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. 1979 Jul;42(7):606–618. doi: 10.1136/jnnp.42.7.606

Pathophysiological mechanisms in cerebral palsy.

H S Milner-Brown, R D Penn
PMCID: PMC490274  PMID: 479900

Abstract

To investigate some of the pathophysiological mechanisms in cerebral palsy, surface electromyograms (EMG) were recorded from pairs of flexor/extensor muscles during both voluntary and passive flexion/extension of upper and lower limbs of 20 patients. Elbow, knee, or ankle joint angles were measured simultaneously, as well as the force required to flex/extend the limbs passively at frequencies of 0.1--1.0 Hz. In addition, single motor units were recorded from the first dorsal interosseous muscles of six of the patients. Almost all patients showed resistance to passive movements (hypertonia). This hypertonia did not necessarily impair voluntary flexion/extension movements if alternating EMG activity was maintained in at least one of the pairs of flexor/extensor muscles involved in the movement. In six severly involved patients, there was a complete breakdown in the reciprocal relationship between reciprocally acting pairs of flexor/extensor motoneurones, which resulted in synchronous activation (co-contractions) of flexor/extensor muscles during both voluntary and passive movements. In these patients the hyperactive segmental reflex added to the disabling effects of co-contractions during voluntary movements. Single motor units recorded from patients with dystonic movements were recruited with variable delays (2--10 s) and usually discharged intermittently at high frequencies (60--120/s). This abnormla motor unit discharge pattern may relate to pathology of the basal ganglia.

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

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