The epileptogenic properties of cefazolin (CFZ) were utilized to induce an electrophysiological pattern of epilepsy in the rabbit. CFZ, cortically applied in different concentrations (2 or 4%), produced epileptic activity in a degree proportional to the concentration of the substance. In this experimental epilepsy model, we evaluated the effects of increasing doses (0.025, 0.05, and 0.1 mg/kg i.v.) of the calcium antagonist nimodipine (Bay e 9736). In the evaluation of nimodipine effects, the spike-and-wave burst frequency per minute was taken into account. These data were compared with those of placebo-treated (Bay e 9736 control test) control groups and statistically evaluated by two-tailed t test. In 2% CFZ-induced epilepsy, nimodipine at the 0.025- and 0.05-mg/kg doses did not produce significant changes in the EEG pattern. A statistically significant reduction (p less than 0.001) in epileptic activity was observed at the 0.1-mg/kg nimodipine dose. This reduction was seen first in the contralateral focus leads and persisted for the entire time of observation. In the more intense epileptic form (4% CFZ), nimodipine at the doses employed did not induce noteworthy EEG modifications. These data indicate that nimodipine exerts an antiepileptic effect. The possible mechanisms involved in this activity of a calcium antagonist are discussed.
Two neuro-Behçet patients have been studied, over a period of several months, by means of peroneal and median somatosensory- (SEP), brainstem auditory- (BAEP), and visual- (VEP) evoked potentials. In both patients, peroneal SEP showed evidence of a pathological reduction in the central conduction velocity without a related deep sensation impairment, while VEP changes were consistent with the visual disorders. Conversely, BAEP and median SEP findings did not show disease-related abnormalities. The observed anomalies were detectable irrespective of the clinical phase of the disease. Thus, evoked potential assessment is useful in providing objective evidence for evaluating and monitoring CNS damage in neuro-Behçet's syndrome.
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