The Etiology of

Psychogenic Non - Epileptic

Seizures : Toward
a Biopsychoso c ial Model
Markus Reuber, MD, PhD, FRCP

KEYWORDS
 Psychogenic non-epileptic seizures  Conversion
 Dissociation  Epilepsy  Pseudoseizures  Etiology

Many paroxysmal neurologic disorders cause impairment of consciousness, but most

patients are diagnosed with one of three: epilepsy, syncope, or psychogenic nonepi-
leptic seizures (PNES). In one study, a neurologist was able to establish a diagnosis in
87% of 158 consecutive patients newly referred to her clinic, with 43% having
epilepsy, 25% syncope, 12% PNES, and 7% other disorders.1 The authors of another
study, which reportedly captured all patients experiencing a blackout who first pre-
sented to a neurologist, emergency room, or primary care physician, believed that
57.4% had epilepsy, 22.3% syncope, and 18.0% PNES.2
Although PNES are therefore among the most important differential diagnoses of
epilepsy, they are not well understood, and are therefore often not well treated.3–5
Diagnostic delay, the mistreatment of PNES as epilepsy (or less commonly of epilepsy
as PNES), and poor communication between patients and doctors remain common-
place. Neurologists have a crucial role in explaining the disorder to patients.
PNES are episodes of altered movement, sensation, or experience resembling
epileptic seizures, but not associated with ictal electrical discharges in the brain.
They are a behavioral response to mental, physical, or social distress characterized
by a temporary loss of control. The most common semiology involves excessive
movement of limbs, trunk, and head resembling tonic–clonic seizures. PNES with stiff-
ening and tremor, or atonia and unresponsiveness also occur.6
Most experts assume that PNES are an unintentional manifestation of emotional
distress. They are called ‘‘dissociative convulsions’’ (F44.5) in the International Classi-
fication of Diseases (ICD-10) and ‘‘conversion disorder with seizures or convulsions’’

Funding support: The author did not receive any funding for this review. There is no conflict of
interest to declare.
Academic Neurology Unit, University of Sheffield, Royal Hallamshire Hospital, Glossop Road,
Sheffield, S10 2JF, UK
E-mail address: [email protected]

Neurol Clin 27 (2009) 909–924

doi:10.1016/j.ncl.2009.06.004 neurologic.theclinics.com
0733-8619/09/$ – see front matter ª 2009 Elsevier Inc. All rights reserved.
910 Reuber

(300.11) in the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR).

However, experts recognize that PNES are occasionally simulated (in malingering
and factitious disorders).7
PNES have been the subject of many recent review articles, which have focused on
the differential diagnosis,8 the process of making the diagnosis,9,10 the relationship
with neurologic pathology,11 the management by neurologists,12 and further treatment
by psychotherapists.13–16 This article focuses on developing an explanatory model for
PNES that integrates the results of a wide range of studies. It is aimed at general
neurologists, psychiatrists, and clinical psychologists who would like to gain a better
understanding of a complex disorder. Reflecting the author’s expertise in the area, it
focuses on adults.

ETIOLOGIC FRAMEWORK

PNES occur in a heterogeneous patient population. No single mechanism or even

contributing factor has been identified that is necessary and sufficient to explain
PNES in all patients. PNES are best understood based on the biopsychosocial, multi-
factorial etiologic model outlined in Fig. 1.
In most patients several interacting causes can be identified. Predisposing factors
increase vulnerability to the development of PNES in later life. Precipitating factors
occur over the days to months before the onset of seizures and seem to cause
PNES to start. Perpetuating factors make it harder for patients to regain control of
seizures or aggravate the problem once seizures have started. Triggering factors
seem to start recurrent seizures within seconds or minutes. Even if one factor seems
to play a predominant role in a particular patient, other factors are likely to have
contributed and should not be ignored.

