Pitfalls of Psychogenic Non-epileptic Status Epilepticus

Transcription

1 Pitfalls of Psychogenic Non-epileptic Status Epilepticus Hulya Karatas, 1 F. Irsel Tezer, 1 Nese Dericioglu, 1 and Serap Saygi 2 1 Hacettepe University, Institute of Neurological Sciences and Psychiatry, Ankara, Turkey 2 Hacettepe University, Faculty of Medicine, Department of Neurology, Ankara, Turkey Objectives and Background: In patients with medically refractory seizures 20 30% do not have epilepsy, and the majority are diagnosed with psychogenic nonepileptic seizures (PNES). Almost one-third of this group has a prolonged episode that is termed as PNES status epilepticus (PNES-SE). The aim of this study was to describe the characteristics of patients with (1) PNES-SE only and (2) PNES-SE with concurrent epileptic seizures. Methods: We screened retrospectively all patients who underwent videoelectroencephalogram (video-eeg) long-term monitoring at our institution between 1996 and Patients with PNES were identified by typical clinical features with no ictal EEG changes. Patients with continuous episodes for at least 30 min that led to intubation were identified as PNES-SE. They were divided into two groups: group 1, pure PNES-SE and group 2, PNES-SE with concurrent epilepsy. Group characteristics were defined with respect to demographic, clinical, electroencephalographic, neuroimaging and psychiatric variables. Results: PNES were recorded in 88/916 patients (10%) of whom 6 (7%) were treated intensively due to misdiagnosis of status epilepticus (SE), with two having coexistent epileptic seizures. All patients had concurrent psychiatric disorder(s), diagnosed by a psychiatrist. Duration of time until correct diagnosis was lengthy in all cases, and particularly for patients with PNES-SE with coexisting epileptic seizures (more than 10 years). Conclusion: To avoid iatrogenic complications and to treat the underlying psychiatric conditions, early diagnosis of PNES is necessary. Understanding the clinical characteristics of PNES-SE leads to early diagnoses, which may avoid iatrogenesis and economic burden. Keywords: epilepsy, psychogenic non-epileptic seizures, psychogenic non-epileptic status epilepticus, video- EEG monitoring, long-term monitoring Introduction Misdiagnosis of epileptic seizures is relatively common. Approximately 20 30% of patients with refractory seizures seen at epilepsy centres are found to be misdiagnosed and the majority of these patients are shown to have psychogenic non-epileptic seizures (PNES) (Benbadis & Allen Hauser, 2000; Krumholz, 1999). The coexistence of epileptic seizures with PNES is a reason for difficulty in diagnosis, and this may occur 5 50% of the patients with PNES (Martin et al., 2003; Sigurdardottir & Olafsson, 1998). In that case, long-term video-electroencephalogram (video- EEG) monitoring is the gold standard for definition of epileptic seizure or PNES (Benbadis & Lin, 2008). Prolonged attacks like status epilepticus are also reasons for misdiagnosis of PNES. Mostly, PNES are rapidly self-terminating attacks. Prolonged (generally longer than 30 min) and dramatic PNES mimicking status epilepticus have been described as PNES status epilepticus (PNES-SE) (Reuber, Pukrop, Mitchell, Bauer, & Elger, 2003). Address for correspondence: Hulya Karatas, MD and F. Irsel Tezer, MD, PhD, Hacettepe University, Institute of Neurological Sciences and Psychiatry, Sihhiye, 06100, Ankara, Turkey. These authors have contributed equally to this article. s: hulyak@hacettepe.edu.tr, irseltezer@yahoo.com.tr BRAIN IMPAIRMENT VOLUME 13 NUMBER 3 DECEMBER pp c The Authors 2013 doi: /BrImp

2 HULYA KARATAS ET AL. The existence of a very limited number of reports about PNES-SE may be the result of difficulty in diagnosis (Dworetzky et al., 2006; Reuber et al., 2003). But PNES-SE is not rare. Rueber et al. (2003) reported 85 PNES patients, 77.6% having at least one seizure lasting more than 30 min (PNES-SE), 38.8% having recurrent hospital admissions, and 27% being admitted to an intensive care unit. In another study of patients with PNES diagnosed during long-term monitoring, 9 of 49 (18%) showed PNES-SE (Dworetzky et al., 2006). Another explanation for the lack of a larger number of studies of PNES-SE is that such patients are mostly admitted to emergency departments or transferred to intensive care units (Dworetzky et al., 2006). According to the study of Dworetzky and colleagues, patients with PNES-SE were more frequently admitted on an urgent basis, compared with patients with PNES without prolonged or repeated events. It is usually the