Disturbed functional brain interactions underlying deficient tactile object discrimination in Parkinson's disease

Somatosensory discrimination of cuboid objects was studied in a group of healthy volunteers and patients with Parkinson's disease using regional cerebral blood flow (rCBF) measurements obtained with positron emission tomography (PET) and 15O labeled water [H215O]. A 6‐[18F]‐fluoro‐L‐dopa (FDOPA) PET scan demonstrated that the patients may be grouped into those with normal and those with abnormally low FDOPA uptake in the caudate nucleus. The categorical group comparisons revealed that task‐induced rCBF increases were deficient in bilateral motor and sensory cortical areas in the Parkinson patients. Moreover, deficient rCBF increases were evident in the mesial and right dorsolateral prefrontal cortex for patients in a more advanced disease state, who showed low FDOPA uptake in the caudate nucleus. A principal component analysis (PCA), performed on the rCBF data, identified three patterns (principal components, PCs) that differentiated patients from normals. The first PC represented a right‐hemisphere dominant, bilateral group of brain areas known to be involved in tactile exploration. A second PC reflected a cortical‐subcortical pattern of functional interactions, comprising cortical areas important for working memory processes. The third group‐differentiating PC revealed a pattern of functional interactions involving bilateral temporo‐parieto‐occipital association cortices, which was consistent with a hypothesized supramodal network necessary for object discrimination. In an additional subgroup analysis, greater expression of the third PC pattern predicted greater caudate FDOPA uptake in patients. Our neuroimaging data revealed a disturbance of distinct patterns of brain functional interactions related to the sensorimotor deficit in Parkinson's disease and to deficits of cognitive information processing deficits in the more advanced stage of Parkinson's disease. Hum. Brain Mapping 11:131–145, 2000. © 2000 Wiley‐Liss, Inc.