PREDISPOSING FACTORS
Genetic factors
The relationship between inherited factors or childhood antecedents of a particular
disorder such as PNES and its later development is typically indirect or probabilistic.
Many other factors codetermine whether PNES will develop in an individual. Little is
currently known about specific genetic factors conferring vulnerability or resilience

Predisposing Precipitating Perpetuating

Early Stressful
experience experience /
(abuse, Conflicts,
Avoidance, isolation,
neglect) dilemmas
distress, anger
anxiety,
Genetic
Usual depression
constitution
(vulnerability / Functioning PNES misattributions,
resilience) (vulnerable state) sick role,
financial disincentives,
Later misdiagnosis,
Physical or
experience mistreatment
mental health
(interpersonal
symptoms /
problems /
models
models)

Fig. 1. Etiology of psychogenic nonepileptic seizures: a multifactorial model.

 Psychogenic Nonepileptic Seizures 911

to adverse life events or the development of mental disorders.17 However, large

studies show that these factors exist, and that they are not always active from birth
but may exert their effects during later periods of development.18,19
The most obvious genetically determined risk factor for the development of PNES is
female gender. Lesser20 examined the sex distribution in 21 studies and found
descriptions of 734 women and 250 men who had PNES. Similar to the sex distribution
in other somatoform disorders,21 women are therefore three times more likely to
develop PNES than men. This gender difference is not fully explained by readily recog-
nizable experiential differences between men and women, such as the higher rates of
sexual abuse experienced by women.22 Similar to other forms of somatization, PNES
may be an acquired and culturally determined predominantly female expression of
helplessness or anger.23,24 However, more direct biologic reasons may exist as to
why women are more likely than men to develop PNES.

Childhood Abuse and Neglect

The relationship between childhood sexual abuse (CSA) and PNES has received
particular attention since Freud25 highlighted a possible link. Although CSA is only re-
ported by a minority of patients who have PNES, it is a good example of the complex
relationship between a distant antecedent and an adult manifestation of psychopa-
thology (see Case A). The largest study comparing CSA in groups of patients who
had PNES (n 5 71) and those who had epilepsy (n 5 140) found significantly higher
rates of both sexual (24.0% versus 7.1%) and physical (15.5% versus 2.9%) childhood
abuse in those who had PNES.26 Although the etiologic relevance of CSA for PNES is
not undisputed, these results have been replicated in most other studies of this
issue.27,28
As with other psychiatric conditions linked to CSA, the adverse childhood experi-
ence probably must combine with other factors to lead to PNES in later life. Although
the effects of CSA can also be reduced by optimal support from at least one parent,29
several recent studies have identified a range of different mechanisms that may link
CSA or physical abuse and neglect in early life with PNES in adulthood. Holman
and colleagues30 showed that (unlike controls affected by epilepsy) patients who
have PNES often have a fearful attachment style, making secure interpersonal
relationships harder for them to develop and maintain in adulthood. The presence of
a fearful attachment style was correlated with a history of adverse experience in early
life.
Salmon and colleagues31 showed that CSA is often associated with childhood
physical abuse, neglect, and a dysfunctional family environment. Patients who had
PNES and reported CSA were also more likely to report adult sexual abuse, suggest-
ing that a history of CSA can be a marker of more extensive and pervasive adverse
experience. Bewley and colleagues32 found that more than 90% of patients who
had PNES scored in the abnormal range on a standardized measure of alexithymia,
meaning that they had difficulties feeling or perceiving emotions. Others have shown
that etiologic links exist between trauma and deprivation in early life and alexithymia in
later life.33
Alexithymia is not the only form of abnormal emotional reactivity related to CSA.
Individuals who have a history of CSA may also experience sudden and extreme
emotional fluctuations in adulthood.34 In two studies using personality inventories,
the largest subgroups of patients who had PNES reported experiencing this form of
emotional dysregulation,35,36 with borderline personality disorder (which is character-
ized by emotional dysregulation) overrepresented.37,38
912 Reuber

Furthermore, Bakvis and colleagues39 showed that patients who have PNES and
a history of sexual abuse have a heart rate variability than healthy controls. In a masked
emotional Stroop test, comparing color-naming latencies for backwardly masked
angry, neutral, and happy faces, patients who had PNES showed a positive attentional
bias for angry faces, suggesting that their previous adverse experience had produced
measurable changes in (preconscious) information processing. These findings
suggest that patients with PNES who have experienced sexual abuse remain in
a persistently hypervigilant state.
The fact that sexual abuse (including CSA) is likely to be relevant to PNES is also
supported by the finding that this history shapes the way in which PNES present.
Those who experienced previous sexual abuse developed their seizures earlier, had
more anxiety prodromes or ictal flashbacks, more severe seizures (with more frequent
injuries, incontinence, and ‘‘pseudostatus’’), and more seizures from apparent sleep
than other patients who have PNES.22

