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. 2010 Mar;39(2):136-42.
doi: 10.3785/j.issn.1008-9292.2010.02.005.

[Role of activated brain regions during tactile stimulation in early Parkinson's disease: a preliminary fMRI study]

[Article in Chinese]
Affiliations

[Role of activated brain regions during tactile stimulation in early Parkinson's disease: a preliminary fMRI study]

[Article in Chinese]
Heng-yi Cao et al. Zhejiang Da Xue Xue Bao Yi Xue Ban. 2010 Mar.

Abstract

Objective: To investigate the role of activated brain regions in Parkinson's disease (PD) during tactile stimulation.

Methods: Twenty-one patients with early PD[mean age (60.43 +/-9.65)y] and twenty-two age-matched healthy controls [mean age (59.23 +/-11.12)y] were enrolled in the study. All the patients were tested by the United Parkinson Disease Rating Scale (UPDRS) as the evaluation of the disease severity. A block design was used when the finger tactile stimulation was given to the subjects. The hypoactive and hyperactive regions of PD patients were confirmed first, which were identified as regions of interest (ROI). ROI analysis was performed to quantify BOLD signal changes when subjects were under tactile stimulation. The correlations of signal changes with disease severity, and correlations of hyperactive with hypoactive regions were analyzed.

Results: Right primary sensory and motor cortex, right supplementary motor area (SMA), bilateral caudates, bilateral precuneus, bilateral occipital visual cortex and left middle temporal gyrus were hypoactivated in PD, while right prefrontal cortex (PFC) and right caudate were hyperactivated. The hypoactivation of right SMA was negatively correlated with disease severity. All the hypoactive and hyperactive regions were positively correlated with activation of caudates. There was a positive correlation between hyperactive PFC and hypoactive regions.

Conclusions: The signal change of SMA is directly related to disease severity in early PD, and caudates may play a significant role in PD tactile processing. The hyperactivation of PFC may be not a compensation but a pathophysiological change related to PD neural dysfunction.

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