case that there is an absence of clear clinical findings of patients with PNES-SE admitted to emergency departments, with the exception of short illness history, normal interictal EEGs despite high-frequency spells, and usage of only a few anti-eplieptic drugs (Dworetzky et al., 2006). Early diagnosis of this clinical condition is important because patients with PNES-SE are at risk of iatrogenic harm due to inappropriate emergency interventions such as mechanical ventilation and high-dose anti-epileptic or anaesthetic drugs (Reuber & Elger, 2003). Furthermore, unnecessary expenses for diagnosis and treatment with excessive anti-epileptic drugs, as well as evaluations in intensive care units, lead to economic problems. Early correct diagnosis of patients with PNES-SE may reduce iatrogenesis and the economic burden. However, we acknowledge the difficulty for a physician in the emergency room when he or she is confronted with a patient who might actually have real SE or PNES-SE. There are a few studies describing the clinical characteristics of patients with PNES and PNES-SE (Dworetzky et al., 2006; Rueber et al., 2003), but to the best of our knowledge the features of patients with PNES-SE and coexistence of epilepsy, which may be a problem for diagnosis and emergent treatment, have not yet been reported. The aim of this study is to describe the characteristics of pure PNES-SE patients and PNES-SE patients with epileptic seizures, and to try to identify clues for early diagnosis of patients with PNES-SE who are at risk of pharmacologic mistreatment. Methods We screened retrospectively all patients who underwent video-eeg long-term monitoring (LTM) at our institution from October 1996 to March A 32-channel EEG recording system was used. Scalp electrodes, including T1 T2 electrodes, were placed according to the system. Patients underwent continuous video-eeg LTM lasting 3 10 days. We identified patients with PNES by video-eeg LTM in which alteration in awareness or bilateral motor involvement and no definite ictal EEG changes were demonstrated (Vanderzant, Giordani, Berent, Dreifuss, & Sackellares, 1986). Patients diagnosed with concurrent epilepsy were included. Three epileptologists reviewed the EEG data for all cases. At least one psychiatrist evaluated the patients when they were diagnosed with PNES through the video-eeg LTM. Patients with continuous or repeated episodes with the aforementioned features, in addition to failure to return to baseline for at least 30 min, which led to intubation, along with absence of associated ictal or post-ictal EEG changes, were identified as PNES- SE, as documented in their past medical history. We only included the PNES patients with a history of PNES-SE. Patients were divided into two groups: group 1, pure PNES-SE; and group 2, PNES-SE with concurrent epilepsy. Group characteristics were defined with respect to demographic, clinical, electroencephalographic, neuroimaging and psychiatric variables. Routinely, informed consent was also obtained from all patients, including those with PNES following long-term video-eeg monitoring. Statistical analysis was not performed, because of the small sample sizes. Results There were 916 video-eeg LTM patients in our department during the study period. PNES were recorded in 88 patients (88/916 = 10%) of whom 6 (6/88 = 7%) had been treated intensively due to misdiagnosis of SE in other centres, according to their past medical history. The age of the patients was between 20 and 41 years at admission, and five were female. All patients had routine laboratory tests, serum anti-epileptic drug levels were checked, cranial magnetic resonance imaging (MRI) and routine and sleep-deprived EEGs were performed. All routine laboratory tests were in the normal range and serum anti-epileptic drug levels were at therapeutic levels. Cranial MRI was normal in five of the patients; there was small heterotopia in the white matter of the left frontal lobe in one patient (see below, patient 2 in group 2). Routine and sleep-deprived EEGs were normal in the pure PNES-SE group. Provocative techniques were 334

