Focus (Am Psychiatr Publ). Fall 2016; 14(4): 422–431.

PMCID: PMC6519589
Published online 2016 Oct 7. doi: 10.1176/appi.focus.20160020: 10.1176/appi.focus.20160020 PMID: 31975822

Clinical Approaches to Psychogenic Nonepileptic Seizures

Sepideh N Bajestan, M.D., Ph.D. and W. Curt LaFrance, Jr., M.D., M.P.H.

Dr. Bajestan is with the Neuropsychiatry Service, Department of Psychiatry and Behavioral Sciences, Stanford University, Stanford,
California. Dr. LaFrance is with the Departments of Psychiatry and Neurology, Division of Neuropsychiatry and Behavioral Neurology,
Rhode Island Hospital, Providence. Send correspondence to Dr. LaFrance (e-mail: william_lafrance_jr@brown.edu).

Copyright ©2016 by the American Psychiatric Association

Abstract

Psychogenic nonepileptic seizures (PNES) are a subtype of conversion disorder (also called functional neuro‐
logical symptom disorder in DSM-5). Patients with PNES are high utilizers of health care and can have disabil‐
ity levels similar to those of patients with epilepsy. PNES is a common, complex neuropsychiatric somatoform
disorder at the interface of neurology and psychiatry disciplines and is largely overlooked and avoided by
mental health providers. Despite advances in establishing accurate diagnosis and evidence-based treatments,
recent knowledge about PNES has not been well translated into clinical practice. Long diagnostic delays have
been associated with poor prognosis. Recent advances in possible neurophysiological biomarkers include
functional MRI studies that show abnormalities in emotional, cognitive, executive, and sensorimotor neurocir‐
cuits. Although the gold standard for diagnosis is video electroencephalograph, this test is underused by psy‐
chiatrists. The International League Against Epilepsy proposed a staged approach to PNES diagnosis using
history, semiologic features, and EEG. Thorough psychiatric assessment can identify relevant biopsychosocial
and predisposing, precipitating, and perpetuating factors, as well as assess the comorbid psychiatric disor‐
ders, which can inform a treatment plan. Clear and thoughtful delivery of diagnosis is the first step in treat‐
ment. Regular follow-up with the patient’s neurologist, in addition to treatment by mental health profession‐
als familiar with somatic symptom disorders, is recommended. Psychotherapy is the mainstay of treatment,
and randomized clinical trials using cognitive-behavioral therapies reveal significant reduction in seizures
and other psychiatric symptoms. After centuries, mental health providers now have access to the tools to di‐
agnose and effectively treat PNES and other conversion disorders.

Keywords: Neuropsychiatry/neurobiology, Somatoform Disorders, Seizures, Treatment assessment &amp,

planning

Psychogenic nonepileptic seizures (PNES) are paroxysmal, involuntary changes in behavior, sensation, motor
activity, cognitive processing (including change in level of consciousness), or autonomic function linked to a
dysfunction in the processing of psychological or social distress (1). PNES are symptoms of conversion disor‐
der, and the most recent version of the Diagnostic and Statistical Manual of Mental Disorders (fifth edition;
DSM-5) has added the title functional neurological symptom disorder (FNSD) (2). Diagnostic criteria for CD-
FNSD are as follows:
1. One or more symptoms of altered voluntary motor or sensory function.
2. Clinical findings provide evidence of incompatibility between the symptom and recognized neurological or
medical conditions.
3. The symptom or deficit is not better explained by another medical or mental disorder.
4. The symptom or deficit causes clinically significant distress or impairment in social, occupational, or other
important areas of functioning or warrants medical evaluation.

The criteria have been revised from DSM-IV in an effort to consider that, although psychological conflicts re‐
main a driving force behind the psychopathologic mechanism of CD-FNSD, psychological symptoms can be
hard to identify in the psychiatrist’s initial, brief encounters with patients (3) and thus have been relegated to
a note in the diagnosis description (2).

Symptoms of CD-FNSD can present as paralysis, gait abnormalities, and tremors (4). When symptoms of CD-
FNSD include seizure-like events that are not explained by epileptic seizures (ES) or other neurological or
medical etiologies, these symptoms are described as psychogenic (or functional) and are given the diagnosis
of PNES. Diagnosis often is confirmed with the use of video electroencephalography (vEEG) monitoring be‐
cause, unlike ES, PNES do not exhibit epileptiform discharges. Also, PNES do not respond to antiepileptic
medications (5, 6). Sigmund Freud conceptualized this disorder in psychological constructs, whereas Jean-
Martin Charcot explored it as a neurological process (7).

