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Journal of Neurology, Neurosurgery, and Psychiatry logoLink to Journal of Neurology, Neurosurgery, and Psychiatry
. 1983 Jan;46(1):45–53. doi: 10.1136/jnnp.46.1.45

Physiological mechanisms of rigidity in Parkinson's disease.

A Berardelli, A F Sabra, M Hallett
PMCID: PMC1027262  PMID: 6842199

Abstract

Electromyographic responses of triceps surae and tibialis anterior produced by dorsiflexion stretch were studied in 17 patients with Parkinson's disease. Most patients showed increased muscular activity when attempting to relax. A few patients showed an increase of short-latency reflexes when relaxed and when exerting a voluntary plantarflexion prior to the stretch. Many patients showed long-latency reflexes when relaxed and all but one showed long-latency reflexes with voluntary contraction; and these reflexes were often larger in magnitude and longer in duration than those seen in normal subjects. Unlike the short-latency reflex, the long-latency reflex did not disappear with vibration applied to the Achilles tendon. The long-latency reflexes and continuous responses to slow ramp stretches were diminished at a latency similar to the beginning of long-latency reflexes when the stretching was quickly reversed. Dorsiflexion stretch also frequently produced a shortening reaction in tibialis anterior. Of all the abnormal behavior exhibited by the Parkinsonian patients only the long-latency reflex magnitude and duration correlated with the clinical impression of increased tone. The mechanism of the long-latency reflex to stretch which is responsible for rigidity is not certain, but the present results are consistent with a group II mediated tonic response.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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