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Perhaps no subject has generated more debate in medicine than the diagnosis of brain death (BD). Writers, philosophers, ethicists, and physicians have focused on different aspects of BD. Nevertheless, no significant advances in the understanding of pathophysiologic mechanisms in BD have occurred over the last decade.
American Academy of Neurology (AAN) Practice Parameters defined BD as “the irreversible loss of function of the entire brain, including the brainstem” with three specific criteria: 1) unresponsiveness, 2) absent brainstem reflexes, and 3) apnea. In addition to these clinical criteria, there are important prerequisites: a) presence of clinical or neuroimaging evidence of acute CNS catastrophe severe enough to explain the condition, b) core temperature greater than 32°C (90°F), c) no drug intoxication or poisoning, and d) absence of confounding medical conditions such as severe electrolyte, acid-base, or endocrine disturbances.1
In this issue of Neurology®, Wijdicks and Pfeifer2 offer a new look at an old condition and attempt to provide an analysis of the neuropathologic features that correlate with a clinical diagnosis of BD. They reviewed macroscopic and microscopic brain pathology for ischemic neuronal damage in 41 patients …
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