNES [28]. Some authors distinguish
between comorbid and etiologic psychiatric conditions in PNES, but this implies a detailed understanding of the
pathophysiology of these symptoms, which is lacking. These disorders overlap, and it is common for patients to
have more than one of these conditions [97]. (See 'Etiology' above.)
Concurrent or past epilepsy — Estimates of the prevalence of concurrent epilepsy among patients with PNES
vary widely, from 5 to over 50 percent, in part because of differing diagnostic criteria used to determine the
coexistence of epilepsy [16,18,21,23,105-109]. When strict diagnostic criteria are applied, the prevalence of
mixed PNES with epilepsy is likely closer to 5 to 10 percent [105,107]. The typical clinical course of adults with
both diagnoses is that the onset of epilepsy predates the onset of PNES by approximately 10 years [92]. It has
been postulated that the patient's own history of epilepsy may be the model for their PNES.
In one case series with video-electroencephalography (EEG) documentation of both PNES and epileptic seizures
in the same patient, most patients (18 of 20) had notably different clinical semiology for PNES compared with
their epileptic seizures [110]. However, another series found that patients with PNES and probable temporal lobe
epilepsy had symptoms that appeared to be more characteristic of temporal lobe seizures, possibly because of
learned behaviors from their own seizures [111].
A few patients (2 to 9 percent) with epilepsy develop PNES after epilepsy surgery [112-114]. These typically
emerge within the first several months, at a time when other psychiatric complications are also most incident.
These patients often manifest other symptoms of psychiatric distress (eg, anxiety, psychosis). The symptoms
may approximate presurgical epileptic events but are often very different. This phenomenon may be due in part
to a paradoxical dependence on seizures and all of its psychosocial ramifications.
Other neurologic and medical disorders — PNES is well described in patients with neurologic developmental
disabilities [16,115,116]. Notably, the prevalence of mixed PNES with epilepsy can be up to 30 percent in this
population [117]. Among these patients, distinguishing PNES from epileptic seizures and other repetitive,
stereotyped behaviors is a particular challenge. In one study, individuals with PNES and learning disabilities were
more likely to have circumstantial triggering of events and more prolonged events than individuals without
learning disabilities [18].
A history of recurrent medical evaluations for other unexplained somatic complaints is common. In one series, 30
percent of PNES patients had a sufficient burden of gastrointestinal complaints, pain, fatigue, and other
complaints to meet criteria for an undifferentiated somatoform disorder [118]. In another study that included over
250 patients with either PNES or epilepsy who underwent video-EEG monitoring over a two-year period, patients
with PNES were significantly more likely than those with epilepsy (66 versus 27 percent) to have one or more of
the following diagnoses: fibromyalgia, systemic exertion intolerance disease (also known as chronic fatigue
syndrome), chronic pain syndrome, headaches, irritable bowel syndrome, asthma, and gastroesophageal reflux
disease (GERD) [119].
An increased risk of prior physical insults has been described in patients with PNES, including antecedent minor
head trauma in 30 to 44 percent of patients [16,23,39,109,118,120,121], health-related complications [18], and
surgical procedures [122]. It has been posited that the provocation of PNES may involve processes that are
physiologic as much as psychologic (ie, biopsychosocial model for functional neurologic symptoms) [123]. Recall
bias may also contribute to the apparent association.
DIFFERENTIAL DIAGNOSIS — The primary consideration in the differential diagnosis of PNES is epileptic
seizures [106]. Seizures arising from the frontal lobe in particular are often mistaken for PNES because of their
unusual semiology. (See 'Ictal features' above.)
Clinical features that suggest frontal lobe seizures rather than PNES are a brief duration (less than one minute),
stereotyped manifestations, eyes open during the ictus, and their occurrence during physiologic sleep [55,72,86].
In one video-electroencephalography (EEG) study, tonic contraction of the upper extremities in abduction was a
feature of 90 percent of 63 supplementary motor seizures and occurred in none of 111 PNES [55]. (See
"Localization-related (focal) epilepsy: Causes and clinical features", section on 'Frontal lobe epilepsy'.)
Other nonepileptic paroxysmal disorders may be mistaken for either epileptic seizures or for PNES [106]. These
vary by age group and include sleep disorders, movement disorders, migraine, and syncope (table 1 and table
3). These are discussed in detail separately. (See "Approach to abnormal movements and behaviors during
sleep" and "Nonepileptic paroxysmal disorders in adolescents and adults" and "Evaluation and management of
the first seizure in adults".)
DIAGNOSIS — Clinical features of events are often not sufficiently sensitive or specific to definitively distinguish
seizures from PNES, and confirmatory video-electroencephalography (EEG) testing is usually required to
supplement the history [124]. An accurate diagnosis is best achieved by assimilating a wide variety of clues,
including a detailed history from the patient and observers, the physical examination, selected testing, and a
psychiatric evaluation.
Levels of diagnostic certainty — Video-EEG is the gold-standard test for the diagnosis of PNES and should be
performed in all patients in whom this diagnosis is suspected [12,125]. Video-EEG results are not always
conclusive, however, and the resource is not readily available to every patient worldwide.
Recognizing these limitations, the Nonepileptic Seizure Task Force of the International League Against Epilepsy
(ILAE) delineates how PNES can be diagnosed with varying levels of certainty according to the combination of
three elements (table 4) [126]:
● Event description by patient and/or witness
● Clinician observation of seizures as an in-person witness or by video recordings
