Hippocampal Damage in the Human Brain after Cardiac Arrest
- 7 January 2000
- journal article
- clinical trial
- Published by S. Karger AG in Cerebrovascular Diseases
- Vol. 10 (1) , 2-7
- https://doi.org/10.1159/000016018
Abstract
Very few reports are available on changes in the human hippocampus after cardiac arrest. The objective of this study was to investigate if specific hippocampal volume losses can be demonstrated in the human brain following reperfusion after cardiac arrest. We assessed the volumes of the hippocampal formation (HF) and temporal lobe excluding HF (TL) as the contrast using magnetic resonance (MR)-imaging-based volumetry in 11 vegetative patients after cardiac arrest and in 22 healthy controls of similar age, sex and body size distribution. The measured volumes were normalized for differences in the head size among subjects by dividing by the total intracranial volume (TICV). The MR images of the 11 patients were obtained between days 8 and 21 after cardiac arrest. The observed volumes of HFs and TLs of both patient and control groups were as follows: right HF volume (HFV): 2.67 +/- 0.19 (mean +/- SD, cm(3)) in patients versus 3.89 +/- 0.44 in controls; left HFV: 2.72 +/- 0.17 versus 3.74 +/- 0.35; right TL volume (TLV): 73.37 +/- 6.54 versus 80.08 +/- 7.62, and left TLV: 72. 45 +/- 6.77 versus 78.59 +/- 6.68. The normalized indices (HFV/TICV and TLV/TICV) were as follows: right HF: 0.0021 +/- 0.0002 (mean +/- SD) in patients versus 0.0031 +/- 0.0001 in controls, p < 0.0001, left HF: 0.0022 +/- 0.0002 versus 0.0030 +/- 0.0001, p < 0.0001, right TL: 0.058 +/- 0.002 versus 0.064 +/- 0.004, p = 0.0007, and left TL: 0.058 +/- 0.002 versus 0.062 +/- 0.004, p = 0.0014. The HFV-TLV ratios (HFV/TICV divided by TLV/TICV) of both groups were: right HFV-TLV ratio: 0.037 +/- 0.004 in patients versus 0.049 +/- 0. 004 in controls, p < 0.0001, left HFV-TLV ratio: 0.038 +/- 0.004 versus 0.048 +/- 0.004, p < 0.0001. The patient group had HFs that were 26.8-30.6% smaller than those of the control group, but in the patient group, the TLs slightly decreased in size by only 7.8-8.2% of the volume of those in the control group within 21 days after cardiac arrest. The volume reductions in the bilateral HFs of patients after cardiac arrest were significantly larger than those in the bilateral TLs. We speculate that this specific rapid hippocampal shrinkage reflects its greater vulnerability to global brain ischemia.Keywords
This publication has 11 references indexed in Scilit:
- Glucocorticoids increase extracellular [3H]d-aspartate overflow in hippocampal cultures during cyanide-induced ischemiaBrain Research, 1994
- Repeated stress causes reversible impairments of spatial memory performanceBrain Research, 1994
- Global ischemia can cause DNA fragmentation indicative of apoptosis in rat brainNeuroscience Letters, 1993
- Neuropsychological sequelae of cardiac arrestPublished by American Medical Association (AMA) ,1993
- Exposure to excess glucocorticoids alters dendritic morphology of adult hippocampal pyramidal neuronsBrain Research, 1990
- Free radical generation during brief period of cerebral ischemia may trigger delayed neuronal deathNeuroscience, 1990
- Hippocampal abnormalities in amnesic patients revealed by high-resolution magnetic resonance imagingNature, 1989
- Ischemia triggers NMDA receptor-linked cytoskeletal proteolysis in hippocampusBrain Research, 1989
- Calcium-mediated neurotoxicity: relationship to specific channel types and role in ischemic damageTrends in Neurosciences, 1988
- Delayed neuronal death in the gerbil hippocampus following ischemiaBrain Research, 1982