Epidemiology and Natural History

PNES are present in up to 20% of the 2.7 million patients diagnosed as having epilepsy in the United States
(8). The diagnosis of PNES is made in 20% to 50% of seizure-monitoring unit (SMU) admissions (9), which
makes PNES as common as multiple sclerosis and Parkinson’s disease (10).

Eighty percent of patients with PNES in the general population are women, who are mostly between age 15
and 35 (11). PNES also is reported in 25% of veterans admitted to the SMU (12), and most of this population
is male, which illustrates the sampling biases of the two environments. PNES has been reported among all
races and different ethnic groups worldwide (13–17). Ataque de nervios in the Hispanic population (18, 19)
and “falling out” in the black American population (20) are cultural variations of PNES.

PNES and epilepsy are associated with similar levels of disability (21). Repeated workups and treatments for
presumed epilepsy are estimated to incur from $100 million to $900 million per year in medical services in
the United States (22). Unnecessarily aggressive treatments for epilepsy may result in oversedation, intuba‐
tion, vagal nerve stimulator placement, and even temporal lobectomy (23). In a follow-up study, 44% of pa‐
tients with PNES had poor outcomes (defined as not being seizure free and remaining dependent) (24).
Diagnosis of PNES was delayed up to nine years in some older studies (25). Delayed diagnosis is associated
with a poor prognosis (26); therefore, timely diagnosis of PNES can be instrumental in the care of these
patients.

Biopsychosocial Underpinnings

Biological Vulnerabilities
Traumatic brain injury (TBI), intellectual disabilities, and epilepsy are frequently reported as coexisting diag‐
noses with PNES (27). In one study of 92 patients with vEEG-confirmed PNES, almost half of patients with
PNES reported TBI, and of those with TBI, 73% met criteria for mild TBI (28). The study found that patients
with TBI and PNES had significantly increased odds for having major depression, behavioral impulsivity, post‐
traumatic stress disorder (PTSD), and a trauma or abuse history. The authors concluded that mild TBI is a
significant risk factor for patients with PNES, because it is associated with increased psychiatric diagnostic co‐
morbidity, symptom severity, poorer functioning, and increased disability. Similar findings emerged in a study
of veterans who reported having a TBI (12).

Neuroimaging studies have revealed that patient groups with PNES showed cortical atrophy in the anterior
cingulate cortex, supplementary motor area, and precentral gyrus regions in quantitative structural brain
magnetic resonance imaging (MRI), compared with a control group (29, 30). Functional MRI (fMRI) studies of
patient groups with PNES have suggested an alteration in the connectivity of brain areas involved in emo‐
tional processing (e.g., the amygdala, insula, and anterior cingulate cortices), areas responsible for executive
function and cognitive processes (e.g., the lateral prefrontal and parietal cortex), and areas involved in motor
function (e.g., the supplementary motor area) (6, 31–36). Connectivity between the supplementary motor
area and the anterior cingulate cortex is correlated with frequency of PNES (36). A sample group with PNES
showed more functional connectivity between insular subregions and the sensorimotor network compared
with a healthy control group (35).

Overall, with the structural and functional abnormalities, it is hypothesized that high emotional arousal of pa‐
tients with PNES, coupled with reduced cognitive-executive control, might influence their motor function and,
consequently, trigger seizures (6, 35, 37). Of note, the connectivity changes may indicate alterations in brain
function rather than the “cause” of the CD-FNSD, just as an epileptiform discharge is a fingerprint of epilepsy
rather than its etiology.

Psychosocial Mechanisms

Psychobiology studies have shown that patients with PNES may be less tolerant of emotional arousal (38)
and show high alexithymic (difficulty in identifying and describing internal emotional experience) (39, 40),
somatization (39), dissociative (41, 42), and avoidance tendencies (41).

Patients with PNES have been described by some researchers as a heterogeneous population (43–45).
However, Kalogjera-Sackellares described two main “causes” of PNES: posttraumatic PNES, from acute or re‐
mote trauma, and developmental PNES, from emotional privation during developmental periods (46). As
noted above, PTSD and history of traumatic events are highly prevalent among patients with PNES (27, 47).
Some authors have conceptualized PNES as manifestations of PTSD (48); however, only half of patients with
PNES have PTSD (49). Their many comorbidities are the rule, including mood, anxiety, personality, pain, cog‐
nitive, sleep, and other somatic symptom disorders, which makes their “heterogeneity” their homogeneity
(50).

