Psychogenic Non-Epileptic Seizures, Prospective Clinical Experience: Diagnosis, Clinical Features, Risk Factors, Psychiatric Comorbidity, Treatment Outcome

Epileptology in Czech Republic

Epileptic Disord 2007; 9 (Suppl. 1): S52-8

Psychogenic non-epileptic seizures, prospective clinical experience: diagnosis, clinical features, risk factors, psychiatric comorbidity, treatment outcome

Jirˇí Hovorka1, Tomáš Nežádal1, Erik Herman1, Iveta Neˇmcová1, Michal Bajacˇek2 1 Neurology, Epileptology and Neuropsychiatry Department, Na Františku Hospital, Prague 2 Neurosurgery Department, 1st Medical School, Charles University, Prague, Czech Republic

ABSTRACT – In our study, we evaluated 249 patients with refractory seizures using video-EEG monitoring. In this sample, we identiﬁed 56 (22.5%) patients with psychogenic non-epileptic seizures – PNES only. Spontaneous seizures were recorded in 49 (87%) patients with PNES. Suggestive seizure induction using intravenous saline placebo was successful in 77.1% of induced PNES cases. Disease duration prior to PNES diagnosis was quite long. Prolonged past and current intake of high number of different antiepileptic drugs was also typical for these patients. We evaluated ictal PNES semiology. Whereas ictal EEG was normal in all PNES patients, interictal EEG was abnormal in 46.4%. Brain MRI was abnormal in 30.4%. Personality disorders were the most frequent psychiatric co-morbidity (in 44.6% of PNES patients), emotionally unstable (borderline) personality disorder was predominant (in 32.1% of PNES patients). Risk factors for epilepsy misdiagnosis and PNES manifestation are discussed. Therapeutic outcome after two years of combined treatment (psychopharmacotherapy and/or psychotherapy) is presented; approximately one third of patients were seizure-free following two years of treatment, one third of patients were responders (≥ 50% reduction in seizure frequency) and one third did not respond to treatment. Key words: psychogenic non-epileptic seizures, dissociative seizures, video-EEG monitoring, MRI ﬁndings, psychiatric co-morbidity, therapeutic outcomes

Patients with psychogenic non-epileptic zures can be very frequent, with dra- seizures (PNES) represent 20 to 30% matic manifestations, including gene- 10.1684/epd.2008.0156 doi: Correspondence: of patients referred to epilepsy centers ralized convulsions, falls and injuries. J. Hovorka as having refractory seizures (Benba- Interictal EEG and MRI abnormalities Neurology, Epileptology and Neuro- dis and Hauser, 2000; Lancman et al. in PNES may be also a risk factor for psychiatry Department, 2001). The differential diagnosis misdiagnosis of epilepsy. Some of Na Františku Hospital, Prague-1, 110 00 Czech Republic between PNES and epilepsy in daily these patients are at times admitted to neurological practice is difficult. Sei- intensive care units with the diagnosis