3 PITFALLS OF PSYCHOGENIC NON-EPILEPTIC STATUS EPILEPTICUS performed during EEG recording and PNES attacks were recorded in 3 out of 6 patients. Among these 6 patients, two had coexistent epileptic seizures that were difficult to differentiate from PNES. The characteristics of group 1 are summarised in Table 1, and the two patients in group 2 are described in detail. Patients in group 2 had more than 10 years duration between PNES onset and video- EEG LTM-documented PNES diagnosis. This duration was longer than for the pure PNES-SE group. Age and gender were similar in each group. Psychiatric diagnoses of patients are discussed in detail below. Group 1: Pure PNES-SE Patients Group 1 contained four patients, all of whom had had seizures for between 1 and 6 years. Past medical history of these patients revealed that all had been hospitalised in an intensive care unit or emergency room with diagnosis and treatment of status epilepticus, leading to intubation or not, depending on the usage of general anaesthetic agents. They had no histories of febrile convulsion, head trauma or family history of epilepsy. They had been using at least two anti-epileptic drugs. All four patients had some link to the medical profession. Neurological examinations, routine laboratory tests, cranial MRI, and routine and sleep-deprived EEGs were normal. During routine EEG recording intravenous saline injection was given for provocation of PNE seizure in two patients and PNE seizure was documented. Only one patient (patient 3) also had a lumbar puncture, with normal findings. Between 1 and 7 years from their first seizures, they were monitored in our video-eeg LTM unit and PNES were documented for all of them. After that, psychiatric evaluation was performed and they were treated with suitable psychiatric medication. Three of the four patients in the pure PNES- SE group had dissociative disorder, and in addition, one also had depression. The remaining patient in group 1 had depression only. All anti-epileptic drugs were discontinued in all patients. Subsequent follow-up was conducted at varying intervals. According to their self-reports, three of the four patients had been free of PNES or PNES-SE attacks at 1 4 years, and in the final patient the frequency and intensity of attacks had decreased at 7-year follow-up. Group 2: PNES-SE Patients with Concurrent Epilepsy Group 2 comprised two patients. The first patient (patient 1 in group 2, see Table 1) had experienced TABLE 1 The clinical characteristics of patients Relationship with medical professional or epilepsy patients Associated psychiatric disorders Time to LTM Diagnosis of concurrent epileptic seizure frequency Number of AEDs Frequency of seizure attacks Duration of seizure attacks (years) Admission age/gender Groups Patients Pure PNES-SE 1 20/F 19 1/week No 2 (VPA, DPH) Dissociative disorder 1 year Nursing student 2 20/F 18 2/week No 2 (CBZ, VPA) Dissociative disorder 2 years Father was a medical doctor 3 26/F 26 2/week No 2 (DPH, PHB) Dissociative disorder, 2 weeks Husband was a medical depression doctor 4 26/M /week No 2 (LVT, CBZ) Depression 7 years Nurse 1 27/F /day Yes, 1 3/year 2 (LVT, VPA) Depression, suicide 12 years Brother epileptic Pure PNES-SE and epilepsy 10 years Sister and daughter epileptic Anxiety disorders and depression 2 41/F /week Yes, 8 10/year 4 (LVT, PHB, CLZ, VPA) PNES-SE, psychogenic non-epileptic seizures-status epilepticus; AED, anti-epileptic drug; LTM, long-term monitoring. CBZ, carbamazepine; CLZ, clonazepam; DPH, phenytoin; LVT, levetiracetam; PHB, phenobarbital; VPA, valproic acid. 335

4 HULYA KARATAS ET AL. frequent daily seizures with myoclonia or staring and a few generalised tonic clonic convulsions (1 per year) from the age of 15 years. But she also had a history of recurrent seizures that led to admission to local emergency services. She suffered from depression and attempted to commit suicide twice when she was 16 and 25 years of age. Her family history revealed the death of five siblings due to non-specific infections or seizures. She experienced instability during walking and amnesia for a few months. In her neurological examination she had mild ataxia and action tremor of the hands. Her anti-epileptic therapy included levetiracetam (2000 mg/day) and valproic acid (1500 mg/day). She had frequent attacks that were diagnosed as status epilepticus and were captured by a hand camera in our clinic, yet the semiology was unusual for an epileptic seizure. Video-EEG LTM revealed 10 attacks that were confirmed as her habitual seizures by her mother, with hand tremors, swinging of the head and brief myoclonia of her arms. These attacks lasted for min. Sometimes she became responsive or she cried during these attacks. Mostly, ictal EEGs did not show epileptic discharges except in a few of the attacks of myoclonus, with generalised multiple spike or spike-wave discharges. Most of her attacks were assumed to be PNES although she had myoclonic seizures. Her background rhythm was slow (5.5 6 Hz) interictally and intermittent generalised