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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Decerebrate rigidity in humans.

Decerebrate rigidity (DR) in humans results from a midbrain lesion and is manifested by an exaggerated extensor posture of all extremities. It is characterized by shortening and lengthening reactions and can be modified by tonic neck, labyrinthine (Magnus-de Kleijn), and phasic spinal reflexes. These criteria, and not extensor posture alone, reflect the observations of Sherrington and should form the basis of the clinical examination; however, the experimental-anatomical lesion and physiological findings can never be reproduced exactly in humans. "Tonic and cerebellar fits" are not the equivalent of DR, but are forms of muscle spasm that result in an extensor attitude. They are caused by irritation and excitation of the brain stem. The most common cause of DR in humans is trauma. The incidence of DR in head-injured patients may be as high as 40%, resulting in an average mortality rate of 80%; the presence of an extensor posture increases the mortality from 20 to 70%. The surgical removal of an intracranial lesion does not improve the high mortality rate in patients with craniocerebral trauma who are decerebrate. Although the Glasgow coma scale (GCS) does not consider the specific type of central nervous system abnormality caused by trauma, it is an accurate and accepted assessment of outcome after coma lasting longer than 6 hours. DR is a factor in the best motor response of the GCS and should be assigned major importance in the prognosis of comatose head-injured patients.[1]


  1. Decerebrate rigidity in humans. Davis, R.A., Davis, L. Neurosurgery (1982) [Pubmed]
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