Recognition of Nonepileptic Events

Mar Carreño, M.D., Ph.D.1

ABSTRACT

Nonepileptic paroxysmal events are behavioral, motor, or sensory episodes that do

not result from abnormal cortical electrical activity. They can mimic any type of epileptic
seizures including simple partial, complex partial, and generalized tonic-clonic seizures.
Nonepileptic paroxysmal events may be physiological or psychogenic in nature. In clinical
practice, the most common imitators of epileptic seizures are syncope and psychogenic
seizures, but transient ischemic attacks, migraine, movement disorders, and metabolic

Downloaded by: Universidad de Barcelona. Copyrighted material.

disturbances must be considered at times in the differential diagnosis. In most cases, the
clinical history is enough to make a correct diagnosis. The clinical features suggestive of
various types of nonepileptic paroxysmal events, together with useful diagnostic tests, will
be reviewed.

KEYWORDS: Psychogenic seizures, epilepsy, syncope, migraine, video-EEG

T he differential diagnosis of epileptic seizures is clinical history. A detailed description of the symptoms
very broad, partly because the symptomatology of epi- and signs exhibited during the paroxysmal episode
leptic seizures is varied, depending on the eloquent is essential to reach a correct diagnosis and classify
cortical areas activated by the epileptic activity (sympto- the epileptic seizures. Accordingly, it is necessary to
matogenic zone). There is a great amount of diseases obtain information from the patient and witnesses,
which can produce focal neurological symptoms and including:
signs, occurring repeatedly in a paroxysmal way, not
unlike epileptic seizures, and which can be mistaken  Triggering factors for the episodes: sleep deprivation,
for epilepsy. Yet, to make a definite diagnosis of epilepsy, alcohol intake, drugs, activity at the time of the onset
it is necessary to demonstrate the epileptiform activity of the event
associated with the recurrent attacks. Nonepileptic seiz-  Prodromal symptoms (e.g., vegetative symptoms, diz-
ures are behavioral, sensory, and motor events that are ziness, stereotyped sensations, etc). Vegetative symp-
not associated with epileptiform activity. However, in toms often precede syncope; other types of stereotyped
the case of some physiologic nonepileptic seizures, like sensations such as rising epigastric sensation, altered
syncope, abnormal electrical activity may be identified at taste or smell, prolonged sense of déjà vu, and formed
the time of the event. Nonepileptic seizures can mimic or unformed visual hallucinations are seen in the
any type of epileptic seizures. context of focal epilepsies. In this case, patients often
The limited duration, the presence of an aura, the report having had these sensations also in isolation,
postictal confusion, and the stereotyped nature of symp- without loss of awareness.
toms are some of the clinical features of epileptic seizures  Loss of awareness, and its duration
that help to make a correct diagnosis. In the majority of  Abnormal movements associated with the loss of
cases, a diagnosis can be made from a properly taken awareness: head-turning and stereotyped proximal

1
Epilepsy Unit, Department of Neurology, Hospital Clı́nic, Barcelona, Epilepsy; Guest Editor, Andres M. Kanner, M.D.
Spain. Semin Neurol 2008;28:297–304. Copyright # 2008 by Thieme
Address for correspondence and reprint requests: Mar Carreño, Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001,
M.D., Ph.D., Director, Epilepsy Unit, Department of Neurology, USA. Tel: +1(212) 584-4662.
Hospital Clı́nic, Villarroel 170, 08036 Barcelona, Spain (e-mail: DOI 10.1055/s-2008-1079334. ISSN 0271-8235.
mcarreno@clinic.ub.es).
297
298 SEMINARS IN NEUROLOGY/VOLUME 28, NUMBER 3 2008

