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• W24992107 abstract "Seizures are a symptom of several neurologic and medical diseases; each with different causes, ictal signs, and neuropathologic substrates. Understanding the epileptogenic process, especially if it is intractable and chronic, requires a knowledge of that syndrome's pathophysiology and pathogenesis. Perhaps one of the best characterized of the chronic human epilepsies is mesial temporal lobe epilepsy (MTLE). Clinical reports have described this syndrome's behavioral and EEG features, and pathologic studies have proposed possible pathophysiologic mechanisms (Weiser et al. , 1993 . For example, MTLE patients who undergo surgery for seizure control most often have focal pathologies in their surgical specimens, and this finding supports the pathophysiologic concept that temporal lobe pathologies, like hippocampal sclerosis, probably “cause” this syndrome ( Babb and Brown, 1987 ; Mathern et al. , 1995d ). Unfortunately, one problem with clinically derived hypotheses is that they are principally generated from retrospectively collected data (i.e., after surgery and pathologic examination), and prospective clinical trials are probably no longer feasible. Hence, “cause-and-effect” hypotheses generated from retrospective clinical studies should be viewed with some caution; however, there is another way to test pathophysiologic concepts and that is with the use of animal models. Nonetheless, in order for animal studies to be relevant to patients with MTLE the model should look like the human syndrome, and several criteria have been proposed ( Ben-Ari, 1985 ; Mathern et al. , 1996d,f ) 1. The hippocampus, amygdala, and other limbic structures should play a central role in the chronic ictal semiology." @default.
• W24992107 created "2016-06-24" @default.
• W24992107 creator A5056220869 @default.
• W24992107 date "1999-01-01" @default.
• W24992107 modified "2023-09-27" @default.
• W24992107 title "Hippocampal Pathophysiology in Experimental Models" @default.
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