Psychogenic nonepileptic seizures
PETER WIDDESS-WALSH1,2*, BARBARA MOSTACCI3, PAOLO TINUPER3, AND ORRIN DEVINSKY1,2
1Comprehensive Epilepsy Center, Institute of Neurology and Neurosurgery at St. Barnabas, Livingston, NJ, USA
2Comprehensive Epilepsy Center, NYU Langone School of Medicine, New York, NY, USA
3IRCCS Istituto delle Scienze Neurologiche, University of Bologna, Bologna, Italy
Psychogenic nonepileptic seizures (PNES) are paroxysmal
episodes of altered consciousness, behavior, or repetitive
movement. They appear similar to seizures but do not
result from excessive neuronal discharges, in contrast to
epileptic or acute symptomatic seizures. They are a subset
of neurological somatoform disorders that includes psy-
chogenic movement disorders and paralysis. Symptoms
are highly variable but usually consist of either positive
(shaking, posturing) or negative (collapse, unresponsive-
ness) components. They must be differentiated from
physiological nonepileptic events such as convulsive
syncope or sleep attacks.
The nomenclature has changed over the years and has
included pseudoseizures, hysterical seizures, and nonepi-
leptic attack disorder (NEAD). Some authors avoid the
use of the term “seizures” to reduce the connection with
epilepsy. The term “pseudoseizure” is no longer used as
it implies falseness. Dichotomies based on semiology,
psychological profiles, and mechanisms have been sug-
PNES have occurred throughout history and across
cultures (Veith, 1965). In other cultures and times, hys-
teria/PNES were interpreted as demonic possession, and
often resulted in exorcism or execution. In the 19th cen-
1859; Janet, 1895) introduced modern concepts of un-
conscious conversion symptoms caused by repression
expanded the role of hysteria, but channeled interest in
PNES within dynamic psychiatry rather than neurology
until the last few decades (Devinsky, 1998).
The prevalence of PNES in the general population is
unclear, as the literature contains series based on refer-
rals to epilepsy centers, where up to 10–20% of children
and 10–22% of adults have PNES (Gates et al., 1985;
Wyllie et al., 1990; Benbadis and Allen Hauser, 2000;
Reuber and Elger, 2003; Wood et al., 2004). Up to
10% of patients with PNES may have comorbid epilepsy
(Widdess-Walsh et al., 2010). Patients with PNES often
present to epilepsy centers due to lack of effect of anti-
epileptic drugs (AEDs); up to 50% of patients with re-
fractory seizures may have PNES (Lesser, 1996;
Hovorka et al., 2007). Historically, in Charcot’s “Quar-
tier des Epileptiques,” 46 (12%) of 385 women in a ward
of epileptic patients were found to have what was
thought to be PNES (Temkin, 1994). An estimated calcu-
lation of prevalence based on known epidemiological
data is 2–33 per 100 000 (Benbadis and Allen Hauser,
2000). The annual incidence of PNES is between 0.91
and 3.03 per 100 000 (Table 17.1). These numbers are
probably underestimated; somatoform disorders are
common and almost 6% of patients with anxiety disor-
ders have somatoform symptoms (Rogers et al., 1996).
“Hysterical symptoms” account for 1% of neurological
diagnoses (Marsden, 1986). The most common age
group is 20–30 years (Krumholz and Niedermeyer,
1983; Gumnit and Gates, 1986). Misdiagnosis is common:
PNES was misdiagnosed as status epilepticus in 27% of
patients with PNES who then received treatment for pro-
longed seizures. Prolonged events (>30 min) were seen
in 77.6% of patients with PNES (Reuber et al., 2003c).
*Correspondence to: Peter Widdess-Walsh, M.B., M.R.C.P.I., Institute of Neurology and Neurosurgery at St. Barnabas, Suite 101,
200 South Orange Avenue, Livingston, NJ 07039, USA. Tel: þ1-973-3227117, Fax: þ1-973-3227505, E-mail: pwiddesswalsh@bar-
Handbook of Clinical Neurology, Vol. 107 (3rd series)
Epilepsy, Part I
H. Stefan and W.H. Theodore, Editors
# 2012 Elsevier B.V. All rights reserved
adverse events such as respiratory arrest, unnecessary
procedures, and drug reactions. (Howell et al., 1989).
PNES are the most common type of conversion reac-
tion in many countries including India, Turkey, and
Oman, where the estimated prevalence may be as high
as 3–4% (Martı ´nez-Taboas et al., 2010). The advent
and availability of video-EEG have influenced the
reporting of PNES.
PNES are3–4times morecommon infemales,except
for patients before puberty and the elderly (Wyllie et al.,
1999; Duncan et al., 2006). Females are more likely
to suffer and report sexual abuse, physical abuse, and
self-harm (Oto et al., 2005). A history of abuse
(particularly sexual) is a common feature of PNES
and is discussed in more detail below. Subjective and/
or functional complaints are more common in women
than in men. In addition, there are physiological differ-
ences between women and men from exposure of the
brain and hypothalamus to sex hormones, which influ-
ence this dichotomy.
Patients with low IQ are at 5–7 times greater risk for
developing PNES (Reuber and Elger, 2003). In a series
of 288 patients with PNES, 8.6% had a learning disability
(Duncan and Oto, 2008a). Patients with PNES and learn-
gender. They have more situational triggers and a higher
proportion of epilepsy (Duncan and Oto, 2008b).
PNES are not confined to young adults. In one series,
and Salinsky, 2010). Patients aged over 65 years repre-
sented 9.6% (9 of 94) of patients with PNES in another
not be underestimated. The lifetime dollar cost of PNES
year could be up to $900 million in the USA alone
(Martin et al., 1998). The cost is magnified by the aver-
age delay in diagnosis of up to 7 years, often until inpa-
tient video-EEG is performed (Reuber et al., 2002a).
ilepsy, who, while representing 10–15% of all patients
with epilepsy, account for over 50% in costs (Begley
et al., 1994). One study showed that diagnosis with
video-EEG monitoring and multidisciplinary manage-
ment reduced healthcare costs in patients with PNES
(emergency room visits, outpatient clinic visits, and
of life is associated with PNES, particularly if the events
are frequent (Al Marzooqi et al., 2004; Lawton et al.,
The most common basis for PNES is the conversion dis-
order, a subconscious “conversion” of internal conflicts
somatization (Brown and Trimble, 2000; Akyuz et al.,
2004) or dissociation (Kuyk et al., 1997; Reuber and
House, 2002; Bowman, 2006), or both, is the underlying
mechanism. The International Classification of Diseases,
tive disorders, whereas the Diagnostic and Statistical
Manual ofMentalDisorders,4th edition (DSM-IV),clas-
sifiesitunder somatoform disorders.Inaddition,contro-
versy exists as to whether PNES should be a separate
disease entity or just a symptom of an underlying psychi-
atric disorder (Reuber and Elger, 2003).
