Showing papers on "Epileptogenesis published in 1982"

Normal Brain Distribution of Carbamazepine in Cat Penicillin Focal Epilepsy

Abstract: Carbamazepine (CBZ) brain distribution was studied in cats rendered epileptic by penicillin topically applied on neocortex. CBZ penetration into the focus did not differ significantly from penetration into the other areas of the brain, with the drug rapidly entering the cerebral tissue (peak at 30 min). As no difference was found between CBZ brain concentrations at 15 and 90 min, substantial early binding of the drug was confirmed in this experimental model of epilepsy. As CBZ was able to decrease rapidly the spike frequency of the penicillin focus, it may be speculated that it was also able to prevent the metabolic alterations associated with severe epileptogenesis that would have caused an impaired CBZ brain distribution.

Clinical Significance of Secondary Epileptogenesis

Abstract: A possible existence of secondary epileptogenesis in humans was examined encephalographically and clinically. In the study of 128 patients with temporal foci who were followed up for about five years, the EEG foci changed from unilateral to bilateral (in 25/84) and from bilateral to unilateral (in 17/44). After status epilepticus, a new focus was found encephalographically in addition to the previous foci in one of the patients. The patients with bitemporal foci were found to be more therapy-resistant than those with a unitemporal focus. The mode of evolution of partial seizures was investigated in long-term histories of four patients with visual seizures and complex partial seizures who had occipital and temporal foci independently in the interictal EEG. In one patient the visual seizure at onset combined with a complex partial seizure after the fifth year, although only former seizure events had been documented on videotape. Through careful observations of a number of simultaneous video recordings of clinical and encephalographic features, not one patient showed two different partial seizures originating at separate foci. Therefore, we failed to obtain the definitive evidence of clinieoencephalographic secondary epileptogenesis, despite the fact that the existence of encephalographic secondary epileptogenesis seemed to be possible.

Therapeutic concentration of antiepileptic drugs and the severity of epileptogenesis.

Abstract: In sodium valproate monotherapy for generalized seizures and carbamazepine for partial seizures, it was found in a within-patient follow-up study that the effect-developing concentrations which were sufficient to suppress the clinical seizures were significantly higher than the effect-sustaining concentrations by which longstanding suppression was maintained. There was a delayed onset of therapeutic effect which worked to suppress the clinical and electrographic seizure manifestations, and the length of the delay depended on the nature of the epilepsy. In animal experiments, the possibility that the severity of epilepsy may become milder as a consequence of successful pharmacotherapy was reconfirmed in amygdaloid-kindled cats on chronic medication in place of kindling animals on acute prophylactic medication. Only when the established generalized seizures were completely suppressed, was the generalized seizure triggering threshold evidently elevated. Since epilepsy is a long-standing condition lasting for years to decades, short-spanned cross-sectional observations are often misleading. Whatever relationship might exist between the blood levels of antiepileptic drugs and the paroxysmal discharges in the EEG, the severity of epileptogenesis as well as the longitudinal time course must always be taken into consideration in the drug treatment of epilepsy.

Binding of [3H]-L-glutamate with synaptic membranes isolated from the cerebral cortex and hippocampus of krushinskii-molodkina rats

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