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Brain Regions Associated With Cognitive Impairment in Patients With Parkinson Disease: Quantitative Analysis of Cerebral Blood Flow Using 123I Iodoamphetamine SPECT

Hattori, Naoya MD, PhD*; Yabe, Ichiro MD, PhD; Hirata, Kenji MD, PhD; Shiga, Tohru MD, PhD; Sakushima, Ken MD, MPH; Tsuji-Akimoto, Sachiko MD, PhD; Sasaki, Hidenao MD, PhD; Tamaki, Nagara MD, PhD

doi: 10.1097/RLU.0b013e3182873511
Original Articles

Purpose: Cognitive impairment is a representative neuropsychiatric presentation that accompanies Parkinson disease (PD). The purpose of this study was to localize the cerebral regions associated with cognitive impairment in patients with PD using quantitative SPECT.

Patients and Methods: Thirty-two patients with PD (mean [SD] age, 75 [8] years; 25 women; Hoehn-Yahr scores from 2 to 5) underwent quantitative brain SPECT using 123I iodoamphetamine. Parametric images of regional cerebral blood flow (rCBF) were spatially normalized to the standard brain atlas. First, voxel-by-voxel comparison between patients with PD with versus without cognitive impairment was performed to visualize overall trend of regional differences. Next, the individual quantitative rCBF values were extracted in representative cortical regions using a standard region-of-interest template to compare the quantitative rCBF values.

Results: Patients with cognitive impairment showed trends of lower rCBF in the left frontal and temporal cortices as well as in the bilateral medial frontal and anterior cingulate cortices in the voxel-by-voxel analyses. Region-of-interest–based analysis demonstrated significantly lower rCBF in the bilateral anterior cingulate cortices (right, 25.8 [5.5] vs 28.9 [5.7] mL per 100 g/min, P < 0.05; left, 25.8 [5.8] vs 29.1 [5.7] mL per 100 g/min, P < 0.05) associated with cognitive impairment.

Conclusions: Patients with cognitive impairment showed lower rCBF in the left frontal and temporal cortices as well as in the bilateral medial frontal and anterior cingulate cortices. The results suggested dysexecutive function as an underlining mechanism of cognitive impairment in patients with PD.

From the Departments of *Molecular Imaging, †Neurology, and ‡Nuclear Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan.

Received for publication April 12, 2012; revision accepted January 8, 2013.

Conflict of interest and sources of funding: none declared.

Reprints: Naoya Hattori, MD, PhD, Department of Molecular Imaging, Hokkaido University Graduate School of Medicine, Sapporo, Japan, Kita15 Nishi 7, Kita-Ku, Sapporo, Hokkaido, Japan, 060-8638. E-mail: nhattori@med.hokudai.ac.jp.

© 2013 by Lippincott Williams & Wilkins