Experiments in which animals were exposed to interruption of blood flow were far removed from the bedside evaluation of patients with anoxic-ischemic brain injury. In the early 1900s, laboratory scientists created “acute anemia” (through ligation of major arteries or removing large volumes of blood) to study the resuscitation of the central nervous system of mammals; they labeled the resulting presentation “anemic decerebration.” Sherrington’s intercollicular lesion decerebration model looked identical to the anemic decerebration model. Clinicians had to wait for a 1946 paper that described a complete neurologic examination, including cranial nerves, motor function, tone, and reflex pattern, along with comprehensive autopsy results showing extensive changes in the basal ganglia, particularly in the caudate nucleus, putamen, and the temporal lobe (cornu ammonis).
The study of the pathophysiology of brain damage has a long history starting with animal experiments and cumulating in autopsy descriptions of patients who died after some days of support. Unsurprisingly, the research tracks of animal experiments and bedside evaluation of anoxic-ischemic brain injury were far apart. However, each provided a foundation for our clinical understanding of what we now know is the most severe type of injury to the brain .