Hippocampal pathology in fatal human head injury without high intracranial pressure.

Publication/Presentation Date

6-1-1994

Abstract

Traumatically induced hippocampal damage is a frequent sequela of fatal human head injury and is traditionally considered to be the result of decreased cerebral perfusion secondary to raised intracranial pressure (ICP). However, in previous studies employing an experimental model of acceleration head injury, hippocampal lesions have been observed in the absence of high ICP. To further elucidate the role of raised ICP in the production of posttraumatic hippocampal neuronal damage, 14 cases of fatal human nonmissile head injury, in which the measured ICP was less than 20 mm Hg, were subjected to light microscopic evaluation for the frequency and anatomic distribution of hippocampal damage. The mean maximal ICP of the 14 patients was 17.6 mm Hg. Detailed light microscopic evaluation revealed hippocampal lesions in 12 of the 14 cases studied (86%). These lesions were typically bilateral foci of selective neuronal loss in the CA1 subfield of the hippocampus. The nature and distribution of hippocampal lesions were similar to those previously reported both in fatal human head injury associated with elevated ICP and in experimental acceleration head injury without raised ICP. These results provide further evidence that the occurrence of hippocampal neuronal loss following head injury is not exclusively dependent on elevated ICP. Other mechanisms, such as pathologic excitation of neurons, may be involved.

Volume

11

Issue

3

First Page

317

Last Page

324

ISSN

0897-7151

Disciplines

Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods

PubMedID

7996585

Department(s)

Administration and Leadership

Document Type

Article

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