● Available ictal and interictal EEG data
More timely recognition of PNES under this graded approach may promote earlier exploration of potential
psychologic underpinnings and treatment options. Meanwhile, for patients whose clinical data meet lower levels
of diagnostic certainty, iterative assessments over time by the treating neurologist remain vital, as emergence of
potential epilepsy-consistent data would refute the initial PNES diagnosis.
History — PNES is important to consider when evaluating patients with episodic neurologic symptoms. Missing
this diagnosis has important consequences, including:
● Inappropriate treatment with antiseizure drugs and potential morbidities of drug toxicity [6,95,127].
Prolonged episodes, psychogenic status epilepticus in particular, are often treated with toxic antiseizure drug
doses, intubation, and iatrogenically induced coma [1,31,91,95,96,127-131].
● Costs and burdens to the individual and health care system due to recurrent visits to the emergency
department and hospitalizations for uncontrolled, unrecognized PNES [132].
● Persistence of conversion and other psychiatric symptoms and delay of needed psychiatric interventions.
While video-EEG improves the ability to recognize PNES, the diagnosis relies heavily on clues obtained by
detailed history from the patient and observers. Suggestive clinical features and relevant comorbidities are
reviewed in detail above. (See 'Clinical features of events' above and 'Common comorbidities' above.)
The diagnosis of PNES can be challenging, with delays as long as 10 to 15 years in some case series [9,75].
This is due in part to the broad diversity of PNES presentations and the lack of one single unifying presenting
symptom. Other sources of misdiagnosis include an inadequate history, co-occurrence of PNES and epilepsy in
the same patient, poor clinician-patient rapport, reliance upon clinical observation of the event, discomfort in
making a psychiatric diagnosis, and reluctance to obtain a psychiatric evaluation before the clinician feels
confident about the diagnosis [133].
Examination findings — Physical examination of patients with PNES may be completely normal, demonstrate
neurologic abnormalities associated with unrelated neurologic disorders, or exhibit classic signs of conversion
disorder. In conversion disorder, the clinician may find a variety of abnormalities that do not make physiologic
sense [25].
A classic sign of conversion disorder is an apparent lack of concern for serious clinical symptoms (so-called
"belle indifference"). However, some believe this finding is overemphasized in PNES patients and may be absent
[134].
Electroencephalography
Routine EEG — Routine EEG is often inadequate for distinguishing epileptic seizures from PNES. One
reason is that a routine EEG records activity for only 20 to 30 minutes and is therefore unlikely to capture an
ictus. A normal interictal EEG does not exclude the possibility of epilepsy or confirm the diagnosis of PNES [135].
At the same time, interictal epileptiform abnormalities do not rule out PNES. While more prevalent among
patients with epilepsy, these are also seen in patients with PNES [75,110,136]. In patients felt to have PNES
alone (without comorbid epilepsy), the prevalence of interictal EEG abnormalities ranges from 10 to 18 percent
[11,75,108,109,121,136]. An abnormal interictal EEG is more common if there is a past or concurrent history of
epilepsy or other underlying neurologic injury or disease. (See "Electroencephalography (EEG) in the diagnosis
of seizures and epilepsy".)
Video-EEG monitoring — Video-EEG monitoring combines extended EEG monitoring with time-locked video
acquisition that allows for analysis of clinical and electrographic features during a captured event. The yield of
monitoring is high; 73 to 96 percent of patients will have typical PNES within the first 48 hours of recording
[12,53,137,138].
Accurate interpretation of video-EEG monitoring requires careful analysis of the clinical events and any changes
in the EEG occurring before, during, and after the seizure. During a clinical event that includes altered
consciousness, a physiologic basis for altered consciousness should be sought on EEG. Cerebral
hypoperfusion, as occurs during syncope, coincides with a stereotyped progression from theta slowing, to delta
slowing, to background suppression (depending on the severity of cerebral hypoxia) [139]. By contrast, an alpha
rhythm on EEG is the neurophysiologic correlate of alertness. Discordant findings (eg, clinical alteration of
consciousness with concurrent alpha rhythm on EEG) are supportive of PNES in the appropriate clinical context.
Beyond these scenarios, the absence of an ictal EEG epileptiform abnormality does not necessarily distinguish
psychogenic from physiologic nonepileptic etiologies. The distinction of psychogenic origin requires the
demonstration of PNES-consistent semiologic features (table 2) in the context of supportive historical and
ictal/peri-ictal physical exam findings.
Failure to see an electrographic seizure on surface EEG during an event does not exclude epilepsy, and caution
is required for interpretation. While the majority of generalized tonic-clonic seizures reveal an ictal EEG correlate,
the tracing may be obscured by muscle artifact. On the other hand, only 15 to 33 percent of simple partial
seizures or seizure auras, which involve a limited brain area and are of deep origin, are associated with surface
EEG abnormalities [140]. Furthermore, in some seizures, the early onset of motor activity results in artifacts that
can obscure EEG changes. (See "Video and ambulatory EEG monitoring in the diagnosis of seizures and
epilepsy".)
When the history suggests more than one independent event type, an occurrence of each type should be
recorded on video-EEG, since each type could reflect a distinct diagnosis. Event types that are not documented
on video-EEG should be diagnosed with a more cautious level of certainty (table 4) [126]. It is also important to
determine from both patients and family members that the event captured on video-EEG is typical of the events
that are being evaluated. It can be helpful to show the captured video of the event to family members who can