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of “cluster epileptic seizures” or “status epilepticus” and come was evaluated after two years. Based on a patient- intensively treated, including ventilatory assistance. Ma- held seizure frequency records, mean monthly PNES sei- nagement of PNES as epileptic seizures can lead to signi- zure frequency was calculated for baseline period ficant iatrogenic harm (Gröppel et al. 2000; Reuber and (3 months before PNES diagnosis). During the treatment Elger, 2003). Early correct diagnosis of PNES is important period (2 years) seizure frequency was recorded and to avoid these hazards and to provide the patients with evaluated individually in each patient. Psychiatric assess- appropriate treatment, usually combined therapeutic pro- ments were conducted at the time of PNES diagnosis and cedures (psychopharmacotherapy and/or psychotherapy). during the subsequent treatment period. These problems represent significant challenge to medical When the diagnosis of PNES was confirmed, the first community thus far. Video-EEG monitoring, including therapeutic step in all patients was to inform the patient of suggestive seizure induction seems to be the most effective the diagnosis, provide educational interview with the pa- diagnostic tool and gold standard in seizure disorders tient with an explanation of principles of dissociation, differential diagnosis (Bazil et al. 1994; Devinsky, 1994; potential triggers, symptoms and treatment options. As Benbadis et al. 1994; Benbadis et al. 2000). part of this interview, video- records of their seizures were The aim of our prospective study was to evaluate, in a presented to the patients. group of patients with PNES, various aspects of diagnosis The second step involved introduction of SSRI antidepres- and treatment: video-EEG diagnosis including suggestive sants (sertraline, citalopram, paroxetine) in patients in seizure induction using intravenous saline placebo, clini- whom SSRIs were indicated. SSRIs were prescribed in cal profile, interictal EEG, MRI, psychiatric co-morbidity, doses normally used for treatment of anxiety or depressive possible risk factors for PNES manifestation and therapeu- disorders. Treatment with a low dose of an atypical antip- tic outcome after two years of treatment. sychotic (risperidone, olanzapine, quetiapine, ziprasi- odone) was started in patients, in whom no clear benefit from treatment with antidepressants was evident. In pa- Methods tients in whom anticonvulsants with positive mood stabilizing or anxiolytic effects were used before the verifica- We evaluated 249 patients admitted to our video-EEG tion of PNES aetiology (lamotrigine, carbamazepine, monitoring unit for refractory seizures in 2001-2003. All pregabaline), treatment with these anticonvulsants was these patients underwent video-EEG monitoring (continu- reintroduced even after establishing the dissociative origin ous 24 hours video-monitoring, 18 EEG channels, 10-20 of seizures. Specific dynamically-oriented psychotherapy system, one ECG channel, Alien commercial system) in- was introduced in patients in whom psychological origin cluding usual activation methods and/or suggestive sei- of seizures was clearly established. zure provocation (in approved patients with signed patient consent). On the video-EEG, we evaluated whether the seizures were “typical” spontaneous seizures, epileptic Results and/or PNES. Diagnosis of PNES with dissociative origin was made in patients with recorded spontaneous and/or PNES only, psychogenic non-epileptic seizures of disso- provoked seizures and negative ictal EEG. ciative origin, was diagnosed in 56 (22.5%) of all 249 In these patients, other parameters, including ictal seizure monitored patients (table 1). Both epileptic and PNES semiology, interictal and ictal EEG, brain MRI, neurologi- were diagnosed and confirmed on the video-EEG in 3 cal and somatic co-morbidity, treatment with antiepileptic (1.2%) cases, and were suspected, based on the personal drugs, personality profile and other potential psychiatric history, in 8 (3.2%) patients. co-morbidities (classified according to ICD-10 system) Spontaneous PNES were recorded in 49 of PNES- were also evaluated by an experienced psychiatrist and/or diagnosed patients. In the remaining 7 patients, PNES psychologist. Risk factors for epilepsy misdiagnosis and for were only diagnosed following suggestive seizure induc- PNES manifestation were identified. tion. Typical seizures were induced in 37 (77.1%) of 48 Patients with epileptic seizures only, with both epileptic induced cases, provocation was negative in 11 (22.9%). seizures and PNES, unclear diagnosis, no recorded sei- Eight patients did not provide consent with seizure induc- zures even after suggestive seizure provocation, patients tion. All patients tolerated PNES induction well, with no with panic attacks only and patients with somatic non- delayed negative experience. epileptic seizures or sleep disorders were excluded from Disease duration prior to PNES diagnosis, age and gender further evaluations. of the patients, seizure frequency per month, mean num- In patients with diagnosed PNES, existing antiepileptic ber of different used antiepileptic drugs in the past thera- drug treatment was withdrawn (except from the patients in peutic history and currently, and other PNES patients’ whom specific treatment with antiepileptic drugs was characteristics are presented in table 1. indicated for psychiatric reason) and psychiatric treatment Neurological co-morbidity was found in 7 patients and/or psychotherapy were introduced. Treatment out- (12.5%). Two patients (3.6%) had epilepsy in family his-