and distal movements (automatisms) are often seen and the presence of pallor and sweating prior to the loss
during seizures. Generalized stiffening and clonic of awareness help to make the diagnosis. Patients recover
jerking may be seen in both seizures and convulsive quickly after syncope; they are initially able to hear, and
syncope. then they recover complete cognitive function, without
 Urinary incontinence, tongue-biting (biting the side ‘‘postsyncopal’’ confusion, and are able to remember the
of the tongue is highly suggestive of epileptic seizure, events preceding the loss of awareness.
biting the tip may be seen in other conditions such as Carotid sinus syncope is defined as syncope, which
syncope) by history, seems to occur in close relationship with
 Degree of confusion after the episode accidental mechanical manipulation of the carotid si-
 Myalgias the next day, suggestive of seizures nuses. Carotid sinus hypersensitivity is a common cause
 Focal neurological signs after the episode of unexplained falls in elderly people. The key presynco-
pal sign is that of the neck turning before the presyncopal
Based on the history, clinicians are able to gen- symptoms and loss of consciousness. This type of syncope
erate an initial diagnostic impression, which determines can be reproduced with carotid sinus massage. Yet, given
the type of studies that should be ordered to reach a final the small risk of stroke, this maneuver is contraindicated
diagnosis. Reasons for misdiagnosis include incomplete in those with known carotid artery stenosis and in
clinical history, excessive importance being given to patients with carotid bruits or recent cerebrovascular
certain symptoms such as jerks or urinary incontinence events where carotid stenosis has not been excluded.3
(which, in addition to epileptic seizures, may also be seen Situational syncope refers to those forms of neu-

Downloaded by: Universidad de Barcelona. Copyrighted material.

in syncope and psychogenic seizures), and the incorrect rally mediated syncope associated with specific scenarios
interpretation as ‘‘epileptiform’’ of normal variants or (e.g., micturition, coughing, defecating, etc.). Urinary
nonspecific findings on the electroencephalogram incontinence, lateral tongue-biting, and other lesions are
(EEG).1 Nonepileptic seizures are classified as physio- uncommon during neurally mediated syncope. A good
logic or psychogenic in origin. The two conditions which history, preferably with a witness account, is usually
are most commonly mistaken for epileptic seizures in enough to make the diagnosis. Sometimes, however,
clinical practice are syncope and psychogenic seizures. neurally mediated syncopes have a ‘‘nonclassical’’ pre-
sentation. Examples of nonclassical vasovagal syncope
include episodes without clear triggering events or pre-
PHYSIOLOGIC NONEPILEPTIC monitory symptoms. These forms are diagnosed by
PAROXYSMAL SEIZURES minor clinical criteria, exclusion of other causes for
syncope (absence of structural heart disease), and pos-
Syncope itive response to carotid sinus massage2 or head-up tilt
Syncope consists of a transitory, brief loss of conscious- table test. For a head-up tilt-test to be positive there
ness accompanied by loss of postural tone, caused by a must be a reproduction of typical symptoms along with
decrease in global cerebral perfusion. Several types of concomitant cardioinhibitory (bradycardic), cardiode-
syncope are identified.2 pressor (hypotensive), or mixed response.3

NEURALLY MEDIATED SYNCOPE SYNCOPE DUE TO ORTHOSTATIC HYPOTENSION

Vasovagal (neurocardiogenic) syncope is caused by an Syncope due to orthostatic hypotension takes place
exaggerated response of normal cardiovascular reflexes. during a postural change due to inability of the auto-
It happens in healthy people, especially young adults and nomic nervous system to compensate for the fall in blood
children. Typical precipitating factors are prolonged pressure with a vasoconstrictive response. There are
periods of time in a standing position, sudden change different causes of this type of syncope, including the
of position from lying down to a standing position, hot use of drugs causing hypotension (such as antihyperten-
or crowded places, pain, or intense emotion. It is sive agents, diuretics, tricyclic antidepressants) and pe-
characteristic that the patient has vegetative prodromal ripheral neuropathies due to diabetes or alcoholism. The
symptoms of variable duration (from 10 seconds up to syncope occurs from a few seconds to a few minutes after
1 to 2 minutes), also known as a presyncope, consisting standing. Unlike vasovagal syncope, cold sweating and
of lightheadedness or a ‘‘faint’’ feeling, cold sweating, bradycardia are usually not seen.
decreased hearing and vision, and pallor. These are
followed by loss of muscle tone and loss of awareness, CARDIOGENIC SYNCOPE
with the patient falling to the ground. Sometimes the This type of syncope results from alterations in the
loss of awareness may be followed by generalized stiffen- cardiac rhythm or cardiac structural abnormalities. It is
ing and some myoclonic jerks (convulsive syncope), important to make a proper diagnosis as this type of
which may be mistaken for the clonic jerks of a gener- syncope may be life-threatening. The alterations of
alized tonic-clonic seizure. The prodromal symptoms cardiac rhythm include both tachy- and bradyarrhythmias
 RECOGNITION OF NONEPILEPTIC EVENTS/CARREÑO 299

