Movement disorders following lesions of the thalamus or subthalamic region


  • M. S. Lee,

    1. University Department of Clinical Neurology, Institute of Neurology, London, U.K.
    2. Department of Neurology, Yongdong Severance Hospital, Yonsei University College of Medicine, Seoul, Korea
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  • Dr. C. D. Marsden

    Corresponding author
    1. University Department of Clinical Neurology, Institute of Neurology, London, U.K.
    • University Department of Clinical Neurology, Institute of Neurology, Queen Square, WC1N 3BG, London, U.K.
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Reports of 62 cases with a movement disorder associated with a focal lesion in the thalamus and/or subthalamic region were analyzed. Thirtythree cases had a lesion confined to the thalamus. Sixteen cases had a thalamic lesion extending into the subthalamic region and/or midbrain. Thirteen cases had a lesion in the subthalamic region or a subthalamic lesion extending into the midbrain. Nineteen cases with dystonia, 18 with asterixis, 17 with ballismchorea, three with paroxysmal dystonia, and five with clonic or myorhthmic movements have been described. No case with isolated tremor has been described. In 53 cases with unilateral thalamic or subthalamic lesions, all but one with bilateral blepharospasm (associated with right posterior thalamic, pontomesencephalic, and bilateral cerebellar lesions) had dyskinesias in the limbs contralateral to the lesion. The other nine cases had bilateral paramedian thalamic lesions; seven developed bilateral dyskinesias, and the remaining two had unilateral dyskinesias. Regarding the 19 patients with dystonia, the two with bilateral blepharospasm had thalamic and upper brainstem lesions, and one with hemidystonia and torticollis had a subthalamic lesion. The other 16 patients all had a unilateral thalamic lesion with contralateral dystonia (10 hemidystonia, five focal dystonia affecting a hand and/or an arm, and one segmental dystonia involving face, arm, and hand). The exact location of the thalamic lesion was mentioned in 10 cases; the posterior or posterolateral thalamus was involved in six and the paramedian thalamus in four. These areas are more posterior or medial to the ventrolateral and ventroanterior thalamic nuclei, which receive pallido-thalamic and nigro-thalamic afferents. Two cases developed dystonia immediately after thalamotomy, and one case developed it 4 days after head trauma. The others initially had a hemiplegia and developed dystonia 1–9 months after the acute insult. Fifteen of the 17 patients with chorea had a unilateral lesion in the subthalamic nucleus or subthalamic region (eight due to infarcts, one to hemorrhage, five to mass lesions, and one to multiple sclerosis). All had contralateral hemichorea or hemiballism. One other case had bilateral chorea of the hands and tongue due to paramedian thalamic infarction. Another case with generalized chorea and thalamic atrophy was complicated by stereotaxic surgery. Thirteen of the 18 cases with asterixis had lesions confined to the thalamus. Eight were associated with thalamotomy, and five others had a stroke (four infarction and one hemorrhage) affecting the contralateral thalamus. The remaining five cases had a thalamic lesion with additional subthalamic or midbrain damage (four due to stroke and one to tumor). Asterixis was detected in all cases at the initial examination and usually resolved within 2–53 days after the acute insult. Three cases of paroxysmal dystonia occurred 19 days to 3 months after an acute thalamic lesions (two due to infarcts and one to multiple sclerosis), as the initial hemiplegia resolved. The attacks were precipitated by voluntary movements. All had discrete focal lesions in the posterolateral or ventrolateral thalamus, with involvement of the internal capsule. No case of pure parkinsonism had been described with thalamic or subthalamic lesions.