Modern theories of PNES emerged in the 19th cen-
tury. In 1853, Carter suggested three etiological factors
for hysteria: temperament, circumstantial triggers, and
concealment (repression) of the exciting cause. Charcot
argued against intentional symptom production. Janet
first attributed PNES to dissociation; he felt that the
traumatized individual enters a state of self-hypnosis
as a reaction to overwhelming or childhood traumatic
events (Moene and Kuyk, 2010). PNES related to post-
traumatic stress disorder (PTSD) was first described by
Janet in war trauma survivors (Janet, 1889). According
to Freud, “these fits are nothing but pantomimically
projected into motility” (Strachey, 1955).
Incidence of psychogenic nonepileptic seizures
ReferenceDetails of studyNo. of patientsIncidenceSexAge (years)
Homogeneous population, single center,
Iceland – 5% of all new-onset
Hamilton county, Ohio, USA – 6.8%
of all seizures
141.4 per 100 000F 79%Range 15–24
Szaflarski et al.,
O’Sullivan et al.,
773.03 per 100 000
F 73%Range 25–44
50 0.91 per 100 000
F 61%Average 32.4
278P. WIDDESS-WALSH ET AL.
A minority of apparent cases of PNES may be pro-
duced intentionally, such as with malingering (if moti-
vated by obvious external gains), factitious disorder/
Munchausen syndrome (if motivated in order to attain
the “sick role”; Savard et al., 1988), or Munchausen syn-
drome by proxy (such as an attempt by a parent or care-
giver to create the impression that the person has
that events are not directly caused by a primary psychi-
atric disorder such as panic attacks, agitation, or hallu-
cinations. Video-EEG may not fully exclude coexisting
epileptic seizures (ES) if the events in question are not
captured or if ES are scalp EEG-negative.
Some evidence exists that the nondominant hemi-
sphere may have a role in the development of PNES.
Abnormalities on magnetic resonance imaging (MRI)
or epileptiform EEG abnormalities in patients with
PNES were found to be more common (72%) in the right
hemisphere (Devinsky et al., 2001). Functional MRI
(fMRI) of psychogenic tremor due to a conversion reac-
tion showed hypoactivity of the right temporoparietal
junction during the tremor. The authors theorized that
the associated lack of sensory feedback to movement
removes “self-agency” (experience that one is the cause
of one’s own actions), so that the patient perceives the
movements as involuntary (Voon et al., 2010). Inhibitory
centers such as the ventromedian prefrontal cortex
showed increased activation on fMRI motor imagery
in conversion paralysis compared with the unaffected
limb (de Lange et al., 2008). Single-photon emission
computed tomography (SPECT) and fMRI studies have
shown abnormalities in the anterior cingulate gyrus and
orbitofrontal cortex in patients with conversion disor-
der. No fMRI data exist for PNES.
Basal hypercortisolism and an abnormal hypotha-
lamic–pituitary axis have been described in patients with
PNES, particularly in those with a history of sexual
trauma, compared with normal controls (Simeon
et al., 2007; Bakvis et al., 2010).
A variety of models and theories exist for PNES. Pre-
cipitants of PNES include abuse, trauma, neglect, be-
reavement, family dysfunction, health anxiety, social
stress, and a history of insecure attachments (Duncan
and Oto, 2008a; Bowman, 2010). One model of PNES
childhood events or abuse, trauma, comorbid condi-
tions), then precipitating events (sickness, emotional
stressor, major life events) triggering the PNES,
then perpetuating events resulting in recurrent PNES
(i.e., conditioning (primary or secondary gain), emo-
tional disorder, illness belief) (Stone et al., 2005). Clas-
sical and operant conditioning theory explain how PNES
tive response to arousal (“panic without panic”)
(Goldstein, 2004). LaFrance and Devinsky (2002)
divided PNES into etiological subsets: 1, anxious; 2a,
abused – borderline personality; 2b, abused afraid
(PTSD); 3, somatic; 4, dysthymic/depressed; 5, mentally
retarded. According to Bowman (1999), there are four
pathways to the development of PNES: a history of
sexual or physical abuse, recent sexual assault, multiple
life stressors that overwhelm coping abilities, and panic
attacks mistaken for PNES.
zure prior to their symptom onset, implying a role for
symptom modeling (Bautista et al., 2008). Symptom
modeling involves the mimicking of another person’s
(or the person themselves’) symptoms to satisfy primary
and secondary gains. This study excluded patients with
comorbid PNES and epilepsy. Only 9 of the 27 patients
had other family members with seizures.
The psychodynamic theory of PNES reflects the con-
flict between the components of personality; the id, the
ego, and the superego. Offensive thoughts and memo-
ries are repressed in order not to be aware of them.
These repressed thoughts may find an outlet in physical
symptoms that allow the patient to relieve their uncon-
scious selves (i.e., the id) and to keep the offending con-
tent or thoughts further repressed – the primary gain.
The primary pathology is the unresolved intrapsychic
conflict. Eventually this leads to secondary gain from
obtaining attention, and avoiding responsibility.
family dynamics such as enmeshment, impaired conflict
resolution, and parental conflict. The physical symp-
toms may reduce responsibility for family conflicts.
It may also relieve the child of going to school, resulting
in secondary gain and worsening the severity of the
problem. The PNES becomes an expression of what is
may be modeling of parental somatizing behaviors
(Plioplys et al., 2007).
History and comorbidities
There has been a previous psychological trauma in
44–100% of patients with PNES (Fleisher et al., 2002;
Fiszman et al., 2004; Duncan and Oto, 2008a). A history
of sexual or physical abuse is particularly common, with
a wide range of prevalence (9–77%) in various studies
(Alper et al., 1993; Rechlin et al., 1997; Reuber et al.,
2000; Abubakr et al., 2003; Binzer et al., 2004; Fiszman
et al., 2004; Duncan and Oto, 2008a). Studies using
careful interviews with psychologists rather than self-
reports found an overall lifetime risk of 84–90%
(Bowman and Markand, 1999; Dikel et al., 2003). Sexual
abuse is more common in female patients (Dworetzky
PSYCHOGENIC NONEPILEPTIC SEIZURES279
et al., 2005; Duncan and Oto, 2008a; Selkirk et al.,
2008). Patients with a history of abuse have poorer men-
tal health, earlier-onset PNES, and their spells are more
severe (Selkirk et al., 2008). One study reported incest in
30% of the patients (Binzer et al., 2004); other traumatic
events include bereavement and bullying (Duncan and
Oto, 2008a). The exact role of abuse or trauma in
the development of PNES remains to be elucidated,
although putative dissociative mechanisms exist.
Childhood factors have also been implicated, and
perceived parental rearing mean scores showed signifi-
cant differences from those in patients with ES. In par-
ticular, in one series, patients with PNES recollected less
parental warmth and more paternal rejection (Binzer
et al., 2004).
