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Effects of disease duration on the clinical features and brain glucose metabolism in patients with mixed type multiple system atrophy.

 C. H. Lyoo  ;  Y. Jeong  ;  Y. H. Ryu  ;  S.Y. Lee  ;  T. J. Song  ;  J. H. Lee  ;  J.O. Rinne  ;  M. S. Lee 
 BRAIN, Vol.131(pt2) : 438-446, 2008 
Journal Title
Issue Date
Aged ; Brain/diagnostic imaging ; Brain/metabolism* ; Brain/pathology ; Brain Mapping/methods ; Cognition Disorders/etiology ; Cognition Disorders/metabolism ; Cognition Disorders/pathology ; Female ; Fluorodeoxyglucose F18 ; Follow-Up Studies ; Glucose/metabolism* ; Humans ; Magnetic Resonance Imaging/methods ; Male ; Middle Aged ; Multiple System Atrophy/diagnostic imaging ; Multiple System Atrophy/metabolism* ; Multiple System Atrophy/pathology ; Multiple System Atrophy/psychology ; Neuropsychological Tests ; Parkinson Disease, Secondary/etiology ; Parkinson Disease, Secondary/metabolism ; Parkinson Disease, Secondary/pathology ; Positron-Emission Tomography ; Radiopharmaceuticals ; Time Factors
multiple system atrophy ; cognitive impairment ; positron emission tomography
To study the effect of disease duration on the clinical, neuropsychological and [(18)F]-deoxyglucose (FDG) PET findings in patients with mixed type multiple system atrophy (MSA), this study included 16 controls and 37 mixed-type MSA patients with a shorter than a 3-year history of cerebellar or parkinsonian symptoms. We classified the patients into three groups according to the duration of parkinsonian or cerebellar symptoms (Group I = <or=1 year; II = 13-24 months; III = 25-36 months). We performed UPDRS, international cooperative ataxia rating scale (ICARS), and a neuropsychological test battery. We compared the FDG PET findings of each group of patients with controls. Group I patients frequently had memory and frontal executive dysfunction. They showed hypometabolism in the frontal cortex, anterior cerebellar hemisphere and vermis. They had parkinsonian motor deficits, but no basal ganglia hypometabolism. Group II and III patients frequently had multiple domain cognitive impairments, and showed hypometabolism in the frontal and parieto-temporal cortices. Hypometabolism of the bilateral caudate and the left posterolateral putamen was observed in Group II, and whole striatum in Group III. In summary, the cortical hypometabolism begins in the frontal cortex and spreads to the parieto-temporal cortex in MSA. This spreading pattern coincides with the progressive cognitive decline. Early caudate hypometabolism may also contribute to the cognitive impairment. Parkinsonian motor deficits precede putaminal hypometabolism that begins in its posterolateral part. Cerebellar hypometabolism occurs early in the clinical courses and seems to be a relevant metabolic descriptor of cerebellar deficits
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1. College of Medicine (의과대학) > Dept. of Nuclear Medicine (핵의학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
Yonsei Authors
Lyoo, Chul Hyoung(류철형) ORCID logo https://orcid.org/0000-0003-2231-672X
Ryu, Young Hoon(유영훈) ORCID logo https://orcid.org/0000-0002-9000-5563
Lee, Myung Sik(이명식) ORCID logo https://orcid.org/0000-0002-8413-1854
Lee, Jae Hyeok(이재혁)
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