indicate how closely it resembles prior events they have witnessed.
One study of inter-rater reliability of video-EEG found only moderate agreement (kappa = 0.57) for the diagnosis
of PNES [141]. Limitations of this study that differ from "real-life" use of this test include a forced choice paradigm
(epileptic versus psychogenic nonepileptic versus physiologic nonepileptic seizures) that was based on the
analysis of a single episode with no access to other clinical data.
Spell induction — Video-EEG monitoring may be supplemented with the administration of a placebo
designed to induce a PNES. This may be helpful if the patient fails to have a spontaneous event during
prolonged video-EEG monitoring.
This maneuver is typically performed by administering a placebo (eg, intravenous saline or rubbing alcohol on
the skin of the patient) with or without simultaneous hyperventilation and photic stimulation. The patient is
instructed that the maneuver may induce an episode. Across studies, approximately 70 to 90 percent of patients
with PNES will have a typical event in this setting [6,31,52,142-145]. The success rate of induction may be higher
among patients with certain clinical characteristics, including hypermotor ictal features, uncommon cognitive and
affective self-reported symptoms, and absence of prior induction exposure [145].
While much less common, epileptic seizures have also been reported to occur with induction [106,108,137,146-
148]. Because of this, induction should be performed while the patient is monitored on video-EEG. It is also
essential to confirm that the elicited episode is representative of the spells under investigation. A patient with
epilepsy may experience new and nonepileptic symptoms under these circumstances, but the features are
usually atypical of their usual seizures and hence have limited clinical relevance [149].
Use of spell induction maneuvers is controversial. While facilitating diagnosis, the inherent deceit in this
approach may jeopardize the clinician-patient relationship and impede future treatment efforts [150]. However,
some experts believe that these considerations are outweighed by the benefits of making an accurate diagnosis
and avoiding future morbidity associated with inappropriate treatments [6,151,152]. Alternative techniques that
do not use a placebo, but instead administer photic stimulation and/or hyperventilation with verbal suggestion,
may obviate the deceitful aspects, as these are routinely used to precipitate epileptic seizures. This approach
may be more acceptable to patients and clinicians. [52,142]. As another alternative, some clinicians report that
they successfully use placebo induction techniques after informing the patient that they are being used to elicit a
possible psychogenic as well as epileptic seizure [153]. This transparency avoids deceit and makes this
technique ethically more acceptable.
Other monitoring techniques — Sometimes, in spite of prolonged video-EEG and use of induction
techniques, no episode is recorded. In such cases, outpatient ambulatory EEG, ideally with concomitant video,
may be helpful. Advising family members to have a phone or video camera ready to record on standby can be
helpful as well. While the absence of concomitant EEG is a significant limitation, direct observation of the clinical
event via video can provide a key criterion to support higher levels of diagnostic certainty in the ILAE's staged
approach to the diagnosis of PNES (table 4) [66,126]. (See 'Levels of diagnostic certainty' above and 'Ictal
features' above.)
Serum testing — Certain laboratory studies can help differentiate PNES from epileptic seizure.
● Prolactin – Depending on the seizure type, prolactin levels may be elevated after an epileptic seizure
[69,70]. The pooled sensitivity of an elevated prolactin (twice the baseline level) from several studies is 60
percent for generalized tonic-clonic seizures and 46 percent for focal seizures with impaired awareness
[154]. The sensitivity is lower for focal seizures with retained awareness as well as for seizures arising from
the frontal lobe [155].
The timing of measuring prolactin is crucial. In typical cases, prolactin levels peak 15 to 20 minutes after the
seizure and return to baseline levels within an hour [154]. Considering the known circadian fluctuation of
serum prolactin [156], the optimal baseline prolactin level for comparison purposes should be drawn at
approximately the same time on the next day after the initial postictal serum prolactin measurement and at
least six hours after the last seizure. Prolactin elevations have not been well characterized in the setting of
repeated seizures or status epilepticus, and have unclear utility in such settings.
Prolactin levels are unlikely to rise after a PNES, but elevations can occur after syncope [154,157]. Thus, an
elevated prolactin level can be helpful in identifying a physiologic episode (epileptic seizure or syncope);
however, a nonelevated prolactin level does not imply PNES. Conditions associated with hyperprolactinemia
may confound the results, even when paired baseline and postictal prolactin measurements are available.
These conditions include pregnancy/lactation, prolactinomas, primary hypothyroidism, and certain drugs (eg,
dopamine antagonists) [154]. (See "Causes of hyperprolactinemia".)
● Other serum markers – Other laboratories that may help distinguish PNES from epileptic seizures and other
physiologic events include creatine phosphokinase (CPK), cortisol, white blood cell count, lactate
dehydrogenase, pCO2, ammonia, and neuron-specific enolase [158-161]. CPK levels in particular are often
elevated after generalized tonic-clonic seizures but not after partial seizures. The later rise and prolonged
elevation of CPK, up to 24 hours postictally, make this test somewhat more useful in the outpatient setting.
However, a defined threshold level for abnormality, sensitivity, and specificity remains to be determined for
CPK, as for other serum markers [162,163].
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Neuroimaging — Given the clinical overlap between epileptic seizures and PNES, a neuroimaging study should
be obtained to evaluate for a culprit structural brain abnormality. In the absence of contraindications (eg,