sharp and sharp slow wave discharges occurred for 1 2 s. The interictal background activity increased to 7 8 Hz after discontinuation of valproic acid. Her mini-mental state test, cranial MRI and lysosomal enzyme screening tests were normal. The patient was referred to the department of psychiatry in our hospital where axis II, disorder of personality was diagnosed. A history of sexual abuse was also identified. Risperidone (2 mg/day) was prescribed and psychotherapy was initiated. During 1 week of treatment as an inpatient in the psychiatry service she had only one PNE attack. Patient 2 had seizures characterised by staring since the age of 5 years. She also had her first generalised seizure at the age of 31 years, after she was divorced. Her daughter also had generalised seizures with eye blinking and her sister was mentally retarded and had generalised seizures. The patient had been on valproic acid therapy for 10 years but she had frequent seizures during the past 2 3 months. Levetiracetam (3000 mg/day), phenobarbital (100 mg/day) and clonazepam (6 mg/day) had been added to her treatment at another hospital during the past 2 months. Also, she had been evaluated in an intensive care unit of that hospital and intravenous midazolam had been given for a day due to her frequent generalised seizures. The patient had been referred to our hospital for evaluation of intractable seizures, apathy and ataxia, with a diagnosis of progressive myoclonic epilepsy. She was apathetic and she had dysarthria and ataxia in her neurological examination. Her routine laboratory tests were normal. The serum levels of valproic acid were between 74 and 95 mg/dl during her hospitalisation, but levels were higher (112 mg/dl) during her evaluation in another hospital approximately 1 month previously. On admission to our video-eeg LTM unit, background activity in EEG was slow, with 6 7 Hz rhythms; there were also generalised Hz spike-wave discharges for less than 2 min interictally. She had two similar attacks; one of them was induced with intravenous saline. She had swinging of head and squeezing of teeth and eyes for 2 3 min. The ictal EEG did not show epileptic discharges. These attacks were diagnosed as PNE attacks. Anxiety disorders and depression were diagnosed after referral to the department of psychiatry. Her lysosomal enzymes, serum levels of ammonia, organic acids in serum or urine, lactic acid and pyruvic acid were in the normal range. But her cranial MRI showed small heterotopia in the white matter of the left frontal lobe. Her antiepileptic drugs were changed to levetiracetam 2000 mg/day and clonazepam 2 mg/day. Her apathy and ataxia disappeared. Her epileptic and psychogenic seizures were infrequent at 2-year follow-up, and in the past year she had no seizures. Discussion In the present study the prevalence of PNES was 10% (88/916) in patients monitored with video- EEG LTM during a 12.5-year period. In these PNES patients the prevalence of PNES-SE was 7% (6/88). PNES-SE was considered an unusual complication of PNES, although recent studies suggest that it is not rare, ranging from 18 to 27% (Dworetzky et al., 2006; Reuber et al., 2003). The prevalence of PNES-SE in our PNES patients was lower (7%) than in previous studies. One explanation for this difference may be the diversity of the study populations and methods used to identify PNES. In the study of Rueber and colleagues (2003) the results (27%) were derived from a questionnaire report from 85 PNES patients, and were not confirmed by medical records. In our study, we identified the PNES-SE according to the information from patients, as well as medical charts declaring whether they received treatment in intensive care units with or without 336

5 PITFALLS OF PSYCHOGENIC NON-EPILEPTIC STATUS EPILEPTICUS intubation, and the recognised gold standard of recordings of PNE seizures by video-eeg LTM. Yet, in another study that also used video-eeg LTM (Dworetzky et al., 2006), the prevalence of PNES patients monitored by video-eeg LTM was higher than our study (49/270, 18% and 88/916, 10%, respectively). In addition, the prevalence of PNES-SE was also higher (9/49, 18%). However, in our reference centre for epilepsy surgery, most PNES patients are diagnosed in the outpatient EEG laboratory. Only patients with difficulty in diagnosis or concurrent epilepsy are monitored in the video-eeg LTM unit. Consequently, the overall ratio of patients with PNES (n = 88) to video-eeg LTM (n = 916) sessions was also lower (10%) than that previously reported in the literature (49/279, 18%) (Dworetzky