Table 1 Typical Clinical Characteristics Associated with movements or bizarre tremor. The frequency is variable,
Various Types of Syncope from only one episode to several a day. The trigger of
Neurally mediated syncope symptoms with maneuvers that decrease cerebral perfu-
 Absence of cardiac disease sion can serve as a clue to the diagnosis, such as standing
 Long history of syncope up or hyperextension of the neck, and there is a short
 Following unpleasant sights, sounds, smells, or pain latency between these triggers and the onset of symptoms
 Prolonged standing or being in crowded, hot places of a few seconds’ duration, in general. The jerks last for
 Nausea, vomiting associated with syncope seconds to minutes, and stop when the patient sits or lies
 During or after a meal down. Other neurological signs suggestive of vascular
 With head rotation, pressure on carotid sinus (shaving, dysfunction may be found in the same patient, such as
tight collars) dysphasia, transitory dysarthria, paresthesias in the limb
 After exertion affected by the jerking or ipsilateral hemiparesis.4 EEGs
Syncope due to orthostatic hypotension do not show epileptiform discharges associated with the
 Following a change from a supine to standing position symptoms, but some patients do have contralateral
 Temporal relationship with start (or dose changes) slowing on the EEG which may increase during the
of medication associated with hypotension episodes provoked by hypoperfusion.
 Prolonged standing especially in crowded, hot places
 Presence of autonomic neuropathy or Parkinsonism
Cardiac syncope GLOBAL TRANSITORY AMNESIA

Downloaded by: Universidad de Barcelona. Copyrighted material.

 Presence of severe structural heart disease Episodes of global transitory amnesia (GTA) have a
 During exertion sudden onset and are characterized by marked alteration
 Preceded by palpitations or accompanied by chest pain of anterograde memory, temporal disorientation, and
 Family history of sudden death occasionally disorientation in space, but orientation to
From Brignole et al,2 with permission from Oxford University Press.
person and recognition of others is always preserved. The
level of consciousness and language functions are main-
(such as Wolf-Parkinson-White, atrioventricular block, tained throughout the episode but the patient looks
and others) which cause a decrease in cardiac output confused, has motor and ideatory perseveration, and
irrespective of the circulatory demands. may get lost. Immediate memory is preserved, as well
Structural heart disease (aortic stenosis, obstruc- as abstract thinking. Patients may repeat series of words
tive myocardiopathy, mitral stenosis, or auricular myx- or numbers and perform complex tasks such as driving,
oma) can cause syncope when circulatory demands reading, writing, or solving arithmetical problems, which
outweigh the impaired ability of the heart to increase is uncommon during nonconvulsive status epilepticus
its output (for example during exercise). The clinical (SE). Around 10% of patients may have headache during
features suggestive of specific causes of syncope are the episode. Amnesia usually lasts several hours (less
summarized in Table 1.2 than 24). GTA must be differentiated mainly from
nonconvulsive, complex partial, and absence SE. Specific
deficits, temporal course, and absence of ictal EEG
CEREBROVASCULAR ACCIDENTS patterns during the episode help to make the diagnosis.
Cerebrovascular accidents, which are most often mis-
taken for epileptic seizures, are transient ischemic attacks
(TIA) which cause neurological signs and symptoms of MIGRAINE
brief duration resembling epileptic seizures. TIA in the Migraine and epilepsy are both chronic disorders char-
territory of the carotid artery usually produce negative acterized by recurrent neurological attacks, with a partial
symptoms, either motor or sensory, generally without clinical and therapeutic overlap and frequently occurring
associated loss of consciousness. TIA in the territory of together. Occipital epilepsy is the type of focal seizure
the vertebrobasilar artery may be accompanied by loss of disorder which is most often mistaken for migraine.
consciousness and must be distinguished from atonic Epileptic auras arising from the occipital lobe may be
seizures, myoclonic seizures, and partial seizures causing mistaken for typical visual migrainous auras. Some
falls. Severe carotid stenosis may produce ‘‘limb-shaking,’’ clinical features may help to distinguish them:
consisting of rhythmic or arrhythmic clonic jerking in the
contralateral hand, arm, and leg (though less frequently).  Visual epileptic auras are usually of short duration, less
Unlike focal motor epileptic seizures, when both the arm than 30 seconds, rarely can reach 1 minute, and only
and the leg are affected, there is not a jacksonian march exceptionally last more than 3 minutes, as opposed to
and the face is not involved. The patient may describe the 5 to 60 minutes of a typical migrainous aura.
these jerks as tremor, inability to control the arm, or ‘‘lack  The perception of multiple circular spots, almost al-
of coordination.’’ Movements may resemble choreic ways brightly colored (but may be also in black and
300 SEMINARS IN NEUROLOGY/VOLUME 28, NUMBER 3 2008

