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as large vessel disease with small vessel embolisation. The anatomical basis of the lesions causing ataxic-hemiparesis have been previously discussed. It is like-ly that interruption of pontocerebellar fibres from pon-tine nuclei plus corticospinal tracts in the basis pontis, is responsible for pontine ataxic-hemiparesis.2 Inter-ruption of cerebral peduncle and the superior cerebel-lar pednucle after it has crossed the midbrain, in the ventral spect of the midbrain may be responsive for a midbrain ataxic-hemiparesis. '•5 Capsular ataxic-hemi-paresis will cause the syndrome by involving the corti-cospinal tract as well as the frontopontine fibres in the posterior limb of the internal capsule. Although cap-sule ataxia hemiparesis seems frequently to be associ-ated with sensory loss, sensory loss is not essential for ataxia to be present, as in Iragui and McCutchen's case, and our case 4. Involvement of cerebellar projec-tion to the cortex appears also possible,1-8 and underlie perhaps the ataxic hemiparesis when the lesion is above the internal capsule