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PURPOSES: A 56-year-old man with mild mental retardation, right congenital hemiparesis, and refractory partial seizures was referred for vagus nerve stimulation (VNS). METHODS: Routine lead diagnostic testing during the surgical procedure (1.0 mA, 20 Hz, and 500 micros, for approximately 17 s) resulted, during the initial two stimulations, in a bradycardia of approximately 30 beats/min. A third attempt led to transient asystole that required atropine and brief cardiopulmonary resuscitation. RESULTS: The procedure was immediately terminated, the device removed, and the patient recovered completely. A postoperative cardiologic evaluation, including an ECG, 24-h Holter monitor, echocardiogram, and a tilt-table test, was normal. CONCLUSIONS: Possible mechanisms for the bradycardia/asystole include stimulation of cervical cardiac branches of the vagus nerve either by collateral current spread or directly by inadvertent placement of the electrodes on one of these branches; improper plugging of the electrodes into the pulse generator, resulting in erratic varying intensity of stimulation; reverse polarity; and idiosyncratic-type reaction in a hypersusceptible individual. The manufacturer reports the occurrence rate in approximately 3,500 implants for this intraoperative event to be approximately one in 875 cases or 0.1%.

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Forty-three patients exhibiting psychogenic seizures with onset before the age of 16 years were studied. All patients underwent intensive electroencephalography and video-electroencephalography monitoring. Thirty-two were female and 11 male. Mean age of the population at seizure onset was 12.4 years (range, 5 to 16 years). Twenty-one patients (48.8%) were taking anticonvulsants. Neurologic past history was abnormal in nine cases. Family history of epilepsy was found in 15 cases (34.9%). Median seizure frequency was one seizure every 5 days. Clinical characteristics of the seizures varied. However, unresponsiveness with generalized violent and uncoordinated movements involving the whole body (n = 19) or with generalized trembling (n = 11) were the most common features. Neuropsychological testing, carried out in 22 cases, failed to show major abnormalities in most of the cases. Significant personal and family distress was found in most of the cases. An important impact on patient's quality of life was evident when the seizures were present as compared to the seizure-free periods. There were no statistically significant predictors of clinical outcome.

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OBJECTIVE: To describe the association of choreiform movements with the use of valproic acid. DESIGN: Case series. PATIENTS: Three patients who developed chorea during long-term treatment with valproic acid. All patients had severe brain damage; one had a preexisting unilateral vascular lesion in the caudate nucleus. At the time chorea developed, two patients were also receiving phenytoin sodium. RESULTS: Chorea developed between 30 minutes and 3 hours after ingestion of valproic acid, and the duration of the episodes varied between 30 minutes and 8 hours. The episodes of chorea occurred frequently for several days followed by asymptomatic periods lasting several weeks. Choreic movements involved the head, mouth, tongue, trunk, and limbs bilaterally in two cases and contralaterally in the patient with the caudate lesion. In one case, it was necessary to withdraw valproic acid treatment, while in the other two cases, replacement of valproic acid by divalproex sodium sprinkles presumably decreased peak concentrations and resulted in resolution with no recurrence of the chorea. CONCLUSIONS: Valproic acid-associated chorea occurred in patients with severe epilepsy and brain damage. It may occur after several years of valproic acid use and may be more likely to develop if valproic acid is taken together with phenytoin. Because valproic acid-associated chorea seemed to be dose related, avoiding excessive fluctuations of serum levels by the use of divalproex sodium sprinkles may be an effective solution in these cases.

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Induction by suggestion has previously been reported to be effective in the diagnosis of psychogenic seizures (PS). However, the sensitivity and specificity of this procedure has not previously been studied. Results of induction of PS by suggestion were analyzed in 93 patients with purely PS. The diagnosis of PS was based on the recording of a clinical event on video-electroencephalography, the absence of clinical or electroencephalography the absence of clinical or electroencephalographic evidence of epilepsy, and the subsequent followup and withdrawal of anticonvulsants supporting the diagnosis of PS. A control-group was composed of 20 patients with epilepsy in which induction was tried. Both groups were comparable for age, sex, and educational level. Induction was performed following a standardized protocol. The test was carried out placing a colored patch on the neck. The test was considered positive when the induced clinical events were typical, according to a witness familiar with the patient's seizures. Induction was positive in 72 of 93 cases with PS and in none with epilepsy. Sensitivity of this test for the diagnosis of PS was 77.4%, specificity 100%, positive predictive value 100%, and negative predictive value 48.7%.

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We reviewed records of 85 patients with juvenile myoclonic epilepsy (JME) for significant asymmetries in clinical seizures or the EEG. We noted asymmetries in 26 of 85 patients (30.6%). Only 2 patients had both clinical and EEG asymmetries; 12 had clinical asymmetries and 12 had EEG asymmetries exclusively. Analysis of patients with and without asymmetries showed no statistically significant differences in comparisons of sex, age at seizure onset, family history of epilepsy, seizure type, or response to treatment. The delay in diagnosis was greater in JME patients with asymmetries (9.5 years) than in JME patients with no asymmetries (7.5 years), but this difference was not statistically significant. Fourteen of the 26 patients with asymmetries (53.8%) were initially misdiagnosed as having partial seizures. Asymmetries in JME patients are not only common, but are also a frequent cause of misdiagnosis.