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Table 1. Clinical characteristics of PNES patients tory and one patient suffered from serious diabetes melli- (n = 56). tus, diagnosed a few months prior to first PNES occurrence (tables 4 and 7). Characteristics Four patients (7.1%) had a history of “pseudo-status epi- Gender lepticus” and two were treated with ventilatory assistance Females 39 (69.6%) (3.6%). Males 17 (30.4%) Seizure semiology in PNES patients was evaluated and is Age (years, ± SD) 29.6 ± 10,1 presented in table 2. Most frequent symptoms were mo- Disease duration (years, ± SD) 6.7 ± 3.4 toric. Non-motoric symptoms were also frequent. Tongue Seizure frequency per month, prior to PNES 10.8 ± 10.8 (tip), lips or buccal biting injuries were found in 10 pa- diagnosis (mean, ± SD) tients; there were no other physical injuries and no urinary Number of antiepileptic drugs (AEDs) in past 4.4 ± 1.7 incontinence (table 2). Thirteen patients (23.2%) had non- history (mean, ± SD) stereotypical, varying semiology from more than one clus- Number of currently used AEDs (mean, ± SD) 2.7 ± 1.2 ter: psychogenic motor seizure, psychogenic minor motor Video-EEG monitoring duration, PNES 3.7 ± 2.2 (days, ± SD) or trembling seizures and psychogenic atonic seizures Number of recorded seizures (mean, ± SD) 3.6 ± 3.3 (Gröppel et al. 2000). Seizure duration (minutes, ± SD?) 6,2 ± 4,1 While ictal changes were lacking on EEGs of all PNES Spontaneous PNES (patients, %) 49 (87%) patients, interictal EEG was abnormal in 26 (46.4%) of the Suggestive seizure provocation done 48 (85.7%) 56 patients with the presence of interictal epileptiform (patients, %) abnormity in 12 (21.4%) cases, non-specific, slow abnor- - positive (patients, %) 37 (77.1%) mality was present in 19 (33.9%) patients’ EEGs and both - negative (patients, %) 11 (22.9%) epileptiform and slow abnormality in 5 (8.9%) patients. Epilepsy in family history (patients, %) 2 (3.6%) Nevertheless, no patient had spike-and-wave, or Neurological co-morbidity (patients, %) 7 (12.5%) polyspike-and-wave abnormality. Types and localization of EEG abnormalities are presented in table 3. Diagnosis of both PNES and epileptic seizures of frontal lobe origin was confirmed in one patient by the means of positive ictal Table 2. Seizure semiology (frequency of individual SPECT correlate in suspected localization of epileptic symptoms) in PNES patients (n = 56, frequency > 5%). seizures. Ictal EEG and interictal SPECT were negative in this patient. Ictal PNES symptoms n (%) Brain MRI was abnormal in 17 (30.4%) PNES patients. Closed eyelids with resistant lid opening 37 (66.1%) Individual MRI findings are presented in table 4. Trembling, rapid limb tremor 30 (53.6%) Personality disorders were the most frequent psychiatric Preictal “pseudosleep” 22 (39.3%) co-morbidity and were found in 25/56 (44.6%) patients Asynchronous “hyper-motor” limb 19 (33.9%) (table 5). The different types of personality disorders movements, out-of-phase present within the sample are summarized in table 6; Opisthotonus 16 (28.6%) emotionally unstable (borderline) personality disorder Pelvic trusting, rhytmic pelvic movements 15 (26.8%) was predominant. Other psychiatric co-morbidities were ”Aura”, preceding other symptoms 14 (25.0%) present in 31/56 (55.4%) patients (table 5); anxiety disor- Head movements, side-to-side head shaking 13 (23.2%) ders (panic disorder, generalised anxiety disorder and post Clonic limb movements 12 (21.4%) traumatic stress disorder) and depression were frequent. Tongue (tip), lip or buccae biting 10 (17.9%) The most frequent potential risk factors associated with Unresponsiveness, areactivity, “staring” - 9 (16.1%) PNES in patients’ psychiatric history are presented in without any motor symptoms table 7. Atonia with unresponsiveness 6 (10.7%) Sounds, screams, vocalization or crying 5 (8.9%) Overall, the effect of combined therapeutic procedures Subjective, sensory changes only 5 (8.9%) (psychopharmacotherapy and/or psychotherapy) was moderate. After 2 years of treatment, 16/56 (28.6%) pa-

Table 3. Type and localization of interictal EEG abnormalities in PNES patients (n = 56).

