Psychogenic nonepileptic seizures

Author

Alan B Ettinger, MD Section Editor

Timothy A Pedley, MD Deputy Editor

Janet L Wilterdink, MD

Last literature review version 17.1: January 2009 | This topic last updated: February 5,
2009 (More)

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, and movement disorders.

Another notable type of episodic behavior is a psychogenic nonepileptic seizure (PNES).

Characterized by sudden and time-limited disturbances of motor, sensory, autonomic,
cognitive, and/or emotional functions, PNES can mimic epileptic seizures. However, in contrast
to epileptic seizures, PNES are not associated with physiological central nervous system
dysfunction but are instead psychogenically determined [1-4] .

Other terms, such as pseudoseizures or hysterical seizures, have been used to describe these
episodes. The term "hysterical" seizures or "hysteroepilepsy" is now discouraged as both
pejorative and oversimplified, failing to capture the broad range of underlying
psychopathology. The term "pseudoseizures" is also discouraged, since the root "pseudo," or
false, invalidates the genuine, even if psychogenic, disorder that a patient experiences.

It is important that clinicians consider PNES when evaluating patients with episodic symptoms.
Missing this diagnosis may result in inappropriate treatment with antiepileptic drugs that are
associated with potential morbidity, especially if drug toxicity is incurred in the attempt to
suppress episodes [5-7] . Prolonged episodes, "psychogenic status epilepticus" in particular,
are often treated with toxic antiepileptic drug doses, intubation, and iatrogenically induced
coma [6-14] . When PNES occur during pregnancy, these treatments pose additional risks to
the fetus [2] . Recurrent visits to the emergency room and hospitalizations for uncontrolled,
unrecognized PNES place a cost burden on the healthcare system [15] . Finally, failure to
recognize psychiatric issues may promote the persistence of conversion symptoms and deny
the patient needed psychiatric interventions.

The diagnosis of PNES can be challenging. In some case series, delay to PNES diagnosis has
been as long as 9 to 16 years [16,17] . 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 physician-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 [18] . While advances in technology,
especially the advent of video-electroencephalography, have greatly advanced our ability to
recognize PNES, 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.

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.
One epidemiologic study in Iceland reported an incidence rate of 1.4 per 100,000 individuals
over age 15 years; a study in Ohio documented a mean incidence of 3 per 100,000 between
1995 and 1998 [3,5,19] . The prevalence of PNES has been estimated to be between 2 to 33
per 100,000 [20] .

Among patients referred to outpatient epilepsy centers, 5 to 25 percent of patients 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 [3,21] .

PNES most commonly presents in the third decade of life [17,22-25] . However, most age
groups can be affected, including young children and the elderly [26-28] . One study suggests
that the age of onset may be influenced by pre-existing features; patients with learning
disabilities had a relatively younger age of onset compared to those with a history of physical
or psychosocial trauma [29] . (See "Nonepileptic paroxysmal disorders in children" and see
"Seizures and epilepsy in the elderly: Diagnosis and treatment").

PNES has a female predominance ranging from 66 to 99 percent in different series

[5,22,23,25,28,30-34] . This is consistent with gender ratios described in conversion disorder,
one of the salient psychiatric conditions underlying PNES [35,36] . (See "Psychosocial history"
below). Race, marital status, and years of education do not appear to influence the prevalence
of PNES [24] .

CLINICAL FEATURES OF EVENTS — Recognizing PNES can be challenging even for experienced
observers, in part because of the broad diversity of PNES presentations. Nonetheless, clues
that arouse suspicion for this diagnosis are often apparent from the clinical history. It is
important to remember that no single feature is either sensitive or specific for PNES.

A history from patients with suspected PNES should elicit information relevant to any
paroxysmal disorder including seizures: Detailed description of the event as perceived by the
patient and as witnessed by others, including prodromal and postictal features Precipitants,
circumstances in which episodes occur Episode frequency, duration Factors that reduce seizure
frequency or attenuate an episode
Precipitants and setting — The setting in which an episode occurs can be helpful in
distinguishing PNES and epilepsy. Most episodes of PNES occur in front of witnesses [37,38] . 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 [37] . PNES tend not to occur during
sleep. In contrast, epileptic seizures can occur during sleep, and in some forms of epilepsy,
nocturnal episodes are most frequent. However, nocturnal seizures are frequently
unwitnessed, and patients with PNES may report (erroneously) that seizures occur during sleep
[39-41] . Patients with PNES may appear to be asleep just before seizure-onset, but the EEG in
these cases demonstrates wakefulness [40] . (See "Video-EEG monitoring" below). While it is
intuitive that PNES would be more likely to be associated with stressful situations, stress is
commonly cited as a seizure precipitant in patients with epilepsy [42,43] . 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 [44] . PNES are often frequent. At the time of evaluation,
most report at least daily episodes; less than one event a week is uncommon
[5,17,23,25,34,38,45] . This observation may reflect a sampling bias.

