There is conjoining experimental and clinical evidence supporting a fundamental role of the basal ganglia as a sensory analyser engaged in central somatosensory control. This study was aimed at investigating the functional anatomy of sensory processing in two clinical conditions characterized by basal ganglia dysfunction, i.e. Parkinson's and Huntington's disease. Based on previously recorded data of somatosensory evoked potentials, we expected deficient sensory-evoked activation in cortical areas that receive modulatory somatosensory input via the basal ganglia. Eight Parkinson's disease patients, eight Huntington's disease patients and eight healthy controls underwent repetitive H(2)(15)O-PET activation scans during two experimental conditions in random order: (i) continuous unilateral high-frequency vibratory stimulation applied to the immobilized metacarpal joint of the index finger and (ii) rest (no vibratory stimulus). In the control cohort, the activation pattern was lateralized to the side opposite to stimulus presentation, including cortical [primary sensory cortex (S1); secondary sensory cortex (S2)] and subcortical (globus pallidus, ventrolateral thalamus) regional cerebral blood flow (rCBF) increases (P < 0.001). Between-group comparisons (P < 0.01) of vibration-induced rCBF changes between patients and controls revealed differences in central sensory processing: (i) in Parkinson's disease, decreased activation of contralateral sensorimotor (S1/M1) and lateral premotor cortex, contralateral S2, contralateral posterior cingulate, bilateral prefrontal cortex (Brodmann area 10) and contralateral basal ganglia; (ii) in Huntington's disease, decreased activation of contralateral S2, parietal areas 39 and 40, and lingual gyrus, bilateral prefrontal cortex (Brodmann areas 8, 9, 10 and 44), S1 (trend only) and contralateral basal ganglia; (iii) in both clinical conditions relative enhanced activation of ipsilateral sensory cortical areas, notably caudal S1, S2 and insular cortex. Our data show that Parkinson's disease and Huntington's disease, beyond well-established deficits in central motor control, are characterized by abnormal cortical and subcortical activation on passive sensory stimulation. Furthermore, the finding that activation increases in ipsilateral sensory cortical areas may be interpreted as an indication of either altered central focusing and gating of sensory impulses, or enhanced compensatory recruitment of associative sensory areas in the presence of basal ganglia dysfunction. Altered sensory processing is thought to contribute to pertinent motor deficits in both conditions.