Physical Factors
The author’s understanding about the mechanisms through which apparently physical
or biologic factors such as epilepsy or learning disabilities predispose to the develop-
ment of PNES is limited.11 Structural or functional brain abnormalities are found more
commonly in patients who have PNES than in the general population.40–42 The
percentage of patients found to have concurrent epilepsy has varied from 3.6% to
58% in different PNES series,43 but the risk for developing PNES is increased in
patients who have epilepsy.
In the author’s own series, the clinical history suggested additional epilepsy in 119 of
329 patients who had PNES (36.2%).43 Similar to other large case series, the develop-
ment of epileptic seizures almost always preceded the manifestation of PNES.44
However, the mechanisms through which epilepsy predisposes to PNES remain
uncertain. In a study comparing patients affected by epilepsy (n 5 90) and those
affected by epilepsy and PNES (E1P, n 5 90), no particular epileptologic features
that made the development of comorbid PNES more likely could be identified. Patients
in the E1P group were more likely to have neuropsychological impairment and low IQ
(see Case B).43
Epilepsy may contribute to the risk for developing PNES not only through biologic
mechanisms but also because the experience (or observation) of epileptic seizures
may provide an opportunity for model learning (see Case C).45 Studies showing that
patients who have PNES are more likely to report a family history than those with
epilepsy and are more likely to have witnessed someone else have a seizure before
developing their own seizure disorder offer some support for this idea.46,47

PRECIPITATING FACTORS
Adult Life Events
Although patients will often state initially that their seizures started ‘‘out of the blue’’
and without any identifiable cause, significant precipitants for the development of
PNES can often be identified. One small study comparing patients who had recent-
onset PNES (n 5 20) with those who had recent-onset epilepsy (n 5 20) found that
the PNES group reported more (typically adverse or traumatic) life events over the
12 months before the onset of the seizures than the epilepsy group.48 The authors
of one descriptive study found precipitating traumatic life events in all but 9% of
patients.49
 Psychogenic Nonepileptic Seizures 913

Factors that have been described as precipitating PNES include rape,50–52 injury,50,53
‘‘symbolic’’ traumatic experience in adulthood after childhood abuse,50,51,54 death of or
separation from family members or friends,50,55 job loss,49,50 road traffic and other
accidents,49,50 giving birth,56 minor surgical procedures,57 earthquakes,58 relationship
difficulties,49,50 and legal action.59 In women, precipitating events are most commonly
linked to sexual abuse (see Case A). In men, loss of employment or enforced role
changes are more important (see Case D).49,50,60 In older people, physical illness is
the most common identifiable precipitant.61
Although approximately 75% to 90% of patients who have PNES report a history of
significant trauma,27,50 and some evidence shows that a history of trauma or adverse
life events is more closely associated with the development of PNES than of other
unexplained neurologic symptoms,50,62 these potential precipitants are clearly not
specific for the development of PNES.
One study showed that in 76% of patients the precipitating event was only signifi-
cant in the context of a history of other trauma or previous or ongoing conflict (see
Case D).49 Another study based on a detailed analysis of 14 video-recorded patient
interviews showed that in 13 of 14 cases, any precipitating events seemed less rele-
vant to the cause of the seizures than the forced choices or unspeakable dilemmas
forced on patients by family or social circumstances.54
Two studies comparing patients who had PNES with those who had epilepsy found
that PNES were not so much explained by stressful life events (which were reported
equally as often by patients who had epilepsy) as by the use of less-effective coping
mechanisms.63,64

Psychopathology
Clinical experience suggests that PNES commonly start in association with or during
a period of exacerbation of another mental disorder. A lifetime history of other somato-
form or dissociative disorders is found in more than 50% of patients who have PNES.
Anxiety or psychotic and bipolar disorders are less common but are found more
frequently in patients who have PNES than in the general population.38,53 Many
patients who have PNES have features of posttraumatic stress disorder (PTSD) and,
according to a range of (small) studies, 22% to 100% of patients who have PNES fulfill
the DSM-IV criteria for PTSD.65

