MAMC Journal of Medical Sciences

: 2019  |  Volume : 5  |  Issue : 1  |  Page : 1--7

Psychogenic nonepileptic seizures (PNES): A review

Neera Chaudhry1, Kamakshi Dhamija2, Vinod Puri3,  
1 Professor and Head, Department of Neurology, VMMC & SJH, New Delhi, India
2 Consultant Neurologist, Kainos Hospital, Rohtak, Haryana, India
3 Senior Director, Department of Neurology and Head, Comprehensive Epilepsy Services, Max Superspeciality Hospital (Saket), New Delhi, India

Correspondence Address:
Kamakshi Dhamija
Consultant Neurologist, Department of Neurology, Kainos Hospital, Rohtak, Haryana (DM Neurology, GIPMER, New Delhi), Delhi bypass Road, Rohtak, 124001, Haryana


Psychogenic nonepileptic seizures (PNES) are observable abrupt paroxysmal changes in consciousness or behaviour that present similar to epileptic seizures but are not accompanied by the electrophysiological changes associated with epilepsy and there is a strong suspicion or positive evidence for existence of a psychogenic cause. There is no single feature that absolutely distinguishes true epileptic events from psychogenic nonepileptic seizures and hence there is considerable diagnostic uncertainty for the condition. This is well evidenced by the fact that there is an average delay of approximately 7 years before the right diagnosis of ‘psychogenic seizures’ is achieved. Hence, this leads to an enormous social and economic burden on the society with costs incurred upon ‘PNES’ approximating that of refractory epilepsy group. This review focusses on the salient clinical pointers to the condition along with possible diagnostic and treatment strategies.

How to cite this article:
Chaudhry N, Dhamija K, Puri V. Psychogenic nonepileptic seizures (PNES): A review.MAMC J Med Sci 2019;5:1-7

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Chaudhry N, Dhamija K, Puri V. Psychogenic nonepileptic seizures (PNES): A review. MAMC J Med Sci [serial online] 2019 [cited 2019 Jun 19 ];5:1-7
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Psychogenic nonepileptic seizures (PNES) involve observable abrupt paroxysmal changes in consciousness or behavior that present similar to epileptic seizures but are not accompanied by the electrophysiological changes associated with epilepsy and there is a strong suspicion or positive evidence for existence of a psychogenic cause.[1] Variably known as pseudoseizures, nonepileptic attacks, hysterical seizures, or psychoseizures, they have been categorized in the Diagnostic and Statistical Manual of Mental Disorders, 5th edition, as a type of conversion disorder.[2] They have been well known to occur throughout history and across all cultures where they have been interpreted as demonic possession and often resulted in exorcism or execution. In the past, various authors have attempted to explain the psychopathology behind the occurrence of these events. Carter attributed it to “unconscious conversion symptoms caused by repression of usually sexual conflicts.”[3] Janet believed their occurrence was due to “self-hypnosis involving a dissociation of sensory and/or motor functions as a reaction to overwhelming or childhood traumatic events.” Kraeplin and Freud also believed a role of hysteria in PNES. Post-traumatic stress disorder has also been linked to it.[4] Despite these theories, it is now well accepted that PNES should be considered as a separate clinical entity and not just a symptom of underlying psychiatric comorbidity


The epidemiological data for PNES is limited as there is considerable uncertainty in the diagnosis of the condition. A community survey in rural India found the incidence of pseudoseizures to be nearly 2.9 per 1000 population.[5] This roughly corroborates with its incidence reported from the developed nations. The prevalence of PNES in the western literature is estimated to be around 33 per 100,000 people.[6]

The most common age group for the disorder is 20 to 30 years, although studies have shown an incidence of about 10% in patients over 55 years of age too.[7] Of the children and adolescents referred to pediatric video-electroencephalogram (EEG) monitoring units, 5 to 20% have been reported to suffer from PNES.[8] Females clearly outnumber the males and in an Indian study, females constituted nearly 90% of the patient group.[9] However, some studies have suggested that there might be a higher prevalence in males than originally thought. Comorbid epilepsy is present in 7 to 32% of patients with PNES and the literature shows that 50% of patients with refractory seizures may have PNES.[10] Patients with a low IQ are five to seven times at more risk for PNES compared to normal IQ population.[11] Individuals who have family members with epilepsy are at a higher risk of developing PNES than individuals without a family history of the same. A family history of epilepsy is reported in up to 35% of patients with childhood-onset PNES.[12]