pacemaker, severe claustrophobia), magnetic resonance imaging (MRI) is preferred over computed tomography
(CT) because it has superior sensitivity for detecting relevant lesions.
When a structural abnormality is seen on brain MRI, it suggests a neuroanatomic substrate for epilepsy and
provides support for a diagnosis of epilepsy. However, many series report abnormal brain MRI in 10 to 38
percent of patients with PNES [11,21,75,121,164]. At the same time, many patients with epileptic seizures have
normal brain MRI. Abnormalities identified in PNES patients include arachnoid cyst, post-traumatic or gliotic
change, hippocampal sclerosis, and venous angioma [121].
The role of functional imaging in the evaluation of suspected PNES is not well established. Abnormalities on
interictal single-photon emission computed tomography (SPECT) have been reported in both PNES and
epilepsy. However, a change in focal perfusion from an ictal or postictal SPECT compared with an interictal
SPECT can help distinguish epileptic seizures from PNES [164-168]. This technique may be particularly useful
when movement-related muscle artifact obscures EEG interpretation. However, this test is not widely available,
and the sensitivity and specificity are uncertain.
Neuropsychological testing — Neuropsychological testing is not an essential part of the diagnostic evaluation
but can be useful in establishing the treatment plan, as it may allow mental health clinicians to integrate
psychiatric diagnoses and therapeutic plans. (See 'Psychiatric evaluation' below.)
Neuropsychological testing typically assesses cognitive functioning as well as some psychologic domains.
Patients with epilepsy as well as those with PNES often exhibit mild cognitive deficits, particularly in attention and
memory [16,99,121,169-171]. Some of these deficits may be related to antiseizure drugs and other medications.
Neuropsychological testing may be suspicious for PNES when a pattern of failure to recognize words presented
repeatedly is exhibited in the face of only rarely making false-positive errors (termed a "negative response bias")
[172,173].
Personality profile testing such as the Minnesota Multiphasic Personality Inventory (MMPI), a common
component of neuropsychological testing, can be helpful in supplementing formal psychiatric evaluations and
highlighting comorbid psychiatric disturbances [174]. Patients with PNES typically have high scores on
somatization, hypochondriasis, and hysteria subscales [12,21,136,174-176]. While it is a helpful adjunct in the
evaluation of patients, studies give varying estimates of its ability to correctly categorize PNES versus epilepsy
patients ranging from 70 to 90 percent.
One group developed a self-administered screening questionnaire that in a validation cohort had an 85 percent
sensitivity and an 85 percent specificity for distinguishing PNES from epileptic seizures [177]. This questionnaire
was based primarily on items that were culled from other psychosocial scales that question patients about
attitudes toward health and lifestyle, self-efficacy, and symptoms of anxiety and depression. This instrument has
not yet been widely validated.
Psychiatric evaluation — While essential in the evaluation of patients with suspected PNES, the role of
psychiatric evaluation is not to establish or refute a PNES diagnosis, but rather to identify comorbid or underlying
psychiatric conditions that will hopefully direct treatment [11,89,104,125].
An experienced clinician in a detailed psychiatric interview will elicit clinical features that may establish a
diagnosis of depression, anxiety, somatic symptom disorder, a dissociative disorder, and other disorders.
Sufficient rapport may also be established in this setting, which allows for a previously unreported history of
sexual abuse or other trauma to be revealed. (See 'Psychopathology' above.)
Findings on neuropsychological testing may supplement the interview in arriving at one or more psychiatric
disorders. (See 'Neuropsychological testing' above.)
PRESENTING THE DIAGNOSIS — Presenting the diagnosis of PNES to patients can be challenging. Most
agree that this should not take place until the clinician feels very definite about the diagnosis [178,179]. Care
providers who take on this role should be well trained in delivering this information.
This conversation is crucially important for the patient's prognosis. Because most serious morbidity associated
with PNES is from inappropriate aggressive treatment of presumed epileptic seizures, it is important for the
patient and family to accept the diagnosis of PNES in order to avoid emergency department visits, as well as to
obtain appropriate psychiatric treatment [132,179].
A useful method for communicating the diagnosis of PNES to patients emphasizes the presentation in a
nonjudgmental fashion that strives to maintain patient dignity [125,180]. Useful techniques and talking points in
this conversation include some of the following [29,180]:
● State that you do not consider the episodes to be caused by epileptic discharges. Rather, these episodes
are akin to "a software problem, while the hardware is alright" [181].
● Emphasize that this problem is as serious as one caused by epilepsy and deserves the attention and
treatment that is accorded any illness.
● Discuss how stress afflicts each of us to variable degrees and in different ways. Note that "the body needs to
blow off steam" in some fashion; some people release this stress with the development of headaches,
others with tremors, and some with nonepileptic seizures.
● Emphasize that the episodes are experienced as real and bothersome, and that although they relate to
emotional or psychologic causes, you do not dismiss the problem, and you do not consider the patient to be
"crazy."
● State that the disorder warrants different treatments than those administered for epilepsy.
● Tell patients that you expect that they may react in many ways to this diagnosis. Many patients become
angry in response to receiving the diagnosis. Some may acknowledge these feelings, while others may not.
An angry reaction may forebode a poor prognosis [9,118].
When a video-electroencephalography (EEG) confirmed diagnosis of PNES has been appropriately

