Abstract
Three cases of hemiballism-hemichorea accompanied by motor weakness in the same limb (s) induced by isolated subcortical infarction were presented and the symptomatic and pathophysiological aspects of dyskinesia associated with focal brain damage were discussed.
Involuntary limb movements observed in these patients consisted of regular, rhythmic flinging movements of ballistic type more prominent in the proximal portions of limbs and also of less regular and more abrupt choreic movements in the distal portions all on one side of the body, namely hemiballism-hemichorea.
Post-apoplectic hemiballism is characterized by a sudden onset, violent nature, long duration and poor prognosis and this dyskinesia may be caused by a destructive lesion located at the subthalamic nucleus as well as other sites as the caudate head, putamen and thalamus. Review of the literature disclosed that cortical or subcortical lesions are among rare causes of hemiballism.
Limb shaking, on the other hand, is considered to be transient involuntary limb movements of a hemiballismhemichorea type manifested as a clinical sign of carotid transient ischemic attacks.
The commonly shared location of the lesions in three cases on CT or MRI is the subcortical white matter underneath the precentral gyrus and the premotor cortex contralateral to dyskinesia. None of these cases were accompanied with lesions in the vicinity of the subthalamic nucleus or basal ganglia.
Voluntarily executed movements are presumed to be checked by the cortico-striato-pallido-subthalamo-pallidothalamo-cortical negative feedback loop. Subthalamic nucleus also receives a direct excitatory neural connection from the precentral gyrus, which may also take part in the inhibitory neural feedback loop mentioned above. The presence of a subcortical damage lying so as to interfere with the neural connections from cortex to striatum or subthalamic nucleus may lead to functional suppression of the subthalamic nucleus and subsequently of the pars interna of the globus pallidus, which in turn “disinhibits” thalamus and cortex, resulting in appearance of involuntary dyskinesia.
Limb paresis caused by a cortical and/or subcortical lesion is known to abolish hemiballism induced by a subthalamic damage in cats. Hemibalism-hemichorea induced by subcortical infarction may have a higher possibility of accompanying motor paresis of the same limbs, which may bring about relatively fair prognosis as in two of the three cases.