The economic burden of PNES is substantial, especially in developing nations, for both the patients and society. The cost incurred upon diagnostic modalities like EEG, video-EEG, imaging studies, antiepileptic drugs (AEDs), and the emergency department visits for patients with PNES approaches that of the refractory epilepsy group.[7] Interestingly, 1 in 10 patients of PNES present with “apparent status epilepticus.”[13] Hence, this condition needs to be carefully investigated and handled upon right from its initiation.


Although a complex disorder with a multitude of risk factors, the majority of PNES cases are caused by traumatic experiences or developmental issues. In children, risk factors include difficulties in school (46%), family discord (42%), and interpersonal conflicts such as bullying (25%).[14] In the adolescent population depression is a frequent accompaniment. A prior history of sexual abuse is frequently present among adult women who develop PNES.[15] Patients with PNES are more likely to be obese than patients with epileptic seizures.[16] “Psychogenic events” are often first precipitated by some major life event, stressor, or sickness. Primary or secondary gain often results in perpetuation of the disorder. Dissociative and anxiety disorders, learning disabilities, post-traumatic stress disorder, and personality disorders are often accompanying comorbidities with the entity. A study also suggested that patients with PNES have more functional somatic syndromes (fibromyalgia, chronic fatigue syndrome, chronic pain syndrome, tension headaches, and irritable bowel syndrome), and have more medical illnesses that are chronic with intermittent attacks (migraines, asthma, and gastro-oesophageal reflux disease).[17]

 Clinical Features

For the majority of patients, a detailed clinical history in combination with video-EEG monitoring, during which a typical event has been recorded, is sufficient for a physician to provide an accurate diagnosis. However, the diagnosis is not always straightforward in patients since no single clinical feature clearly distinguishes epileptic from non-epileptic events. It is important to consider the fact that there is an average delay of 7 years before a diagnosis of PNES is reached.[18] Frontal lobe epilepsy with its hypermotor manifestations poses specially significant diagnostic dilemma. Hence, it has been repeatedly attempted to delineate clinical features that may be helpful to distinguish epileptic from “pseudoepileptic” events.

Patient’s Description

Taking account of the event from both the patient and the caregiver is important. Patients with epilepsy and those with PNES talk differently about their seizures and it is important to have an interactional and linguistic analysis of patients’ description. Linguists can accurately distinguish PNES from epileptic seizures in 85% of cases through assessment of how patients interact with an interviewer and describe their episodes during a 30 min video-taped interview.[19] A patient with a true seizure will usually discuss subjective symptoms in detail and strategies they use to interrupt or prevent seizures. They would be willing to know what happens during their periods of reduced consciousness, whereas the patient with PNES would concentrate on the circumstances in which the seizure occurred rather than on the seizure itself and would discuss sparingly and with difficulty the subjective symptoms. At times, the patient would just name unconsciousness without further description.

Semiology of Events

Onset and Duration

Epileptic seizures are stereotyped events reflecting their origin from a particular area of brain. PNES can also be stereotypical, but often the features, sequence, and time course of such seizures lack consistency. True seizures have an abrupt onset and a gradual recovery. In contrast, in patients with PNES the events do not have an abrupt onset. The duration is also variable and have a waxing and waning character.[20] They are also in general more prolonged than true seizures. PNES are also more likely to terminate abruptly than epileptic seizures, which are typically associated with gradual increases in the interval between jerks at the end of a convulsion.