et al., 2006). Diagnosis of PNES is difficult, and time delay for the diagnosis was reported as 7.2 years by Reuber, Fernandez, Bauer, Helmstaedter and Elger (2002). In group 1 of the present study, it took between 1 and 6 years to diagnose PNES and all patients were on anti-epileptic medication. In group 2, the coexistence of epileptic seizures led to difficulty and time delay in diagnosis, and because of this, diagnosis of PNES took more than 10 years for the two patients in this group. Time delay for correct diagnosis may lead to misdiagnosis of status epilepticus and intensive treatment of these patients in the emergency room, because a detailed history, advanced experience in seizure phenomenology and ictal EEG recordings (video- EEG LTM) are often not available. Intensive treatment with or without respiratory support may be harmful and even cause death in patients with PNES-SE (Reuber, Baker, Gill, Smith & Chadwick, 2004). Thus it is important to refer these patients to video-eeg LTM units to find out the correct diagnosis beneath their status epilepticus. Iatrogenically induced overdose of multiple antiepileptic drugs due to frequent seizures may result in drug toxicity (Neidermeyer, Blumer, Holscher & Walker, 1970; Weaver, 2004), apathy or ataxia, or slowing background activity in the EEG. As an example, the clinical presentation of our two patients in group 2 mimicked more serious problems, such as progressive myoclonic epilepsy or other degenerative diseases associated with seizures. The suspicion of a diagnosis of degenerative or more complicated disorders may lead to excessive costs in evaluation of such patients, in addition to causing iatrogenic harm with excessive anti-epileptic drugs. In these patients, we decreased the toxic dosages of the drugs. This led to normalisation of EEG and clinical presentation. That important and practical point must be considered while evaluating these patients. Abnormal EEG and MRI findings are especially misleading factors, adding to the time delay for diagnosis of PNES with true epileptic seizures (Reuber & Elger, 2003). In group 2, both patients had abnormal interictal EEGs. Patient 2 also had MRI abnormalities with a small heterotopic nodule in the frontal lobe, which did not exclude the diagnosis of idiopathic generalised epilepsy (Betting et al., 2006) or PNES. Although that was not the case in our patients, the overreading of EEGs often led to erroneous diagnosis of epilepsy in PNE seizures (Benbadis & Lin, 2008). Provocative techniques may be useful in the diagnosis of PNE seizures (Benbadis, 2001). There is a debate in the literature about the use of provocative techniques, such as intravenous saline injection, for the diagnosis of PNE attacks (Benbadis, 2001; Gates, 2001). Saline injection has been used to bring out these attacks whenever the presence of PNES was suspected during outpatient EEG recording (Benbadis, 2001; Dericioglu, Saygi, & Ciger, 1999; Krumholz & Niedemeyer, 1983; Slater, Brown, Jacobs, & Ramsay, 1995). In our three patients, we used a provocative technique during the stay in the emergency room as soon as we suspected PNE attacks. These attacks included the ictal behavioural characteristics consisting of irregular out of phase clonic movements in the extremities, closed eyes, side to side head movements or pelvic thrusting (Dworetzky et al., 2006; Krumholz, 1999; Saygi, Katz, Marks, & Spencer, 1992). For final diagnosis, all of our patients were admitted to the video-eeg LTM unit. Video-EEG monitoring is necessary to record the coexistence of seizures and also for the diagnosis of frontal lobe seizures that mimic PNE attacks. The correct and early diagnosis of PNES may help patients and physicians to address the underlying or associated psychological issues, as the outcome of psychiatric disorders is better in patients with a shorter history of PNES (Reuber & Elger, 2003; Vanderzant et al., 1986). Psychiatric diagnoses in PNES patients include somatoform and dissociative disorders, depression, anxiety disorders, post-traumatic stress disorders and personality disorders. In our study three of four patients in the pure PNES-SE group (group 1) had dissociative disorder, which was not a feature in either of the two patients in the PNES-SE with concurrent epilepsy group. Moreover, while both patients in the PNES-SE with concurrent epilepsy group (group 2) had a diagnosis of depression, only two of the patients in the pure PNES-SE group had depression. We can only speculate that this difference might be important in the ontogenesis of PNES- SE. During the 1 12 years of follow-up, our patients had no recurrence of PNES-SE and they were 337

