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Further Investigations into the Speed of Cerebral Swelling Following Blunt Cranial Trauma

Authors

  • Roger W. Byard M.D.,

    1. Adelaide Centre for Neuroscience Research, School of Medical Sciences, The University of Adelaide, Frome Road, Adelaide, SA 5005, Australia.
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  • Levon Gabrielian M.D.,

    1. Adelaide Centre for Neuroscience Research, School of Medical Sciences, The University of Adelaide, Frome Road, Adelaide, SA 5005, Australia.
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  • Stephen C. Helps Ph.D.,

    1. Adelaide Centre for Neuroscience Research, School of Medical Sciences, The University of Adelaide, Frome Road, Adelaide, SA 5005, Australia.
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  • Emma Thornton Ph.D.,

    1. Adelaide Centre for Neuroscience Research, School of Medical Sciences, The University of Adelaide, Frome Road, Adelaide, SA 5005, Australia.
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  • Robert Vink Ph.D.

    1. Adelaide Centre for Neuroscience Research, School of Medical Sciences, The University of Adelaide, Frome Road, Adelaide, SA 5005, Australia.
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  • Funded, in part, by the Neurosurgical Research Foundation (Australia) and by a grant from the National Health and Medical Research Council of Australia.

Additional information and reprint requests:
Roger W. Byard, M.D.
School of Medical Sciences
The University of Adelaide
Frome Road
Adelaide
SA 5005
Australia
E-mail: roger.byard@adelaide.edu.au

Abstract

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.

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