Clinical Approaches to Psychogenic Nonepileptic Seizures

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 disorder, 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:

The criteria have been revised from DSM-IV in an effort to consider that, although psychological conflicts remain 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 because, 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, intubation, vagal nerve stimulator placement, and even temporal lobectomy (23). In a follow-up study, 44% of patients 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 diagnoses 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, posttraumatic 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 comorbidity, 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 emotional 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 patients 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 remote 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, cognitive, 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 dysregulation (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 comorbid 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 tendencies, patients with PNES manifest their underlying psychological distress in a somatized, seizure-like behavior (1).

Assessment and Establishing the Diagnosis

The diagnosis of PNES can be challenging and requires a multidisciplinary approach involving both neurology 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 consistent 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 assessment considering biopsychosocial and predisposing, precipitating, and perpetuating factors (52) to understand 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 symptoms can emerge (54). During monitoring, tapering of antiepileptic drugs needs to be gradual and done under 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 biting, 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 monitoring. 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 differentiated (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 emotions; 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 cardiovascular 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 diagnosis, the International League Against Epilepsy’s Nonepileptic Seizure Task Force published a staged approach 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 discharges 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 generalized tonic-clonic ES and in some focal ES (72). Studies have reported conflicting results for the use of prolactin 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 comorbidities need to be carefully assessed. Prior studies have reported a nine-year delay in establishing the correct 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 systematic 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 increased 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 usually 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 after 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 history, 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 physical abuse by her alcoholic father. Her parents divorced when she was young, and, consequently, the family experienced 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 abortion. 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, precipitating, 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 neuropsychiatric 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 attention 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 experiences 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 physician 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 disorder seizures are real, not fake—they just are not caused by epilepsy. In speaking with the patient and family, clinicians should clearly and positively acknowledge that antiepileptic drugs do not treat PNES, that antidepressant 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 neuropsychiatric 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 controlled data (89, 90). Conventional CBT for PNES is being studied presently in a multicenter randomized controlled 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 approaches to the known pathologies among patients with somatoform disorders, the CBT-ip addresses somatoform, mood, and anxiety disorders. The two CBT-ip–containing arms in the CBT-ip pilot RCT showed reduction 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 somatic distress and emotion regulation difficulties among patients with PNES (78). Psychodynamic psychotherapy 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 significant commonalities in the psychophysiological mechanisms seen among patients with PNES and among patients 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 psychological 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 address 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 significant 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 venlafaxine for patients with PNES and anxiety disorders, depression, or both, the frequency of seizures and depression and anxiety scores were significantly reduced (98). A selection of textbooks and guides including different psychotherapeutic approaches for therapists and patients is listed in Box 1.

Patients with PNES have poor outcomes if left untreated and seem to have poorer outcomes than those diagnosed 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, associations, and research institutes, however, have not attended to the treatment needs of this population or devoted 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 conversion 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.