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Sparing of Motor Function After Cortical Injury:  A New Perspective on Underlying Mechanisms

Michael G. Boyeson, PhD; Jennifer L. Jones, MS; Robert L. Harmon, MD
Arch Neurol. 1994;51(4):405-414. doi:10.1001/archneur.1994.00540160107014.
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Historically, many theories have been offered to explain recovery of function following permanent brain injury. Because specific functional deficits often occur after injury to certain neuroanatomical locations, it has been tempting to suggest that within the brain, structure equals function (this interpretation, of course, has its roots in "phrenology," the 19th-century practice of detecting mental and behavioral traits by examining the skull's shape). Views that were common until recently emphasized structural and functional rigidity in the brain, which would seem to provide little opportunity for the occurrence of compensation. However, the observation that a considerable amount of spontaneous functional recovery occurs after many permanent brain lesions requires some explanation for the recovery that involves modification of intact portions of the brain. Recent research has provided data that reveal several forms of brain plasticity, including changes in neurotransmitter sensitivity, collateral sprouting, and diaschisis. Evidence supporting claims that beneficial behavioral recovery occurs through such physiological modifications in the brain are abundant in the literature,1-4 although, in general, there has not been any empirical establishment of causality.

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