A number of case reports have highlighted the occurrence of parkinsonism following strategic infarcts affecting the basal ganglia but the prevalence of parkinsonism after striatal infarcts (SI) has not been assessed. Therefore, we evaluated the clinical features and prevalence of parkinsonism in a large series of patients admitted to the Stroke-Unit of the Department of Neurology Innsbruck. Cerebral scans were retrospectively screened for SI, defined as a lesion larger than 1.5 cm involving the basal ganglia and the internal capsule. Out of 622 patients, 27 met the criteria for SI (4.3%) and 11 patients were available for follow-up. All patients presented contralateral motor weakness. Bilateral akinetic-rigid parkinsonism was found in only one patient whose [(123)I]beta-CIT-SPECT showed a decrease of the ligand uptake following the limits of the vascular lesion. Overall, parkinsonism does not appear to be a frequent consequence of striatal infarcts. Multiple lacunar subcortical infarcts interrupting thalamocortical drive may be more critical for the development of vascular parkinsonism.