Ictal Phase

The generalized tonic–clonic phase of a true epileptic seizure is characterized by whole-body rigidity and “in-phase” body movements. Eyes remain open in 92 to 100% of true seizures and the mouth is also often agaped. By contrast, at the onset of convulsive PNES, the eyes of patients are typically closed. Although eye closure can be observed during epileptic seizures, eye closure throughout the entire ictal episode is considered a characteristic feature of PNES. Forced eye closure—resistance to the eyes being pulled open by an examiner—during psychogenic unresponsiveness is also a sign of PNES. If eyes are open during these “pseudoevents,” evidence of fixation can be sought by the examiner. The patient is rolled onto his/her side. If fixation is maintained, the patient’s eyes would generally be deviated to the ground. When the patient is rolled onto the other side, the eyes remain still directed on the ground (Henry and Woodruff sign).[21] Alternatively, the examiner may place a mirror in front of the patient and look for evidence of convergence and fixation. Further on, the patient’s mouth is often tightly clenched during PNES attacks.

Complex movements such as writhing, flailing, and whole-body thrashing are commonly associated with PNES. However, evidence of flailing and thrashing alone cannot be used to distinguish between PNES and epileptic seizures, since these complex movements can also occur as a consequence of frontal lobe seizures.[22] Same is true for side-to-side head movements or body turning (jacitation) that suggest a possibility of PNES, although they are not diagnostic for it. Asynchronous body movements (alternate clonic movements, usually of the arms) are not typically associated with convulsive epileptic seizures, but can occur during convulsive PNES. Furthermore, pelvic thrusting is much more likely to occur in PNES than in epileptic seizures. Opisthotonic posturing, also termed “arc en cercle,” has also been shown to occur in up to 28% of patients with PNES.[23] Thus, distinguishing between frontal lobe seizures and PNES can be challenging. Certain features as brief (5–45 s) seizures and nocturnal clustering favor epileptic seizures. Turning to prone position during seizures is also an unusual occurrence during PNES. Patients with pseudoevents may just be unresponsive or stare during the event and automatisms are typically absent. There may be periods of prolonged body flaccidity, associated with eye blinking, swallowing, or slumping forward.

A precise temporal sequence of events must always be elicited. Variable, random, or nonphysiological events (e.g., thumb jerking followed by toe jerking followed by eye jerking) should raise the suspicion of PNES. Nocturnal clustering favors epileptic seizures, but it is prudent to remember that psychogenic events may also occur during the period of “pseudosleep.”[24]


Vocalization and the speech of the patient during the ictus can also be useful in distinguishing the two. A true ictal vocalization has a monotonous quality and is often “empty” and typically comprises meaningless phrases or sounds that are repeated. Vocalization usually happens at the beginning of the ictus and is related to respiratory muscular contractions. Speech is primitive and has no emotional expression. In PNES, however, the speech tends to contain more emotion and evokes more feelings of sadness or pain.[25] It is often intelligible and the patient frequently responds to questions during episodes. Postictally, the patient may respond in whispers.

Accompanying Injuries

Injuries requiring sutures, bone fracture, or tongue biting are reported in as high as 40% of PNES patients. Of note is the fact that true events usually have lateral tongue bite, whereas tongue bite in pseudoevents is usually on the tip of the tongue.[26] Interestingly, burns have not been reported by patients with PNES. It is important to consider that events like urinary incontinence, although known to occur so characteristically in true seizures, are also self-reported during pseudoevents in as much as 44% of patients.[27]

Postictal Phase

In the postictal phase, patients with epileptic seizures have altered breathing patterns in the form of “stertorous breathing.” Focal neurological deficits, postictal headache (38%), and fatigue (56%) can occur.[28] Corneal reflex is absent and plantar response is usually extensor after the true event. In contrast, in PNES, postictal breathing is rapid, shallow and soft, irregular, and associated with pauses.[29] Although headache and fatigue can occur after a “pseudoevent,” these patients usually also have refractory interictal headache and other pain syndromes. They can often recall events that occurred during a seizure and usually adopt an avoidance behavior after the event.

