ISCHEMIC BRAIN-DAMAGE AND MEMORY IMPAIRMENT - A COMMENTARY

Authors
Citation
Lr. Squire et Sm. Zola, ISCHEMIC BRAIN-DAMAGE AND MEMORY IMPAIRMENT - A COMMENTARY, Hippocampus, 6(5), 1996, pp. 546-552
Citations number
50
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
10509631
Volume
6
Issue
5
Year of publication
1996
Pages
546 - 552
Database
ISI
SICI code
1050-9631(1996)6:5<546:IBAMI->2.0.ZU;2-H
Abstract
Studies in humans and monkeys have identified structures in the medial temporal lobe essential for memory (the hippocampal region, i.e., the dentate gyrus, the hippocampus, and the subicular complex, and the ad jacent perirhinal, entorhinal, and parahippocampal cortices). Addition al work has revealed that for both species, damage limited to the hipp ocampal region produces less severe memory impairment than damage that includes additional structures within the medial temporal robe. This work has been based on both neurosurgical lesions and on lesions produ ced by global ischemia or anoxia. An important issue about ischemic da mage is whether the damage identifiable in histopathological examinati on provides an accurate estimate of direct neural damage or whether ad ditional direct damage might be present that is sufficient to disrupt neuronal function in areas important for memory and sufficient to impa ir behavioral performance, but not sufficient to progress to cell deat h and to be detectable in conventional histopathology. This commentary explores the issue of ischemic damage and memory impairment. Although few studies have addressed this issue directly, the currently availab le data from global ischemia in rats, monkeys, and humans are consiste nt with the hypothesis that the detectable neuronal damage is responsi ble for the severity of the observed behavioral impairment. Yet it is also true that this hypothesis has not been the target of very much sy stematic work. We encourage additional experimental work, especially i n rats, that could further illuminate how to evaluate the behavioral e ffects of ischemic lesions. (C) 1996 Wiley-Liss, Inc.