Type/Localization Regional Bilateral Generalized/diffuse n (%) n (%) n (%) Non-epileptiform abnormality 6 (10.7%) 11 (19.6%) 2 (3.6%) Epileptiform abnormality (sharp waves or spikes, 4 (7.1%) 5 (8.9%) 3 (5.4%) no spike and wave complexes or polyspikes)

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Table 4. MRI abnormalities in PNES patients (n = 56). Table 7. Risk factors in psychiatric history in PNES patients (n = 56). Total number of abnormal 17 (30.4%) MRIs Risk factor n % Unspecified gliosis 8 Problems in family relations (divorce, death 16 28.6 Cavum septi pellucidi 2 of a family member, traumatic relationship Multiple sclerosis 2 with an important family member, etc.) Arnold-Chiari malformation 1 Reaction to onset of serious somatic illness 8 14.3 (neurological co-morbidity; multiple Lateral ventricular lipoma 1 sclerosis 2 pts, brain contusion 1 pt, Subarachnoideal cyst 1 Arnold-Chiari malformation 1 pt, migraine Brain contusion 1 2 pts, diabetes mellitus 1 pt) Cortical atrophy 1 Sexual or physical abuse in childhood or 6 10.7 early adulthood Table 5. Psychiatric co-morbidity in patients with PNES History of uncontrolled aggressive 5 8.9 of dissociative origin (n = 56). behaviour Substance abuse or dependency 4 7.1 Psychiatric co-morbidity n % History of head injury without somatic 3 5.4 Personality disorders 25 44.6 consequences (no brain contusion, normal CT, MRI finding) Anxiety disorders (panic disorder, 17 30.4 generalised anxiety disorder, Job loss 1 1.8 post-traumatic stress disorder) Absence of obvious risk factors 13 23.2 Depressive disorder 5 8.9 Total 56 100 Somatization disorder 3 5.4 Munchhausen syndrome 2 3.6 Schizoaffective disorder 1 1.8 Table 8. Therapeutic outcome over the past 12 months Eating disorder 1 1.8 in PNES patients following two years of treatment Mental retardation 1 1.8 (n = 56). Malingering 1 1.8 Total 56 100 Therapeutic outcome over n% the past 12 months Seizure free 16 28.6 Table 6. Personality disorders (n = 25). Responders (> 50% seizure reduction but 19 33.9 not seizure free) Type of personality disorders n % No response 18 32.1 Emotionally unstable (borderline) 18 72 Lost to follow up 3 5.4 personality disorder Total 56 100 Dependent personality disorder 3 12 Organic personality disorder 2 8 Avoidant personality disorder 1 4 Schizotypal personality disorder 1 4 free after two years without any other specific treatment, Total 25 100 except from routine neurological and psychiatric follow-up examinations. The best pharmacological treatment results were found in tients were seizure free for at least the last 12 months, the group of PNES patients suffering from co-morbid anxi- 19/56 (33.9%) were responders (reduction of seizures by ety or depressive symptoms, and treated with antidepres- at least 50%), 18/56 (32.1%) patients did not respond to sants. Following relief of anxiety or depression we any treatment and 3/56 patients (5.4%) were lost to follow noted ≥ 50% seizure reduction (responders) in 7/56 up (table 8). Four non-responders (7.1%) with no evidence (12.5%) patients, and absence of seizures in 5/56 (8.9%) of epilepsy additional to PNES were prescribed, by neu- patients (table 9). The combined treatment with SSRI and rologists other then our center neurologists, a “new” anti- low dose of atypical antipsychotic (risperidone, olanzap- convulsive medication. These patients remained non- ine, quetiapine, ziprasidone) in resistant patients had responders. moderate effect (table 9). The video-presentation of PNES seizures and education The most problematic group to treat were the patients were somewhat effective: we experienced immediate re- suffering from PNES with co-morbid personality disorders, duction of seizures by at least 50% (responders) in 4/56 predominantly emotionally unstable (borderline) disorder. (7.1%) patients, and consequent absence of seizures in In these patients, we first introduced treatment with SSRI 3/56 (5.4%) patients; these 3 patients remained seizure- antidepressants and, in case of the lack of response, a

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Table 9. Positive therapeutic outcome over the past 12 months in PNES patients with different psychiatric co-morbidity after 2 years of treatment (n = 56).