white) appearing in a temporal hemifield and moving tions (hallucinations upon arousal) may help to make the
horizontally toward the opposite side while increasing correct diagnosis.5
in size, is suggestive of epileptic auras, a pattern very
different from the ‘‘fortification spectrum’’ or the PERIODIC LEG MOVEMENTS OF SLEEP
‘‘scintillating scotoma,’’ slowly spreading from a point Periodic leg movements of sleep are repetitive and stereo-
of fixation to one hemifield and leaving variable typed movements of the legs, predominantly during
degrees of blindness in its way that characterize a nonrapid-eye-movement (NREM) sleep. The typical
visual aura. movement is the extension of toe and dorsiflexion of
 Epileptic seizures may be frequent, as opposed to a the ankle, frequently associated with knee and hip flexion.
few episodes per year to a few per month commonly They may be uni- or bilateral and occur in an almost
observed in migraine patients. periodic fashion, within 20- to 40-second intervals.6
There is significant overlap with restless legs syndrome.
In addition to the visual symptoms, occipital lobe Clinical features which help in the diagnosis are presen-
seizures (and other focal and generalized seizures) are tation during the first half of the week, occurrence in
often accompanied by headache with migrainous fea- clusters, involvement of both lower limbs, and possible
tures, which may be preictal or postictal. association with insomnia or hypersomnia.
Basilar migraine, which may cause confusion and
loss of consciousness, may also be mistaken for epileptic AROUSAL DISORDERS
seizures. The diagnosis of basilar type migraine is based Disorders of arousal usually occur during slow wave

Downloaded by: Universidad de Barcelona. Copyrighted material.

on the finding of two migraine attacks accompanied by a sleep. They include the parasomnias, which are the
specific aura, with dysarthria, vertigo, tinnitus, impaired most frequently encountered in clinical practice, and
hearing, double vision, ataxia of a cerebellar type, loss are commonly mistaken for epilepsy. This type of sleep
of consciousness, and bilateral paresthesias. Acute con- disorder starts during childhood and usually disappears
fusional migraine (episodes of agitation and confusion in adolescence. They are characterized by paroxysmal
with decreased awareness during seconds or minutes motor activity with partial or total loss of awareness, and
preceding the actual pain) may also be mistaken for have a great variety of clinical manifestations. In clinical
epilepsy. When doubts about the nature of the episode practice, three groups are distinguished: confusional
persist, patients may be referred for video-EEG. arousals, which are associated with few motor or auto-
It is important to bear in mind that certain EEG nomic manifestations; somnambulism, associated with
abnormalities have been associated with certain types motor activity but little autonomic activation; and noc-
of migraine; for example, slowing and periodic lateral- turnal terrors, in which the autonomic activation is the
ized epileptiform discharges have been described in main clinical feature and is accompanied by motor
basilar migraine, hemiplegic migraine, and prolonged manifestations of variable intensity. REM arousal dis-
migrainous auras. In acute confusional migraine, EEG orders may be mistaken for nocturnal frontal lobe
may show diffuse slowing. seizures. Clinical features that help to distinguish be-
tween them are shown in Table 2.7

Sleep Disorders PARASOMNIAS ASSOCIATED WITH REM SLEEP

REM sleep behavior disorder is characterized by loss of
CATAPLEXY muscle atonia during sleep. Patients display different
Attacks of cataplexy may be mistaken for epileptic motor behaviors in response to the content of their
seizures. They are brought on by emotional stimuli and dreams. The motor manifestations may consist of speak-
are characterized by a sudden loss of muscle tone, which ing, screaming, and kicking. Patients are not conscious
may be generalized and trigger a fall to the ground, or during these episodes, but they may be awakened, and
partial, which give rise to head or jaw drops or sensation most often they can recall the content of their dreams.8
of intermittent leg weakness. Sometimes the patient is The duration of the episodes ranges from several minutes
dysarthric during the attack or has difficulty speaking. to half an hour and may happen once or several times
Patients may grimace and have myoclonic jerks. Unlike every day. They occur preferentially during the second
many epileptic seizures, consciousness is always pre- half of the night, when most REM sleep takes place.
served and there is no amnesia for the episode. Falls,
unlike epileptic falls, are gradual, and lesions are rare.
The duration of the episodes varies between several Endocrine Alterations
seconds and, more rarely, several minutes. The frequency Various hormonal or metabolic alterations which may
is variable and is usually stable over time. The presence of cause paroxysmal signs and symptoms or decrease the
other narcolepsy symptoms, such as excessive daytime level of consciousness may imitate epileptic seizures.
somnolence, sleep paralysis, or hypnagogic hallucina- The following entities may cause a decreased level of
 RECOGNITION OF NONEPILEPTIC EVENTS/CARREÑO 301

