Abstract
Decerebrate rigidity (DR) in animals is caused by a release of spinal neurons from supraspinal inhibition, which results in a caricature of reflex standing and includes tonic neck and labyrinthine reflexes. The reticular formation, cerebellum, vestibular complex, spinal cord, and muscle spindle system and their neurophysiological interaction are critical to DR. Its discovery and investigation were essential to Sherrington's concept of the integrative action of the nervous system. There are two types of DR with different anatomical and physiological bases. Intercollicular decerebration yields rigidity in extensor muscles that results from bilateral destruction of the central tegmental tracts, is abolished by posterior root section, and is due to a facilitation of gamma motoneuron discharge (gamma animal). Anemic decerebration is characterized by excessive extensor rigidity, depends upon the release of tonic labryinthine reflexes from cerebellar inhibition, is independent of posterior root section, and is caused by excessive alpha motoneuron discharge (alpha animal). DR has provided an insight into the mechanisms of posture and standing, but the correlation of laboratory observations and results from animals to humans must be made with caution.
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