Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014547 (focal epilepsy)
 1,627 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article has three goals: (1) to review the evidence that bears upon the occurrence of secondary epileptogenesis in man, (2) to set forth the criteria that distinguish secondary epileptogenesis from multifocal epilepsy--both clinically and by pharmacologic means--and (3) to indicate the importance of an understanding of the pathophysiology of secondary epileptogenesis to clinical decision making in the care of epileptic patients. In Section I, the three different developmental stages of secondary epileptogenesis defined in experimental preparations are outlined, and particular emphasis is placed on the remarkable similarity in the electrographic manifestations reported from animal species ranging from reptile to baboon. The clinical manifestations differ depending, within species, on exactly where in the brain the primary focus is situated and, between species, on the different organizations of the neural substrate within which epileptiform discharge is engendered. Section II is devoted to a review of three separate series of patients whose presenting symptom was epilepsy and in whom the etiology proved to be a histologically verified brain tumor or malformation. The choice of patient material was dictated by the conclusion that the main barrier to acceptance of human secondary epileptogenesis is the difficulty of distinguishing between multiple primary lesions maturing at different rates and those secondarily induced by an already existing single one. In the vast majority of patients where trauma, infection, anoxia, and vascular disease represent the most common etiologies, multiple primary structural injury is an ever-present possibility. Restricting our analysis to tumors of neural, glial, or vascular origin eliminates, as far as practicable, the issue of multiple primary lesions. A significant number of patients with focal epilepsy develop secondary epileptogenic lesions. The evidence presented shows that a primary epileptogenic lesion in man may induce a trans-synaptic and long-lasting alteration in nerve cell behavior characterized by paroxysmal electrographic manifestations and clinical seizures. Furthermore, the more frequent the seizures, the more likely is a secondary focus to become permanent. These observations underscore the importance of rigorous seizure control (electrographic as well as behavioral) and raise the question of earlier surgical intervention where medicinal therapy fails.
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PMID:Varieties of human secondary epileptogenesis. 250 38

It is difficult to prove the existence of secondary epileptogenesis in man. In the majority of cases of human focal epilepsy, where the cause is likely to be trauma, infection, or vascular disease, the occurrence of additional or new epileptogenic foci is usually attributed to multiple primary injuries (maturing at different rates), or to progressive disease. Cerebral tumor is the only common cause in which the probability of multiple primary lesions is vanishingly low. Therefore, a personally followed series of cases of cerebral tumor seen as epilepsy are reviewed in which clinical, electrophysiologic, and pharmacologic data are analyzed for evidence of secondary epileptogenesis. Such evidence was found in 34% of our tumor patients. It was possible to demonstrate, in humans, the three stages of secondary epileptogenesis previously documented in animals. A pharmacologic test is described that separates the reversible from the irreversible stage of secondary epileptogenesis and allows prediction of the results of surgical removal of the primary focus.
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PMID:Secondary epileptogenesis in man. 392 Oct 8