Physical Factors
In some patients (at least potentially), physical precipitating factors can be identified.
PNES have been observed after epilepsy surgery and other neurosurgical procedures.
Although some studies suggest that patients who have right-sided brain abnormalities
were at particular risk,42,66 this was not confirmed by other studies.40,67–69 A history of
head injuries is given by 24% to 65% of patients.70–72 In most cases, investigations fail
to show any physical sequelae of injury, although PNES have also been reported more
after traumatic brain injury.73 PNES may also be facilitated by antiepileptic drugs
(AEDs) or AED intoxication (see Case C).74

TRIGGERS

Clinical experience suggests that PNES often also have more immediate triggers.75
PNES have been observed in patients emerging from general anesthesia.57,67,76–78
Video-EEG studies with intracranial electrodes have shown that PNES can develop
from focal epileptic seizures79 or even EEG-documented sleep.80
914 Reuber

Much more commonly, however, an episode of apparent loss of consciousness is

directly preceded by physical symptoms of arousal (eg, dry mouth, racing heart,
increased sweating, hand tremor, shortness of breath), suggesting panic as a trigger
(even if the patient was unaware that the symptoms were associated with anxiety) (see
Case D).81 Some patients describe PNES when exposed to a sudden sensory stim-
ulus, or during sensory overload when many things seemed to occur simultaneously.
Not uncommonly, an increasing number of different sensations (eg, flashing lights,
stepping into dark rooms, sudden noises) seem to trigger seizures as the disorder
becomes more chronic (see Case A). Many patients seem to become so weary of trig-
gering their seizures that they begin to make great efforts to avoid all emotional fluc-
tuations, perhaps best described as emotion phobia. In keeping with this observation,
a study comparing patients who had PNES, those who had epilepsy, and healthy
controls found evidence of increased fear sensitivity in the PNES group.82
Patients may also become highly sensitized to (and avoidant of) physical sensa-
tions, such as mild presyncopal symptoms, perhaps as a consequence of an initial
blackout fully explained by syncope. Unfortunately, whether an initial blackout may
have been truly syncopal is difficult to determine because the semiology of PNES
can be hard to distinguish from that of syncope.83,84 The phenomenon of PNES
directly arising from simple partial (epileptic) seizures observed with video-EEG could
be explained by a similar phobic/dissociative mechanism (although different explana-
tions have also been proposed).85 This mechanism could also explain why some
PNES are triggered by manifestations of psychopathology, such as visual flashbacks
in PTSD or hallucinations in psychotic disorders.

PERPETUATING FACTORS
Avoidance
Once PNES have developed, it is usually possible to identify perpetuating factors that
inhibit ability to gain control over seizures. Perhaps the most important of these is
anxiety/avoidance. In a study describing etiologic factors in patients who had PNES
and other functional symptoms, the authors identified anxiety (including health anxiety
or hypochondriasis) as a relevant perpetuating factor in more than 50% of patients in
both groups.50
Comparative studies have shown that patients who have PNES feel more strongly
than healthy controls or those affected by epilepsy that their health is determined
by factors beyond their own control, and that they have a stronger tendency to escape
or avoid dealing with problems (see Cases B and D).86,87 Perhaps persistent avoid-
ance causes patients who have PNES to be less likely to consider negative life events
relevant to the cause of their seizures than patients affected by epilepsy,86 although
they report these adverse experiences more commonly.48 Avoidant behavior and
the failure to consider life events as relevant may also explain why nearly 50% of
patients who have PNES (or other functional neurologic disorders) fail to engage in
psychotherapy.88
Avoidant behavior may even be apparent in the communication between doctors
and patients. Several studies have shown that if the doctor adopts a receptive stance,
avoids early interruption, and opens the encounter with an open question (eg, ‘‘how
can I help you today?’’ or ‘‘what was your expectation when you came to see
me?’’), patients who have epilepsy will focus on their subjective seizure experiences
without any further prompting.89–91 In contrast, patients who have PNES and who
are approached in this way avoid talking about seizure symptoms and focus on the
situations in which their seizures occur or the consequences.92
 Psychogenic Nonepileptic Seizures 915

