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Titolo:
Neuroprotection: A new therapeutic option in the treatment of epilepsy?
Autore:
Schurks, M; Wiegand, F; Diener, HC;
Indirizzi:
Univ Essen Gesamthsch Klinikum, Neurol Klin & Poliklin, D-45122 Essen, Germany Univ Essen Gesamthsch Klinikum Essen Germany D-45122 5122 Essen, Germany Janssen Gilag, Neuss, Germany Janssen Gilag Neuss GermanyJanssen Gilag, Neuss, Germany
Titolo Testata:
AKTUELLE NEUROLOGIE
fascicolo: 7, volume: 28, anno: 2001,
pagine: 326 -
SICI:
0302-4350(200109)28:7<326:NANTOI>2.0.ZU;2-7
Fonte:
ISI
Lingua:
GER
Soggetto:
TEMPORAL-LOBE EPILEPSY; HIPPOCAMPAL NEURONAL DAMAGE; TRANSIENT CEREBRAL-ISCHEMIA; RESISTANT KINDLED RATS; GLOBAL-ISCHEMIA; ANTICONVULSANT EFFICACY; FOREBRAIN ISCHEMIA; GERBIL MODEL; BRAIN-DAMAGE; CA1 NEURONS;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
59
Recensione:
Indirizzi per estratti:
Indirizzo: Schurks, M Univ Essen Gesamthsch Klinikum, Neurol Klin & Poliklin, Hufelandstr 55, D-45122 Essen, Germany Univ Essen Gesamthsch Klinikum Hufelandstr 55 Essen Germany D-45122
Citazione:
M. Schurks et al., "Neuroprotection: A new therapeutic option in the treatment of epilepsy?", AKT NEUROL, 28(7), 2001, pp. 326

Abstract

The primary aim in treating patients with epilepsy is the suppression of seizures. Apart from this symptomatic treatment so far no pharmacological approach exists to alter the natural course of the disease ("disease modification"). There is clinical, as well as pre-clinical evidence that neuronal damage and an impairment of cognitive function frequently occurs during the course of epilepsy. It seems logical to investigate the feasibility of new therapeutic approaches in which neuroprotection plays a major role. The prevention of neuronal damage induced either by the pathophysiological cellular alterations generated by the disease itself, by repetetive seizures, or astatus epilepticus is of major interest. Unfortunately so far data concerning the neuroprotective potential of anticonvulsive drugs is only availablein preclinical studies. The four basic mechanisms by which neuronal damageusually occurs are (1) increased Na+-influx, (2) increased Ca2+-influx, (3) diminished GABA-ergic activity and (4) increased glutamatergic excitotoxicity through massive stimulation of ionotropic Glutamat-receptors (especially non-NMDA-receptors). This review reflects the current literature regarding the protective effects of anticonvulsive drugs.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 20:21:11