The overall number of life events, especially nega-
tive, unexpected events related to personal health issues
and with adjustment problems in the year preceding dis-
ease onset, is significantly higher in patients with PNES
traumatic experiences are particularly common in late-
onset PNES (Duncan et al., 2006).
Psychiatric comorbidities are reported in 50–100% of
patients with PNES (Rechlin et al., 1997; Reuber et al.,
ality disorders, prominently borderline type, are reported
in up to 65% of patients (Smith et al., 1992; Jawad et al.,
1995; Binzer et al., 2004). Depression is significantly
more common than in the general population, but its
prevalence is comparable to that of patients with ES
(Rechlin et al., 1997; Binzer et al., 2004; Dworetzky
et al., 2005; O’Sullivan et al., 2007; Asmussen et al.,
2009). However, depression in PNES is more likely to
(Asmussen et al., 2009). Conversion disorder was diag-
nosed in all patients with pseudostatus in one series
than in ES and occurs in 9–100% of patients with PNES
(Fiszman et al., 2004; Dworetzky et al., 2005). Anxiety
and somatoform disorders were also reported (Binzer
et al., 2004; Dworetzky et al., 2005; O’Sullivan et al.,
2007). The prevalence of suicide attempts was 11–46%
in PNES (Meierkord et al., 1991; Peguero et al., 1995;
Lesser, 1996; Binzer et al., 2004) and up to 60–67% in
pseudostatus (Rechlin et al., 1997; Reuber et al., 2000).
reported in 37–80% of patients (Meierkord et al., 1991;
De Wet et al., 2003; Mellers, 2005; O’Sullivan et al.,
2007). Chronic pain is very common (Dworetzky
et al., 2005), and a history of chronic pain and fibromy-
algia was highly predictive of PNES in a population of
patients with refractory epilepsy (Benbadis, 2005).
Asthma, of possible psychogenic origin, was reported
in 26.5% of patients in one study (De Wet et al., 2003).
Although the absence of risk factors for ES may be
reassuring, their presence may be misleading: family
history of epilepsy, learning disability, and head trauma
are not uncommon in these patients (Mellers, 2005;
O’Sullivan et al., 2007; Duncan and Oto, 2008a).
Of particular complexity is the co-occurrence of
PNES and epilepsy in the same patient, estimated to oc-
cur in up to 10% of patients with PNES (Lesser et al.,
1983; Benbadis et al., 2001). This co-occurrence is more
common in the learning disabled population (Duncan
and Oto, 2008a, b). The PNES will typically start after
the ES, and may present as a new seizure type or as
“pseudoresistance” to AEDs and in association with
psychiatric instability. There is often a longer time to di-
agnosis and higher use of AEDs. There are few charac-
teristic features compared with those in patients with
PNES alone, and the seizure types often appear similar.
Clinicians, patients, and families must differentiate
PNES from ES, as the treatments are divergent. In these
cases, video-EEG or home video analysis is extremely
valuable. Sitting down to review events with family
and caregivers can help them determine which ones
are true PNES; when they subsequently call to report
events, the physician is more likely to make the correct
management decision. Although PNES and ES occur at
separate times, PNES may occur in the early phase of an
epileptic seizure, or the epileptic seizure can facilitate
PNES. This group is at risk for overtreatment of pseu-
dostatus, due to the established diagnosis of epilepsy
and assumption that the PNES is actually an epileptic
seizure (Widdess-Walsh et al., 2010). PNES can occur
de novo after epilepsy surgery, and need to be differen-
tiated from recurrent ES and presumed surgical failure
(Parra et al., 1998).
PNES presents in various forms, and some authors clas-
ileptic seizure types. Others question this division,
claiming that the processes underlying PNES are distinct
from those of epilepsy and that classification based on
superficial resemblance to ES is misleading (Leis et al.,
1992). Several authors have grouped PNES according to
semiology, the most consistent division being prominent
limpness or collapse versus prominent motor behavior
(Meierkord et al., 1991; Chen and Izadyar, 2010).
Attacks with only subjective symptoms can occur
(DeToledo and Ramsay, 1996; Hovorka et al., 2007),
but are more difficult to diagnose definitely as they
are frequently excluded from video-EEG semiological
studies because their nonepileptic origin cannot be
demonstrated – the EEG is often normal during simple
partial seizures with sensory symptoms. Therefore, we
280P. WIDDESS-WALSH ET AL.
focus on PNES presenting with objective alterations in
consciousness and/or motor behavior.
The onset of PNES is usually gradual, contrasting
with the abrupt onset of ES (Gulick et al., 1982; Meier-
orexclusively occursduring wakefulness(Gowers,1901;
Luther et al., 1982; Kanner et al., 1990; Saygi et al., 1992;
Raymond et al., 1999) (Table 17.2). However, one study
described PNES arising from stage II–III sleep or a
few seconds after awakening (Orbach et al., 2003).
Moreover, PNES may occur during behavioral sleep,
with EEG revealing normal waking activity. Benbadis
et al. (1996) named this condition “pseudosleep,” a very
specific feature of PNES (Thacker et al., 1993; Benbadis
et al., 1996; Hovorka et al., 2007).
Precipitating factors implicating anxiety and stress
situations are commonly found in PNES (Luther et al.,
1982; Slater et al., 1995; Lesser, 1996) as well as ES,
although stress is less prominent as a provocative
factor (Slater et al., 1995; Lesser, 1996). PNES tend to
Clinical features of psychogenic nonepileptic seizures (PNES) versus epileptic seizures (ES)
Clinical featuresPNES ES
Occurrence in presence of
Occurrence during sleep
Response to verbal
Movements of upper and
“arc de cercle”
Thrashing, violent movements
of the body
Unilateral head turning
Pelvic thrusting forward
Possible but less obvious
Rarely reported; pseudosleep
Variable, often >2 min
Up to 1–2 min
Never preserved in GTCS. Rarely and only
partially preserved in CPS
Out of phase In-phase in GTCS
Occasional/common Occasional/common in FLS; very rare in
Occasional/common in FLS; rare in other typesOccasional/common
Occasional/common (especially in
May be absent in PNES
Common before GTCS
Occasional/common in FLS; very rare in
Always present in the tonic phase of GTCS Whole-body rigidity
Fluctuating course; pauses
in motor activity
without prominent motor
Occasional Very rare (absence status)
Emotional: moans, screams, gasps, “ictal
weeping”; understandable statements
Common/very common, sustained,
forceful, with opposition to opening
Very uncommon, but may be reported
Very uncommon, but may be reported
Very rare, on the tip
Monotonous epileptic cry in GTCS; continuous,
moans, animal-like noises, uttering in FLS
Very rare, partial, never forceful, never
throughout the spell
Common, especially in GTCS
Occasional/common in GTCS, on the side
Bite to the tongue
Fatigue or lethargy
PSYCHOGENIC NONEPILEPTIC SEIZURES 281
occur in the presence of “significant” others (Luther
et al., 1982) and the occurrence of a paroxysmal be-
havioral change during a clinic visit predicts PNES
Prodromal feelings are frequent, generally neither
specific nor lateralized, and include dizziness or funny
feelings, as well as olfactory, auditory, visual, or com-
plexsensations and focal numbness (Gulick et al., 1982;
Luther et al., 1982; Hovorka et al., 2007). Symptoms
suggesting hyperventilation include lightheadedness,
acral paresthesias, and palpitations (Lesser, 1996).