Ictal features — Unresponsive behavior with motor manifestations mimicking a generalized

convulsion or a complex partial seizure is the most common manifestation of a PNES
[22,23,28,32,38,45-47] . Less common are events that mimic atonic, absence, or simple partial
seizures. A variety of clinical behaviors may occur during PNES, some of which are useful in
distinguishing them from epileptic seizures (show table 1). However, no single semiologic
feature is either sensitive or specific for PNES [5] . A variety of convulsive-like motor activity
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 wax and wane over the
course of the ictus [21,22,48] . Specific movements such as writhing, thrashing, pelvic thrusts,
opisthotonus (arched back), and jactitation (rolling from side to side) suggest a PNES, but these
are not always present [22,38,46,48] . Moreover, some epileptic seizures, such as those of
frontal lobe origin, can produce unusual-appearing motor activities similar to PNES [21,39,49-
54] . Stereotyped and consistent lateralization of motor features usually, but not always,
suggests epilepsy [39,47] . (See "Localization-related epilepsy: Causes and clinical features",
section on Frontal lobe epilepsy). 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 [16,17,22,23,34,45,55] . A tongue bitten on the side is
more specific for epileptic seizure, than when bitten on the tip [56] . Incomplete loss of
consciousness during the episode, suggested either by responsiveness to stimuli or by later
recall of events during the ictus, suggests PNES [22,57] . Weeping, ictal stuttering, and
vocalizations are relatively uncommon in epileptic seizures and suggest PNES [58-61] . When
vocalization occurs in an epileptic seizure, it usually occurs at seizure onset, not during the
convulsion. A seizure aura is frequently reported in PNES (25 to 60 percent) and may be a
more common symptom than in epilepsy [32,34,38] . Autonomic manifestations during an
ictus (eg, tachycardia, cyanosis) suggest epileptic seizure, and their absence, particularly during
a major convulsion, suggests PNES [48,61,62] . Eyes are usually open during the ictus of a
generalized convulsive seizure [56,63] . 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
[48] . 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 [64] . In
this report, patient and observer reports of ictal eye closure were not reliable. Ictal atonia is
not a common PNES manifestation, however, when prolonged, this almost always represents
PNES, not epileptic seizure [46] . 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
[22-24,39,47,53,65,66] . Prolonged episodes (ie, psychogenic status epilepticus) are not rare. In
one series, 78 percent of patients with PNES reported at least one event longer the 30
minutes, and half of these patients had recurrent episodes of psychogenic status epilepticus
[14] .

Postictal symptoms: Rapid alerting and reorientation is common after PNES but uncommon
with epileptic seizures, except for certain seizure types, such as absence or frontal lobe
seizures [38,39,49] . However, in some case series, half or more of patients with PNES
exhibited postictal confusion or drowsiness [32,38] . Postictal headache occurs in up to half of
patients with epileptic seizures, but is rare in PNES [43] . 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, compared with shallow,
rapid respirations in patients after a PNES [63] . 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 [48] . Postictal nose-wiping or coughing is a rare but somewhat
specific feature of mesial temporal lobe seizures [67] .

Response to treatment — Most patients with PNES have seizures for many years prior to
diagnosis, and most are treated unsuccessfully with antiepileptic drugs [5,16,23,28,32,38,46] .
A failure to make even small improvements in seizure frequency despite vigorous antiepileptic
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 [7,10,13] .