communicated, up to one-third of patients may experience improvement in their seizure burden with short-term
follow-up, often without having received any additional intervention [101,182]. On the other hand, some patients
with PNES exhibit exacerbations of their episodes after the diagnosis is revealed, and we often warn patients not
to be surprised if this were to occur [9].
One study used a semistructured interview and a printed leaflet that emphasized many of these points, among
others, in communicating a new diagnosis of PNES to 50 patients [183]. The investigators felt that these patients
responded more positively and had better outcomes than those in whom this approach was not utilized, but there
was no control group in this study for direct comparison.
NEUROLOGIC FOLLOW-UP — A frequent error on the part of neurologists is the immediate discharge of
patients with PNES, with the rationale that the diagnosis is psychiatric and not neurologic. In fact, some experts
advise instead that patients with PNES should not be discharged from the neurologist's care until patients and
families accept the fact that they do not have epilepsy, have transitioned to psychiatric care, and have agreed on
the time to discontinue neurologic care [2,179].
Premature discharge can exacerbate episodes and increase resistance to accepting the diagnosis. Patients
often report a poor understanding of the diagnosis and may complain in a follow-up that they did not receive a
clarification of diagnosis even if a thorough discussion was rendered [9,184].
During the transition toward establishing mental health care, neurologists should continue to pursue important
roles that include the following:
● Make sure that the diagnosis of PNES does not change (ie, no new clinical data emerge that are supportive
of epilepsy)
● Limit invasive investigation of other symptoms for which a medical cause has been ruled out
● Supervise cautious discontinuation of antiseizure drug therapy
Ideally, a close dialogue should also be developed and maintained between neurologic, psychiatric, and primary
care providers, who may sometimes disagree about the diagnosis and the accuracy of video-
electroencephalography (EEG) monitoring [9,102,125,179,185]. This communication may limit mixed and
conflicting messages from different clinicians that can contribute to the overall poor prognosis [9].
Cautious discontinuation of antiseizure drug therapy should be coordinated where possible [125]. It is not
infrequent for episodes to increase during this time period. Some antiseizure drugs have mood-stabilizing
properties, and their discontinuation may exacerbate an underlying affective or panic disorder. On the other
hand, early withdrawal of antiseizure drugs may be associated with some benefits, including decreased use of
rescue antiseizure drug treatment and higher employment rates at 18 months [186].
We use EEG data to help inform the duration of neurologic follow-up. For patients with known interictal or ictal
epileptiform EEG findings, we advise long-term neurologic follow-up. For patients without known epileptiform
EEG findings, we advise neurologic follow-up for at least six months after discontinuation of antiseizure drug
therapy. The rationale for this practice is the small but present possibility of coexisting epilepsy and the fact that
the highest risk for seizure relapse in patients with epilepsy is within the initial several months after
discontinuation of antiseizure drug therapy [187].
For patients with recurrent events in the setting of antiseizure drug discontinuation, repeat video-EEG monitoring
may be needed if there is doubt that these episodes are different in nature than those documented to be PNES.
TREATMENT — While some patients relinquish episodes soon after the diagnosis is revealed, most will continue
to have episodes and will require long-term psychiatric interventions [10,16,101,178,188,189].
Barriers to effective treatment of PNES patients include poor compliance and financial and insurance-related
limitations for ongoing treatment. Another challenge is the difficulty finding psychiatric clinicians who are well
acquainted and comfortable dealing with PNES.
Psychotherapy — Psychiatric interventions are the hallmark of treatment for PNES, although response is often
incomplete [125]. These are individualized according to the underlying psychiatric diagnosis.
Treatment recommendations in PNES are mostly based upon clinical experience and observational studies;
there have been few randomized treatment trials for PNES. One challenge in designing treatments and trials to
assess their efficacy relates to the heterogeneous combinations of psychiatric disorders that underlie PNES
[178].
Cognitive behavioral therapy (CBT) is a brief psychosocial intervention that is composed of a variety of
therapeutic approaches. All of the approaches share the basic assumption that therapeutic change can be
effected by targeting changes in thoughts (beliefs and attitudes) and behaviors that contribute to emotional
distress. An approach based upon a fear-avoidance model may be especially successful for patients who have
PNES as a dissociative response in stressful circumstances. Observational case series and small randomized
trials suggest that CBT may be helpful in reducing episodes and improving psychosocial functioning [190-193].
● A randomized trial compared CBT with standard medical care in 66 patients with PNES [192]. After four
months of treatment, patients on active treatment had a lower median monthly frequency of seizures than
patients in the control group (2.0 versus 6.8) and a trend toward benefit in three-month seizure remission
rates (odds ratio [OR] 3; 95% CI 0.85-11.5). There was no effect of treatment on psychosocial function,
health service use, or employment.
● In a multicenter pilot trial, 38 patients with PNES were randomly assigned to receive CBT-informed
psychotherapy with or without sertraline, sertraline alone, or usual treatment for 16 weeks [193]. This study
was not sufficiently powered to analyze for differences between treatment groups. Compared with baseline
conditions within each group, seizure frequency was reduced by 51 percent in those who received CBT
alone and 59 percent in those who received CBT plus sertraline; seizures were not reduced in those treated
with sertraline alone or usual care. CBT was also associated with improvements in depression, anxiety,
quality of life, and global functioning. Notably, however, only a minority of patients became episode free in
either of the CBT groups, and the durability of response beyond four months is not known.
Traditional psychotherapy has been used in patients with PNES with mixed success [188,194,195]. Group
therapy sessions also employ traditional psychodynamic or psychoeducational techniques, and small studies
have reported decreased episode frequency and/or improvement in psychosocial comorbidities in some patients
with PNES [196-200]. The high prevalence of family problems in patients with PNES offers promise that family-
related education and interventions may be useful, but these have not been systematically studied [44].
Psychodynamic interpersonal therapy is an alternative form of psychotherapy. In a case series of 47 patients with
PNES, this intervention was associated with seizure remission in 25 percent, and a >50 percent seizure
reduction in 40 percent [201].
Role of medications — Antidepressants and anxiolytics may be prescribed on an individualized basis. These
may better address psychiatric comorbidities of depression and anxiety rather than an underlying causative
psychiatric disorder.
These medications have had mixed results in open-label studies of PNES [196,202,203]. In a pilot study, 38
patients with PNES were randomly assigned to treatment with flexible-dose sertraline or placebo [204]. Active
treatment was associated with a nonsignificant reduction in PNES frequency. Another pilot study found no benefit
of sertraline except when combined with CBT [193].
Driving — There are few data regarding driving safety in patients with PNES. While many clinicians recommend
driving restrictions to their patients with PNES, the little available evidence has not demonstrated that patients
with PNES are at increased risk of motor vehicle crashes [205-209]. In the absence of data supporting that
patients with PNES are at increased risk of crashes, we suggest that such decisions be individualized based on
the nature of the episodes, the diagnostic certainty, any precipitating factors or situations, and the patient's
overall neuropsychiatric condition.
PROGNOSIS — Most studies that have assessed the prognosis in patients after PNES diagnosis suggest that
only a minority (25 to 38 percent) of patients achieve seizure freedom [9,11,21,101,182,210]. Children have a
better prognosis than adults, with 70 to 80 percent achieving seizure remission [211].
While outcome is often reported as a percent of those with seizure remission, this narrow measure does not
necessarily reflect the overall clinical outcome with respect to psychiatric and psychosocial status
[11,190,210,212]. As an example, in one study, 56 percent of patients overall continued to depend on state-
supported financial benefits at four years after PNES diagnosis [11,210]. The percentage was lower, but still
substantial (43 percent), among those in episode remission. Other studies have also found that occupational
status, while more likely to improve if PNES cease, often does not improve, even when episodes remit [62,213].
Some studies suggest that psychosocial issues and depression, rather than persistent PNES, are more directly
related to disability and reduced quality of life [190,214].
Both attempted and successful suicides have been reported in some series with follow-up [62,190,215]. In one of
these cohorts, suicide attempts were equally frequent (11 of 56 patients overall) in those with or without seizure
remission [62]. Limited evidence suggests that there may be a modest increase in premature mortality in patients
with PNES [216].
Some patients may develop new somatic complaints after remission of PNES, especially headaches [59]. Other
studies suggest that development of new somatic complaints is uncommon and similarly frequent in those with
persistent PNES versus PNES in remission [101,217].
Some of the risk factors inconsistently associated with a worse prognosis include
[2,6,10,11,29,59,62,101,146,182,194,218,219]:
● Longer duration of symptoms
● Older age at onset
● Lower educational level, lower intelligence quotient (IQ)
● More isolation, more limited family support
● Dependent lifestyle
● No formal treatment plan
● Unrelieved stressors (eg, ongoing abuse, family conflict)
● Anger, rejection of PNES diagnosis
● More severe underlying psychiatric disorder, especially severe or generalized somatization or dissociative
symptoms
Some studies have associated clinical semiology with prognosis [2,11,219]. Patients with more dramatic motor
features, self-injury, and prolonged episodes have a lower likelihood of remission than those with more passive
or catatonic-like behaviors. This finding is not universal, however, and PNES event semiology can change over
time [10,220].
SUMMARY AND RECOMMENDATIONS
● Psychogenic nonepileptic seizures (PNES) are events derived from psychologic underpinnings that clinically
mimic epileptic seizures, but are not associated with abnormally excessive neuronal activity. (See
'Introduction' above and 'Etiology' above.)
● PNES include a variety of clinical manifestations, some of which are suggestive, although not independently
diagnostic, in distinguishing PNES from epileptic seizures (table 2). (See 'Clinical features of events' above.)
● The diagnosis of PNES is generally established by video-electroencephalography (EEG) monitoring, in

