Open AccessNeuronal Apoptosis in the Dentate Gyrus in Humans with Subarachnoid Hemorrhage and Cerebral Hypoxia
Author(s) -
MD Roland Nau,
Haase Sabine,
Bunkowski Stephanie,
MD Wolfgang Brück
Publication year - 2002
Publication title -
brain pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.986
H-Index - 132
eISSN - 1750-3639
pISSN - 1015-6305
DOI - 10.1111/j.1750-3639.2002.tb00447.x
Subject(s) - dentate gyrus , subarachnoid hemorrhage , hypoxia (environmental) , medicine , pathology , autopsy , apoptosis , cerebral hypoxia , hippocampus , neuroscience , biology , chemistry , ischemia , organic chemistry , oxygen , biochemistry
Apoptosis of dentate granule cells is a typical feature of several animal models of disease. In 20 autopsy cases of subarachnoid hemorrhage (SAH) and global cerebral hypoxia caused by protracted shock or respiratory failure, we evaluated by light microscopy and in situ tailing whether this pattern of neuronal damage also occurs in humans. In subarachnoid hemorrhage, 4.0/mm 2 (0–13.0/mm 2 ) a poptotic neurons were observed in the dentate gyrus, in cerebral hypoxia 3.6/mm 2 (0–19.9/mm 2 ) (p>0.05), and in 10 aged‐matched control cases dying rapidly from non‐neurological diseases 0/mm 2 (0–0/mm 2 ) (median [range]) (p<0.001 versus SAH and hypoxia). Neuronal apoptosis in the dentate gyrus was most frequent, when death occurred later than 24 hours and less than 11 days after disease onset. Neuronal damage in the hippocampus was always necrotic. It was more severe in hypoxia than in SAH (median neuronal damage score 3 [range: 0–3] versus 0 [0–3], p<0.001). Apoptosis appears to be the predominant mechanism of death in dentate granule cells irrespective of the underlying disease, whereas neuronal death in the hippocampus generally is of necrotic morphology.