[[Table 1]] summarizes salient distinction points between true epileptic seizures and PNES.{Table 1}

In a study defining age-related differences in semiology of PNES, it was highlighted that ictal eye closure, motor phenomenon lasting more than 2 minutes, vocalization during the “tonic–clonic” phase, postictal speech change, and pelvic thrusting were less frequent in children and adolescents with PNES as compared to adults. Biting the tip or side of the tongue and opisthotonus were found to be rare and only present in adults. As for the semiological categories, major motor activity was concluded to be the main feature in adults, and minor motor activity was more prevalent among children (52.9 and 38.1%, respectively; p = 0.01). The study emphasized that recognizing differences of ictal features of PNES in children and adults is important and also useful in promoting earlier recognition of PNES in pediatric population.[30]

 Role of Investigations

Home Video Recordings

Home video alone may have a high specificity and sensitivity in selected patients, especially when reviewed by an experienced observer with reported sensitivity of 93% and specificity of 94%.[31] But this has its own limitations. Home video recordings often capture only a partial view of the patient. Facial expression, limb position, and movement are often not included or obscured by bedsheets or family members. Some phone cameras have a low frame rate, which can make smooth physiological movements look jerky and epileptic. Moreover, postictal phase of some epileptic seizures may look like PNES. However, they undoubtedly are helpful for screening before video-EEG recording, especially in patients with few events. Family members must be taught about the importance of focusing on face, limb, and trunk movements of the patient and also to assess the response of the patient to commands during the event.


EEG alone cannot diagnose PNES. It should be remembered that on one hand a single routine EEG is normal in 30% of patients with epileptic seizures,[32] while 15% of the normal population may have nonspecific abnormalities on EEG. Less than 1% of normal population may also have epileptiform discharges on EEG.[33] On the other hand, abnormalities in EEG are more common in patients with PNES. According to a study, up to 37% of patients with PNES had a report of an epileptiform baseline EEG, which later turned out to be some normal EEG variants when re-evaluated at an epilepsy center.[34] Hence, relying on EEG for diagnosis and exclusion of PNES should be done with caution.


Video-EEG remains the “gold standard” investigation. The combination of observed semiology and a normal background EEG before, during, and after the attack is sine qua non for PNES. A true epileptic pattern has evolving rhythms in the frequency of delta and beta with a stable frequency of rhythmic movements. PNES often have a “stuttering” pattern of rhythmic motor activity, where “rest periods” between the periods of motor activity correspond to normal background electrical activity on EEG. This “on–off–on” pattern of motor activity (alternating periods of rest and rhythmic motor movement) during a seizure is common in patients with PNES, but is hardly ever seen during epileptic seizures.[35] However, motion artifacts can obscure the EEG or be mistaken for ictal discharges. Moreover, in some epileptic patients, ictal scalp-EEG often shows no epileptiform features. Adding to the dilemma, generalized epileptiform discharges can also occur during drug withdrawal (especially barbiturates) even in patients with PNES.[36]

It must be borne in mind that before concluding that a particular subject has PNES, the event must be visually confirmed from a family member as some patients may have both epileptic seizures and pseudoevents further complicating the situation. As already emphasized, comorbid epilepsy is present in 7 to 32% of patients with PNES. Thus, careful consideration must be given and all relevant information must be sought before any decision regarding discontinuation of AEDs is taken.

Outpatient video-EEG monitoring is an interesting and promising modality that can capture PNES events in more than 50% patients in the outpatient setting, especially in patients with infrequent events and situational triggers.[37]

Psychogenic Nonepileptic Seizures Induction

When a spontaneous episode is not recorded, PNES can be induced by hyperventilation, photic stimulation, verbal suggestion, compression of body parts, placing a tuning fork or moistened patches on the skin, intravenous administration of saline, or other placebo or hypnosis. Protocols to induce PNES during EEG are used by nearly 40% of American Epilepsy Society members.[38] Induction reduces the time to diagnosis and avoids the hazards of an inappropriate diagnosis of epilepsy.[39] In a study focusing on the impact of provocation methods in PNES, it was concluded that such seizures occurred significantly more often in the patients who had been informed prior to EEG about the increased seizure risk during hyperventilation and photic stimulation as compared to patients who were not informed (38 vs. 10.0%; p = 0.001). The results implied that simply providing correct and explicit information about provocation techniques substantially increased the PNES rate.[40]