6 HULYA KARATAS ET AL. continued with psychiatric treatment with less frequent PNE attacks. It has been documented that PNES occur between the ages of 15 and 35 years, with greater frequency in women (Krumholz, 1999). Supporting this report, 5 out of 6 patients were young females. An interesting feature of group 1 (four patients) was the relationship with the medical profession. Two were nurses and the other two patients were relatives of medical doctors. Physicians in the emergency rooms are usually not suspicious about the diagnosis of epilepsy and do not investigate seizure history in detail if there is a companion. Having a relationship with a medical professional, or a relative having epilepsy, may be a risk factor for PNES, as in our patients who were familiar with epileptic seizures. Although it is speculative, given the very small sample size, we believe it is worth reporting this interesting observation. We were unable to identify any publications in the English literature indicating that a relationship with the medical profession may lead to misdiagnosis of PNE attacks as epileptic seizures. In conclusion, incorrect diagnosis of PNES, as well as intensive treatment of prolonged PNE attacks as status epilepticus, is still a problem in the emergency room and has potential risks. To avoid iatrogenic complications and treat underlying psychiatric conditions, early diagnosis of PNES is necessary. Further research is warranted to identify risk factors for misdiagnosis in addition to those suggested by this study. References Benbadis, S.R. (2001). Provocative techniques should be used for the diagnosis of psychogenic nonepileptic seizures. Archives of Neurology, 58(12), Benbadis, S.R., & Allen Hauser, W. (2000). An estimate of the prevalence of psychogenic non-epileptic seizures. Seizure, 9(4), Benbadis, S.R. & Lin, K. (2008). Errors in EEG interpretation and misdiagnosis of epilepsy. Which EEG patterns are overread? European Neurology, 59(5), Betting, L.E., Mory, S.B., Lopes-Cendes, I., Li, L.M., Guerreiro, M.M., Guerreiro, C.A.,... Cendes, F. (2006). MRI reveals structural abnormalities in patients with idiopathic generalized epilepsy. Neurology, 67(5), Dericioglu, N., Saygi, S., & Ciger, A. (1999). The value of provocative methods in patients suspected of having non-epileptic seizures. Seizure, 8(3), Dworetzky, B.A., Mortati, K.A., Rosetti, A.O., Vaccaro, B., Nelson, A., & Bromfield, E.B. (2006). Clinical characteristics of psychogenic seizure status in long term monitoring unit. Epilepsy and Behavior, 9, Gates, J.R. (2001). Provocative testing should not be used for nonepileptic seizures. Archives of Neurology, 58, Krumholz, A. (1999). Nonepileptic seizures: diagnosis and management. Neurology, 53(Suppl 2), S76 S83. Krumholz, A., & Niedermeyer, E. (1983). Psychogenic seizures: a clinical study with follow-up data. Neurology, 33, Martin, R., Burneo, J.G., Prasad, A., Powell, T., Faught, E., Knowlton, R.,... Kuzniecky, R. (2003). Frequency of epilepsy in patients with psychogenic seizures monitored by video-eeg. Neurology, 61(12), Neidermeyer, E., Blumer, D., Holscher, E., & Walker, B.A. (1970). Classical hysterical seizures facilitated by anticonvulsant toxicity. Psychiatria Clinica, 3, Reuber, M., Baker, G.A., Gill, R., Smith, D.F., & Chadwick, D.W. (2004). Failure to recognize psychogenic nonepileptic seizures may cause death. Neurology, 62(5), Reuber, M., & Elger, C. (2003). Psychogenic nonepileptic seizures: review and update. Epilepsy and Behavior, 4, Reuber, M., Fernandez, G., Bauer, J., Helmstaedter, C., & Elger, C.E. (2002). Diagnostic delay in psychogenic nonepileptic seizures. Neurology, 58, Reuber, M., Pukrop, R., Mitchell, A.J., Bauer, J., & Elger, C.E. (2003). Clinical significance of recurrent psychogenic nonepileptic seizure status. Journal of Neurology, 250, Saygi, S., Katz, A., Marks, D.A., & Spencer, S.S. (1992). Frontal lobe partial seizures and psychogenic seizures. Neurology, 42, Sigurdardottir, K.R., & Olafsson, E. (1998). Incidence of psychogenic seizures in adults: a population-based study in Iceland. Epilepsia, 39(7), Slater, J.D., Brown, M.C., Jacobs, W., & Ramsay, R.E. (1995). Induction of pseudoseizures with intravenous saline placebo. Epilepsia, 36, Vanderzant, C.W., Giordani, B., Berent, S., Dreifuss, F.E., & Sackellares, J.C. (1986). Personality of patients with pseudoseizures. Neurology, 36, Weaver, D.F. (2004). Organic pseudoseizures as an unrecognized side-effect of anticonvulsant therapy Seizure, 13(7),