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Circling seizures (CS) have been described in association with focal lesions as well as with generalized EEG discharges. We report 1 patient with juvenile myoclonic epilepsy (JME) who developed CS. There were no focal findings on clinical examination, EEG, or imaging studies. We propose that CS in this patient may represent a profound asymmetry in expression of an idiopathic generalized epilepsy rather than a partial condition.

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A 30-year-old man with long-standing localization-related epilepsy and mental retardation had seizures that were partially controlled with valproate (VPA) 500 mg four times daily. Routine examination showed severe thrombocytopenia with mild leukopenia and chronic low-grade hemolytic anemia. Pertinent laboratory results included positive ANA, rheumatoid factor, anti-NIA, circulating immune complexes, and antihistone antibody. The patient was treated with high dosage prednisone with partial improvement, but continued to have exacerbations at lower dosages. Fourteen months later, VPA was discontinued, and rapid improvement ensued. Prednisone was subsequently discontinued, and the patient has now maintained normal platelet counts for 18 months.

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The clinical characteristics, psychosocial background, neuropsychological testing, clinical and social outcome were analysed in 93 adults with psychogenic seizures (PS). Thirteen (14%) were males and 80 (86%) were females. Mean age was 31.7 years (range 16 to 55 years). Lack of responsiveness associated with motor activity was the most common finding. Neuropsychological testing done in 46 cases revealed hysteroid traits and coping mechanisms and depression to be the most prevalent underlying problems. History of sexual abuse was evident in 10 (10.7%) cases. Social impact analysis revealed that of 62 patients who were working at the onset of PS, 34 were not working at the time of the diagnosis of PS. In 25 cases, PS were the reason for not working. After a mean follow-up of 60.7 months done in 63 patients, 16 (25.4%) patients were seizure-free. There were no obvious significant predictors of poor prognosis.

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A developmentally normal 4-year-old white female who presented with pain in the right hand as the only manifestation of epilepsy is reported. Two years later, she developed complex partial seizures following right-hand pain. Computed tomography and magnetic resonance imaging were unremarkable. Prolonged ambulatory electroencephalography (EEG) as well as video-EEGs with ictal pain episodes failed to reveal abnormalities. Only a full night video-EEG performed after antiepileptic drug withdrawal demonstrated 2 right-hand pain episodes followed by a complex partial seizure with ictal epileptiform activity on the scalp EEG in the left parasagittal area, rapidly generalized and interictal discharges in the C3-P3 area. This patient had a very unusual presentation of epilepsy.

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To assess the clinical characteristics of valproate (VPA)-associated pancreatitis, information from three sources was gathered: (a) a survey among 507 physicians with a special interest in treatment of epilepsy, (b) a review of the authors' patient population, and (c) a review of the literature. Of 366 physicians answering the survey, 53 (14.5%) reported a case of pancreatitis. Thirty-nine cases were available for review (24 from the medical literature, 12 from the survey, and 3 from the authors). Pancreatitis appeared to be more frequent in young persons (mean age 16.4 years) but may occur at any age. The highest risk appears to exist during the first months of treatment: 43.8% of the cases developed during the first 3 months, and 68.8% developed during the first year. Seventy-six percent of patients were receiving polytherapy, and 41% had some form of associated chronic encephalopathy. In most patients, the reaction was rapidly reversible when VPA was discontinued. It was severe in 6 patients, with 3 deaths reported. Rechallenge with VPA was attempted in 9 patients, with a high incidence of relapses. Asymptomatic elevation of serum amylase in patients receiving VPA was reported by 40 (10.9%) of the physicians surveyed. Awareness of the problem and early discontinuation of VPA may be effective in preventing serious reactions.

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Strokes are the most common cause of epilepsy in the elderly. Seizures after an acute stroke have been estimated to occur in 5% to 10% of cases. A distinction between early and late seizures should be made. Early seizures are more common, occur very early in the evolution of the stroke, and tend to be focal motor, brief, and isolated. They are likely to be the result of an acute local brain metabolic alteration induced by the cerebrovascular event, and once these derangements are reversed, seizures disappear. Epilepsy usually does not follow early seizures, but the risk is probably increased. Late seizures occur months to years after the stroke and are probably due to structural brain abnormalities leading to the development of an epileptic focus. The majority of these cases develop epilepsy. The risk of seizures is markedly increased when the cerebrovascular event involves the cerebral cortex. Deep-seated hemispheric or infratentorial lesions rarely produce seizures or epilepsy. It is possible that hemorrhagic stroke carries a higher incidence of seizures, but the issue remains controversial. It has also been suggested that embolic infarction has a higher incidence of seizures that does thrombotic infarction, but definitive evidence is lacking. The presence of seizures in an acute stroke does not seem to correlate with the size of the lesion, functional outcome, or mortality. Prophylactic treatment with antiepileptic drugs is probably not indicated in most types of strokes, except for subarachnoid hemorrhage after a ruptured intracranial aneurysm. When early seizures develop, treatment is indicated but may not be necessary for a prolonged period of time. If late seizures develop, chronic anticonvulsant therapy is recommended.

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