Type of patients Explanation, education, SSRI SSRI + AAP video-EEG presentation PNES patients with co-morbid anxiety or depressive disorder 1SF 5SF 2SF (n = 22) 2 responders 7 responders

PNES patients with a personality disorder (n = 25) 1 SF 2SF 3SF 1 responder 3 responders 4 responders

Other PNES patients (n = 9) 1 SF 1 responder 1 SF 1 responder 1 responder combination of an SSRI and low doses of atypical antipsy- duction, to be the most effective and safe diagnostic tool in chotic were prescribed. The best results it this group of seizure disorder differential diagnosis. patients were achieved with a combination of an SSRI and The most frequent ictal symptoms were motoric, while low doses of atypical antipsychotics (table 9). non-motoric symptoms were also rather frequent (Lanc- Anticonvulsants with positive mood stabilizing or anxi- man et al. 2001). Tongue (tip), lips or buccal biting were olytic effect were continued in 5/56 (8.9%) patients, two of relatively more frequent than we expected. Large propor- whom suffered from emotionally unstable (borderline) tion of patients had non-stereotypical, varying semiology personality disorder. from more than one of the previously defined clusters: Specific dynamically-orientated psychotherapy was intro- psychogenic motor seizure, psychogenic minor motor or duced in 16/56 (28.6%) patients; in all patients this was in trembling seizures and psychogenic atonic seizures combination with psychopharmacological treatment. (Gröppel et al. 2000). Our study included all PNES pa- Positive additive effect of psychotherapy was observable tients, not only those with consistent seizure semiology, as in approximately half of the patients. was the case in the above cited study. This is why we did not use the seizure classification based on the analysis of symptom clusters (Gröppel et al. 2000). This classification Discussion assumes relatively stereotypical semiology of PNES, al- most identical to the description of epileptic seizures. However, the results of our study suggest, that pleomorhic, Our study confirms high proportion of PNES patients with non-stereotypical and varying semiology may be more dissociative non-epileptic seizures in the population of typical for patients with PNES. Recognition of this fact patients treated for refractory epilepsy. Mean age and sex could become one of the most important factors for PNES distribution in our sample, with predominating female population, were typical of PNES patients. These findings diagnosis. are consistent with previously published data (Devinski et Disease duration prior to establishing the diagnosis of al. 1996; Benbadis and Hauser, 2000; Litwin and Cardenˇa, PNES was, in our opinion, surprisingly long. As was the 2000; Lancman et al. 2001). prolonged intake of high number of different antiepileptic Both epileptic and PNES were confirmed by the means of drugs in the patients’ history and currently. Moreover, 4 video-EEG in only a smaller number of evaluated patients. patients (7.1%) had a history of “pseudostatus epilepti- Nevertheless, this combination of seizures was suspected cus”, and 2 (3.6%) were treated with ventilatory assis- in other patients in our sample based on their personal tance. These data are alarming from many points of view: history. Spontaneous PNES were recorded in 87% of the delay between the first manifestation of PNES and PNES-diagnosed patients. Suggestive seizure induction correct diagnosis remains unacceptably long, patients using intravenous saline placebo was highly positive with PNES are treated inappropriately with anticonvul- (77.1% of induced patients) and effective for PNES diag- sants for a long time, and some patients are treated with nosis confirmation (Bazil et al. 1994; Devinsky, 1994; inappropriate emergency interventions. Our findings are Benbadis et al. 1994; Benbadis et al. 2000 ; Dericioglu consistent with published data (Gröppel et al. 2000; Reu- et al. 1999). These findings are in line with previously ber and Elger, 2003). Management of PNES as epileptic published data (Lancman et al. 2001; Benbadis et al. seizures can lead to significant iatrogenic harm (Reuber 2000). All patients tolerated PNES induction well, with no and Elger, 2003). Early correct diagnosis of PNES is impor- consequent subjective negative experience or damaging tant to avoid these hazards and provide the patients with effect on the physician-patient relationship. We consider appropriate treatment, usually with combined therapeutic video-EEG monitoring, including suggestive seizure in- procedures. These issues have so far been challenging.