PNES usually last for more than 2 minutes and may
be longer than 30 minutes, which is very unusual for ES
Meierkord et al., 1991; Saygi et al., 1992; Raymond et al.,
1999; Hovorka et al., 2007; Azar et al., 2008).
A motor behavior is frequently reported as part of
the attack. The features most often reported include
asynchronous out-of-phase limb movements, or absence
of in-phase limb movements in attacks resembling gen-
eralized tonic–clonic seizures (GTCS) (Gates et al., 1985;
Leis et al., 1992; Hovorka et al., 2007; Azar et al., 2008).
The absence of whole-body rigidity during the entire du-
ration of an attack “mimicking” GTCS is highly specific
for PNES according to Gates et al. (1985). Side-to-side
head/body turning is common in PNES, whereas these
patients seldom show unilateral head turning, as may
seizure (Gates et al., 1985; Leis et al., 1992; Saygi et al.,
1992). Pelvic thrusting is commonly described (Gates
et al., 1985; Leis et al., 1992; Saygi et al., 1992; Flu ¨gel
et al., 1996; Geyer et al., 2000; Abubakr et al., 2003;
Hovorka et al., 2007; Azar et al., 2008), especially in
women (Meierkord et al., 1991; Abubakr et al., 2003),
and according to some authors it is typically forwards,
whereas when it occurs during GTCS it is generally
backwards (Gates et al., 1985). Thrashing and grabbing
behavior is another typical feature (Gulick et al., 1982;
Kanner et al., 1990; Raymond et al., 1999; Abubakr
et al., 2003). In contrast to supplementary motor area
(frontal lobe) seizures (FLS), the movements in PNES
generally involve the head and neck, whereas FLS are
generalized or mainly involve the lower limbs and trunk
(Kanner et al., 1990). All of the motor patterns reported
in PNES can occur in FLS, especially those involving the
mesial structures, including maintenance of conscious-
ness during bilateral motor attacks, lack of postictal
signs, and normal ictal EEGs (Kanner et al., 1990; Saygi
et al., 1992; Geyer et al., 2000; Azar et al., 2008). There-
fore, the differential diagnosis of PNES and FLS can be
challenging. Features that strongly suggest FLS include:
turning toa prone position (Saygi et al., 1992), tonic pos-
turing in abduction of upper extremities (Kanner et al.,
1990), short duration, highly stereotyped pattern, and
frequent or exclusive occurrence during sleep (Kanner
et al., 1990; Mellers, 2005). Tonic posturing and opistho-
tonus can occur with PNES (Gulick et al., 1982; Luther
et al., 1982; Kanner et al., 1990; Hovorka et al., 2007),
Clinical featuresPNES ES
Rapid, shallow, irregular, with pauses,
Deep, prolonged, regular, loud, snoring
(stertorous breathing) in GTCS
Absent Inappropriate events sequence
Hypnosis, placebo, suggestion
Cognitive assessment (PNES
versus partial seizures)
Recall of memory items
Extensor plantar response
May be inducedNot inducible
Very common and commonly >50%
Rare and always <50%
May be impaired
Rare (depending on kind of seizure)
Common after GTCS
Values for the frequency of these features are approximate: very common, >70%; common, 30–70%; occasional, 10–30%; rare, 5–10%;
very rare, <5%.
CPS, complex partial seizures; FLS, frontal lobe seizures; GTCS, generalized tonic–clonic seizures.
282P. WIDDESS-WALSH ET AL.
even though the “arc de cercle” considered pathogno-
monic for psychogenic disorder by Charcot and Richer
(1887) is seldom encountered nowadays. PNES often ex-
hibit a discontinuous pattern with motor activity alter-
nated with brief periods of rest, in contrast to the
epileptic pattern (Gulick et al., 1982; Meierkord et al.,
1991; Mellers, 2005).
Figure 17.1 shows frames of several psychogenic
Istituto delle Scienze Neurologiche, University of
Bologna, Bologna, Italy.
Semipurposeful behavior can occur with PNES
(Gulick et al., 1982; Luther et al., 1982; Meierkord
et al., 1991) and occurs de novo, unlike ES in which
patients can continue purposeful activity begun before
the attack. The activity is generally goal-directed with
a dramatic or violent element (Gulick et al., 1982). Less
frequent features of PNES include alimentary phe-
nomena (Gulick et al., 1982), trembling (Gulick et al.,
1982; Hovorka et al., 2007), whole-body flaccidity
(Gates et al., 1985; Leis et al., 1992), grimacing (Gulick
et al., 1982), and jerking (Gulick et al., 1982; Raymond
et al., 1999).
Vocalization is common in both PNES and ES, but
differs in quality. Vocalization in GTCS is invariably
the typical “epileptic cry,” whereas vocalization during
or animal noises and sometimes containing understand-
able words. Vocalization during PNES is variable and
emotional sadness or pain (Gulick et al., 1982; Luther
et al., 1982; Gates et al., 1985; Kanner et al., 1990; Saygi
Fig. 17.1. (A) Patient covering her face with her hands. Pseudodystonic posture of the inferior limbs. (B) Tonic posturing and
facial grimace. (C) Opisthotonic posture. (D) Prolonged unresponsiveness without prominent motor features, resistance to eye
opening. (E) Pseudodystonic posturing of the neck. (F) Prolonged unresponsiveness without prominent motor features.
PSYCHOGENIC NONEPILEPTIC SEIZURES283
et al., 1992; Slater et al., 1995; Hovorka et al., 2007; Azar
et al., 2008). Note that many ES can include similar
sistent between seizures. Ictal stuttering was described
in 8.5% of patients with PNES but in no patients with
ES in a large series (Vossler et al., 2004). Some degree
of verbal responsiveness can occur in PNES resembling
complex partial seizures (CPS) (Bell et al., 1998) and,
when present during apparent GTCS, is pathognomonic
for PNES (Gulick et al., 1982). However, FLS can cause
bilateral motor phenomena with preserved conscious-
ness, leading to the misdiagnosis of PNES.
