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Showing papers on "Epileptogenesis published in 1979"


Journal ArticleDOI
TL;DR: Evidence is presented suggesting that the neural effect of iron released from hemoglobin may be causally related to the development of a trauma-induced epileptiform focus in humans.

105 citations


Journal ArticleDOI
08 Jun 1979-Science
TL;DR: The results suggest that alteration of synaptic sensitivity to acetylcholine may contribute to kindling and epileptogenesis.
Abstract: Kindling is an experimental model of epilepsy in which periodic brain stimulation induces the progressive development of electrical and behavioral seizures. A kindling-induced electrical seizure (afterdischarge) in the rat hippocampus produces prolonged neuronal supersensitivity to microiontophoretically applied acetylcholine after a latency of 40 to 60 minutes. Neuronal acetylcholine supersensitivity is correlated with the further progression of kindling. A larger hippocampal after-discharge is elicited by a subsequent kindling stimulus delivered in the presence of acetylcholine supersensitivity, but not by one delivered before the onset of the supersensitivity. The results suggest that alteration of synaptic sensitivity to acetylcholine may contribute to kindling and epileptogenesis.

78 citations


Journal ArticleDOI
TL;DR: The hypothesis that 5-HT neurons can serve to inhibit seizures is supported, as the lack of robustness across parameters of epileptogenesis as well as discrepant findings related to 5- HT depletion mode suggest that kindled seizures affect other neuronal populations in addition to those under serotonergic influence.

67 citations


01 Sep 1979
TL;DR: Defined alterations in restricted neuronal pathways of the mouse brain produced by single locus mutations can be used to infer general principles of inherited epileptogenesis, and may provide specific biological test systems for the development of more selective chemical antagonists of seizure activity.
Abstract: The neurological expression of mutations at defined gene loci in isogenic mice provides a singular opportunity to investigate the developmental pathophysiology of inherited central nervous system (CNS) diseases Analysis of the single locus mutants that are currently available shows that CNS diseases that include spontaneous seizures as symptoms can be inherited as simple recessive traits Mutant gene dose is highly correlated with the spontaneous occurrence of seizures Single gene defects at one of multiple chromosomal loci may give rise to similar epileptic patterns One mutation, tottering (tg, chromosome 8, recessive) produces in young mice a focal motor seizure pattern with a somatotopic progression, and behavioral absence seizures accompanied by abnormal bursts of bilaterally synchronous, spike-wave discharges in the electrocorticogram Spontaneous electrographic and clinical seizures of this general pattern bear close resemblance to common forms of human epilepsy Defined alterations in restricted neuronal pathways of the mouse brain produced by single locus mutations can be used to infer general principles of inherited epileptogenesis, and may provide specific biological test systems for the development of more selective chemical antagonists of seizure activity

44 citations


Journal ArticleDOI
TL;DR: The results seem to support the hypothesis that accumulation of [K+]0 is related to development of early epilepsy, and high K+ solutions directly applied to the cortex produced spiking and seizures.
Abstract: Clinical studies indicate that early epilepsy after head injury may be associated with some transient and reversible pathophysical processes of the brain. It has been proposed that epileptogenesis ...

8 citations


Journal ArticleDOI
TL;DR: An important role of specific and nonspecific factors of epileptogenesis in the formation of experimental photogenic epilepsy is indicated.
Abstract: The character of formation of an experimental syndrome of photogenic epilepsy, obtained by creating a generator of pathologically enhanced excitation in the lateral geniculate body by local injection of tetanus toxin, was studied in chronic experiments on rats. The initial manifestations appearing in the animals were shown to be due to pathological enhancement of specific sensory excitation in the lateral geniculate body and to be accompanied by a marked increase in amplitude of the evoked potential in the visual cortex. The subsequent development of a neuropathological syndrome was connected with diffuse disturbances of rhythmic electrical activity of the brain, characteristic of a state of increased epileptic predisposition in the experimental animals. The results of these experiments indicate an important role of specific and nonspecific factors of epileptogenesis in the formation of experimental photogenic epilepsy.

1 citations