An improved test of motor coordination in the lower limbs

Fisher, Casey

doi:10.1212/wnl.11.4.335

Cited by 2 publications

(1 citation statement)

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“…This abnormality is rather frequent, and often much more severe, in patients with cerebellar deficits where it was thought possibly to be related to dysdiadochokinesis (Hallett et al, 1975b). There is quite often in Parkinson's disease a clumsiness in alternating movements that is not very well defined and not clearly separable from clumsiness seen in other movement disorders (Fisher, 1960(Fisher, , 1961Schwab, 1972); this abnormality in antagonist inhibition may occasionally underlie some aspects of 'clumsiness'. The results of this experiment dispute the claim that slowness of movement in Parkinson's disease is due to 'failure to relax' or rigidity of the antagonist muscles.…”

Section: Discussionmentioning

confidence: 99%

Analysis of stereotyped voluntary movements at the elbow in patients with Parkinson's disease.

Hallett¹,

Shahani²,

Young³

1977

Journal of Neurology, Neurosurgery & Psychiatry

218

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S U M M A R Y Patients with Parkinson's disease performed several different stereotyped elbow flexion tasks, and the electromyographic (EMG) patterns from biceps and triceps were compared with previously established normal standards. The EMG pattern during a smooth flexion task was almost always abnormal and was characterised by alternating activity in biceps and triceps. The EMG patterns during a fast flexion task were also usually abnormal although they were always composed of bursts of EMG activity of normal duration appearing alternately in the agonist and antagonist muscles. These bursts, associated with movements of the limb, have a superficially similar appearance to the EMG bursts seen with tremor-at-rest, but certain physiological differences are demonstrated. This study demonstrates that both slow (ramp) and fast (ballistic) movements are clearly abnormal in these patients with disease of the basal ganglia. In a task designed to investigate antagonist inhibition before agonist activity, a majority of the patients performed normally. This suggests that, contrary to previous claims, slowness of movement (akinesia/bradykinesia) is not due either to failure to relax or to rigidity of antagonist muscles.

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Section: Discussionmentioning

confidence: 99%