Several video-EEG studies have found that the eyes
are closed during 55–96% of PNES (Gulick et al.,
1982; DeToledo and Ramsay, 1996; Flu ¨gel et al., 1996;
Alhalabi and Verma, 1994; Chung et al., 2006; Hovorka
et al., 2007; Azar et al., 2008; Syed et al., 2008). Con-
versely,theeyes are openatthebeginning orthroughout
92–100% of ES, including episodes arising from sleep
(Alhalabi and Verma, 1994; DeToledo and Ramsay,
1996; Chung et al., 2006; Azar et al., 2008). The eyes
are characteristically forcefully closed with active oppo-
sition to opening in PNES (DeToledo and Ramsay, 1996;
Hovorka et al., 2007). Purely sensory PNES probably
constitute an exception: in one series, eyes were closed
in 11% and patients always opened their eyes when
told to do so (DeToledo and Ramsay, 1996). Some stud-
ies found that most (82–88%) patients with PNES have
no ictal eye manifestation (Gates et al., 1985; Leis et al.,
1992); in one series this was significantly different
from GCTS (Gates et al., 1985). Notably, self and ob-
server reports of eye closure were unreliable in one
study, identifying only half of the events correctly
(Syed et al., 2008).
Prolonged limpness without motor symptoms often
accompanied by apparent atonia is another common
form of PNES (Gulick et al., 1982; Luther et al., 1982;
Meierkord et al., 1991; Leis et al., 1992; Raymond
et al., 1999; Abubakr et al., 2003; Hovorka et al.,
2007). In some of these prolonged atonic PNES, there
is intermittent eye blinking, swallowing, or mouthing
movements (Gulick et al., 1982), slumping forward
(Gulick et al., 1982), staring (Hovorka et al., 2007), or
avoidance behavior (Luther et al., 1982). This PNES pat-
tern does not parallel any seizure type other than ab-
sence status, but atonia is rare in this epileptic seizure
type. Other etiologies are also unlikely, as episodes last-
ing more than 5 minutes that completely reverse suggest
PNES, not other organic disorders (Meierkord et al.,
1991; Mellers, 2005).
Urinary incontinence is very rare during video-EEG
recorded PNES (Luther et al., 1982; Meierkord et al.,
1991; Slater et al., 1995; Abubakr et al., 2003; Hovorka
et al., 2007; Oliva et al., 2008), although it may be
self-reported (44% in one study) (Peguero et al., 1995;
Dworetzky et al., 2005).
Self-injury was uncommon during video-EEG re-
cordings of PNES (Meierkord et al., 1991; Benbadis
et al., 1995; Abubakr et al., 2003; Hovorka et al.,
2007; Oliva et al., 2008), although it is more commonly
one study, 40% of patients with PNES reported some
ing bone fracture, or tongue biting. Interestingly burns
were never reported by patients with PNES, but only by
patients with epilepsy (Peguero et al., 1995). Tongue bit-
ing is rare in PNES (Luther et al., 1982; Meierkord et al.,
1991; Benbadis et al., 1995; Hovorka et al., 2007; Oliva
et al., 2008) and, when it occurs, is typically on the tip
(Hovorka et al., 2007) and not in the lateral or anterolat-
eral tongue as in GTCS (DeToledo and Ramsay, 1996;
Oliva et al., 2008).
Uncommon but relatively specific features of PNES
include ictal weeping (Bergen and Ristanovic, 1993), the
“teddy bear sign” of age-inappropriate behavior, such as
bringing a teddy bear or similar item to the epilepsy mon-
itoring unit (Burneo et al., 2003), and responding to ques-
tions in a whispering voice and to commands with partial
motor responses postictally (Chabolla and Shih, 2006).
The postictal breathing pattern after PNES is often
rapid, shallow and soft, irregular, and associated with
in GTCS when postictal breathing is deep, with pro-
longed inspiratory and expiratory phases, regular, loud,
usually with snoring (“stertorous”), and impaired for
longer, and in FLS when it is usually shallow, regular,
and quiet (Sen et al., 2007; Azar et al., 2008).
Postictal agitation, confusion, headache, and fatigue
are uncommon after PNES (Ettinger et al., 1999a; Azar
et al., 2008). Ability to recall the seizure is frequent in
PNES, contrasting with GCTS and CPS (Leis et al.,
1992; Bell et al., 1998; Mellers, 2005).
Although stereotypy is usually considered specific
for ES, stereotyped events were recorded in 67–90%
of video-EEG studies recording multiple PNES in the
same patient (Gulick et al., 1982; Meierkord et al.,
1991; Raymond et al., 1999; Hovorka et al., 2007).
Individual ictal features occasionally mimic a spe-
cific epileptic seizure type, but rarely does a complete
PNES closely resemble a single epileptic seizure type
(Luther et al., 1982; Meierkord et al., 1991; Leis et al.,
1992). Thus, the precise temporal sequence of events
should always be elicited, and variable, random, or non-
physiological (e.g., thumb jerking followed by toe jerk-
ing followed by eye jerking) sequences should raise the
suspicion of PNES.
tus. Patients may present with all the features described
284P. WIDDESS-WALSH ET AL.
above without returning to normal state for a long time.
Psychogenicstatus may be the first manifestationor com-
plicate ahistory ofPNES, anda single episodeof “status”
occurred in up to 78% of patients with PNES (Reuber
et al., 2003b).
Ictal testing during video-EEG recording or observed
PNES can be helpful. Corneal reflex is usually impaired
mal after PNES. Unilateral or bilateral extensor plantar
response, common within5minutes ofGTCS is not seen
in PNES (Walczak and Rubinsky, 1994).
Avoidance maneuvers consist of evaluating the pa-
tient’s resistance to eye opening, avoiding placing his
or her hand on the face, or avoiding placing a heel on
the opposite shin. Avoidance can occur in up to 100%
of PNES (Luther et al., 1982). When eyes are open,
searching for evidence of fixation can be useful. One
maneuver consists of rolling the patient onto his or
her side: if fixation is maintained, the patient’s eyes
are generally deviated to the ground; when the patient
is rolled onto the other side, the eyes should be directed
on the ground again (“Henry and Woodruff sign”).
Alternatively the examiner may place a mirror in front
of the patient and look for evidence of convergence
and fixation (Henry and Woodruff, 1978; Mellers, 2005).
Much of the psychological research in patients with
PNES has used the Minnesota Multiphasic Personality
Inventory (MMPI) and MMPI-2, where patients score
higher on scales related to hypochondriasis, hysteria,
and, to a lesser extent, schizophrenia and depression.