which captured clinical events are examined in conjunction with EEG activity. Most patients with PNES will
have an event within a few days of monitoring. Other tests (interictal EEG, neuroimaging,
neuropsychological tests, and laboratory studies) are used primarily to investigate alternative etiologies and
are not diagnostic of PNES in isolation. (See 'Diagnosis' above.)
● Frontal lobe seizures can have atypical clinical features and can be confused with PNES, especially when
there is no correlate on surface EEG. Features that suggest that the events are frontal lobe seizures include
short duration, stereotyped features, and occurrence during physiologic sleep. (See 'Differential diagnosis'
above.)
● The diagnosis of PNES, once established, should be presented to patients and their families in a supportive,
nonjudgmental fashion. (See 'Presenting the diagnosis' above.)
● Neurologic follow-up should be maintained after a diagnosis of PNES to monitor the safe withdrawal of
antiseizure drugs, answer patient questions, and communicate with other treating clinicians until such time
as the patient has been fully transitioned to psychiatric care. (See 'Neurologic follow-up' above.)
● For patients with PNES, we suggest psychotherapy (Grade 2B). We generally prefer cognitive behavioral
therapy (CBT) because it is the best-studied option in this patient population; reasonable alternatives include
interpersonal therapy and group therapy. (See 'Treatment' above.)
● Pharmacotherapy should be individualized according to the comorbid psychiatric diagnosis. (See 'Role of
medications' above.)
● The prognosis for patients with PNES is guarded. Many patients will continue to have seizure-like events.
Patients with and without PNES remission may have substantial psychiatric morbidity and functional
limitations on follow-up. Further studies are needed to identify effective psychiatric interventions for these
patients. (See 'Prognosis' above.)
ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge Alan Ettinger, MD, MBA,
who contributed to an earlier version of this topic review.
Use of UpToDate is subject to the Subscription and License Agreement.
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Topic 2227 Version 20.0
GRAPHICS
Imitators of epilepsy: Nonepileptic paroxysmal disorders
Neonates
Apnea
Jitteriness
Benign neonatal sleep myoclonus
Hyperekplexia
Infants
Breath-holding spells
Benign myoclonus of infancy
Shuddering attacks
Sandifer syndrome
Benign torticollis in infancy
Abnormal eye movements (eg, spasmus nutans, opsoclonus-myoclonus)
Rhythmic movement disorder (head banging)
Children
Breath-holding spells
Vasovagal syncope
Migraine
Benign paroxysmal vertigo
Staring spells
Tic disorders and stereotypies
Rhythmic movement disorder
Parasomnias
Adolescents and young adults