It has been conventionally thought that induction might have a negative effect on doctor–patient relationship. However, if induction is done in a healthy and supportive manner, there is increased receptiveness on part of the patients for their condition and potential hazards of long-term AED treatment could be prevented. It has been found useful for both adults and children. The induction maneuvers have a high sensitivity and are 100% specific for the diagnosis of PNES, although there are also concerns about triggering “true seizures” with such induction techniques in a handful of patients.[41]

Serological Markers

Elevated serum prolactin (>500 IU/ml) is seen in 90% of patients after generalised tonic clonic seizures, and in 60% of patients after complex partial seizures 10 to 20 minutes after the attack.[42] Absence of postictal prolactin rise predicts PNES with a mean sensitivity of 89%. The American Academy of Neurology Therapeutics and Technology Assessment Subcommittee has emphasized that a twice normal relative or absolute serum prolactin increase, from blood drawn 10 to 20 minutes after the onset of the ictus, compared against a baseline nonictal prolactin, is a useful adjunct for diagnosis of PNES.[43] However, it should be remembered that positive results are possible in PNES and are also commonly found after syncope. Also, the criteria for abnormal levels are not standardized. False positive tests may also result from usage of dopamine antagonists, tricyclic antidepressants, and breast stimulation. Similarly, the test may be falsely negative in dopamine agonist usage, status epilepticus, and frontal lobe epileptic seizures.

Serum cortisol and dexamethasone suppression test have not reliably differentiated PNES or epilepsy. Also, elevations in peripheral white blood count, creatine kinase, neuron-specific enolase, capillary oxygen saturation on pulse oximetry, and brain-derived neurotrophic factor have got a limited discriminative power.[44]


Neuroimaging has got a modest differential diagnostic value as epilepsy patients may have normal MRI studies and significant numbers with lone PNES may have abnormal MRI studies. In a study up to 30% of patients with PNES were identified as having MRI abnormalities most often in the form of nonspecific gliosis.[25] Hence, the presence or absence of MRI abnormalities alone cannot be reliably used to distinguish true seizures and pseudoevents.

Some authors have studied the role of quantitative perfusion changes on ictal SPECT in patients with nonepileptic seizures. No blood flow changes were noted on quantitative SPECT analysis in such patients.[45]


Patient Counseling

Counseling the patient about the condition is of utmost importance. Patients must be counseled that events are not due to abnormal or harmful brain activity/brain damage and no AEDs are needed. They must be assured that the physician believes that these episodes are not volitional and no one believes that they are “faking.” Patients and caregivers must understand that a psychological basis for the events exist despite the patient’s lack of awareness of coexistent stress or emotional upset. Help from psychiatrist must be sought. Frequent follow-ups reduce need to produce more or severe symptoms to get medical attention, emergency room admission, and feelings of abandonment. Other comorbidities as major depressive disorder, post-traumatic stress disorder, and personality disorder must be identified and treated. Family should also be advised on how to manage events.

Role of Psychodynamic Psychotherapy

If patients have insight into their disease and are intelligent and motivated enough to introspect the disorder, psychodynamic psychotherapy should be offered to them. The targets of the therapy are to reduce shame, explore trauma, and identify emotions raised by trauma. Group therapy has also been used by researchers with good outcome.[46]

Cognitive Behavioral Therapy

Targets of the treatment therapy include focusing on avoidance behavior, explore the sequelae of prior traumatic experiences, and manage symptom anxiety.[47] PNES is viewed as a learned maladaptive behavior that is reinforced by the environment. Patients are reinforced that the inappropriate behavior is no longer rewarded, even can be punished. This therapy has got the advantage that normal intelligence and insight are not necessary for success. In the study by Lafrance et al., 11 of 17 patients were seizure-free at the end of a 12-week course of cognitive behavioral therapy (CBT).[48] In a study by Goldstein et al. in 2010, CBT was found to reduce PNES by 20% after a 4-month course in a group of 64 patients randomized to CBT or standard medical care.[49] However, controlling environmental conditions is a major obstacle in the success of this modality.

Other Modalities

Family therapy, eye movement desensitization and reprocessing, biofeedback, and hypnosis can be employed for treatment as per individual patients’ need.