Isolation and ‘‘sick role’’

Perhaps the increasing avoidance of potential seizure triggers and normal social inter-
action causes patients to become isolated and their social contact group to
contract.93 Some become angry,94 and a substantial number (22% in the author’s
study) become depressed.50 Many develop additional physical symptoms, such as
fatigue or pain (see Cases A and D),95,96 with the number of additional symptoms
correlating to the degree of emotional distress and severity of PNES disorder.97
Many patients become disabled and dependent on others. One study showed that
69% of 84 patients were employed at the start of their seizure disorder, and only 20%
were still working by the time they were referred for video-EEG.98 Four years after
diagnosis, 56.4% were receiving health benefits.99 In fact, two studies suggest that
patients who have PNES are more likely than those who have similarly disabling
epileptic seizures to be receiving health-related benefits, providing them with a finan-
cial disincentive to getting better.100,101 For some patients the ‘‘sick role’’ becomes an
important part of their identity (see Cases A, B, and D).24
The fact that patients and doctors commonly misattribute PNES to physical causes
(especially epilepsy) means that the psychodynamic causes are not addressed. Misdi-
agnosis rates between 5% and 50% have been reported in different settings.102–105
Patients’ misplaced belief that there must be something physically wrong may be
strengthened by repeated cycles of investigation and the prescription of more and
more drugs (see Case D).106,107
In a study describing more than 300 patients, the authors found that the diagnosis of
PNES was delayed by a mean of more than 7 years after the manifestation of seizures
and that three quarters of the patients had been treated inappropriately with AEDs by
the time the correct diagnosis was made.108 More than 20% of these patients had at
least one hospital admission with prolonged PNES (‘‘pseudostatus’’). Repeated
admissions with prolonged PNES can lead to significant iatrogenic harm, including
death.109,110 Even patients who have been formally diagnosed with PNES commonly
report being confused by their physicians’ explanations of their diagnosis.93,111

SUMMARY

This account shows how a wide range of nonspecific factors collude to cause PNES,
which is a very particular manifestation of psychopathology. The case reports show in
what complex ways a predisposing traumatic experience, such as CSA, can be inti-
mately linked to precipitating and perpetuating experiences in later life, or how one
factor, such as comorbid epilepsy, can predispose to, precipitate, and perpetuate
PNES. Although considering the cause of PNES in terms of the etiologic framework
described in this article can help clinicians understand their patients,75 and perhaps
to communicate the diagnosis more credibly,112 the identification of particular etio-
logic factors is not directly linked to specific interventions. Often the interaction of
different factors is more readily addressed with psychotherapy than the specific
factors themselves.
The fact that current understanding of the cause of PNES is limited to such
a complex model of interacting etiologic factors, and that no specific pathogen has
been identified, does not mean that the cause of the disorder remains unknown. In
clinical practice, psychodynamic factors explain the presence of PNES to the satisfac-
tion of experienced psychologists or psychotherapists in 95% of cases,50,113 which
means that individually adapted variants of psychotherapy are the preferred treat-
ment.75,114,115 However, other forms of intervention may also prove useful in the
future. The biologic underpinning of an increased vulnerability to PNES is just
916 Reuber

beginning to be understood.39 This work may enable better targeted medical interven-
tions to be developed in the future.