Uliaszek et al. found that patients with PNES cluster into two groups on the basis of levels of emotional dys‐
regulation (43). The first of these is the emotionally underregulated group, which Uliaszek and colleagues
found to be significantly associated with several measures of psychiatric symptoms and higher rates of co‐
morbid psychiatric diagnoses, and the second is the emotionally overregulated cluster who underreport
emotional difficulties (43). Difficulty in processing emotional experiences and lower tolerance for emotional
arousal may result in emotional dysregulation in the presence of conscious or subconscious psychological
triggers or somatosensory stimuli (e.g., auditory or visual triggers). With somatization and dissociation ten‐
dencies, patients with PNES manifest their underlying psychological distress in a somatized, seizure-like be‐
havior (1).

Assessment and Establishing the Diagnosis

The diagnosis of PNES can be challenging and requires a multidisciplinary approach involving both neurol‐
ogy and psychiatry disciplines. The first step in diagnosis is differentiating nonepileptic seizures from ES, and
the gold standard for diagnosis is the recording of the typical seizures on vEEG. A history and semiology con‐
sistent with PNES, with the absence of epileptiform discharges on the EEG before, during, and after the event,
establish the diagnosis of PNES (5). If the patient has several types of seizures, all types need to be described
in the history to assist with recording the various semiologies, to rule out ES or physiologic nonepileptic
events. The ictal semiologic features are key because certain signs are more likely to be associated with ES or
with PNES (51), as described below. The consulting psychiatrist needs to do a thorough psychiatric assess‐
ment considering biopsychosocial and predisposing, precipitating, and perpetuating factors (52) to under‐
stand several factors involved in symptom initiation and maintenance. Psychiatric comorbidities need to be
carefully assessed and targeted during the treatment (53).

Clinicians must consider the possibility of comorbid neurologic diseases and the possibility that new symp‐
toms can emerge (54). During monitoring, tapering of antiepileptic drugs needs to be gradual and done un‐
der the care of the neurologist, who is also monitoring the emergence of any new type of seizures (55). Once
diagnosis is established and psychiatric and psychological treatments are initiated, patients should continue
regular follow-up with their neurologist (56).

Semiologic Features

No single sign or symptom differentiates ES from PNES. Abrupt onset, short duration, stertorous breathing,
occurrence from EEG-physiologic sleep, stereotypical movements, ictal-onset eye opening, lateral tongue bit‐
ing, and postictal confusion are more suggestive of ES. Long duration, fluctuating course, asynchronous
movements, pelvic thrusting, side-to-side head or body movements, forced eye closure, and memory recall
during the seizure are more in favor of a diagnosis of PNES (57, 58).

Induction Strategies

The use of triggers reported by patients and family members, routine EEG activation procedures (photic
stimulation, hyperventilation), and hypnosis have been reported as useful induction strategies during moni‐
toring. All of these strategies increase the probability of capturing seizures and therefore may facilitate the
diagnosis.

Seizure induction through hypnosis to differentiate between ES and PNES has relatively high sensitivity
(77%) and specificity (95%) (59). In all induction strategies, it is important to determine whether the induced
events are “typical.” If the typical events are induced under hypnosis, self-hypnosis can be taught as a readily
available and inexpensive treatment tool (see more information on hypnosis in the Treatment and Outcome
section of this article) (59). The purpose and process of the induction should be explained to patients before
any induction strategy is used. These strategies need to be applied in a respectful and sensitive manner, with
the goal not only of making a diagnosis but also of empowering patients and fostering a sense of control and
hope. The use of deceptive placebos, such as saline injection or alcohol wipes, for seizure induction has been
questioned for ethical concerns and its potential to compromise physician-patient trust (60).
Differential Diagnosis

Approximately 10% of patients with PNES also have ES (61), and this percentage is reported to be higher
among patients with learning disabilities (62). EEG has low sensitivity for capturing simple partial ES (focal
ES without loss of consciousness) and frontal lobe ES (55, 63). The presence of psychological stress as a
seizure trigger does not differentiate PNES from ES, given that stress also has been reported as a trigger for
ES (55).

