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Visual Hallucinations and Cognitive Impairment in Parkinson's Disease

Published online by Cambridge University Press:  23 September 2014

Hee Kyung Park
Affiliation:
Department of Neurology, Inje University Ilsan-Paik Hospital, Goyang Department of Neurology, University of Ulsan College of Medicine Department of Neurology, College of Medicine, Hanyang University
Jae Seung Kim
Affiliation:
Department of Neurology, Inje University Ilsan-Paik Hospital, Goyang
Ki Chun Im
Affiliation:
Sogang Institute of Advanced Technology, Sogang University, Seoul
Mi Jung Kim
Affiliation:
Department of Neurology, University of Ulsan College of Medicine
Jae-Hong Lee
Affiliation:
Department of Neurology, University of Ulsan College of Medicine
Myoung C. Lee
Affiliation:
Department of Neurology, Cheongshim International Medical Center, Gapyeong, Korea
Juhan Kim
Affiliation:
Department of Neurology, College of Medicine, Hanyang University
Sun Ju Chung*
Affiliation:
Department of Neurology, University of Ulsan College of Medicine
*
Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, 88 Olympic-ro 43-gil, Poongnap-dong, Songpa-gu, Seoul, 138-736, Korea. E-mail: sjchung@amc.seoul.kr
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Abstract:

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Background:

Visual hallucination (VH) is a common psychotic symptom in patients with Parkinson's disease (PD) and may be a significant predictor of cognitive impairment (CI) in such patients.

Objective:

This study aimed to investigate the pattern of glucose metabolism of VH and the relationship between VH and CI in PD.

Methods:

We studied 28 PD patients, including 15 with VH (PD-VH) and 13 without VH (PD-NVH). Of the 15 PD-VH patients, 8 patients had cognitive impairment (PD-VHCI) whereas 7 did not (PD-VHNCI). All patients underwent [18F] fluorodeoxyglucose positron emission tomography ([18F] FDG PET) followed by statistical parametric mapping (SPM) analyses.

Results:

Compared to the patients with PDNVH, PD-VHNCI patients showed glucose hypometabolism in the inferior and middle temporal cortices, fusiform gyri, and frontal areas, suggesting the involvement of the ventral visual pathway. Compared to the patients with PDNVH, PD-VHCI patients showed glucose hypometabolism in the temporoparietal association cortices with scattered frontal areas.

Conclusion:

Dysfunction of ventral visual pathway involving the temporal lobe may play a key role in VH development in PD patients. The evolving distribution from the ventral visual pathway to more extensive posterior cortices in PD-VHCI patients suggests that VH may be a prodromal symptom occurring prior to CI in PD patients.

Type
Original Article
Copyright
Copyright © The Canadian Journal of Neurological 2013

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