Epilepsia
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Clinical Trial
Electrophysiological studies of cervical vagus nerve stimulation in humans: I. EEG effects.
Evidence from studies of experimental animals indicates that electrical stimulation of the vagus nerve alters EEGs under certain stimulus parameters. We report EEG effects of electrical stimulation of the vagus nerve in 9 patients with medically intractable seizures as part of a clinical trial of chronic vagal stimulation for control of epilepsy. ⋯ The left vagus nerve in the neck was stimulated with a programmable implanted stimulator. Stimulation at various stimulus frequencies and amplitudes had no noticeable effect on EEG activity whether the patient was under general anesthesia, awake, or asleep, but vagus nerve stimulation may interrupt ongoing ictal EEG activity.
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Case Reports
Prolonged ictal amnesia with transient focal abnormalities on magnetic resonance imaging.
A previously healthy woman had a prolonged amnestic state caused by complex partial status epilepticus with bilateral mesiotemporal lobe involvement confirmed by EEG with nasopharyngeal electrodes. A magnetic resonance imaging (MRI) scan obtained shortly after recovery from the amnesia showed reversible focal abnormalities consisting of increased signal intensity on T2-weighted scan in the mesiotemporal lobe.
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We studied 36 drop seizures in 5 patients with myoclonic astatic epilepsy of early childhood (MAEE) with simultaneous split-screen video recording and polygraph. Sixteen were falling attacks and 20 were either less severe attacks exhibiting only deep head nodding or seizures equivalent to drop attacks in terms of ictal pattern but recorded in the supine position. All seizures except those that occurred in patients in the supine position showed sudden momentary head dropping or collapse of the whole body downward. ⋯ The AT seizure showed abrupt atonic falling, with and without transient preceding facial expression change and/or twitching of extremities. The ictal EEGs of all 36 seizures exhibited generalized bilaterally synchronous single or multiple spike(s) and wave discharges. Atonic drop attacks appear to be a common cause of ictal epileptic falling in MAEE.
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The brain uptake index (BUI) method of Oldendorf was used to examine blood-brain barrier (BBB) drug transport in mice, rats, and rabbits; felbamate (FBM) extraction (E) in a single transcapillary passage was 5-20%, and drug uptake in rat brain was not concentration-dependent. Like diazepam, FBM was retained in mouse brain. To ensure that radioactivity measurements reflected the disposition of parent drug and not some metabolite, extracts of mouse brain were prepared for further analysis. ⋯ Differences between newborn and adult rabbit BBB FBM extraction and between different anesthetic agents are attributable to cerebral blood flow (CBF) rates. The permeability-surface area products (PS = [CBF].[E]) for FBM in rats, rabbits, and mice were 0.09, 0.16 and 0.30 ml/min/g, respectively. Preliminary autoradiographic analyses of frozen brain sections suggest that [14C]FBM distributes relatively uniformly throughout the brain and that minor variations apparently are a function of differing CBF rates.
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Clinical Trial
Gamma-vinyl GABA (vigabatrin) in epilepsy: clinical, neurochemical, and neurophysiologic monitoring in epileptic patients.
We report long-term clinical, neurochemical, and electrophysiologic data of gamma-vinyl GABA (GVG, vigabatrin) in three groups of patients. GVG was started as add-on therapy for 75 patients with refractory complex partial seizures (group A) and for 36 mentally handicapped patients with severe epilepsy (group B). The third group (C) consisted of 20 patients with carbamazepine (CBZ) monotherapy, in half of whom GVG monotherapy was substituted. ⋯ After 6 (group A) and 3 years (group B) of follow-up, 27 and 33% of the patients, respectively, still had good response to GVG. Neurochemical measurements showed a twofold increase in CSF GABA concentrations and minimal or no changes in other neurotransmitter-related parameters. In group C, substitution of GVG as medication tended to normalize the lengthened latencies in somatosensory evoked potentials (SEPs) observed during CBZ treatment.