Table 2 Clinical Differences between Parasomnias and Frontal Lobe Seizures

Non-REM Parasomnias
(Somnambulism,
Nocturnal Terrors) Nocturnal Frontal Lobe Epilepsy

Age of onset Usually < 10 years Variable, generally childhood

or adolescence
Positive family history 60–90% < 40%
Mean number of attacks per day 1–2 >3
Monthly frequency of episodes Less than 1–4 20–40
Clinical course over time Tendency to disappear Frequency of episodes generally
in adolescence stable over time
Mean duration of disorder Around 7 years Around 20 years
Duration of the episodes Seconds to 30 minutes Seconds to 3 minutes (usually
less than 2 minutes)
Clinical features of the episodes Variable complexity; not Very stereotyped in video
stereotyped in video recordings recordings, frequently vigorous
or even violent movements
Triggering factors Sleep deprivation, fever, alcohol, stress Frequently no triggering factors are identified

Downloaded by: Universidad de Barcelona. Copyrighted material.

Associated conditions Obstructive apneas of sleep Frequently none are identified
Ictal EEG Slow waves, no epileptiform activity Frequently normal or obscured by muscle
artifact; clear EEG ictal pattern associated
to episodes in < 10% of patients
Temporal occurrence during sleep First half of the night, generally after At any time during sleep, may happen in
90 minutes of sleep first 30–60 seconds
PSG stage Stage III–IV Generally stage II sleep, occasionally in
stages III or IV
REM, rapid eye movement; EEG, electroencephalogram; PSG, polysomnogram.
From Derry et al,7 with permission from Blackwell Publishing.

consciousness: hypo- or hyperglycemia, hypo- or hyper- than 1 minute), preservation of consciousness, absence of
natremia, hyperthyroidism, and pheochromocytoma. pain, good response to antiepileptic drugs (AEDs), age
Hyperglycemia, hypocalcemia, hypothyroidism, etc., of onset between 1 and 20 years, and exclusion of other
may give rise to abnormal involuntary movements. organic disease.9
Vegetative symptoms may be caused by hypoglycemia,
pheochromocytoma, porphyria, carcinoid syndrome, or
hypo- or hyperthyroidism. Different metabolic altera- PSYCHOGENIC NONEPILEPTIC SEIZURES
tions may cause delirium, which can be mistaken for
complex partial SE. These include hepatic insufficiency, Panic Attacks
porphyria, Cushing’s or Addison’s disease, hypo- or Panic attacks may be mistaken for epileptic seizures,
hyperparathyroidism, hypo- or hypercalcemia, hypo- or particularly complex partial seizures. In addition, it is
hypernatremia, and hypo- or hyperkalemia. possible that a patient with a panic attack may end up
having syncope because of hyperventilation. The fear
seen during a panic attack must be differentiated from
Movement Disorders the ictal fear that may be a prominent symptom in
It may be difficult to distinguish between a movement certain partial seizures arising from the temporal
disorder and an epileptic seizure with predominantly lobe.10 The differences between panic attacks and ictal
motor symptoms. Some examples are myoclonus and fear are summarized in Table 3.
paroxysmal movement disorders, such as paroxysmal
dystonia or hyperplexia, and some types of tremor, tics,
or hemifacial spasms. The diagnosis is usually based on Psychogenic Nonepileptic Seizures or
the clinical features, although recording of cerebral Pseudoseizures
electrical activity may be necessary in some cases to Psychogenic nonepileptic seizures, also known as pseu-
rule out an epileptic seizure. In the case of paroxysmal doseizures, are nonepileptic paroxysmal events without
kinesogenic dystonia, a list of recently proposed diag- an organic or somatic cause. They consist of paroxysmal
nostic criteria include: triggering factors (generally brus- behavioral, motor, or sensory episodes associated with a
que movements), short duration of the episodes (less variety of other phenomena (e.g., vocalizations, crying,
302 SEMINARS IN NEUROLOGY/VOLUME 28, NUMBER 3 2008