V” profile among patients with PNES (Griffith et al.,
2007; LaFrance, 2008). Patients with “motor” events gen-
erally have more severe psychopathology than those with
“catatonic” events (Wilkus and Dodrill, 1989; Griffith
et al., 2007). MMPI-2 outcomes coupled with clinical
variables yielded 48–80% sensitivity and 68–80% speci-
ficity for a diagnosis of PNES (Cragar et al., 2003;
Schramke et al., 2007). The MMPI alone or with other
measures can help identify personality or etiology-based
PNES subtypes, suggesting potential therapeutic ap-
proaches. Results are equivocal and will not be consid-
ered here (Gumnit and Gates, 1986; Barrash et al., 1989;
Cragar et al., 2005).
Harden et al. (2009) compared patients with PNES to
patients with ES with respect to personality clusters,
using the Structured Clinical Interview Personality
Disorders Modules for DSM-IV-TR (SCID-II). Overall,
personality disorders were common in both groups: 75%
in patients with ES and 81% in those with PNES. Patients
with PNES were more likely to meet criteria for a per-
sonality disorder in Cluster A (paranoid, schizoid, schi-
narcissistic) compared with patients with ES, who were
more likely to have Cluster C criteria (avoidant, depen-
dent, obsessive–compulsive). The difference was statis-
Intelligence measures and cognitive testing
Binder et al. (1998) found no significant differences be-
tween patients with ES and PNES on several IQ tests of
intelligence or learning and memory, but scores were
significantly inferior to those of control subjects. An-
other study found that performance IQ ranged from de-
ficient to very superior in patients with PNES, but the
distribution was skewed toward the low normal range
and 41.5% of the patients had full-scale IQ scores in
the low average or borderline range. Scores on the Hal-
stead Reitan Neuropsychological Test Battery showed
impairment in 63% of patients with PNES. Impaired
performance involved diverse cognitive functions such
as mental flexibility and ease of learning in novel
problem-solving situations, spatial localization memory,
auditory perception and discrimination, motor speed,
and coordination. However, the sample considered
had a high incidence of closed head injury and substance
abuse, which could account for the abnormal findings
(Kalogjera-Sackellares and Sackellares, 1999).
Abnormal neuropsychological performance in pa-
of psychopathology on the MMPI-2, suggesting that im-
paired cognition may be linked to emotional rather than
organic factors in these patients (Cragar et al., 2005).
Reduced motor speed and grip strength were found in
patients with PNES compared with healthy controls
(Sackellares and Sackellares, 2001), although these fea-
tures could be signs of lack of motivation (LaFrance,
Patients with PNES score lower than those with ES on
some motivational measures, although not necessarily
in an intentional manner, and this could affect neuro-
psychological test results (Brown et al., 1991; Binder
et al., 1994, 1998; Drane et al., 2006). This finding is con-
troversial, as others failed to find impaired motivational
effort, claiming that patients with PNES produce trust-
worthy findings in neuropsychological tests (Cragar
et al., 2006; Dodrill, 2008).
PSYCHOGENIC NONEPILEPTIC SEIZURES
Health-related quality of life (HRQoL)
HRQoL, measured with different validated scales, is
lower inpatients with PNES than in patients withepilepsy
or depression. Low scores are due mainly to depression,
AED side-effects, somatization, and psychological dis-
tress (Szaflarski et al., 2003; Szaflarski and Szaflarski,
2004; Testa etal., 2007; LaFrance and Syc, 2009).Seizure
frequency is not independently related to quality of life,
other physical symptoms (LaFrance and Syc, 2009).
Patients with epilepsy and those with PNES talked dif-
ferently about their seizures in studies conducted in
German- and English-speaking patients. Thus, interac-
tional and linguistic analysis of patients’ description
of their seizures allows a correct diagnosis of ES or
PNES in 85–100% of cases (Schwabe et al., 2007; Plug
et al., 2009a; Reuber et al., 2009). Patients with ES dis-
cuss subjective symptoms in detail and focus more easily
on description, whereas patients with PNES discuss spar-
ingly and with difficulty; patients with ES attempt to fill
gaps and are willing to know what happens during
periods of reduced consciousness, whereas those with
Patients with PNES tend to concentrate on the circum-
stances in which the seizure presented rather than on
the seizure itself. Moreover, patients with ES often give
self-initiated hints at strategies they use to interrupt or
prevent seizures, such as focusing on a particular
thought, whereas patients with PNES do not.
conceptualization of seizures, which are likely to reflect
differences in subjective seizure experience between pa-
tients with PNES and those with epilepsy: ES are concep-
tualized as a more external, self-directed entity (i.e., an
or place patients go through (Plug et al., 2009b).
Studies in languages other than English or German
EEG alone cannot diagnose PNES, as it may not make
nor exclude the diagnosis of epilepsy. A single routine
EEG is normal in 30% of patients with ES (Chadwick,
1994; Mellers, 2005). In addition, up to 15% of the nor-
mal population have nonspecific abnormalities and less
than 1% have epileptiform discharges on EEG. Abnor-
malities are more common in patients with PNES inde-
pendent of comorbid epilepsy (Reuber et al., 2002b;
Woollacott et al., 2010), as well as in borderline
personality disorder and in relatives of patients with ep-
ilepsy, which are common conditions in PNES (Luther
et al., 1982; Lesser, 1996; De la Fuente et al., 1998;
Mellers, 2005). Up to 37% of patients with PNES had
a report of an epileptiform baseline EEG, generally
made by neurologists who were not epileptologists or
electroencephalographers (Benbadis and Tatum, 2003;
Lobello et al., 2006). When tracings were re-evaluated
at an epilepsy center, the epileptiform abnormalities
were found to be normal variants (Benbadis and
contrasting with a true epileptic pattern, characterized
by rhythms in the frequency of delta and beta range
evolving from one to the other during the course of
the seizure. Brief pauses in rhythmic movement during
a seizure, followed by resumption of movement at the
same frequency, were highly specific for PNES (“on–
off–on” pattern) (Vinton et al., 2004).
Video-EEG monitoring remains the “gold standard” in-
vestigation for PNES: the patient undergoes aprolonged
simultaneous EEG and video recording to record the ha-
bitualevent. Notably,onestudyshowedonly amoderate
interrater reliability of video-EEG for PNES (Benbadis
et al., 2009). The combination of observed semiology
and normal background EEG before, during, and after
the attack is usually diagnostic. There are some impor-
tant limitations. First, motion artifacts can obscure the
EEG or be mistaken for ictal discharges. Second, ictal
scalp-EEG often shows no epileptic features during sim-
ple partial seizures and FLS, a type that can easily be
clinically mistaken for PNES. Third, as many patients
may have both ES and PNES, it is very important for
diagnosis that the captured event is the habitual one,
so the video should always be shown to someone who
has witnessed the patient’s attacks before establishing
a diagnosis. For similar reasons, if more than one type
of seizure is reported, try to record each type. Fourth,
generalized epileptiform discharges can occur during
drug withdrawal (especially barbiturates) even in pa-
tients with PNES. Finally, in patients with rare attacks,
it may be very difficult to record a spontaneous seizure.