ASSOCIATED FEATURES AND CONDITIONS

Psychosocial history — 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 [17,22,24,25,34,65,68-70] . It is also true
that 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 [32,34,45,69-75] : Depression Anxiety

Somatoform disorder Post-traumatic stress disorder Dissociative disorder Personality
disorders, especially borderline personality disorder, but also obsessive-compulsive,
narcissistic, histrionic, and antisocial personalities A history of sexual or physical abuse is also
prevalent in patients with PNES; in various cohorts, this is reported in one-third to one-half of
patients [17,29,32-34,68,76] . 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 [77] . In another series they were also more likely to exhibit self-harming behaviors
and other medically unexplained symptoms in addition to PNES [29] . Dysfunctional family
relationships (poor communication or support, interpersonal conflict, trauma) are also
reported by many PNES patients and/or family members [32,78-80] .

In contrast, depression with major psychosis and schizophrenia are relatively uncommon in
patients with PNES [28] .

Some authors distinguish between comorbid and etiologic psychiatric conditions, 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 [69] . As an example, dissociation is often associated with post-traumatic stress
disorder and/or a history of physical or sexual abuse.

Dissociative disorders and somatoform/conversion disorders are felt to underlie most PNES,
but this remains unproven [81] . In these conditions, physical symptoms occur in response to
psychosocial stress, and are not intentionally produced [34,74] . This contrasts with factitious
disorder or 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 assumed that patients
with PNES are "faking" their symptoms.

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
[2,17,32,34,71] . In children, separation anxiety, school avoidance, and parental discord or
divorce may also play a role [26,82] . 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 [83] .

Concurrent or past epilepsy — Estimates of the prevalence of concurrent epilepsy among

patients with PNES vary from 5 to 56 percent, in part because of differing diagnostic criteria
used to determine the coexistence of epilepsy [28,29,32,34,84-88] .

In one case series with video-EEG documentation of both PNES and epileptic seizures in the
same patient, there was notably different clinical semiology for PNES compared to epileptic
seizures in 18 of 20 patients [89] . 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 [90] .

A few patients (2 to 9 percent) with epilepsy develop PNES after epilepsy surgery [91-93] .
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.

Seizure model — Patients with PNES have often witnessed epileptic events that may serve as a
clinical model. A seizure history in a friend or relative, or an occupation as a healthcare worker
is not uncommon [32] . In one study, patients with PNES were significantly more likely to have
witnessed an epileptic seizure prior to their event than were patients with epilepsy (66 versus
11 percent) [94] . Alternatively, a patient's own history of epilepsy may be the model for their
PNES.

Comorbid neurologic and medical disease — While underlying neurologic disease is more
prevalent among patients with epilepsy than PNES, a history of neurologic insults, particularly
minor head trauma, is common (30 to 44 percent) in PNES patients [28,34,68,88,95-97] . It is
not clear why such an association should exist. The head injury may be associated with
psychological as well as physical trauma, which may serve as a precipitant for PNES. In some
series, a patient's disability status or litigation for damages appeared to provide a source of
secondary gain for PNES [68] . Recall bias may also contribute to this apparent association.

PNES is also well-described in patients with neurologic developmental disabilities [28,98,99] .

In this population, distinguishing these events 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 [29] .

A history of recurrent medical evaluations for other unexplained somatic complaints should be
examined [69] . As examples, a history of chronic pain or fibromyalgia is common among
patients with PNES [37,43,97] . 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. (See "Somatization", section on Definitions).

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 the latter circumstance, the clinician may find
a variety of abnormalities that do not make physiologic sense [36] .

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 [100] .

DIFFERENTIAL DIAGNOSIS — The primary consideration in the differential diagnosis of PNES

are epileptic seizures [85] . 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 [39,53,63] . In one video-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 [39] . (See "Localization-related epilepsy: Causes
and clinical features", section on Frontal lobe epilepsy).

Other nonepileptic paroxysmal disorders may be mistaken for either epileptic seizures or for
PNES [85] . These include sleep disorders, movement disorders, and syncope. These are
discussed in detail separately. (See "Nonepileptic paroxysmal disorders in adolescents and
adults").

DIAGNOSIS — While not without limitations, video-electroencephalography (EEG) is the gold

standard test for the diagnosis of PNES [24] . However, patients with PNES are likely to
undergo other diagnostic testing during the course of their evaluation. Some tests can provide
support for the diagnosis, others may provide misleading information. Other testing, while not
helpful in diagnosis of PNES, is potentially useful in evaluating comorbidities and choosing
subsequent treatment.

