Parieto-cerebellar loop impairment in ataxic hemiparesis: proposed pathophysiology based on an analysis of cerebral blood flow.

Sixteen stroke patients suffering from ataxic hemiparesis syndrome were studied with regional cerebral blood flow measured by 133-Xenon inhalation technique (12 patients) and by SPECT (HMPAO) (9 patients). The causative lesions (hematoma in 7 and infarct in 9), unilateral in 15 patients and bilateral in 1, were located in the posterior two-thirds of the corona radiata, thalamo-capsular and subthalamus regions, or cerebral peduncle. Ataxia of the cerebellar type was unilateral in 15 patients and bilateral in 1 with similar, deep, bilateral causative lesions. Four patients presented some characteristics of proprioceptive ataxia (mixed ataxia). Associated cognitive disturbances were present in 9 patients and absent in 7. Eleven of the 12 subjects studied by 133-Xenon inhalation technique showed limited centro-parietal hypoperfusion, mainly in the inferior parietal lobule, ipsilateral to the causative lesion and bilaterally in the patient with bilateral lesions and ataxia. Ipsilateral hypoperfusion was confirmed in 7/9 patients studied by SPECT, which also demonstrated contralateral cerebellar hypoperfusion in 4 patients. These findings suggest that ataxic hemiparesis syndrome results from functional depression (diaschisis) consequent to the interruption at many levels of an "inferior parietal associative cortex-cerebellar anterior lobe" circuit.