Showing papers on "Epileptogenesis published in 1983"

The current status of taurine in epilepsy.

Abstract: The part played by taurine in epileptogenesis is still controversial. A cortical deficit of the amino acid has been confirmed only in certain types of human and animal epilepsy, and the effects of an artificial change of taurine cortical concentration are inconclusive. An increase is associated with a reduced susceptibility to epileptogenic agents but not with the prevention of epilepsy, while a decrease may precipitate seizure activity in genetically susceptible rats but does not bring about spontaneous epileptic activity in normal animals. The role of taurine in synaptic transmission is uncertain (specific inhibitory neurotransmitter, indirect modulator of membrane excitability), and its antiepileptic action, confirmed in several models of experimental epilepsy and in short-term clinical studies, does not seem to possess major clinical relevance since trials with a longer follow-up gave unsatisfactory results. Taurine's limited diffusibility across the blood-brain barrier may be the main factor restricting the antiepileptic effect of this compound.

Mechanisms of epileptogenesis in brain-slice model systems.

Abstract: Studies of the mechanisms of epileptogenesis in brain-slice model systems have indicated that there are three underlying processes which interact with one another and lead to the development of interictal discharge. These include (a) intrinsic burst activity, (b) disinhibition, and (c) excitatory synaptic coupling. Intrinsic membrane excitability may be altered by neuromodulators, injury, genetic, and other factors. Disinhibition in effect releases intrinsic burst generating capacities in populations of neurons, and may become an important factor following cortical injury or repetitive activation of inhibitory circuits. Excitatory synaptic coupling is required for evoking intrinsic burst discharges, and also to synchronize populations of neurons. EPSPs also serve as one of the generators for slow depolarization shifts. The contribution of each of these factors to epileptogenesis presumably varies with a type of pathological process and the properties of the involved neuronal population.

Anti-epileptic effects of TRH-T and DN-1417.

Abstract: Antiepileptic effects of both TRH tartrate (TRH-T) and its derivative, γ-butyrolactone-γ-carbonyl-L-histidyl-L-prolinamide citrate (DN-4417) have been evaluated using the amygdaloid kindling cat preparation. The results reported are: 1) transient anticonvulsant effects unrelated to dose for both TRH-T and DN-1417, 2) long-term elevation of the final electroconvulsive threshold in some cats after TRH-T and DN-1417 treatment, 3) prophylactic effects on kindling seizure development as well as effects to prevent positive transfer of the kindling to the contralateral amygdala after daily treatment with DN-1417, 4) a shortened postictal behavioral depression and EEG silence with DN-1417 and 5) a prolonged postictal seizure inhibition period with DN-1417. It is hypothesized that endogenous TRH inhibits seizure activity and reduces the establishment of epileptogenesis in the brain.

Posttraumatic early epilepsy and minor head injury.

Abstract: The mechanism of “early epilepsy” sometimes observed after trivial head injury is controversial. Also, the risk of developing late epilepsy after these convulsions, so far, have not been clear.In order to clarify the mechanism of this posttraumatic early epilepsy after trivial head injury, an attempt was made to observe the role of extracellular potassium ion concentration ([K+]o) in initiation of seizure discharges, in both adult cats and kittens, with K-sensitive microelectrodes.It was concluded that an increase of [K+]o was not a simple factor for epileptogenesis but minor head injury actually increased seizure slisceptability of immature cat cortex.