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 [101] . 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 [16,89,102] . In patients felt to have PNES alone (no
comorbid epilepsy), the prevalence of interictal EEG abnormalities ranges from 10 to 18
percent [16,23,87,88,96,102] . An abnormal interictal EEG is more common if there is a past or
concurrent history of epilepsy or other underlying neurologic injury or disease.

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 first 48 hours [24,103] .

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 [104] . As a
result, failure to see an electrographic seizure does not exclude epilepsy. (See "Video and
ambulatory EEG monitoring in the diagnosis of seizures and epilepsy").

Accurate interpretation of video-EEG monitoring requires careful analysis of the clinical events
with any changes in the EEG occurring before, during, and after the seizure. As one example, a
finding of "preictal pseudosleep", the appearance of clinical sleep while the EEG tracing
demonstrates wakefulness is a very specific, although insensitive, indicator of PNES [40] .

Patients with diverse episode types may have both epileptic seizures and PNES. It is 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 video of the event
to family members who can indicate how closely it resembles prior events they have
witnessed.

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 intravenous saline or rubbing alcohol on

the skin of the patient and telling the patient that this may induce an episode. Between 67 to
90 percent of patients with PNES will have a typical event in this setting [2,5,38,105-107] .
While much less common, epileptic events have also been reported to occur in this setting
[85,87,103,108-110] . Because of this, induction should be performed during video-EEG. It is
also essential to confirm that the elicited episode is representative of the spells under
investigation. A patient with epilepsy may have a PNES under these circumstances, but the
features are usually atypical of their usual events [111] .

Use of this technique is controversial. While facilitating diagnosis, the inherent deceit in this
approach may jeopardize the physician-patient relationship and impede future treatment
efforts. However, many experts believe that these considerations are outweighed by the
benefits of making an accurate diagnosis and avoiding future morbidity associated with
inappropriate treatments [5,112] . Alternative techniques that employ photic stimulation
and/or hyperventilation with suggestion may obviate the deceitful aspects, as these are
routinely used to precipitate epileptic seizures. As a result, these may be more acceptable to
patients and physicians, although special care is required as an epileptic seizure is more likely
to be precipitated with these techniques, than with placebo [38,105] . Some physicians report
successful use of induction techniques when they inform the patient that they are being used
to elicit a possible psychogenic as well as epileptic seizure [113] .

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 video
camera ready to record on stand-by can be helpful as well. While the absence of concomitant
EEG is a significant limitation, direct observation of the clinical event can provide the physician
with valuable information that aids in the diagnosis [48] . (See "Ictal features" above).

Serum testing — Certain laboratory studies can help differentiate PNES from epileptic seizure.
Prolactin levels are often elevated after an epileptic seizure, depending on the seizure type
[50,51] . Pooled sensitivity from several studies report prolactin level elevations (twice the
baseline level) in 60 percent of generalized tonic clonic seizures and 46 percent of complex
partial seizures [114] . The sensitivity is lower for simple partial seizures. Prolactin levels are
less likely to rise after seizures that do not involve mesial temporal areas, making this a less
sensitive test for epileptic seizures arising from the frontal lobe [115] .

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 [114] . A baseline
prolactin level should be determined from a blood sample drawn six hours after the event.
Prolactin elevations have not been well characterized in the setting of repeated seizures or
status epilepticus, and have unclear utility in this setting.

Prolactin levels are unlikely to rise after a PNES, but elevations can occur after syncope
[114,116] . Dopamine antagonists (eg, neuroleptic agents) can elevate prolactin levels and
confound the results. 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. Other serum markers have been used to help distinguish PNES from epileptic
seizures and other physiologic events. These include: creatine phosphokinase (CPK), cortisol,
white blood cell count, lactate dehydrogenase, pCO2, and neuron specific enolase [117-119] .
CPK levels in particular are often elevated after generalized tonic-clonic seizures, but not after
partial seizures. The later rise and prolonged elevation, up to 24 hours postictally, makes this
test somewhat more useful in the outpatient setting. However, a defined threshold level for
abnormality, sensitivity, and specificity remain to be determined for CPK, as for other serum
markers [120] .

Neuroimaging — 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
[16,23,32,96,121] . 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 [96] .