Psychiatric medications may be indicated for axis 1 disorders. Selective serotonin reuptake inhibitors (SSRIs) may be helpful for somatization or dissociation.[50] A pilot randomized controlled trial of sertraline in 38 patients with PNES revealed a 59.3% seizure reduction in the combined CBT and drug arm compared to the conventional treatment group.[51] Neuroleptics and propranolol may be employed for severe dissociative disorders.


The prognosis of the disorder depends on a number of factors. In general, younger age at the onset and diagnosis, higher IQ, educational and social status, attacks with less dramatic features or motionless spells, multiple seizure types, lower level of negativism (self-avoidant behavior), fewer additional somatoform complaints, lower dissociation scores, and lower scores of the personality dimensions confer a good prognosis with rates of remission reaching 16 to 51% in adults and up to 82% in children and adolescents.

On the other hand, longer duration and older age at the onset and diagnosis, chronic abuse, recurrent major depression, dissociative and personality disorder, head injury, attacks with positive motor features, tongue biting, incontinence, abnormal findings on MRI, and recurrent pseudostatus portend a poor prognosis.[52]


It must be borne in mind that there is an average delay of 7 years in the diagnosis of PNES. The large magnitude of the problem combined with a delay in the rightful diagnosis of the condition poses significant economic and psychological burden on the society. Hence every attempt should be made to diagnose the disorder at the earliest. Patients and their families must be counseled about the condition in a supportive manner. Treatment for PNES must be individualized. A combination of approaches is probably the most beneficial. Focus should be on removing maladaptive PNES behavior, learning new coping skills, and removing secondary gains. If with therapy PNES persists, therapy should be reevaluated.

 Take-Home Message

Psychogenic seizures pose a great mental as well as economic burden on patients and their family. Moreover, a high index of suspicion is required on the treating physician’s part involved in the management of such cases. Given the long-term antiepileptic drug-treatment-related adverse effects, it is important that the condition be realized and addressed early in order to avoid PNES becoming a chronic “way of life.”

