title: Neuron tolerance during hydrocephalus.
abstract: Whether or not neuron death plays a major role in pathophysiology during hydrocephalus is not well known. The goals of this study were to determine if neural degeneration occurred during hydrocephalus, and to determine if neuron tolerance developed during this pathophysiologic procedure.Neural damage as visualized by a sensitive staining technique, silver impregnation, was observed in three experimental groups: (1) adult hydrocephalic rats induced by kaolin injection into the cisterna magna, (2) adult rats with chronic hydrocephalus for 10 weeks subjected to acute forebrain ischemia induced by four-vessel occlusion, and (3) adult rats without hydrocephalus subjected to acute forebrain ischemia. The magnitude of hydrocephalus was also evaluated during this time. In mild or moderate hydrocephalus, little cell death was found. In severe hydrocephalus, axon and neuropil degeneration was extensively distributed, but cell death was still rarely observed. Although some neuron degeneration was found after acute forebrain ischemia in hydrocephalic rats, the extensive cell death in cortical layers III and V, and in hippocampal areas CA1 and CA4 that is commonly observed in the ischemic brain without hydrocephalus, was not seen. This study suggests that neuron death was not a major pathological change in the brain during hydrocephalus, with cerebral ventricles being enlarged during the development of hydrocephalus. Less neuron death in hydrocephalic rats after acute forebrain ischemia suggests that neuronal tolerance to ischemia occurs during hydrocephalus.
authors.affiliation: Department of Neurological Surgery, Wayne State University School of Medicine, Detroit, MI 48201, USA. yding@neurosurgery.wayne.edu
authors.forename: Y
authors.initials: Y
authors.lastname: Ding
authors.forename: J P
authors.initials: JP
authors.lastname: McAllister
authors.forename: B
authors.initials: B
authors.lastname: Yao
authors.forename: N
authors.initials: N
authors.lastname: Yan
authors.forename: A I
authors.initials: AI
authors.lastname: Canady
mesh_terms: D000818:Animals; D001369:Axons / Q000473:pathology; D001921:Brain / Q000473:pathology / Q000503:physiopathology*; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology*; D002470:Cell Survival / Q000502:physiology*; D002540:Cerebral Cortex / Q000473:pathology / Q000503:physiopathology; D002552:Cerebral Ventricles / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology*; D003712:Dendrites / Q000473:pathology; D006624:Hippocampus / Q000473:pathology / Q000503:physiopathology; D006849:Hydrocephalus / Q000473:pathology / Q000503:physiopathology*; D007616:Kaolin / Q000494:pharmacology; D009410:Nerve Degeneration / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D009474:Neurons / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D016622:Silver Staining
chemical_list: D007616:Kaolin