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MRI and EEG abnormal findings were, according to pa- psychotherapy) was moderate; when evaluated for the last tients’ medical reports, considered by general practitioners 12 months, 28.6% of patients in our sample were seizure and neurologists as significantly suggestive of “epilepsy free, 33.9% were responders and 32.1% patients did not diagnosis” in most of our PNES patients. Therefore, we respond to treatment (5.4% of patients were lost to follow perceive these MRI and interictal EEG abnormalities as up). These findings support previous data indicating poor important “organic” risk factors for “epilepsy misdiagnosis”. prognosis of PNES patients (Conder and Zasler, 1990; Some authors did not find interictal epileptiform abnor- Reuber et al. 2003, Reuber and Elger, 2003). malities in all PNES patients with consistent seizure semi- Delivery of the diagnosis, video-presentation of PNES ology (Gröppel et al. 2000). Our findings, in a method- seizures and education formed the first step of therapy. ologically distinct study, are different. In agreement with They were well-tolerated but effective in only a small our findings, other authors have described EEG and brain proportion of PNES patients. Only 5.4% of patients re- abnormalities in PNES patients (Lelliot and Fenwick, mained seizure-free after two years without any other 1991; Reuber et al. 2002, Reuber et al. 2002a,b). specific treatment, except routine neurological and psy- Our study has also indicated potential factors in patient chiatric follow-up examinations. history that might have contributed to the development of The best pharmacological treatment results were found in PNES. Most frequently in our study these were: family and the subgroup of PNES patients suffering from co-morbid relationship problems, history of sexual and physical anxiety or depressive symptoms. In these patients, we abuse in childhood and conversion of uncontrolled ag- have successfully used treatment with SSRI antidepres- gression. Furthermore, a reaction to manifestation of a sants and, in resistant patients, combined treatment with serious neurological and other somatic illness was identi- SSRI antidepressants and low doses of an atypical antipsy- fied as a potential underlying PNES precipitating factor chotic. This pharmacotherapy was well tolerated, without and may thus be of importance. No obvious risk factors serious side effects. The most problematic group to treat were identified in only 23.2% of our sample. Somatic and was the patients suffering from PNES with co-morbid psychogenic risk factors for PNES manifestation have also personality disorders, predominantly emotionally un- been described in other studies (Conder and Zasler, 1990; stable (borderline) disorder. The best results in this group Devinski et al. 1996; Abubakr et al. 2003). of patients were achieved with a combination of an SSRI To ensure identification and appropriate interpretation of and low doses of atypical antipsychotics. the above-mentioned potential risk factors for develop- Where anticonvulsants with positive mood stabilizing or ment of PNES, we recommend close neuro-psychiatric anxiolytic effect were prescribed before the verification of cooperation with correct neurological and psychiatric PNES diagnosis (carbamazepine, lamotrigine, pregaba- diagnoses. line), treatment with these anticonvulsants was continued Psychiatric disorders in our study were classified accord- after establishing PNES diagnosis. This was the case for 5 ing to ICD-10 system. Personality disorders were the most (9.3%) patients, two of whom suffered from emotionally frequent psychiatric co-morbidity, particularly the emo- unstable (borderline) personality disorder. tionally unstable (borderline) personality disorder. Simi- Specific dynamically-oriented psychotherapy was intro- larly, this type of personality disorder has been reported in duced in about one third of PNES patients. In all of them PNES patients by other authors (Bowman and Markand, this was in combination with psychopharmacological 1996; Kalogjera-Sackellares and Sackellares, 1997; Kuyk treatment. Positive additive effect of psychotherapy we et al. 2003). In a recently published study, personality observed in approximately half of the patients. disorder cluster A (paranoid, schizoid, schizotypical), Therapeutic outcome achieved in our study was consis- classified according to DSM-IV system, was found as the tent with other published data concerning PNES patients most prevalent in the group of PNES patients (Kuyk et al. (McDate and Brown, 1992, Buchanan and Snars, 1993; 2003). These types of personality disorders have been Reuber et al. 2003); approximately one third of patients found in only a small proportion of patients in our study. In were seizure-free after two years, one third of patients the study by Kuyk et al. (2003), personality disorders were were responders and one third of patients did not respond assessed by self-reported questionnaire. Psychiatric diag- to treatment. noses in our study were established on clinical bases, by psychiatrist and psychologist, both experienced in clinical diagnostics. Therefore, we believe our results are clini- Conclusions cally valid and reliable. Similarly to reports by other authors (Kuyk et al. 2003), anxiety disorders (panic disor- Our study contributes evidence for a topical and challeng- der, generalised anxiety disorder, post traumatic stress ing paradigm: “If we consider 5 patients sitting around a disorder) and depression were also frequent psychiatric table and treated for refractory epilepsy, it is very likely co-morbidities in our sample. that one does not have epilepsy at all”. The correct recog- After two years of treatment, the overall effect of combined nition of “who is who” and subsequent appropriate treat- therapeutic procedures (pychopharmacotherapy and/or ment is hitherto challenging task for epileptologists, even

