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Psychiatric symptoms typical of patients with dementia with Lewy bodies – similarity to those of levodopa-induced psychosis

Published online by Cambridge University Press:  24 June 2014

Eizo Iseki*
Affiliation:
Department of Psychiatry, Yokohama City University School of Medicine, Yokohama Japan
Wami Marui
Affiliation:
Department of Psychiatry, Yokohama City University School of Medicine, Yokohama Japan
Namiko Nihashi
Affiliation:
Department of Psychiatry, Yokohama City University School of Medicine, Yokohama Japan
Kenji Kosaka
Affiliation:
Department of Psychiatry, Yokohama City University School of Medicine, Yokohama Japan
*
Eizo Iseki MD PhD, Department of Psychiatry, Yokohama City University School of Medicine, 3–9 Fukuura, Kanazawa-ku, Yokohama 236–0004, Japan. Tel: +81-45-787-2667; Fax: +81-45-783-2540; E-mail: iseki@med.yokohama-cu.ac.jp

Abstract

We examined psychiatric symptoms in eight cases with dementia with Lewy bodies (DLB), which included visual hallucination of persons or small animals, visual illusion, metamorphosia, leibhaftige Bewusstheit, personal or topographical misidentification, Capgras' syndrome and reduplicative paramnesia as well as depressive state and delusion of persecution. These psychiatric symptoms are identical to those of levodopa-induced psychosis, although these symptoms appeared before medication with anti-Parkinson drugs. The hypersensitivity of the dopamine receptor in the meso-limbic dopaminergic system has been presumed in levodopa-induced psychosis. We previously showed disturbance of the nigro-amygdaloid dopaminergic connections in DLB brains on pathological studies. Hypoperfusion or glucose hypometabolism in the occipital lobe has been demonstrated in DLB patients using SPECT or PET. The amygdala has reciprocal connections with the visual cortex in the occipital lobe. From these findings, it is supposed that the disturbance of the nigro-amygdaloid connections induces hypersensitivity of the dopamine receptor in the amygdala, causing psychiatric symptoms with dysfunction of the visuo-amygdaloid connections.

Type
Original Article
Copyright
Copyright © Acta Neuropsychiatrica 2002

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