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NEUROLOGY 1987;37:1281
© 1987 American Academy of Neurology

Delayed hippocampal damage in humans following cardiorespiratory arrest

Carol K. Petito, MD, Edward Feldmann, MD, William A. Pulsinelli, MD, PhD and Fred Plum, MD

Departments of Pathology (Neuropathology) (Dr. Petito) and Neurology (Drs. Feldmann, Pulsinelli, and Plum), The New York Hospital-Cornell Medical Center, New York, NY.

Transient ischemia in animals produces delayed cell death in vulnerable hippocampal neurons. To see if this occurs in humans, we reexamined brain slides from all patients with anoxic-ischemic encephalopathy and a well-documented cardiorespiratory arrest. Eight patients dying 18 hours or less after cardiac arrest had minimal damage in hippocampus and moderate damage in cerebral cortex and putamen. Six patients living 24 hours or more had severe damage in all four regions. The increase in damage with time postarrest was significant only in the hippocampus. Delayed hippocampal injury now documented in humans provides a target for possible therapy that can be initiated after cardiopulmonary resuscitation.

Address correspondence and reprint requests to Dr. Petito, Department of Pathology, New York Hospital-Cornell Medical Center, 525 East 68th Street, New York, NY 10021.

Supported in part by NIH grant NS-003346.

Received September 10, 1986. Accepted for publication in final form December 11, 1986.




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