Table 3 Clinical Differences between Ictal Fear and Panic Attacks

Ictal Fear Anxiety (Panic Attack)

Generally brief (less than Longer duration (5–20 minutes,

30 seconds’ duration) up to several hours)
Stereotyped signs and symptoms Not so stereotyped symptoms,
may change from one episode to another
No clear triggering factors Stressful situations may precipitate episodes
Light to moderately intense fear Intense fear
Associated with other ictal Associated with autonomic symptoms
symptoms (confusion, loss of (tachycardia, sweating, difficulty breathing);
awareness, automatisms) patient may report ‘‘loss of awareness’’
due to extreme anxiety

other expressions of emotion) that do not result from  Flurries of seizures or recurrent pseudo-SE that lead
abnormal electrical activity from the brain. The seizures to multiple emergency department visits or hospitali-
can mimic any kind of epileptic seizure and thus can be zations. These patients usually receive high doses of
mistaken for generalized tonic-clonic seizures, absence benzodiazepines before events stop or respiratory
seizures, or simple or complex partial seizures. Early depression takes place. Serum creatine kinase incre-

Downloaded by: Universidad de Barcelona. Copyrighted material.

recognition and appropriate treatment of nonepileptic ments following a convulsive pseudostatus are lower
seizures can prevent significant iatrogenic harm and may than the ones seen during epileptic SE.13
result in a better outcome.11 Some clinical features that  High seizure frequency
may help to distinguish psychogenic nonepileptic seiz-  History of sexual or physical abuse
ures from epileptic seizures are as follows:  Lack of concern or excessive or exaggerated emotional
response
 Long duration of psychogenic nonepileptic seizures  Multiple unexplained physical symptoms
and relatively fast recovery  No history of injury from seizures
 Variable symptomatology from one episode to  No response to AEDs or paradoxical increase in
another seizures with AED treatment
 Arrhythmic motor phenomena which do not follow  Personal, family, or professional experience with
the logical sequence of motor activity in hemiclonic, epilepsy
clonic, or generalized tonic-clonic seizures
 Gradual onset, waxing and waning course Not all events with these clinical or historical
 Bizarre movements of the entire body features are psychogenic nonepileptic seizures. Special
 Bilateral motor activity with preserved consciousness care must be taken with frontal lobe seizures, which are
 Pelvic movements (especially pelvic thrusting) often mistaken for pseudoseizures because of their dra-
 Opisthotonic posturing matic motor and vocal outbursts, preserved conscious-
 Weeping and complaining during the event ness, and short postictal period. Frontal lobe seizures
 Eye closure during the event may be distinguished by their brief duration, stereotyped
 Avoidance behavior during the event nature, and tendency to occur during sleep. Other types
 Rarely, tongue biting (if so, the tip of the tongue and of epileptic seizures which may be mistaken for psycho-
not the side) genic nonepileptic seizures are gelastic seizures (in which
 Side-to-side head movements the primary automatism is laughter), reflex epilepsies,
 Postictal whispering voice or partial motor responses and myoclonic jerks. One study reported that patients
to commands during recovery12 with at least two events a week, which have been
 Seizures provoked by suggestion refractory to at least two AEDs, and who have had at
 Resistance to physical exam during the event, espe- least two EEGs without epileptiform abnormalities have
cially resistance to eyelid opening an 85% chance of having psychogenic nonepileptic
seizures.14 Elevated serum prolactin assay, when meas-
Some historical features suggesting psychogenic ured within 10 to 20 minutes after a suspected event, is a
nonepileptic seizures include11: useful adjunctive test in the differentiation of psycho-
genic nonepileptic seizures and generalized tonic-clonic
 Events triggered by emotional or situational factors or complex partial seizures of temporal, but not of
 Episodes usually witnessed by family members/friends frontal, lobe origin among adults and older children.15
or seizures that occur only when the patient is alone However, it is not useful to distinguish between epileptic
 Associated psychiatric disorders seizures and syncope.
 RECOGNITION OF NONEPILEPTIC EVENTS/CARREÑO 303

