dc.creatorCendes F.
dc.creatorSakamoto A.C.
dc.creatorSpreafico R.
dc.creatorBingaman W.
dc.creatorBecker A.J.
dc.date2014
dc.date2015-06-25T17:49:29Z
dc.date2015-11-26T15:22:56Z
dc.date2015-06-25T17:49:29Z
dc.date2015-11-26T15:22:56Z
dc.date.accessioned2018-03-28T22:32:03Z
dc.date.available2018-03-28T22:32:03Z
dc.identifier
dc.identifierActa Neuropathologica. Springer Verlag, v. 128, n. 1, p. 21 - 37, 2014.
dc.identifier16322
dc.identifier10.1007/s00401-014-1292-0
dc.identifierhttp://www.scopus.com/inward/record.url?eid=2-s2.0-84903819427&partnerID=40&md5=bce0de0ab37d48546b38d63cce5690c2
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/85668
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/85668
dc.identifier2-s2.0-84903819427
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1260432
dc.descriptionHippocampal sclerosis (HS) is considered the most frequent neuropathological finding in patients with mesial temporal lobe epilepsy (MTLE). Hippocampal specimens of pharmacoresistant MTLE patients that underwent epilepsy surgery for seizure control reveal the characteristic pattern of segmental neuronal cell loss and concomitant astrogliosis. However, classification issues of hippocampal lesion patterns have been a matter of intense debate. International consensus classification has only recently provided significant progress for comparisons of neurosurgical and clinic-pathological series between different centers. The respective four-tiered classification system of the International League Against Epilepsy subdivides HS into three types and includes a term of "gliosis only, no-HS". Future studies will be necessary to investigate whether each of these subtypes of HS may be related to different etiological factors or with postoperative memory and seizure outcome. Molecular studies have provided potential deeper insights into the pathogenesis of HS and MTLE on the basis of epilepsy-surgical hippocampal specimens and corresponding animal models. These include channelopathies, activation of NMDA receptors, and other conditions related to Ca2+ influx into neurons, the imbalance of Ca2+-binding proteins, acquired channelopathies that increase neuronal excitability, paraneoplastic and non-paraneoplastic inflammatory events, and epigenetic regulation promoting or facilitating hippocampal epileptogenesis. Genetic predisposition for HS is clearly suggested by the high incidence of family history in patients with HS, and by familial MTLE with HS. So far, it is clear that HS is multifactorial and there is no individual pathogenic factor either necessary or sufficient to generate this intriguing histopathological condition. The obvious variety of pathogenetic combinations underlying HS may explain the multitude of clinical presentations, different responses to clinical and surgical treatment. We believe that the stratification of neuropathological patterns can help to characterize specific clinic-pathological entities and predict the postsurgical seizure control in an improved fashion. © 2014 Springer-Verlag.
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dc.languageen
dc.publisherSpringer Verlag
dc.relationActa Neuropathologica
dc.rightsfechado
dc.sourceScopus
dc.titleEpilepsies Associated With Hippocampal Sclerosis
dc.typeArtículos de revistas


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