A typical event occurred within the first 48 hours of
video-EEG monitoring in 88–98.5% of patients with
PNES (Lobello et al., 2006; Woollacott et al., 2010). This
suggests that outpatient monitoring can be cost-effective.
When a spontaneous episode is not recorded, induction
sion of body parts, photic stimulation, hyperventilation,
286P. WIDDESS-WALSH ET AL.
verbal suggestion, placing a tuning fork or moistened
patches on the skin, intravenous administration of saline
or other placebo, and hypnosis. However, the use of these
especially when a placebo is used, and some have ques-
tioned their specificity (Devinsky and Fisher, 1996; Gates,
2001). However, induction can reduce the time to diagno-
and avoiding the hazards of an inappropriate diagnosis of
epilepsy (Benbadis, 2001). Moreover, when the procedure
was disclosed to the patient in a supportive manner after
successful induction, the physician–patient relationship
was not altered and patients agreed to further interven-
maneuvers have a high sensitivity and a specificity
approaching 100% for PNES (Slater et al., 1995; Barry
et al., 2000; Benbadis et al., 2000; Benbadis et al., 2004;
Lancman et al., 1994; Walczak et al., 1994). Hypnosis
may be used also for children (Olson et al., 2008).
Home video recording
Video alone may have a high specificity and sensitivity
in selected patients when reviewed by experienced ob-
server (respectively 94% and 93% in a recent study)
(Chen et al., 2008). However, the onset of the seizure
is generally missed in home videos. Caregivers should
also be instructed to capture limb and face movements
in order to obtain useful information. Nevertheless,
home video recording may be helpful for screening be-
fore video-EEG recording, especially in patients with
Serum prolactin assay
Serum prolactin levels rise to concentrations greater
than 500 IU/mL in more than 90% of patients after
GCTS and 60% of patients after CPS, 10–20 minutes af-
ter the attack (Trimble, 1986; Mellers, 2005). Positive re-
sults are possible in PNES and are commonly found
after syncope (Trimble, 1986; Oribe et al., 1996; Alving,
1998; Shuklaet al.,2004).Littleisknownaboutprolactin
levels after other organic imitators of seizures. The use
of serum prolactin assay has not been established in the
evaluation of status epilepticus, repetitive seizures, and
seizures different from CPS and GTCS. A baseline pro-
lactin test should be available to exclude from evalua-
tion conditions associated with hyperprolactinemia.
a seizure are not standardized and different authors
have used different cutoffs. Despite these limits, serum
prolactin assay is a useful adjunctive test for the differ-
entiation ofGCTSorCPS from PNES (Chen etal.,2005)
Data on SPECTin PNES are limited. The few studies are
small and usually retrospective, and often lack a control
group. Moreover, timing and method of analyzing the
examinations are not standardized, probably affecting
the results. When available, the specificity of a
negative SPECT study in PNES was 70–73%, sensitivity
64–80% (Varma et al., 1996; Ettinger et al., 1998).
Subtraction ictal SPECT coregistered to MRI
(SISCOM) has been used in cases of probable PNES
when other procedures were insufficient for diagnosis
(Neiman et al., 2009). As expected, SISCOM demon-
strated no localizing or lateralizing hyperperfusion or
hypoperfusion changes in 85% of PNES cases. Sensitiv-
ity was 70%. The authors also reported that, combining
their data with those of the previous studies, 89% of pa-
tients with PNES had a negative SPECT examination.
Therefore, SPECT scans can help in diagnosing chal-
lenging cases of PNES.
There are few evidence-based reports on the treatment
of PNES (Baker et al., 2007; Brooks et al., 2007). In
one large study 71 of 187 patients (38%) became
“spell-free” just with communication of the diagnosis
(McKenzie et al., 2010). The way that the diagnosis is
presented is of paramount importance (Shen et al.,
1990). The data on this topic thus far support that early
diagnosis and intervention are important to avoid PNES
1990; Betts and Boden, 1992; Mace and Trimble, 1996).
Once the diagnosis is established, usually by video-
EEG, the patient can be told that there is “good news”
regarding the seizures. These events are not due to ab-
normal or harmful brain activity and are not the result
of brain damage. The importance of knowing what
ing. In a supportive manner, the patient should be in-
formed that the episodes are not volitional and no one
believes that they are “faking.” The patient should be
told that these episodes usually have a psychological ba-
sis despite the patient’s lack of awareness of coexistent
stress or emotional upset. This serves to dispel some of
the common arguments presented by patients or their
families that these seizures are absolutely not psycho-
logical. Withthis information thepatient can betoldthat
they will not require potentially harmful antiepileptic
medications. The use of AEDs by patients with PNES
is common, and elimination of these medications and
their side-effects is a critical part of the treatment plan
(Hantke et al., 2007). The patient should be reassured
that he or she can continue to work together with
PSYCHOGENIC NONEPILEPTIC SEIZURES287
the physician on eliminating these spells so that the
can then be told that further help may be needed by a
ing with upsetting emotions, a frequently discovered
cause for these events. The power of suggestion can
be used as part of the cure. The patient should be told
that these spells may resolve spontaneously and that
they can take an active role in the resolution process
by consciously trying to abort the event when they feel
one is coming on. The patient should be advised not to
become discouraged if breakthrough events occur.
Healthcare utilization after video-EEG diagnosis re-
duced emergency room visits by 97%, outpatient visits
by 80%, and diagnostic tests by 76% in the short term
(Martin et al., 1998).
Comorbidities, such as major depressive disorder,
PTSD, personality disorder, trauma, and family disor-
ders, should be diagnosed and treated. Any suicidal risk
high prevalence of comorbid epilepsy and this should be
evaluated thoroughly even if current events are clearly
nonepileptic. The family should be advised on how to
manage events after discharge. It is often helpful to
show patients or family the video of the events to im-
prove insight and recognition. Visits to the emergency
room should be avoided as they can reinforce dysfunc-
tional seizure-related beliefs and behaviors. Healthcare
or inappropriate treatment; practitioners who see these
must make decisions based on only history or fragmen-
tary descriptions from family, nurses or caregivers. The
follow-up should include the neurologist, psychiatrist,
and psychotherapist, in close collaboration with an epi-
ularly can reduce the need for the patient to produce
more or severe symptoms to get medical attention, re-
duce emergency room admission or inappropriate
testing, and reduce patient feelings of abandonment.
Treatment is often limited, however, by the resources
available to the team, and the team’s experience. Na-
tional resource centers for PNES treatment and referral
plore trauma, and identify emotions raised by trauma.
The symptoms can be understood, for instance that
shaking represents a release of energy, unresponsive-
ness represents a “freezing” response, and falling can
represent “sham death.” Group therapy with a psycho-
dynamic focus reduced PNES in 12 patients (Barry
et al., 2008). However, some patients require alternate
methods because they are poor candidates for insight-
oriented therapy due to borderline intelligence, lack of
motivation or introspection capabilities, important sec-
ondary gains, or a tendency for behavioral acting out.
