Citation

Byard RW, Gabrielian L, Helps SC, Thornton E, Vink R. J. Forensic Sci. 2012; 57(4): 973-975.

Affiliation

Adelaide Centre for Neuroscience Research, School of Medical Sciences, The University of Adelaide, Frome Road, Adelaide, SA 5005, Australia.

Copyright

(Copyright © 2012, American Society for Testing and Materials, Publisher John Wiley and Sons)

DOI

10.1111/j.1556-4029.2012.02109.x

PMID

22372694

Abstract

An anesthetized sheep model of traumatic brain injury (TBI) has been developed to assess early changes in intracranial pressure (ICP) following closed head injury. Immediately after TBI, a transient (<10 min) hypertensive response occurred, followed by significant and prolonged systemic hypotension. ICP demonstrated a biphasic response, being seven times baseline values of 8 ± 2 mm Hg 10 min after injury, decreasing to 25 ± 2 mm Hg by 30 min, and then increasing to values exceeding 30 mm Hg by 4 h postinjury. ICP was always significantly higher than baseline values, which combined with hypotension, reduced cerebral perfusion pressure to less than 60% of normal. This early and sustained increase in ICP after craniocerebral trauma acutely alters cerebral perfusion pressure and brain oxygenation and provides a potential pathophysiological explanation for immediate clinical manifestations in humans following significant TBI.

Language: en