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1Szabo L, Siegler Z, Zubek L, Liptai Z, Korhegyi I, Bansagi B et al. A detailed semiologic analysis of childhood psychogenic nonepileptic seizures. Epilepsia 2012;53:565-70.
2Stone J, LaFrance WC Jr, Brown R, Spiegel D, Levenson JL, Sharpe M. Conversion disorder: Current problems and potential solutions for DSM-5. J Psychosom Res 2011;71:369-76.
3Carter RB. On the Pathology and Treatment of Hysteria. London: J Churchill; 1853.
4Devinsky O. Nonepileptic psychogenic seizures: Quagmires of pathophysiology, diagnosis, and treatment. Epilepsia 1998;39:458-62.
5Kokkat AJ, Verma AK. Prevalence of seizures and paralysis in a rural community. J Indian Med Assoc 1999;96:43-5.
6Benbadis SR, Hauser WA. An estimate of the prevalence of psychogenic nonepileptic seizures. Seizure 2000;9:280-1.
7Widdess-Walsh P, Mostacci B, Tinuper P, Devinsky O. Psychogenic nonepileptic seizures. In: Stefan H, Theodore WH, editors. Epilepsy Part I: Basic Principles and Diagnosis, Handbook of Clinical Neurology. Vol. 107. Amsterdam, The Netherlands: Elsevier; 2012. p. 278.
8Ostrowsky-Coste K, Montavont A, Keo-Kosal P, Guenot M, Chatillon CE, Ryvlin P. Similar semiology of epileptic and psychogenic nonepileptic seizures recorded during stereo-EEG. Seizure 2013;22:897-900.
9Patidar Y, Gupta M, Khwaja GA, Chowdhury D, Batra A, Dasgupta A. Clinical profile of psychogenic nonepileptic seizures in adults: A study of 63 cases. Ann Indian Acad Neurol 2013;16:157-62.
10Holmes MD, Wilkus RJ, Dodrill CB, Batzell L, Wilensky AJ, Ojemann LM. Coexistence of epilepsy in patients with nonepileptic seizures. Epilepsia 1993;34:13.
11Reuber M, Elger CE. Psychogenic nonepileptic seizures: Review and update. Epilepsy Behav 2003;4:205-16.
12Patel H, Scott E, Dunn D, Garg B. Nonepileptic seizures in children. Epilepsia 2007;48:2086-92.
13Zincir SB, Yenel A, Semiz UB. Approach to patients with ‘psychogenic non-epileptic seizures’: A review. Dusunen Adam: J Psychiatry Neurosci 2012;25:170-8.
14Duncan R, Oto M. Predictors of antecedent factors in psychogenic nonepileptic attacks: Multivariate analysis. Neurology 2008;71:1000-5.
15Duncan R, Oto M, Martin E, Pelosi A. Late onset psychogenic nonepileptic attacks. Neurology 2006;66:1644-7.
16Marquez AV, Farias ST, Apperson M, Alsaadi T. Psychogenic nonepileptic seizures are associated with an increased risk of obesity. Epilepsy Behav 2004;5:88-93.
17Dixit R, Popescu A, Bagic B, Ghearing G, Hendrickson R. Medical comorbidities in patients with psychogenic nonepileptic spells (PNES) referred for video-EEG monitoring. Epilepsy Behav 2013;28:137-40.
18Reuber M, Fernandez G, Bauer J, Helmstaedter C, Elger CE. Diagnostic delay in psychogenic nonepileptic seizures. Neurology 2002;58:493-5.
19Reuber M, Fernandez G, Bauer J, Singh DD, Elger CE. Interictal EEG abnormalities in patients with psychogenic non-epileptic seizures. Epilepsia 2002;43:1013-20.
20Desai BT, Porter RJ, Penry JK. Psychogenic seizures. A study of 42 attacks in six patients, with intensive monitoring. Arch Neurol 1982;39:202-9.
21Henry J, Woodruff GA. A diagnostic sign in states of apparent unconsciousness. Lancet 1978;2:920-1.
22Avbersek A, Sisodiya S. Does the primary literature provide support for clinical signs used to distinguish psychogenic nonepileptic seizures from epileptic seizures? J Neurol Neurosurg Psychiatry 2010;81:719-25.
23Hovorka J, Nezadal T, Herman E, Nemcova I, Bajacek M. Psychogenic non-epileptic seizures, prospective clinical experience: Diagnosis, clinical features, risk factors, psychiatry comorbidity, treatment outcome. Epileptic Disord 2007;9:52-8.
24Benbadis SR, Lancman ME, King LM, Swanson SJ. Preictal pseudosleep: A new finding in psychogenic seizures. Neurology 1996;47:63-7.
25Luther JS, McNamara JO, Carwile S, Miller P, Hope V. Pseudoepileptic seizures: Methods and video analysis to aid diagnosis. Ann Neurol 1982;12:458-62.
26Devinsky O, Sanchez-Villasenor F, Vazquez B, Kothari M, Alper K, Luciano D. Clinical profile of patients with epileptic and nonepileptic seizures. Neurology 1996;46:1530-3.
27Peguero E, Abou-Khalil B, Fakhoury T, Matthews G. Self-injury and incontinence in psychogenic seizures. Epilepsia 1995;36:586-91.