It is important to note that lack of epileptiform correlates for the seizures does not automatically implicate a
psychogenic nature of the episodes. Most physiologic nonepileptic events do not generate an ictal discharge.
Syncope is commonly misdiagnosed as epilepsy, especially if it is associated with convulsive or tonic-clonic
movements (64, 65). Many other physiologic conditions, such as paroxysmal movement disorders, cardiac
arrhythmias, autonomic dysfunctions, and electrolyte abnormalities can also present as nonepileptic seizures
that are physiologic in origin (65). Variants of panic attacks can manifest as PNES and need to be differenti‐
ated (55). Consequently, medical conditions that induce autonomic paroxysms similar to panic attacks need
to be ruled out (e.g., endocrine abnormalities, especially disorders of the thyroid and hypothalamic-pituitary-
adrenal axis) (66). The most common medical conditions that can manifest as physiologic nonepileptic events
are described below.

Paroxysmal Neurological Disorders

Paroxysmal movement disorders, postural orthostatic tachycardia syndrome (a disorder of the autonomic
nervous system), cerebrovascular disorders (e.g., stroke, transient ischemic attacks), migraine headaches, and
vertigo can mimic ES (51, 65).

Sleep Disorders

Cataplexy and parasomnias are the most common sleep disorders that may get confused with epilepsy (65,
67). Cataplexy is sudden loss of muscle tone or falls that are triggered by strong positive or negative emo‐
tions; it is usually a symptom of narcolepsy (68). Parasomnias are complex or bizarre behaviors that arise
from sleep state (67). Somnambulism, sleep terrors, and rapid-eye movement behavior disorders (dream-
enacting behavior) are common parasomnias that could be mistaken for nocturnal epilepsy (69).

Cardiovascular and Cerebrovascular Disorders

Cardiac arrhythmias, orthostatic hypotension, and vasovagal syncope are among the most common cardio‐
vascular etiologies of syncope.

Metabolic and Endocrine Abnormalities

Thyroid hormone abnormalities, abnormalities of the hypothalamic-pituitary-adrenal axes, hypoglycemia,

electrolyte imbalances, and hypocalcemia can induce episodes similar to ES or panic attacks (65).

Diagnostic Levels of Certainty for Diagnosis of PNES

vEEG is not accessible to all patients, and even if it is available, some types of seizures may not be captured
during the patient’s admission to the SMU. Delayed diagnosis of PNES is related to poor outcome (24, 56, 70)
and exposes patients to unnecessary treatment with antiepileptic drugs. Given these obstacles to PNES diag‐
nosis, the International League Against Epilepsy’s Nonepileptic Seizure Task Force published a staged ap‐
proach to PNES diagnosis. Three components—history and seizure semiology that are consistent with PNES
and ictal EEG recordings without epileptiform activity—together inform the diagnosis levels, which include
possible, probable, clinically established, and documented PNES (5).

Given the lack of availability of vEEG to some patients in nontertiary care environments, many researchers
have tried to find biomarkers for PNES (71). Neuroimaging, autonomic nervous system markers, prolactin
level, enzyme levels, neurotrophins, and fMRI have been studied; however, lack of psychiatric comparators,
study size, and research methodological issues have limited the use of these studies in clinical practice to
definitively differentiate PNES from epilepsy at the individual patient level (71). Autonomic profiles have been
suggested as the possible biomarkers; however, more research is warranted.

Prolactin is a polypeptide that is secreted from the anterior pituitary gland. The spread of epileptic dis‐
charges to the hypothalamus in ES is believed to result in postictal prolactin releases. The epileptic discharge
raises the plasma prolactin level, which is detectable from 10–20 minutes to two hours postictally in general‐
ized tonic-clonic ES and in some focal ES (72). Studies have reported conflicting results for the use of pro‐
lactin level as a diagnostic tool (71, 72); however, a rise in postictal prolactin in generalized tonic-clonic ES
and some focal epilepsies can be helpful in distinguishing ES from PNES.

Researchers have also studied autonomic profiles of ES and PNES as potential biomarkers to distinguish the
two. Ponnusamy et al. reported increased ictal sympathetic tone in ES and not in PNES (73). A recent study
showed increased preictal sympathetic tone followed by increased parasympathetic tone during the seizure
and postictally in PNES. The authors suggested that the emotional arousal preceding the seizure is likely the
etiology of increased preictal sympathetic tone (74).

