TY - JOUR
T1 - Cerebral metabolic changes in early multiple system atrophy
T2 - A PET study
AU - Taniwaki, Takayuki
AU - Nakagawa, Makoto
AU - Yamada, Takeshi
AU - Yoshida, Tsuyoshi
AU - Ohyagi, Yasumasa
AU - Sasaki, Masayuki
AU - Kuwabara, Yasuo
AU - Tobimatsu, Shozo
AU - Kira, Jun Ichi
N1 - Funding Information:
We thank Katherine Ono for comments on the manuscript. This study was partly supported by grants from the Ministry of Health and Welfare.
PY - 2002/8/15
Y1 - 2002/8/15
N2 - Previous positron emission tomography (PET) studies have shown widespread hypometabolism in the brain of advanced MSA but the time course of these metabolic abnormalities is largely unknown. In order to clarify the principal disease processes in multiple system atrophy (MSA) in the early stage, we investigated regional cerebral glucose metabolism (rCMGglc) and nigral dopaminergic function in nine patients with early stage of MSA using [18F]fluorodeoxyglucose (FDG) and 6-L-[18F]fluorodopa (18F-Dopa) positron emission tomography (PET) (two men and seven women; age, 59.3±5.4 years; disease duration, 29.7±14.6 months). The rCMRglc in the early MSA patients significantly decreased in the cerebellum, brainstem, and striatum compared with that in nine normal subjects. A significant correlation was found between the severity of autonomic dysfunction and rCMRglc within the brainstem. The severity of extrapyramidal signs also correlated with the decline of F-Dopa uptake but not that of rCMRglc within the striatum. The degree of atrophy on MRI has correlated with neither the clinical symptoms nor rCMRglc at the cerebellum and the brainstem. Our PET studies demonstrated widespread metabolic abnormalities except for the cerebral cortex in the brain of MSA even in the early stage. The hypometabolism in the brainstem was tightly linked to the autonomic dysfunction. Not the striatal dysfunction but the nigral damage may be responsible for the extrapyramidal symptoms in early MSA.
AB - Previous positron emission tomography (PET) studies have shown widespread hypometabolism in the brain of advanced MSA but the time course of these metabolic abnormalities is largely unknown. In order to clarify the principal disease processes in multiple system atrophy (MSA) in the early stage, we investigated regional cerebral glucose metabolism (rCMGglc) and nigral dopaminergic function in nine patients with early stage of MSA using [18F]fluorodeoxyglucose (FDG) and 6-L-[18F]fluorodopa (18F-Dopa) positron emission tomography (PET) (two men and seven women; age, 59.3±5.4 years; disease duration, 29.7±14.6 months). The rCMRglc in the early MSA patients significantly decreased in the cerebellum, brainstem, and striatum compared with that in nine normal subjects. A significant correlation was found between the severity of autonomic dysfunction and rCMRglc within the brainstem. The severity of extrapyramidal signs also correlated with the decline of F-Dopa uptake but not that of rCMRglc within the striatum. The degree of atrophy on MRI has correlated with neither the clinical symptoms nor rCMRglc at the cerebellum and the brainstem. Our PET studies demonstrated widespread metabolic abnormalities except for the cerebral cortex in the brain of MSA even in the early stage. The hypometabolism in the brainstem was tightly linked to the autonomic dysfunction. Not the striatal dysfunction but the nigral damage may be responsible for the extrapyramidal symptoms in early MSA.
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U2 - 10.1016/S0022-510X(02)00151-X
DO - 10.1016/S0022-510X(02)00151-X
M3 - Article
C2 - 12127681
AN - SCOPUS:0037102723
SN - 0022-510X
VL - 200
SP - 79
EP - 84
JO - Journal of the Neurological Sciences
JF - Journal of the Neurological Sciences
IS - 1-2
ER -