Abnormalities on interictal single photon emission computed tomography (SPECT) are also
reported in PNES as well as epilepsy cases. However, a change in focal perfusion from in an
ictal or postictal SPECT compared to an interictal SPECT can help distinguish epileptic seizures
from PNES [121-124] . 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 typically assesses both cognitive

functioning as well as some psychological domains. The common occurrence of cognitive
deficits, particularly in attention and memory, in both PNES and epilepsy patients limits the
utility of neuropsychological testing for distinguishing between them [28,96,125,126] . Some of
these deficits may be related to antiepileptic 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") [127] .

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 [128] . Patients with
PNES typically have high scores on hypochondriasis and hysteria subscales [24,32,102,128-130]
. While 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.
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
[23,65] .

An experienced clinician in a detailed psychiatric interview will elicit clinical features that may
establish a diagnosis of depression, anxiety, somatoform, dissociative, and other disorders.
Sufficient rapport may also be established in this setting, that allows for a previously
unreported history of sexual abuse or other trauma to be revealed. (See "Psychosocial history"
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 is a challenge.

Most agree that this should not take place until the clinician feels very definite about the
diagnosis [131,132] . Care providers who take on this role should be well-trained in delivering
this information. Clinicians may prefer to reveal the diagnosis in a separate outpatient meeting
rather than in the video-EEG monitoring unit.

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 room visits, as well as to obtain appropriate psychiatric treatment
[15,132] .

A useful method for communicating the diagnosis of PNES to patients emphasizes the
presentation in a nonjudgmental fashion that strives to maintain patient dignity [133] .
Techniques and talking points that we and others have found useful in this conversation
include some of the following [74,133] : We state that we do not consider the episodes to be
caused by epileptic discharges, but rather represent "the mind playing tricks on the body." We
emphasize that this problem is as serious as one caused by epilepsy and deserves the attention
and treatment that is accorded any illness. We discuss how stress afflicts each of us to variable
degrees and in different ways. We 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. We emphasize that the episodes are
experienced as real and disabling, and that although they relate to emotional or psychological
causes, we do not dismiss the problem, and we do not consider the patient to be "crazy." We
state that their disorder warrants different treatments than those administered for epilepsy.
We tell our patients that we 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 [17,97] . In
my experience, it is useful to anticipate these feelings at the time of revealing the diagnosis.
We and others have also found that patients may exhibit exacerbations of their episodes after
the diagnosis is revealed and we often warn the patients not to be surprised if this were to
occur [17] .
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 PNES patients 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 [132,134] .

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 [17] .

Ideally, a close dialogue should also be developed and maintained between neurologic,
psychiatric, and primary care providers, who often disagree about the diagnosis and the
accuracy of video-EEG monitoring [17,75,132,135] . This communication may limit mixed and
conflicting messages from different doctors that can contribute to the overall poor prognosis
[17] .

Cautious discontinuation of antiepileptic drug (AED) therapy should be coordinated where

possible. It is not infrequent for episodes to increase during this time period. In some cases,
epileptic seizures as well as PNES emerge during this interval [136] . Repeat video-EEG
monitoring may be needed if there is doubt that these episodes are different in nature than
those documented to be PNES. Some AEDs have mood stabilizing properties and their
discontinuation may exacerbate an underlying affective or panic disorder.

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
[22,28,73,131,137,138] .

Treatment recommendations in PNES are based upon anecdotal experience or small case
series [139-141] . There are no published, large, randomized, double-blind treatment trials for
PNES, although a few such trials are underway. One problem in designing treatments and trials
to assess their efficacy relates to the heterogeneous combinations of psychiatric disorders that
underlie PNES [131] . Additionally, patients with PNES often do not adhere to treatment
recommendations or return for follow-up, and may be particularly disinclined to enroll in
treatment trials.

Psychiatric interventions are the hallmark of treatment for PNES. These are individualized
according to the underlying psychiatric diagnosis. One common psychiatric intervention is
traditional psychotherapy. Reports on the success of this intervention are mixed [137,142] .
Group therapy sessions also employ traditional psychodynamic techniques and have had
mixed results in open-label studies of PNES [141,143,144] . The high prevalence of family
problems in patients with PNES offer promise that family-related education and interventions
may be useful, but these have not been systematically studied [78] .
Cognitive behavioral therapy (CBT)is an approach based upon a fear avoidance model and may
be especially successful for patients who have PNES as a dissociative response in stressful
circumstances. CBT employs progressive exposure to feared situations, and emphasizes
problem solving techniques. In one study, 16 of 20 patients with "dissociative seizures"
entered an open-label trial of 12-session CBT. Six months later, there was a reduction in
episodes and some improvement in psychosocial functioning [145] .

