Sensory processing in Parkinson's and Huntington's disease - Investigations with 3D (H2O)-O-15-PET

There is conjoining experimental and clinical evidence supporting a fundame ntal role of the basal ganglia as a sensory analyser engaged in central som atosensory control. This study was aimed at investigating the functional an atomy of sensory processing in two clinical conditions characterized by bas al ganglia dysfunction, i.e. Parkinson's and Huntington's disease. Based on previously recorded data of somatosensory evoked potentials, we expected d eficient sensory-evoked activation in cortical areas that receive modulator y somatosensory input via the basal ganglia. Eight Parkinson's disease pati ents, eight Huntington's disease patients and eight healthy controls underw ent repetitive (H2O)-O-15-PET activation scans during two experimental cond itions 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 activati on pattern was lateralized to the side opposite to stimulus presentation, i ncluding cortical [primary sensory cortex (S1); secondary sensory cortex (S 2)] and subcortical (globus pallidus, ventrolateral thalamus) regional cere bral blood flow (rCBF) increases (P < 0.001), Between-group comparisons (P < 0.01) of vibration-induced rCBF changes between patients and controls rev ealed differences in central sensory processing: (i) in Parkinson's disease , decreased activation of contralateral sensorimotor (S1/M1) and lateral pr emotor cortex, contralateral S2, contralateral posterior cingulate, bilater al prefrontal cortex (Brodmann area 10) and contralateral basal ganglia; (i i) in Huntington's disease, decreased activation of contralateral S2, parie tal areas 39 and 40, and lingual gyrus, bilateral prefrontal cortex (Brodma nn areas 8, 9, 10 and 44), S1 (trend only) and contralateral basal ganglia; (iii) in both clinical conditions relative enhanced activation of ipsilate ral sensory cortical areas, notably caudal S1, S2 and insular cortex. Our d ata show that Parkinson's disease and Huntington's disease, beyond well-est ablished deficits in central motor control, are characterized by abnormal c ortical and subcortical activation on passive sensory stimulation. Furtherm ore, the finding that activation increases in ipsilateral sensory cortical areas may be interpreted as an indication of either altered central focusin g and gating of sensory impulses, or enhanced compensatory recruitment of a ssociative sensory areas in the presence of basal ganglia dysfunction. Alte red sensory processing is thought to contribute to pertinent motor deficits in both conditions.