[Involuntary movements caused by thalamic lesion]
- PMID: 7994988
[Involuntary movements caused by thalamic lesion]
Abstract
We described two types of involuntary movement accompanied with a well-located thalmaic lesion shown by MR imaging in five patients. All patients had the involuntary movements of an upper limb contralateral to the thalamic lesion. Two patients (1 and 2) had choreoathetosis that became most prominent when their index finger approached their nose, where irregular and dysynchronous oscillation occasionally superimposed. This choreoathetosis was differentiated from pseudoathetosis caused by disturbance of proprioceptive sensations. The MRI lesion was located at the middle level of thalamus including nucleus centromedianus. The other three patients (3, 4 and 5) had a regular and rhythmic oscillation in their forearm. The oscillation began to appear after their index finger reached their nose on finger-to-nose test. We considered the oscillation as a postural tremor based on its rhythmicity and regularity. Patient 4 had additional tremor in movement. Their postural tremor continued while the arm kept the position. Surface electromyogram showed the reciprocal discharges between the forearm extensor and flexor muscles with a frequency of 3 to 4 Hz. This tremor was not accentuated during limb movement toward the nose nor was coarse, and was distinguished from intention tremor described by Charcot and Dejerine. This tremor was also different from hyperkinesis volitionnelle and movement oppositionist. The "rubral tremor" differed from the tremor shown in our cases for a lack of resting tremor. The responsible lesion shown by MRI located at caudal posterior thalamus including pulvinar in patient 3, or located at the upper level of thalamus in patient 4 and case 5 that was more rostral than the lesion of the choreoathetosis cases. In cases of cerebrovascular accidents, both types of involuntary movement appeared after several months from the stroke. This delayed appearance suggests that these involuntary movements were the result not only of functional disturbance of thalamus, but of secondary repairing mechanism occurring at the lesion.
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