28Ettinger AB, Weisbrot DM, Nolan E, Devinsky O. Postictal symptoms help distinguish patients with epileptic seizures from those with non-epileptic seizures. Seizure 1999;8:149-51.
29Azar NJ, Tayah TF, Wang L, Song Y, Abou-Khalil BW. Postictal breathing pattern distinguishes epileptic from nonepileptic convulsive seizures. Epilepsia 2008;49:132-7.
30Alessi R, Vincentiis S, Rzezak P, Valente KD. Semiology of psychogenic nonepileptic seizures: Age-related differences. Epilepsy Behav 2013;27:292-5.
31Chen DK, Graber KD, Anderson CT, Fisher RS. Sensitivity and specificity of video alone versus electroencephalography alone for the diagnosis of partial seizures. Epilepsy Behav 2008;13:115-8.
32Mellers JD. The approach to patients with “non-epileptic seizures”. Postgrad Med J 2005;81:498-504.
33Gregory RP, Oates T, Merry RT. Electroencephalogram epileptiform abnormalities in candidates for aircrew training. Electroencephalogr Clin Neurophysiol 1993;86:75-7.
34Benbadis SR, Tatum WO. Overintepretation of EEGs and misdiagnosis of epilepsy. J Clin Neurophysiol 2003;20:42-4.
35Vinton A, Carino J, Vogrin S, Macgregor L, Kilpatrick C, Matkovic Z et al. “Convulsive” nonepileptic seizures have a characteristic pattern of rhythmic artifact distinguishing them from convulsive epileptic seizures. Epilepsia 2004;45:1344–50.
36Fernández-Torre JL. De novo absence status of late onset following withdrawal of lorazepam: A case report. Seizure 2001;10:433-7.
37Rowan AJ, Siegel M, Rosenbaum DH. Daytime intensive monitoring: comparison with prolonged intensive and ambulatory monitoring. Neurology 1987;37:481-4.
38Schachter SC, Brown F, Rowan AJ. Provocative testing for nonepileptic seizures: Attitudes and practices in the United States among American Epilepsy Society members. J Epilepsy 1996;9:249-52.
39Benabadis SR, Agrawal V, Tatum WO. How many patients with psychogenic non-epileptic seizures also have epilepsy. Neurology 2001;57:915-7.
40Hoepner R, Labudda K, Schoendienst M, May TW, Bien CG, Brandt C. Informing patients about the impact of provocation methods increases the rate of psychogenic nonepileptic seizures during EEG recording. Epilepsy Behav 2013;28:457-9.
41Gates JR. Provocative testing should not be used for nonepileptic seizures. Arch Neurol 2001;58:2065-6.
42Bell WL, Park YD, Thompson EA, Radtke RA. Ictal cognitive assessment of partial seizures and pseudoseizures. Arch Neurol 1998;55:1456-9.
43Chen DK, So YT, Fisher RS. Use of serum prolactin in diagnosing epileptic seizures: Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology 2005;65:668-75.
44Willert C, Spitzer C, Kusserow S, Runge U. Serum neuron-specific enolase, prolactin, and creatine kinase after epileptic and psychogenic non-epileptic seizures. Acta Neurol Scand 2004;109:318-28.
45Spanaki MV, Spencer SS, Corsi M, MacMullan J, Seibyl J, Zubal IG. The role of quantitative ictal SPECT analysis in the evaluation of nonepileptic seizures. J Neuroimaging 1999;9:210-6.
46Baryy JJ, Wittenberg D, Bullock KD, Michaels JB, Classen CC, Fisher RS. Group therapy for patients with psychogenic non-epileptic seizures: a pilot study. Epilepsy Behav 2008;13:624-9.
47Deary V, Chalder T, Sharpe M. The cognitive behavioural model of medically unexplained symptoms: A theoretical and empirical review. Clin Psychol Rev 2007;27:781-97.
48LaFrance W, Miller I, Ryan C, Slum A, Solomon D, Kelley J et al. Cognitive behavioral therapy for psychogenic nonepileptic seizures. Epilepsy Behav 2009;14:591-6.
49Goldstein L, Chalder T, Chigwedere C, Khondoker M, Moriarty J, Toone B et al. Cognitive-behavioral therapy for psychogenic nonepileptic seizures: A pilot RCT. Neurology 2010;74:1986-94.
50O Malley PG, Jackson JL, Santoro J, Tomkins G, Balden E, Kroenke K. Antidepressant therapy for unexplained symptoms and symptom syndromes. J Fam Pract 1999;48:980-90.
51LaFrance WC Jr, Baird GL, Barry JJ, Blum AS, Frank Webb A, Keitner GI et al. Multicenter pilot treatment trial for psychogenic nonepileptic seizures: A randomized clinical trial. JAMA Psychiatry 2014;71:997-1005.
52Widdess-Walsh P, Mostacci B, Tinuper P, Devinsky O. Psychogenic nonepileptic seizures. In: Stefan H, Theodore WH, editors. Epilepsy Part I: Basic Principles and Diagnosis, Handbook of Clinical Neurology. Vol. 107. Amsterdam, The Netherlands: Elsevier; 2012. p. 289.