Psychiatric Assessment

PNES is a complex neuropsychiatric disorder and needs careful psychiatric assessment. Psychiatric comor‐
bidities need to be carefully assessed. Prior studies have reported a nine-year delay in establishing the cor‐
rect diagnosis of PNES. Therefore, the assessing and the treating clinicians (if different) should be aware of
factors that maintain and perpetuate the symptoms. As noted above, researchers have recommended a sys‐
tematic biopsychosocial approach that assesses predisposing, precipitating, and perpetuating factors (52) to
assess several individual, family, and professional factors involved in the clinical presentation (53, 54). It is
important to involve the family members in the discussion of the diagnosis and throughout the treatment. An
assessment approach for the case example below is provided in Table 1.

Case Example

Ms. J is a 35-year-old single woman with a past medical history of chronic back pain, migraine headaches, and
major depressive disorder. She also carries the diagnosis of treatment-resistant epilepsy, with seizure onset
in her early 20s. She is now referred for admission to the SMU for differential diagnosis, given the recent in‐
creased frequency of her seizures and multiple failed trials of antiepileptic medications. She describes two
types of seizures. The first type of seizure is episodes of unresponsiveness during which her whole body
shakes, described by others as “flopping like a fish,” with all her limbs flailing rhythmically. Her eyes are usu‐
ally closed during the episodes. She can hear what happens around her but is unable to respond. She denies
any head injury, tongue biting, or loss of bladder or bowel control. The episodes last between five and 30
minutes. She usually feels exhausted after the seizures. The frequency of these episodes has increased to
about four per week from two months ago. Her second type of seizure is episodes of brief “staring” that last
for about one to five minutes on a daily basis; these have increased in frequency from six months ago.

Ms. J has been taken to the emergency department multiple times over the past two months, where she was
told that she “fakes” the seizures. She reports daily migraine headaches and worsening of her depression af‐
ter she lost her job six months ago. She has been isolating herself at home with minimal activities for fear of
having a seizure in public and reports worsening back pain.

Both types of her typical episodes are captured during her hospitalization, with no abnormal epileptiform
EEG correlates before, during, or after the ictus. The semiology of the events, her symptoms, her medical his‐
tory, and the medical assessment are consistent with PNES, and the events are not associated with other
medical etiologies.

During psychiatric assessment, Ms. J reports symptoms of a major depressive episode. She also reports a
long history of depression but is not on any psychiatric medication currently. She reports a history of physi‐
cal abuse by her alcoholic father. Her parents divorced when she was young, and, consequently, the family ex‐
perienced significant financial hardship. Her mother struggled with major depressive disorder as well. Ms. J
reports that her childhood was lonely, because her mother was either working or withdrawn when she was
at home. Ms. J finished high school but dropped out of college when she became pregnant and had an abor‐
tion. She had been working in retail stores until her recent job loss. She has a two-year-old daughter from a
prior relationship and lives with her boyfriend. She reports recent conflicts and verbal arguments with her
boyfriend, mostly around financial problems. Her boyfriend started to work double shifts to pay the bills, and
Ms. J is in the process of applying for disability. In this case example, conceptualization of predisposing, pre‐
cipitating, and perpetuating factors can inform diagnostic formulation and treatment targets (Table 1).

Psychiatric Comorbidities

As noted above, along with having other psychiatric comorbidities, patients with PNES report more somatic
symptoms, compared with a healthy control group or with patients with ES. Examples of such symptoms are
higher rate of somatic syndromes (fibromyalgia, chronic pain, chronic fatigue syndrome, migraine
headaches) (76), mood and anxiety disorders (including PTSD), and personality disorders (27, 47, 77). These
comorbid conditions can and should be addressed along with the seizures in comprehensive neuropsychi‐
atric treatment.

Treatment and Outcome

PNES literature continues to grow, and evidence-based treatments have begun to emerge; however, there is
yet to be a universally accepted protocol for treating the disorder (78). Although the literature continues to
build on the psychological field’s understanding of PNES and its treatment options, the disorder lacks the at‐
tention given to other psychiatric disorders by psychiatrists, other mental health providers, and associations
(79). In terms of treatment, various psychotherapy and pharmacologic treatments have been examined for
PNES (43, 56).

