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Postmortem findings from Scotland have emphatically addressed ischemic brain damage in non-missile severe acute brain trauma. Such findings from dead brains, however, were documented under circumstances that do not reproduce physiological parameters in alive brains, such as during intensive care.
Indeed, as a general rule in neurotrauma acute care, prolonged periods of hours or even days will have elapsed between the moment when clinical signs of brain death are first documented and the time when supportive measures are finally discontinued. Accordingly, the brains evaluated by neuropathologists will have almost invariably sustained ultra-prolonged periods of very low or even absent cerebral perfusion, because of very high intracranial pressure (ICP), low blood pressure, or a combination of both; that is, cerebral perfusion pressure (CPP) will have approached zero for prolonged periods.
Accordingly, it is not surprising that postmortem studies in severe acute brain trauma may frequently disclose ischemic damage. In alive brains, however, adequate ICP and blood pressure levels are frequently found during intensive care and, therefore, factors other than CPP are expected to play a relevant role, insofar as cerebral hemodynamics and metabolism are concerned. From the above discussion, extrapolation from cadaver brains to alive patients during most of the acute phase of injury is largely inappropriate.
According to the author, it is surprising that postmortem studies in severe acute brain trauma may frequently disclose ischemic damage.