Up to 30% of patients referred for video-EEG to methods, including intravenous saline infusions pre-
a tertiary epilepsy center are found to have psychogenic sented to patients as ‘‘epileptogenic medication,’’ the
nonepileptic seizures.16 From 5 to 10% of outpatient placement of a tuning fork on the forehead with the
epilepsy patients have nonepileptic seizures, compared suggestion that vibration may facilitate seizure occur-
with 20 to 40% of inpatient epilepsy populations (hos- rence, application of an alcohol pad over the lateral
pitals and specialty epilepsy centers).11,17 The mean time aspect of the neck, or the use of head-up tilting.21 The
to reach the correct diagnosis may be up to 7.2 years.18 use of these induction procedures raises clinical and
Delay in diagnosis has negative consequences and is ethical problems. Among the clinical ‘‘adverse reactions’’
associated with a worse outcome.19 the following must be considered: nonepileptic status
that may require the use of intravenous sedation; de novo
nonepileptic events in highly suggestionable patients
Diagnosis resulting in a false-positive diagnosis of psychogenic
Inpatient video-EEG monitoring is the preferred test nonepileptic seizures; atypical psychogenic seizures mak-
for the diagnosis of psychogenic nonepileptic seizures. ing the test inconclusive; and occurrence of epileptic
The definitive diagnosis is achieved with the recording seizures. The potential ethical problem associated with
of a ‘‘typical’’ event for the patient without accompa- the induction procedures is that the doctor is not
nying EEG abnormalities. Family members or wit- informing the patient about the true nature of the
nesses who are familiar with the patient’s seizures procedure, and this may compromise the patient-physi-
must agree that the recorded episodes are typical cian relationship. Other induction procedures that are

Downloaded by: Universidad de Barcelona. Copyrighted material.

events. Ideally, several spontaneous events should be acceptable are those that rely on the use of regular
recorded. It should be mentioned, however, that some activation methods in EEG, such as intermittent photic
types of epileptic seizures, like simple partial seizures stimulation, hyperventilation, or both combined.22,23
(auras) or seizures arising from deep midline brain Some experts recommend recording exclusively sponta-
regions (for example, seizures arising from the mesial neous events,21 as most psychogenic seizures are likely to
frontal or parietal regions), may fail to demonstrate an occur spontaneously within 24 to 48 hours of admission.
ictal pattern or interictal epileptiform discharges on They recommend video-EEG without induction
scalp EEG recordings or these may be obscured by procedures for the initial 48 hours, paying special
abundant muscle artifact. Discontinuation of AEDs attention to the interictal EEG recording to detect
to facilitate propagation of the epileptic activity when any possible epileptiform abnormalities. In the absence
no electrographic ictal pattern is identified may help to of a spontaneous event after 48 hours, induction
establish the epileptic nature of these episodes. Ictal protocols may be considered with intermittent photic
single photon emission computed tomography may stimulation and/or hyperventilation or hypnosis in
also be useful, as epileptic seizures may display an certain cases, following full disclosure of the rationale
area of hyperperfusion in the presumed epileptogenic and nature of the technique.21
zone. Video-EEG may also help to rule out psycho- In situations with more restricted access to video-
genic seizures in those patients with unusual or bizarre EEG, selected patients may benefit from short-term
seizure semiology (for example, patients with hyper- outpatient video-EEG recordings, combined with sim-
motor epileptic seizures originating or involving me- ple suggestion techniques if necessary.24
sial frontal regions), and also to establish seizure
frequency in those patients who have both epileptic
seizures and psychogenic seizures (around 5 to 40% of REFERENCES
all patients with psychogenic nonepileptic seizures).
In a prospective study to determine the frequency with 1. Benbadis SR, Tatum WO. Overinterpretation of EEGs and
which video-EEG changes the suspected clinical misdiagnosis of epilepsy. J Clin Neurophysiol 2003;20:42–44
2. Brignole M, Alboni P, Benditt DG, et al. Guidelines on
diagnosis of paroxysmal events, epileptic seizures
management (diagnosis and treatment) of syncope—update
were misdiagnosed as nonepileptic phenomena more 2004. Executive summary. Eur Heart J 2004;25:2054–2072
frequently than the reverse (57% vs. 12%).20 Because 3. McKeon A, Vaughan C, Delanty N. Seizure versus syncope.
of the risk of failing to identify epileptic seizures Lancet Neurol 2006;5:171–180
mimicking psychogenic nonepileptic seizures or epi- 4. Ali S, Khan MA, Khealani B. Limb-shaking transient
leptic seizures in remission, it is recommended that all ischemic attacks: case report and review of literature. BMC
suspected psychogenic seizures be confirmed with Neurol 2006;6:5
5. Scammell TE. The neurobiology, diagnosis, and treatment of
video-EEG.21
narcolepsy. Ann Neurol 2003;53:154–166
The use of induction procedures to trigger psy- 6. Coleman RM, Bliwise DL, Sajben N, Boomkamp A, de
chogenic seizures during video-EEG is a controversial Bruyn LM, Dement WC. Daytime sleepiness in patients
point in clinical practice. Induction procedures consist with periodic movements in sleep. Sleep 1982;5(suppl 2):
of the use of suggestive techniques with a variety of S191–S202
304 SEMINARS IN NEUROLOGY/VOLUME 28, NUMBER 3 2008