Vasovagal syncope
Narcolepsy
Periodic limb movements of sleep
Sleep starts
Paroxysmal dyskinesia
Tic disorders
Hemifacial spasm
Stiff-person syndrome
Migraine
Psychogenic nonepileptic seizures
Hallucinations
Older adults
Cardiogenic syncope
Transient ischemic attack
Drop attacks
Transient global amnesia
Delirium or toxic-metabolic encephalopathy
Rapid eye movement sleep behavior disorder
Graphic 81289 Version 6.0
More common features distinguishing epileptic seizures and psychogenic

nonepileptic seizures (PNES)*
Sign Epileptic PNES
Duration Usually brief, less than 1 to 2 minutes Usually longer than 2 minutes
Eyes Eyes usually open during event Eyes often closed

Forced eye closure suggests PNES
Motor activity Stereotyped Variable

Synchronized Forward pelvic thrusting, rolling side
Build, progress to side, opisthotonus
Wax and wane
Vocalization Uncommon, especially during May occur

convulsion
Prolonged ictal atonia Very rare May occur
Incontinence Common in convulsive seizures Less common
Autonomic signs Cyanosis, tachycardia common with Uncommon

major convulsion
Postictal symptoms Usually confused, drowsy May rapidly awaken and reorient
Headache common Headache rare
* No single feature is sensitive or specific for epileptic versus psychogenic nonepileptic seizures.
Clinical features of seizures, syncope, and other paroxysmal neurologic events in

adults
Recall of the
Clinical features Duration Diagnostic tools
event
Focal seizure Initial symptoms Usually <2 minutes; Variable depending EEG may show
depend on location in can be difficult to on whether interictal spikes (poor
brain; motor and distinguish ictal from consciousness is sensitivity);
visual symptoms postictal phase impaired ambulatory EEG if
usually "positive" (eg, episodes are frequent
shaking, jerking, enough; MRI may
flashing lights, or show structural lesion
visual distortion);
may have anatomic
"march" over
seconds; some
progress rapidly to
GTC
Generalized seizure Sudden alteration or <5 minutes (for Complete amnesia; EEG may show
loss of consciousness GTC); <1 minute for patient may recall generalized spike-
without warning; absence initial focal symptoms and-wave
some have myoclonic characteristic of
jerks or staring; specific syndrome;
tongue-biting and MRI usually normal
urinary incontinence for generalized
may occur (for GTC) epilepsy syndromes,
may show structural
lesion if focal onset
Psychogenic Fluctuating, Rarely <1 minute; Variable Video-EEG monitoring

nonepileptic asynchronous motor often prolonged (>30
seizure activity, often with minutes)
eye closure, side-to-
side head or body
movements, pelvic
thrusting; most occur
in front of a witness;
fully or partially alert
despite bilateral
motor activity;
tongue-biting is rare
Syncope Transient loss of 1 to 2 minutes Patient can recall ECG;

consciousness prodromal symptoms, echocardiography if
resulting in loss of if present; lack of structural cardiac
postural tone; warning may suggest disease is suspected;
prodrome of cardiac source ambulatory ECG
lightheadedness, monitoring if
warm or cold feeing, arrhythmia is
sweating, suspected;
palpitations, pallor; orthostatic blood
myoclonic jerks or pressure
tonic posturing may measurements
occur, especially if
patient is kept
upright; no or
minimal post-event
confusion
Transient ischemic Rapid loss of Several minutes to a Usually complete MRI/MRA, CTA,
attack (TIA) neurologic function few hours unless language vascular risk factors
due to interrupted areas involved
blood flow; symptoms
depend on vascular
territory but are
typically "negative"
(eg, weakness,
numbness, aphasia,
visual loss); intensity
is usually maximal at
onset; consciousness
usually preserved
Migraine aura Positive and/or Up to 1 hour Complete Personal or family

negative neurologic history of migraine
symptoms, most
often visual and
sensory, evolving
gradually over ≥5
minutes (slower onset
than TIA or focal
seizure); slow spread
of positive followed
by negative
symptoms, if present,
is very characteristic;
usually followed by
headache
Panic attack Palpitations, dyspnea, Minutes to hours Complete History of anxiety or

chest pain, depressive
lightheadedness, symptoms, triggering
sense of impending events or stressors
doom; associated
hyperventilation may
result in perioral and
distal limb
paresthesias
Transient global Prominent 1 to 10 hours Complete amnesia for Clinical diagnosis;

amnesia anterograde amnesia (mean 6 hours) the main episode; negative MRI and
(inability to form new retrograde amnesia toxicology screens
memories) and resolves within 24
variable retrograde hours
amnesia; patient is
disoriented in time,
asking repetitive
questions; other
cognitive and motor
functions spared; rare
in adults younger
than 50 years
GTC: generalized tonic-clonic; EEG: electroencephalography; MRI: magnetic resonance imaging; ECG: electrocardiogram;
MRA: magnetic resonance angiography; CTA: computed tomography angiography.
Overview of proposed diagnostic levels of certainty for psychogenic nonepileptic

seizures (PNES)*
History Witnessed event EEG
Diagnostic level
Possible History characteristics By witness or self- No epileptiform activity in