Presenting the diagnosis to the patient and family is the first step and a key component of treatment.
Education about the diagnosis can influence the patient’s understanding of his or her condition, potential
treatment options, and overall feelings of optimism and self-compassion (80–82). Patients with PNES often
score high on assessments for alexithymia and have difficulty understanding the possibility of emotional ex‐
periences affecting what seems to them to be a purely neurologic disorder (56). When patients with PNES
are not properly educated about their disorder, they tend to experience continued distress and stigma and
may not comply with the providers’ treatment recommendations. If they have a lack of insight about their
condition, patients with PNES remain high utilizers of health care, with frequent visits to emergency rooms
(5, 10, 83). For these reasons, it is important that neurologists, mental health providers, and other clinicians
clearly and confidently communicate the diagnosis of PNES in a thoughtful, nonjudgmental manner using
nonpejorative language (e.g., PNES are no longer referred to as “pseudoseizures,” because, as a conversion
disorder, there is nothing false about them) (56).

If a patient’s typical seizure has been captured during vEEG monitoring, it is helpful for the diagnosing physi‐
cian to review the EEG with the patient when explaining the diagnosis. It is also helpful to include family
members in the review of the vEEG and explanation of the diagnosis to decrease confusion in translation of
the diagnosis and increase social support (56). Multiple conversations concerning diagnosis may be needed
to solidify understanding and to increase treatment adherence during the transition into mental health care.
Increased understanding and legitimization of PNES can lead to more acceptance of the diagnosis as well as
to a reduction in health care costs (55, 84).

Several suggested strategies exist for presenting the diagnosis of PNES to a patient, such as emphasizing the
“good news” of establishing a PNES diagnosis, educating patients on the serious side effects of antiepileptic
drugs, discussing the subconscious occurrence of seizures, and giving a thorough explanation of unique
avoidance and maintenance factors. In presenting the diagnosis as good news, clinicians can stress that there
is treatment, rather than focusing on the diagnosis, because some patients say that they would rather have
epilepsy than PNES.

It is important for the clinician to acknowledge to the patient and to the patient’s family that conversion dis‐
order seizures are real, not fake—they just are not caused by epilepsy. In speaking with the patient and fam‐
ily, clinicians should clearly and positively acknowledge that antiepileptic drugs do not treat PNES, that antide‐
pressant medications may help with comorbid symptoms, and that counseling and targeted psychotherapy
are the main treatment (11, 56, 65, 85, 86). Some diagnostic presentation approaches from the literature
have described that the triggers and stressors may not be identified easily; however, a comprehensive neu‐
ropsychiatric evaluation incorporating a developmental and psychosocial history yields stressors and past or
present abuse and trauma for most patients.

As previously noted, individuals with PNES have been shown to display differing emotional regulation styles,
varying symptomatology and personality subtypes, and high rates of psychiatric comorbidity. Accordingly, a
variety of psychotherapy approaches have been described (43, 87, 88). Among such treatments, cognitive-
behavioral therapy (CBT) and CBT-informed psychotherapy (CBT-ip) are the treatments with the most con‐
trolled data (89, 90). Conventional CBT for PNES is being studied presently in a multicenter randomized con‐
trolled trial (RCT) in the United Kingdom. PNES present as a somatic symptom disorder, and some patients
with PNES can display emotion regulation styles that resemble those described in PTSD and panic attacks.
Anxiety disorders have been shown to be treated effectively with CBT (88). Incorporating targeted ap‐
proaches to the known pathologies among patients with somatoform disorders, the CBT-ip addresses so‐
matoform, mood, and anxiety disorders. The two CBT-ip–containing arms in the CBT-ip pilot RCT showed re‐
duction in PNES and psychiatric comorbidities and improvement in quality of life and functioning (89) with
use of a psychotherapy workbook and manual for either ES or nonepileptic seizures (91). Therapists were
trained in the multimodal therapy, which has components of traditional CBT, psychodynamic psychotherapy,
motivational interviewing, psychoeducation, interpersonal therapy, dialectical-behavioral therapy (DBT), and
mindfulness (50).
Other forms of psychotherapy have promise; however, none have been studied in RCTs. Certain modalities
may benefit subsets of patients with PNES. In open-label, uncontrolled trials, psychodynamic psychotherapy
has been shown to significantly reduce patients’ seizure frequency and health care use and to improve so‐
matic distress and emotion regulation difficulties among patients with PNES (78). Psychodynamic psychother‐
apy was shown to be helpful in reducing the seizure frequency in a group psychotherapy setting as well (92).

