A pathogenetic hypothesis of temporal lobe epilepsy. 1993

M Simonato
Institute of Pharmacology, University of Ferrara, Italy.

Temporal lobe epilepsy is the most common type of epilepsy in adults. It frequently develops in previously normal nervous tissue, secondary to trauma, tumour or stroke. The disease has a tendency to progress toward generalization and neurologic deficits. The pathogenesis of temporal lobe epilepsy is still unclear. In this article, a hypothesis is proposed suggesting that a cascade of biological events may underlie its development and progression. These include increased excitatory amino acid release, NMDA receptor activation, influx of calcium into neurones, activation of calcium-dependent enzymes (including phospholipase A2), immediate early gene expression, and synthesis of new proteins. Positive and negative feedback loops as well as other events, taking place in parallel, are also hypothesized. The clinical and pharmacological ramifications of this working hypothesis are discussed.

UI MeSH Term Description Entries
D007696 Kindling, Neurologic The repeated weak excitation of brain structures, that progressively increases sensitivity to the same stimulation. Over time, this can lower the threshold required to trigger seizures. Kindlings, Neurologic,Neurologic Kindling,Neurologic Kindlings
D008954 Models, Biological Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment. Biological Model,Biological Models,Model, Biological,Models, Biologic,Biologic Model,Biologic Models,Model, Biologic
D004833 Epilepsy, Temporal Lobe A localization-related (focal) form of epilepsy characterized by recurrent seizures that arise from foci within the TEMPORAL LOBE, most commonly from its mesial aspect. A wide variety of psychic phenomena may be associated, including illusions, hallucinations, dyscognitive states, and affective experiences. The majority of complex partial seizures (see EPILEPSY, COMPLEX PARTIAL) originate from the temporal lobes. Temporal lobe seizures may be classified by etiology as cryptogenic, familial, or symptomatic. (From Adams et al., Principles of Neurology, 6th ed, p321). Epilepsy, Benign Psychomotor, Childhood,Benign Psychomotor Epilepsy, Childhood,Childhood Benign Psychomotor Epilepsy,Epilepsy, Lateral Temporal,Epilepsy, Uncinate,Epilepsies, Lateral Temporal,Epilepsies, Temporal Lobe,Epilepsies, Uncinate,Lateral Temporal Epilepsies,Lateral Temporal Epilepsy,Temporal Lobe Epilepsies,Temporal Lobe Epilepsy,Uncinate Epilepsies,Uncinate Epilepsy
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D015870 Gene Expression The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION. Expression, Gene,Expressions, Gene,Gene Expressions
D016194 Receptors, N-Methyl-D-Aspartate A class of ionotropic glutamate receptors characterized by affinity for N-methyl-D-aspartate. NMDA receptors have an allosteric binding site for glycine which must be occupied for the channel to open efficiently and a site within the channel itself to which magnesium ions bind in a voltage-dependent manner. The positive voltage dependence of channel conductance and the high permeability of the conducting channel to calcium ions (as well as to monovalent cations) are important in excitotoxicity and neuronal plasticity. N-Methyl-D-Aspartate Receptor,N-Methyl-D-Aspartate Receptors,NMDA Receptor,NMDA Receptor-Ionophore Complex,NMDA Receptors,Receptors, NMDA,N-Methylaspartate Receptors,Receptors, N-Methylaspartate,N Methyl D Aspartate Receptor,N Methyl D Aspartate Receptors,N Methylaspartate Receptors,NMDA Receptor Ionophore Complex,Receptor, N-Methyl-D-Aspartate,Receptor, NMDA,Receptors, N Methyl D Aspartate,Receptors, N Methylaspartate

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