consistent with PNES report/description routine or sleep-deprived
interictal EEG
Probable History characteristics By clinician who reviewed No epileptiform activity in

consistent with PNES video recording or in routine or sleep-deprived
person, showing semiology interictal EEG
typical of PNES
Clinically established History characteristics By clinician experienced in No epileptiform activity in

consistent with PNES diagnosis of seizure routine or ambulatory ictal
disorders (on video or in EEG during a typical
person), showing semiology ictus/event in which the
typical of PNES, while not semiology would make ictal
on EEG epileptiform EEG activity
expectable during
equivalent epileptic seizures
Documented History characteristics By clinician experienced in No epileptiform activity

consistent with PNES diagnosis of seizure immediately before, during,
disorders, showing or after ictus captured on
semiology typical of PNES, ictal video EEG with typical
while on video EEG PNES semiology
EEG: electroencephalography.
* Additional tests may affect the certainty of the diagnosis (eg, self-protective maneuvers or forced eye closure during
unresponsiveness or normal postictal prolactin levels after convulsive seizures).
From: LaFrance WC Jr, Baker GA, Duncan R, et al. Minimum requirements for the diagnosis of psychogenic nonepileptic
seizures: A staged approach: A report from the International League Against Epilepsy Nonepileptic Seizures Task Force.
Epilepsia 2013; 54(11):2005-18. https://onlinelibrary.wiley.com/doi/abs/10.1111/epi.12356. Copyright © 2013 The
International League Against Epilepsy. Reproduced with permission of John Wiley & Sons Inc. This image has been provided
by or is owned by Wiley. Further permission is needed before it can be downloaded to PowerPoint, printed, shared or emailed.
Please contact Wiley's permissions department either via email: permissions@wiley.com or use the RightsLink service by
clicking on the 'Request Permission' link accompanying this article on Wiley Online Library (http://onlinelibrary.wiley.com).
Contributor Disclosures
David K Chen, MD Nothing to disclose Paul Garcia, MD Grant/Research/Clinical Trial Support: Medtronic
[Thalamic stimulation (Deep brain stimulation therapy)]. Consultant/Advisory Boards: Biogen [Epilepsy (Phase II
DSMC; natalizumab)]; Otsuka [Epilepsy (Preclinical consultant; OPC-214870)]. John F Dashe, MD,
PhD Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform to
UpToDate standards of evidence.
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27/8/2018 Psychogenic nonepileptic seizures - UpToDate

Official reprint from UpToDate®

Psychogenic nonepileptic seizures

Author: David K Chen, MD

● Precipitants and circumstances in which episodes occur

● Tongue-biting and self-injury – Classic symptoms of epileptic seizures such as tongue-biting,

Psychiatric conditions associated with PNES include [21,23,29,32,62,97,98,100-104]:

● Somatic symptom and related disorders

● Post-traumatic stress disorder

● Event description by patient and/or witness

● Clinician observation of seizures as an in-person witness or by video recordings

● Available ictal and interictal EEG data

When a video-electroencephalography (EEG) confirmed diagnosis of PNES has been appropriately

● Supervise cautious discontinuation of antiseizure drug therapy

● Longer duration of symptoms

● Older age at onset

● Lower educational level, lower intelligence quotient (IQ)

● More isolation, more limited family support

● No formal treatment plan

● Unrelieved stressors (eg, ongoing abuse, family conflict)

● Anger, rejection of PNES diagnosis

SUMMARY AND RECOMMENDATIONS

● The diagnosis of PNES is generally established by video-electroencephalography (EEG) monitoring, in

Use of UpToDate is subject to the Subscription and License Agreement.

Topic 2227 Version 20.0

Imitators of epilepsy: Nonepileptic paroxysmal disorders

Benign neonatal sleep myoclonus

Benign myoclonus of infancy

Benign torticollis in infancy

Abnormal eye movements (eg, spasmus nutans, opsoclonus-myoclonus)

Rhythmic movement disorder (head banging)

Benign paroxysmal vertigo

Tic disorders and stereotypies

Rhythmic movement disorder

Adolescents and young adults

Periodic limb movements of sleep

Psychogenic nonepileptic seizures

Transient ischemic attack

Transient global amnesia

Delirium or toxic-metabolic encephalopathy

Rapid eye movement sleep behavior disorder

Graphic 81289 Version 6.0

More common features distinguishing epileptic seizures and psychogenic

Sign Epileptic PNES

Eyes Eyes usually open during event Eyes often closed

Motor activity Stereotyped Variable

Vocalization Uncommon, especially during May occur

Prolonged ictal atonia Very rare May occur

Incontinence Common in convulsive seizures Less common

Autonomic signs Cyanosis, tachycardia common with Uncommon

Graphic 77773 Version 4.0

Clinical features of seizures, syncope, and other paroxysmal neurologic events in

Psychogenic Fluctuating, Rarely <1 minute; Variable Video-EEG monitoring

Syncope Transient loss of 1 to 2 minutes Patient can recall ECG;

Migraine aura Positive and/or Up to 1 hour Complete Personal or family

Panic attack Palpitations, dyspnea, Minutes to hours Complete History of anxiety or

Transient global Prominent 1 to 10 hours Complete amnesia for Clinical diagnosis;

Graphic 111740 Version 2.0

Overview of proposed diagnostic levels of certainty for psychogenic nonepileptic

History Witnessed event EEG

Possible History characteristics By witness or self- No epileptiform activity in

Probable History characteristics By clinician who reviewed No epileptiform activity in

Clinically established History characteristics By clinician experienced in No epileptiform activity in