An available and cost-effective precursor or adjunct to treatment for PNES is hypnosis (93, 94). Hypnosis can
be applied easily, and self-hypnosis can be taught easily in SMUs as well as outpatient clinics. There are signif‐
icant commonalities in the psychophysiological mechanisms seen among patients with PNES and among pa‐
tients who have undergone hypnosis. Patients with PNES can use these similarities to present their symptoms
and gain self-soothing techniques, which can lead to feelings of validation, empowerment, and further psy‐
chological treatment adherence (94). Hypnosis could be considered as an adjunct to psychotherapy because,
although it may significantly improve motor conversion symptom severity and impairment, it does not ad‐
dress underlying psychopathology (95).

Group therapy is another emerging area of PNES treatment research. Group therapy can be cost-effective
and provides therapeutic opportunities for patients who are of a lower socioeconomic status and who lack
insurance benefits (96), because it can expand the treatment of one therapist to multiple members of the
group. In the group environment, members provide psychoeducation for each other and are able to share
their personal experience of treatment procedures and outcomes (96). Often, the influence of a group
member’s personal experience can have a greater effect than the influence of a therapist, and success for
one member frequently leads others in the group to mimic that member’s coping strategies. Group therapy is
a place to examine alexithymia, avoidance, and dissociative tendencies in a safe interpersonal environment.
Psychodynamic group therapy focusing on interpersonal issues (92) or DBT group therapy teaching coping
skills (97) may benefit patients with PNES.

Another potential adjunctive therapy is mindfulness-based psychotherapy (95), which shares many of the
principles of CBT and may be an appropriate complement to such therapy. With limited skills in emotion
identification and regulation, patients with PNES could benefit from mindfulness-based psychotherapy, which
has been used to treat other psychiatric disorders, many of which present comorbidly with PNES (95).
Mindfulness also plays a large role in other psychotherapeutic approaches, such as DBT, acceptance and
commitment therapy, mindfulness-based stress reduction therapy, and mindfulness-based cognitive therapy.
Patients with PNES may benefit from mindfulness training that focuses on recognition and management of
their emotions (95). However, mindfulness-based psychotherapy for PNES requires continued exploration in
controlled trials. A summary of selected trials of psychotherapy approaches is listed in Table 2.

Finally, psychopharmacologic interventions also are used to address comorbid conditions of PNES. In a pilot,
multicenter randomized clinical trial, the CBT-ip and combined arm (CBT-ip with sertraline) showed signifi‐
cant reduction of seizure frequency, whereas the sertraline-only arm showed a significant improvement in
depression but only a trend toward seizure reduction (89). In an open-label, noncontrolled trial of venlafax‐
ine for patients with PNES and anxiety disorders, depression, or both, the frequency of seizures and depres‐
sion and anxiety scores were significantly reduced (98). A selection of textbooks and guides including differ‐
ent psychotherapeutic approaches for therapists and patients is listed in Box 1.

BOX 1. GUIDEBOOKS FOR THERAPISTS AND PATIENTS FOR INFORMATION ON PSYCHOGENIC

NONEPILEPTIC SEIZURES
 Cognitive-behavioral–informed approach:

Overcoming Functional Neurological Symptoms: A Five Areas Approach, by Chris Williams, 2011.
Taking Control of Your Seizures: Workbook, by Joel M. Reiter, Donna Andrews, Charlotte Reiter, W.
Curt LaFrance, Jr., 2015
Treating Nonepileptic Seizures: Therapist Guide, by W. Curt LaFrance, Jr., Jeffrey Peter Wincze, 2015

Psychodynamic approach:

Psychodynamics and Psychotherapy of Pseudoseizures, by Dalma Kalogjera-Sackellares, 2004

Psychoeducation approach:

Nonepileptic Seizures: A Guide, by Lorna Myers, 2014

Textbook containing various approaches:

Gates and Rowan’s Nonepileptic Seizures, edited by Steven Schachter and W. Curt LaFrance, Jr., 2010

Patients with PNES have poor outcomes if left untreated and seem to have poorer outcomes than those diag‐
nosed with ES (99, 100). In follow-up studies of patients with PNES, one-third reported reduction of seizures,
whereas another third of the patients remained chronically ill (24, 99, 100). Coexisting epilepsy or psychiatric
comorbidities, dependent lifestyle, and poor relationships have been related to poor prognosis (99, 101,
102). Delayed diagnosis was also reported as another factor related to poor outcome in some studies (24,
70). Continued follow-up care with both neurology and mental health disciplines also remains important in
maintenance management.

