Secondary dystonias due to ischemic and/or hemorrhagic lesions of the basal ganglia and thalamus are rare. Among 2369 patients with stroke, only 12 patients (0.5%) developed posthemiplegic dystonia, which constituted 4.9% of 506 patients with dystonia. Posthemiplegic dystonia appeared as slow, twisting clonic spasms (mobile dystonia) in eight patients who had the distal parts of their extremities affected. On the other hand, in case of an arm or leg involved as a whole, posthemiplegic dystonia appeared as prolonged abnormal postures (fixed dystonia), as observed in our four patients. The latency till the appearance of dystonia following stroke was significantly shorter in mobile dystonia (9 months versus 61.5 months, p=0.05). The fixed dystonia resulted from thalamic involvement in all four cases. On the other hand, mobile dystonia developed in three patients with thalamic involvement, but in all five patients with infarctions in putamen, caudate and lentiform nuclei. The rather low number of cases with basal ganglia/capsular lesions resulting in hemiplegia and leading to subsequent dystonia may be due to selective lesioning and blockade of selective neurotransmitter systems.