APPENDIX: CASES
Case A
History
Mrs. A was referred to a specialist epilepsy clinic by a general neurologist at 55 years
of age. Her seizures did not respond to several antiepileptic drugs (AEDs). She
described blank spells for which she had no memory (duration: seconds to minutes;
onset: 36 years of age; frequency: daily) and episodes involving loss of conscious-
ness, shaking, incontinence, and tongue biting (duration: 5 to 20 minutes; onset: 36
years of age; frequency: two per week).
She had a history of medically unexplained fatigue, which caused her to use a wheel-
chair for 2 years (19 years of age); depression and a deliberate medication overdose
(31 years of age); asthma (33 years of age); and a hysterectomy for dysfunctional
bleeding (35 years of age). Her first blackout occurred during an episode of shortness
of breath and anxiety triggered by an argument with her partner. An interictal EEG
showed a ‘‘very considerable amount of sharp wave activity’’ with a ‘‘possible left-
sided sharp wave focus’’ amounting to ‘‘strong support for the diagnosis of epilepsy.’’
AED treatment was started, but her family doctor never observed any relationship
between changes in her drug treatment and seizure frequency, although he noticed
that seizures got worse during times of ‘‘social difficulty.’’
When she was 36 years old, she was admitted to the hospital after a seizure left her
with a weak and stiff left arm and walking difficulties. The neurologic symptoms were
considered functional and resolved without treatment after 3 months. The timing of
these symptoms coincided with child custody proceedings.
Further emergency admissions occurred with prolonged seizures. When she was 46
year old, she had another admission with left-sided weakness. An MRI scan of the
head showed no abnormalities. Emergency admissions continued as a result of
seizures.
When she was 54 years of age, a typical convulsive seizure (without epileptic EEG
changes) was captured during an admission for video-EEG. The interictal EEG
showed nonspecific changes in the left temporal leads. After the diagnosis of psycho-
genic nonepileptic seizures was discussed with the patient, she stopped having
seizures completely for 1 year, although her AEDs were withdrawn.
Her blank spells later returned (frequency: fewer than one per week), but did not
cause much anxiety or disability, and 3 years later she remains disabled by medically
unexplained facial and joint pains. A state-funded caregiver takes her out once
a week. Twenty sessions of psychotherapy have revealed sexual abuse by several
family members starting in childhood, and followed by sexually and physically abusive
relationships in adulthood with a range of partners. Seizure exacerbations often
seemed to be triggered by close contact with her son (who looked like one of her
abusers) or her daughter (who was abused by a neighbor when the patient was too
unwell to look after her).

Formulation
Predisposing factors: Childhood sexual abuse and neglect; somatization disorder with
inappropriate medical and no psychological interventions; attachment problems with
exploitative and abusive relationships in adulthood.
Precipitating factors: Ongoing sexual abuse and emotional exploitation; court
proceedings.
 Psychogenic Nonepileptic Seizures 917

Perpetuating factors: Inappropriate AED treatment; establishment of codependent

relationship with new (‘‘nice’’) partner; constant reminders of previous abuse through
ongoing contact with children; other functional symptoms; perceives self as chroni-
cally disabled; receives long-term disability benefits.
Triggers: Flashing lights; sudden noises; seeing son or daughter; flashbacks of
abuse.

Case B
History
Mr. B presented to a specialist epilepsy clinic at 56 years of age. He was a nursing home
resident with a lifelong history of epilepsy and severe learning disability. He was able to
feed himself with a spoon but unable to communicate verbally, was doubly incontinent,
and had recently become unable to walk unaided. Mr. B had stopped undergoing
regular neurologic follow-up 5 years previously. His antiepileptic drugs (AEDs)
(phenytoin, 500 mg/d; carbamazepine, 1000 mg/d; phenobarbitone 180 mg/d) had
not been altered since.
He experienced three different seizure types:
(1) Blank spells with head flopping to one side and drooling. The patient could slap
himself on head or face when disturbed (duration: 5–10 minutes; onset: uncertain;
frequency: several per week).
(2) Attack during which the patient would throw himself on floor, banging his head
repetitively until it bled (duration: 5–10 minutes; onset: recent; frequency: several
per week).
(3) Sudden collapse, rigidity, violent shaking followed by limp unresponsive state
with recovery over 10 minutes (duration: 5–10 minutes; onset: always; frequency: 2
per year).
Examination showed the facial appearance of fragile-X (later confirmed with genetic
testing), downbeat nystagmus, refusal to walk, normal tone, tendon reflexes, and
plantar responses.
Diagnosis: Severe learning disability and epilepsy (seizure type 3) secondary to
fragile-X. Additional psychogenic nonepileptic seizures (PNES) facilitated by antiepi-
leptic drug toxicity.
Treatment: Withdrawal of phenytoin followed by withdrawal of phenobarbitone and
introduction of levetiracetam. Encouragement of care staff to ignore PNES and reward
appropriate interpersonal behavior.
Outcome: Type 1 and 2 seizures stopped when phenytoin was discontinued,
walking unaided. At 2 years later, he experienced three type 3 seizures per year.