Cognitive behavioral therapy (CBT) can address
avoidance behavior, deal with the sequelae of prior trau-
matic experiences, and reduce health and symptom anx-
are viewed as a learned maladaptive behavior that is
reinforced by the environment. The inappropriate be-
havior (i.e., PNES) is no longer rewarded or may even
be punished. An advantage of this method is that neither
normal intelligence nor insight is necessary for success.
A disadvantage is that behavioral therapy relies on con-
trolling environmental conditions, which may be impos-
sible to monitor. In the LaFrance study, 11 of 17 patients
were seizure-free at the end of a 12-week course of
CBT. CBT and family therapy can improve quality-of-
life measures (LaFrance, 2008; LaFrance et al., 2008,
2009a, b). CBT reduced PNES by 20% after a 4-month
course in a group of 64 patients randomized to CBT or
standard medical care (Goldstein et al., 2010).
Family therapy is beneficial in many cases because
PNES may largely result from problems related to the
dysfunctional family (LaFrance and Bj?rnaes, 1993).
In this form of therapy, the dysfunction of the family,
rather than the individual patient, is emphasized. Family
therapy can follow different approaches including psy-
Biofeedback was helpful at preventing events in one
adolescent (Pop-Jordanova et al., 2005). Eye movement
desensitization and reprocessing (EMDR) can reduce
PNES, particularly if there is a history of PTSD or an
abusive experience (Chemali and Meadows, 2004). Hyp-
nosis may also have an adjunctive role (Glenn and
Simonds, 1977; Miller, 1983), especially if the PNES is
part of a dissociative disorder (Kluft, 1992).
Psychiatric medications may be indicated for Axis I
(SSRIs) have been used for somatization or dissociation
(O’Malley et al., 1999) with some success. A pilot ran-
domized controlled trial of sertraline in 38 patients with
PNES showed seizure reduction of 45% from baseline
compared with 8% in the placebo group, although the
result was not statistically significant (LaFrance et al.,
2010). Neuroleptics and propranolol can be effective
for severe dissociative disorders (Soloff, 1998).
tion of approaches is probably the most beneficial for
improvement. Treatment should not simply emphasize
removing maladaptive PNES behavior, but should also
288P. WIDDESS-WALSH ET AL.
focus on learning new coping skills and removing sec-
ondary gains. If PNES persist, therapy should be re-
Limited information is available on the outcome after
diagnosis and treatment of PNES. Many studies have
a short follow-up, and a considerable proportion of
the patients are lost to follow-up. Moreover, few studies
included social issues and psychiatric comorbidities as
measures of outcome, although these are more strongly
associated with a poor quality of life and disability than
the seizures themselves (Walczak et al., 1995; Reuber
et al., 2005). Rates of remission have ranged from
16% to 51% in different adult series (Walczak et al.,
1995; Ettinger et al., 1999c; Jongsma et al., 1999; Kanner
et al., 1999; Reuber et al., 2003a; Thompson et al., 2005;
Arain et al., 2007; Bodde et al., 2007; O’Sullivan et al.,
2007) and are much higher (up to 82%) in children and
adolescents (Gudmundsson et al., 2001). An improve-
ment in symptoms has been reported in 55–80% of pa-
tients (Walczak et al., 1995; Ettinger et al., 1999b;
Jongsma et al., 1999).
Seizure reduction was related to an improvement
in different levels of psychological function: reduction
in psychological distress and in feelings of dissatisfac-
tion and passive avoidant behavior, a more active atti-
tude towards social contact, a reduction in dissociative
features such as amnesia, and an increase in self-control
(Bodde et al., 2007). However, at follow-up, unemploy-
ment, dependence on social security, and psychiatric
comorbidities are often still present irrespective of sei-
zure remission (Reuber et al., 2003a, 2005; Arain
et al., 2007). The mean proportion of patients living in-
dependently in a range of outcome studies was 43%
(Reuber et al., 2005).
Favorable predictors of outcome are younger age
at onset and diagnosis, higher IQ, educational and
social status, being accompanied to the first clinic visit,
attacks with less dramatic features or motionless
spells, alowerlevelofnegativism (self-avoidantbehav-
ior), fewer additional somatoform complaints, lower
dissociation scores, and lower scores of the personality
dimensions “inhibitedness,” “emotional dysregula-
tion,” and “compulsivity” (Selwa et al., 2000; Reuber
et al., 2003a; Arain et al., 2007; Bodde et al., 2007).
In children and adolescents favorable predictors are
younger age at presentation, female sex, having more
types of seizure (possibly because they allow an earlier
suspicion of PNES), and not receiving both inpatient
and outpatient treatment (possibly reflecting minor se-
verity) (Gudmundsson et al., 2001).
Longer duration and older age at PNES onset and di-
agnosis are associated with poor outcome, as are higher
to Kanner et al. (1999), a history of chronic abuse, recur-
rent major depression, dissociative and personality dis-
1993; Walczac et al., 1995; Kanner et al., 1999; Selwa
et al., 2000; Reuber et al., 2003a). Head injury was
associated with poor long-term outcome, including
long-lasting disability, despite being relatively mild
(Westbrook et al., 1998). Semiological features associ-
gue biting, and incontinence (Selwa et al., 2000; Reuber
et al., 2003a). Other negative prognostic factors include
abnormal findings on MRI (Kanner et al., 1999) and re-
current pseudostatus (Reuber et al., 2003a).
Comorbid epilepsy, if present, does not significantly
affect outcome (Walczak et al., 1995; Jongsma et al.,
1999; Kanner et al., 1999; Reuber et al., 2003a).
It is difficult to assess the role of therapy, which has
been associated with improved PNES outcome in sev-
eral, but not all, outcome studies, also due to the fact
that presentation of a diagnosis is sometimes sufficient
and removes the need for any specific intervention to
the individual patient. Acceptance of psychotherapy
ranges from 12.5%to47%(Arainet al.,2007;O’Sullivan
et al., 2007), and is related to acceptance of diagnosis,
the most important step towards a favorable outcome
both in adults and in children and adolescents. In this
sense, a definitive and expert diagnosis, good and re-
spectful information, and a specific educational ap-
proach are of great value (Gudmundsson et al., 2001;
Thompson et al., 2005; Bodde et al., 2009).
Thesignificance ofPNES should not beunderestimated.
These episodes can significantly impair quality of life,
and lead to unnecessary therapies and invasive diagnos-
tic studies that can be dangerous and expensive. Unrec-
serious consequences, mainly due to iatrogenic injury,
and can be fatal (Reuber et al., 2004). Early detection
utilizing video-EEG monitoring can avoid misdiagnosis
and direct the patient towards appropriate care.
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