When neurointensivists go in for brain cutting their deceased patient will often display herniation of the uncus of the temporal lobe. We can see compression of the third nerve that is often pointed out by the scalpel. As expected, the mass bearing down on the brainstem and cerebellum causes cerebellar tonsils to descend. Case closed!
Both clinical and laboratory knowledge contributed to understanding of mass effect. In the laboratory, the vital signs of acute mass effect were well known after Cushing’s classic experiments . During Cushing’s year in Europe as a young 31-year-old surgeon, he would study the effects of sudden increased intracranial pressure, and although he looked at cortical vessels through a burr hole, he did not study brain tissue shift (he would do that much later). Others studied the mechanics of brain shift and cranial nerve compression in animals and recorded unexpected findings. The clinicopathological correlation in brain herniation turned out far more ambiguous. Most of these experiments began in the early 1900s and similarly, as in Cushing’s experiments, involved the introduction of rapidly inflated intracranial balloon catheters. The combination of previously known abnormal vital signs and close clinical observation of change in responsiveness of the exposed animal led to the understanding of how rapid inflation could cause brainstem shift. The phenomenon has been the focus of a long history of curiosity-driven animal experiments, which later had important clinical applications. One could argue that this article should be dedicated to all the monkeys, cats and dogs to which we owe so much.
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