Formulation
Predisposing factors: Epilepsy, AED treatment, communication difficulties caused by
learning disabilities.
Precipitating factors: AED toxicity.
Perpetuating factors: Failure to recognize PNES, inappropriate response to seizures
by caregivers.
Triggers: ‘‘Not getting his own way,’’ frustrations.

Case C
History
Mrs. C was referred to a specialist epilepsy clinic at 41 years of age for consideration
of epilepsy surgery. From 3 years of age, she experienced seizures that occurred with
a warning, allowing her to sit down (but which the patient was unable to recall);
918 Reuber

unresponsiveness; drooling of saliva; chewing and fumbling movements; shuddering

of arms and legs; and gradual recovery after 5 minutes, followed by confusion for 30
minutes. Seizures continued at a rate of two to three per month despite treatment with
different AEDs.
At 40 years of age, the seizure frequency suddenly rose to ten per month. The
patient ensured that she was with her mother 24 hours a day. An MRI scan of the
head showed left mesial temporal sclerosis. Further history in the epilepsy clinic sug-
gested that eight of ten attacks had a different semiology (slumping to the ground with
closed eyes, unresponsiveness, appearing asleep for 10 to 20 minutes followed by
immediate recovery). The new seizure type had started 1 year after she found her
husband had died in bed beside her, and days after her son married and moved out.
Video-EEG captured one nocturnal complex partial seizure with left temporal
seizure onset and one PNES manifesting as a limp, unresponsive state. PNES stopped
after two sessions with a clinical psychologist. The patient underwent a left selective
amygdalohippocampectomy 2 years later. All seizures have been controlled for more
than 1 year.

Formulation
Predisposing factors: Epilepsy since childhood; fostering a codependent relationship
with the patient’s mother; chronic anxiety disorder.
Precipitating factors: Traumatic discovery of husband’s death; loss of husband’s
support; conflict between perceived abandonment by son and unwillingness to stand
in the way of son’s happiness.
Perpetuating factors: Ongoing epilepsy; failure to recognize PNES; reestablishment
of codependent relationship with mother.
Triggers: Being left alone; panic attacks; flashbacks.

Case D
History
Mr. D presented to a specialist epilepsy clinic at 46 years of age. His symptoms had
started 5 years previously. Before his first blackout, he had come under increasing
pressure as an information technology project manager. His memory seemed poor
and he was taking increasingly more notes. His first blackout occurred at a business
meeting. He struggled to get his words out although he knew what he wanted to say.
He could not recall the names of the people around him and felt hot and tired. He
developed blurred and double vision and collapsed after these symptoms had been
present for 4 to 5 hours. He looked like he was asleep but lost control of his bladder.
No shaking or injury was present. He recovered after 1 minute. He returned to his hotel
room on his own but had no recollection of doing so. The next day he felt confused and
experienced chest pain. He went to the hospital for a checkup, where a doctor noticed
a droopy left eyelid.
He was unable to return to work for 6 months because of persisting fatigue. His
attempt to return to work on a part-time basis failed because of fatigue, double vision,
and further collapses (3–4 per year). Treatment for myasthenia was started after an
equivocal edrophonium test. Further investigations for myasthenia failed to confirm
this diagnosis. Other tests for muscle diseases were unremarkable. In 20 sessions
of psychotherapy, the patient was able to link his driven work habits and tendency
to avoid emotional experiences with his symptoms. He learned to pace himself and
recognize his limits. He stopped having blackouts. Pyridostigmine treatment was
stopped without a significant worsening of symptoms, but withdrawal of steroid treat-
ment (prednisolone) below 5 mg/d caused a marked increase in lethargy.
 Psychogenic Nonepileptic Seizures 919

Formulation
Predisposing factors: Strict and competitive but emotionally deprived upbringing with
awards only for achievements; tendency to avoid emotional challenge in his own
family through excessive commitment to work.
Precipitating factors: Exhaustion; inability to manage work demands to own satis-
faction; inability to recruit support; panic attacks.
Perpetuating factors: Other functional symptoms (with chronic fatigue offering the
opportunity to avoid emotional challenges); unhelpful medical tests and treatments;
delayed psychological intervention.
Triggers: Fatigue; overactivity; demanding social situations.

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