Conclusions and Future Directions

Conversion disorders, including PNES, are common and disabling. Modern psychiatry practitioners, associa‐
tions, and research institutes, however, have not attended to the treatment needs of this population or de‐
voted substantial institutional funding to PNES research, as they have with other serious mental illnesses.
Psychiatrists have avoided this disorder, likely as a result of the lack of effective treatment options for conver‐
sion disorders in the past. In the past decade, however, neuropsychiatric approaches have yielded definitive
diagnosis with the use of vEEG monitoring and RCTs demonstrating effective cognitive-behaviorally informed
treatments. High-quality RCTs are warranted for other treatment modalities proposed for PNES to broaden
the armamentarium. Studying the biological and psychological mechanisms of response to treatment may
also help in the understanding of conversion disorders.

Acknowledgments

The authors thank Shelby L. Scott, M.A., for assistance with manuscript preparation.
Footnotes

Dr. LaFrance serves on the Epilepsy Foundation Professional Advisory Board; has served as a clinic development consultant for the
Cleveland Clinic, Emory University, Spectrum Health, and the University of Colorado Denver; and has provided expert medicolegal
testimony. He receives editor’s royalties from Cambridge University Press and author’s royalties from Oxford University Press and
has received research support from the American Epilepsy Society, the Epilepsy Foundation, the Matthew Siravo Memorial
Foundation Inc., the National Institutes of Health, the Veteran’s Administration, Brown University, and Rhode Island Hospital. Dr.
Bajestan reports no financial relationships with commercial interests.

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Figures and Tables

TABLE 1.

Biopsychosocial Formulation for Diagnosing Psychogenic Nonepileptic Seizures (PNES)a

Factor Bio Psycho Social

Predisposing Biological susceptibility to major
depressive disorder (family history of
major depressive disorder)
Precipitating Worsening migraine headaches;
worsening depression
Poor attachment (as a result of
childhood adversity); poor coping
style
Worsening depression; anxiety with
increased interpersonal conflicts
Childhood abuse and neglect; poor
family functioning; childhood
financial hardship
Early unwed pregnancy and abortion;
recent unemployment

Perpetuating Deconditioning; worsening back pain
and migraine headaches
Avoidance of seizure triggers;
dysfunctional psychological defenses
and traits (somatization, dissociation,
alexithymia); perception of having
epilepsy; feelings of rejection by
medical professionals; possibility of
formation of sick role
Social isolation; stigma of PNES
diagnosis from medical professionals;
lack of accurate diagnosis and
uncertainty; availability of
compensation for being sick

aSource: Based on formulation model by LaFrance and Bjørnæs (75)

TABLE 2.

Summary of Psychotherapy Approaches for Psychogenic Nonepileptic Seizures a

 Study Psychotherapy Type of N Completed Treatment Duration Follow-Up Comments
Intervention Study of After
Treatment Treatment
Completion

Goldstein CBT versus standard Pilot RCT 29 of 33 12 weekly Six months CBT arm showed
et al. medical care outpatient significantly lower
2010 sessions seizure frequency
(90) compared with control
group (standard
medical care) at the
end of treatment
(p<.002) but not at six-
month follow-up
(p<.08)
LaFrance Four arms: CBT-ip, Multisite 34 of 38, with 8 of 9 for 12 weekly N/A CBT-ip showed 51.4%
et al. sertraline, CBT-ip + pilot RCT CBT-ip, 9 of 10 for CBT-ip + outpatient seizure reduction
2014 sertraline, treatment sertraline, 9 of 9 for sessions (p=.01); CBT-ip +
(89) as usual sertraline only, and 7 of 10 sertraline showed
for control 59.3% seizure
reduction (p=.008); the
two therapy-containing
groups also showed
significant reduction
in psychiatric
comorbidities and
improvement in
quality of life; the
sertraline-only and
control groups did not
show significant
reduction in seizures

Mayor et Brief augmented Open-label, 47 of 66 20 weekly 12–61 25.5% of patients

al. 2010 psychodynamic noncontrolled months became seizure free;
(78) interpersonal therapy 40.4% achieved a
seizure reduction of
>50%

Barry et Psychodynamic Open-label, 7 of 12 32 weekly Several Six patients

al. 2008 group psychotherapy noncontrolled sessions months experienced a decrease
(92) in seizure frequency;
a
CBT, cognitive-behavioral therapy; RCT, randomized controlled trial; CBT-ip, CBT-informed psychotherapy