Faculty Bibliography

BACKGROUND: Epileptic and nonepileptic seizures can occur in the same patient, but usually occur at different times. In 1885, Gowers suggested that minor seizures can elaborate into hysterical seizures, but the concurrence of epileptic and nonepileptic seizures is not well documented. METHODS: We reviewed all patients with nonepileptic seizures documented with video-EEG recordings at our center to identify those with temporally associated epileptic seizures. RESULTS: Four patients were identified in whom video-EEG-documented epileptic seizures were temporally associated with nonepileptic seizures. In one woman, the nonepileptic event followed an absence seizure. Given the high frequency of absence seizures, the occurrence of the nonepileptic seizure may have been coincidental. In three patients, the seizures were partial and arose from right frontotemporal regions. In these patients, epileptic seizures were infrequent. CONCLUSIONS: Epileptic and nonepileptic seizures can be temporally related, and in patients with partial seizures, there may be a pathophysiologic relation in which ictal changes facilitate the development of conversion symptoms. Ictal activation or disinhibition of emotions or impulse control may contribute to these nonepileptic events

PURPOSE: To examine the role of head injury as a risk factor in the development of nonepileptic seizures (NES). Specifically, we will determine the relative frequency of head injury among NES patients referred to our center and will describe several pertinent clinical features and personal characteristics. METHODS: Retrospective record review of patients referred to our center for evaluation of seizures over a 4-year period. All patients with NES were evaluated as in a previously described protocol, which included intensive video EEG monitoring, provocation by suggestion, and psychiatric interview. All NES patients with a history of head injury were extracted for this report. RESULTS: Of 102 patients with NES, nearly one-third (32%) had an antecedent head injury; 52% were male, mean age was 34 years, and 12% had coexisting epilepsy. Multiple psychiatric disorders were not uncommon (79%), and a history of abuse was found in 35%. All but four patients had documented financial gain from their injury. Follow-up at 1 year found poor long-term outcome with lasting disability; despite that, the majority (91%) of head injuries were minor. CONCLUSIONS: Our preliminary findings suggest that prior head injury is associated with the development of NES and may contribute to the pathogenesis of NES in vulnerable patients. Head injury and sexual or physical abuse appear to occur in comparable proportions in patients with NES. This suggests that head injury and abuse may be equally important risk factors in the development of NES

The electroencephalographic abnormalities seen in Landau-Kleffner syndrome (LKS) (language deterioration) are non-specific, and consist of a variety of epileptiform discharge patterns including continuous slow spike-wave discharges during sleep, focal sharp waves with spikes, and centrotemporal (rolandic) spikes. Similarly, the EEG abnormalities seen in autistic epileptiform regression (language and social/behavioral deterioration) are non-specific and overlap with those seen in LKS. By contrast, distinct epilepsy syndromes in otherwise normal children occur in the EEG-defined benign focal epilepsies of childhood. Occipital spikes or spike-wave present either in the older child with visual symptoms and headache or in the younger child with autonomic symptoms followed by brief or prolonged partial motor seizures. Seven young children (five from a consecutive series of 42) presenting clinically with autism or autistic regression and possible or definite seizures, whose EEGs revealed occipital spikes or spike-wave characteristic of the benign epilepsies, are reported. Although occipital spikes are commonly seen in young children as an age-dependent EEG-defined benign focal epilepsy, their high frequency in this population with cognitive difficulties suggests a possible causal relation. The effects of the epileptiform discharge on cognitive functioning presumably reflect extension into temporal and parietal lobes, rather than occipital disturbances per se

The pharmacokinetics and adverse effects of an oral loading dose of carbamazepine administered in tablet or suspension form were studied. Patients on a hospital epilepsy unit who were to receive carbamazepine as a discharge medication were randomly assigned to receive either an oral 8-mg/kg loading dose of the tablet formulation or the same dose of the suspension on an empty stomach. Blood samples were drawn before and at intervals up to 12 hours after the loading dose. Adverse effects were evaluated subjectively and objectively. Total and free serum carbamazepine and carbamazepine-10, 11-epoxide (CBZE) concentrations were determined by high-performance liquid chromatography. Six adult patients were enrolled in and completed the study. All the patients achieved therapeutic total carbamazepine levels; the suspension group did so within two hours and the tablet group within five hours. Maximum serum carbamazepine concentrations ranged from 7.10 to 9.92 mg/L, area under the concentration-versus-time curve from 54.85 to 82.23 micrograms.hr/L, and terminal elimination half-life from 14.05 to 15.71 hours. Adverse effects were mild, few, and short-lived; none of the patients developed gastrointestinal toxicity. Adverse effects were not associated with total or free carbamazepine and CBZE concentrations or with total or free CBZE:carbamazepine ratios. An oral loading dose of carbamazepine 8 mg/kg achieved therapeutic levels within two hours when given as a suspension and within five hours when given as tablets and was well tolerated in all patients