7. Derry CP, Duncan JS, Berkovic SF. Paroxysmal motor 16. Benbadis SR, O’Neill E, Tatum WO, Heriaud L. Outcome
disorders of sleep: the clinical spectrum and differentiation of prolonged video-EEG monitoring at a typical referral
from epilepsy. Epilepsia 2006;47:1775–1791 epilepsy center. Epilepsia 2004;45:1150–1153
8. Fantini ML, Corona A, Clerici S, Ferini-Strambi L. 17. Benbadis SR, Agrawal V, Tatum WO. How many patients
Aggressive dream content without daytime aggressiveness with psychogenic nonepileptic seizures also have epilepsy?
in REM sleep behavior disorder. Neurology 2005;65:1010– Neurology 2001;57:915–917
1015 18. Reuber M, Fernandez G, Bauer J, Helmstaedter C, Elger
9. Bruno MK, Hallett M, Gwinn-Hardy K, et al. Clinical CE. Diagnostic delay in psychogenic nonepileptic seizures.
evaluation of idiopathic paroxysmal kinesigenic dyskinesia: Neurology 2002;58:493–495
new diagnostic criteria. Neurology 2004;63:2280–2287 19. Selwa LM, Geyer J, Nikakhtar N, Brown MB, Schuh LA,
10. Biraben A, Taussig D, Thomas P, et al. Fear as the main Drury I. Nonepileptic seizure outcome varies by type of spell
feature of epileptic seizures. J Neurol Neurosurg Psychiatry and duration of illness. Epilepsia 2000;41:1330–1334
2001;70:186–191 20. Parra J, Iriarte J, Kanner AM. Are we overusing the
11. Alsaadi TM, Marquez AV. Psychogenic nonepileptic seiz- diagnosis of psychogenic non-epileptic events? Seizure 1999;
ures. Am Fam Physician 2005;72:849–856 8:223–227
12. Chabolla DR, Shih JJ. Postictal behaviors associated with 21. Iriarte J, Parra J, Urrestarazu E, Kuyk J. Controversies in the
psychogenic nonepileptic seizures. Epilepsy Behav 2006;9: diagnosis and management of psychogenic pseudoseizures.
307–311 Epilepsy Behav 2003;4:354–359
13. Holtkamp M, Othman J, Buchheim K, Meierkord H. 22. Benbadis SR. Provocative techniques should be used for the
Diagnosis of psychogenic nonepileptic status epilepticus in diagnosis of psychogenic nonepileptic seizures. Arch Neurol
the emergency setting. Neurology 2006;66:1727–1729 2001;58:2063–2065

Downloaded by: Universidad de Barcelona. Copyrighted material.

14. Davis BJ. Predicting nonepileptic seizures utilizing seizure 23. Parra J, Kanner AM, Iriarte J, Gil-Nagel A. When should
frequency, EEG, and response to medication. Eur Neurol induction protocols be used in the diagnostic evaluation of
2004;51:153–156 patients with paroxysmal events? Epilepsia 1998;39:863–
15. Chen DK, So YT, Fisher RS. Use of serum prolactin in 867
diagnosing epileptic seizures: report of the Therapeutics and 24. McGonigal A, Russell AJ, Mallik AK, Oto M, Duncan R.
Technology Assessment Subcommittee of the American Use of short term video EEG in the diagnosis of attack
Academy of Neurology. Neurology 2005;65:668–675 disorders. J Neurol Neurosurg Psychiatry 2004;75:771–772