Antidepressants and anxiolytics may be prescribed. 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 [140,141] .

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 providers who are well-acquainted and comfortable dealing with PNES.

PROGNOSIS — Most studies that have assessed the prognosis in patients after PNES diagnosis
suggest that only a minority (25 to 33 percent) of patients achieve seizure freedom
[4,17,23,32,73] . Children have a better prognosis than adults, with 70 to 80 percent achieving
seizure remission [146] .

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 [4,23,145,151] . 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 [4,23] . 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 even when episodes do remit [45,147] . In another
study, psychosocial issues, not persistent PNES, were the primary cause of disability [145] .

Both attempted and successful suicides have been reported in some series with follow-up
[45,145,148] . In one of these cohorts, suicide attempts were equally frequent (11 of 56
patients overall) in those with or without seizure remission [45] .

Some patients may develop new somatic complaints after their PNES remit. A structured
interview of 56 patients, six or more months following PNES diagnosis, revealed moderate to
severe pain syndromes, especially headaches, in 77 percent [43] . Twenty-six of 27 patients
who stopped experiencing PNES still experienced moderate pain. While the etiologies or other
details about these pain symptoms were not studied, it is possible that pain developed de
novo or became more serious after the PNES diagnosis. Another study, however, suggested
that the development of new somatic complaints was rare, at least within the first six months
after PNES diagnosis [73] .

Some of the risk factors inconsistently associated with a worse prognosis include
[5,22,23,43,45,73,74,108,134,142,149,150]: Longer duration of symptoms Older age at onset
Lower educational level, lower IQ More isolation, more limited family support Dependent
lifestyle Male gender 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 [23,134,150] . 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. However, the reason
behind this association is unclear, and this finding is not universal [22] .

SUMMARY AND RECOMMENDATIONS — Psychogenic nonepileptic seizures (PNES) are events

that clinically mimic epileptic seizures, but are not associated with physiological central
nervous system dysfunction and are instead psychogenically determined. PNES include a
variety of clinical manifestations, some of which are suggestive, although not diagnostic, in
distinguishing PNES from epileptic seizures. (See "Clinical features of events" above). The
diagnosis of PNES is generally established by video-EEG monitoring, in which captured clinical
events are examined in conjunction with electroencephalographic activity. Most patients with
PNES will have an event within a few days of monitoring. The use of techniques to induce
events is somewhat controversial, but can be helpful diagnostically, when patients do not have
an event on monitoring. Other tests (interictal EEG, neuroimaging, neuropsychological tests,
and laboratory studies) can be helpful in the evaluation of patients, but are generally not
diagnostic of PNES. (See "Diagnosis" above). Frontal lobe seizures can have atypical clinical
features and a normal ictal EEG and can be confused with PNES. 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). We believe that neurologic follow-up should
be maintained after PNES diagnosis to monitor the safe withdrawal of antiepileptic drugs,
answer patient questions, and communicate with other treating physicians until such time as
the patient has been fully transitioned to psychiatric care. (See "Neurologic follow-up" above).
Psychiatric interventions are individualized according to the underlying psychiatric diagnosis
and are coordinated by the treating psychiatrist. (See "Treatment" 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).

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More common features distinguishing epileptic seizures and psychogenic nonepileptic

seizures*

Sign Epileptic PNES

Duration Usually brief, less than 1-2 minutes Usually longer than 2 minutes

Eyes Eyes usually open during event

Eyes often closed

Forced eye closure suggests PNES

Motor activity

Stereotyped

Synchronized

Build, progress

Variable

Forward pelvic thrusting, rolling side to side, opisthotonus

Wax and wane

Vocalization Uncommon, especially during convulsion May occur

Prolonged ictal atonia Very rare May occur

Incontinence Common in convulsive seizures Less common

Autonomic signs Cyanosis, tachycardia common with major convulsion Uncommon

Postictal symptoms

Usually confused, drowsy

Headache common

May rapidly awaken and reorient

Headache rare

* No single feature is sensitive or specific for epileptic versus psychogenic nonepileptic

seizures.