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Titolo:
Biochemical changes in multiple system atrophy detected with positron emission tomography
Autore:
Gilman, S;
Indirizzi:
Univ Michigan, Hlth Syst, Dept Neurol, Ann Arbor, MI 48109 USA Univ Michigan Ann Arbor MI USA 48109 Dept Neurol, Ann Arbor, MI 48109 USA
Titolo Testata:
PARKINSONISM & RELATED DISORDERS
fascicolo: 3, volume: 7, anno: 2001,
pagine: 253 - 256
SICI:
1353-8020(200107)7:3<253:BCIMSA>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
STRIATAL MONOAMINERGIC TERMINALS; OLIVOPONTOCEREBELLAR ATROPHY; CONSENSUS STATEMENT; CLINICAL-FEATURES; AUTONOMIC FAILURE; NATURAL-HISTORY; DIAGNOSIS; DEGENERATIONS; CEREBELLAR; PATHOLOGY;
Keywords:
sporadic olivopontocerebellar atrophy; multiple system atrophy; autonomic failure; parkinsonism; cerebellar ataxia; positron emission tomography;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: Gilman, S Univ Michigan, Hlth Syst, Dept Neurol, 1500 E Med Ctr Dr,1914TC,Ann Arbor, MI 48109 USA Univ Michigan 1500 E Med Ctr Dr,1914TC Ann Arbor MI USA 48109 SA
Citazione:
S. Gilman, "Biochemical changes in multiple system atrophy detected with positron emission tomography", PARKINS R D, 7(3), 2001, pp. 253-256

Abstract

Multiple system atrophy (MSA) is a sporadic neurodegenerative disorder manifested by parkinsonism and dysfunction of autonomic, cerebellar, urinary, and pyramidal systems. The most frequent presentation is with a combinationof parkinsonism and autonomic dysfunction, but cerebellar ataxia with autonomic failure occurs frequently as well. Striatonigral degeneration (SND) and sporadic olivopontocerebellar atrophy (sOPCA) can progress to include autonomic failure and thus may be forms of MSA, but it is not known whether all such cases progress to MSA. Utilizing positron emission tomography (PET)with various ligands, my colleagues and I have investigated the biochemical changes in sOPCB and MSA to understand the relationship between these disorders. An initial study revealed decreased local cerebral metabolic rates for glucose in the brainstem, cerebellum, putamen, thalamus and cerebral cortex in both MSA and sOPCA, suggesting that many sOPCA patients would evolve to develop MSA. Later studies confirmed this by demonstrating decreased monoaminergic nigrostriatal terminals in both sOPCA and MSA patients. The studies suggest that the ligand used might be helpful in determining the riskthat an individual patient with sOPCA will progress to develop MSA. An investigation of the course of sOPCA patients observed clinically over severalyears revealed that approximately one-fourth of them progress to MSA within five years. Studies of gamma-aminobutyric acid type A/benzodiazepine neurotransmitter receptors revealed that these sites are largely preserved in sOPCA and MSA. indicating that symptomatic pharmacological therapy may be possible in these disorders. (C) 2001 Elsevier Science Ltd. All rights reserved.

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Documento generato il 17/09/19 alle ore 23:34:24