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those working in epilepsy centers operating with complex Dericioglu N, Saygi S, Ciger A. The value of provocation meth- diagnostic and therapeutic tools. Early diagnosis and man- ods in patients suspected of having non-epileptic seizures. Sei- agement of PNES patients is even more challenging task zure 1999; 8: 152-6. for general practitioners and primary care neurologists. To Devinsky O. Provocation of nonepileptic seizures by suggestion ensure appropriate early management of PNES patients; in a general seizure population. Epilepsia 1994; 35: 768-70. the “hidden” patients should be, as early as possible, Devinski O, Sanchez-Villasenor F, Vasquez B, et al. Clinical pro- consulted in epilepsy centers. file of patients with epileptic and nonepileptic seizures. Neurol- Appropriate early diagnosis and treatment of PNES ogy 1996; 46: 530-3. patients are of the same urgency as, for example, early Gröppel G, Kapitany T, Baumgartner C. Cluster analysis of clini- identification of epilepsy surgery candidates. M cal seizure semiology of psychogenic nonepileptic seizures. Epi- lepsia 2000; 41: 610-4. Acknowledgements. Supported by an investigational grant VZ 002160816: Pathophysiology of neuropsychiatric disorders and its Kalogjera-Sackellares D, Sackellares JC. Personality profile of clinical applications. patiens with pseudoseizures. Seizure 1997; 6: 1-7. Kuyk J, Swinkels WAM, Spinhoven PH. Psychopathologies in patients with nonepileptic seizures with and without comorbid References epilepsy:how different are they? Epilepsy Beh 2003; 4: 13-8. Lancman ME, Lambrakis CHC, Steinhardt MJ. Psychogenic Abubakr A, Kablinger A, Caldito G. Psychogenic seizures:clini- pseudoseizures. A general overview. In: Ettinger AB, Kanner AM, cal features and psychological analysis. Epilepsy Behav 2003; 4: eds. Psychiatric issues in epilepsy. Philadelphia: Lippincott Wil- 241-5. liams & Wilkins, 2001: 341-54. Bazil CW, Kothari M, Luciano D, et al. Provocation of nonepi- Lelliot PT, Fenwick P. Cerebral patology in pseudoseizures. Acta leptic seizures by suggestion in a general seizure population. Neurol Scand 1991; 83: 129-32. Epilepsia 1994; 35: 768-70. Litwin R, Cardenˇa E. Demographic and seizure variables but not Benbadis SR, Stagno SJ, Kosalko J, Friedman AL. Psychogenic hypnotizability or dissociation differentiated psychogenic from seizures: a guide for patients and families. J Neurosci Nurs 1994; organic seizures. J Trauma & Dissociation 2000; 1: 99-122. 26: 306-8. McDate G, Brown SW. Non-epileptic seizures: management and Benbadis SR, Hauser WA. An estimate of the prevalence of psy- predictive factors of outcome. Seizure 1992; 1: 7-10. chogenic non-epileptic seizures. Seizure 2000; 9: 280-1. Reuber M, Fernandez G, Bauer J, Singh DD, Elger CE. Interictal Benbadis SR, Johnson K, Anthony K, et al. Induction of psy- EEG abnormalities in patients with psychogenic nonepileptic chogenic nonepileptic seizures with placebo. Neurology 2000; seizures. Epilepsia 2002; 43: 1013-20. 55: 1904-5. Reuber M, Fernández G, Helmstaedter C, Qurishi A, Elger CE. Bowman ES, Markand ON. Psychodynamics and psychiatric diag- Evidence of brain abnormality in patients with psychogenic noses of pseudoseizure subjects. Am J Psychiatry 1996; 153: 57. nonepileptic seizures. Epilepsy Beh 2002; 3: 246-52. Buchanan N, Snars J. Pseudoseizures (non epileptic attack disor- Reuber M, Pukrop R, Bauer J, Helmstaedter C, Tessendorf N, der): clinical management and outcome in 50 patients. Seizure Elger CE. Outcome in psychogenic nonepileptic seizures: 1 to 10 1993; 2: 141-6. year follow up in 164 patients. Ann Neurol 2003; 53: 305-11. Conder RL, Zasler ND. Psychogenic seizures in brain injury: Reuber M, Elger CHE. Psychogenic nonepileptic seizures: diagnosis, treatment and case study. Brain Inj 1990; 4: 391-7. review and update. Epilepsy Behav 2003; 4: 205-16.

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