Movement Disorders (revue)

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Brain parenchyma sonography detects preclinical parkinsonism

Identifieur interne : 003D91 ( Main/Exploration ); précédent : 003D90; suivant : 003D92

Brain parenchyma sonography detects preclinical parkinsonism

Auteurs : Uwe Walter [Allemagne] ; Christine Klein [Allemagne] ; Ruediger Hilker [Allemagne] ; Reiner Benecke [Allemagne] ; Peter P. Pramstaller [Italie] ; Dirk Dressler [Allemagne]

Source :

RBID : ISTEX:769495CF95B685EB89CE82DC55B762FABE1D9898

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English descriptors

Abstract

Substantia nigra (SN) hyperechogenicity on brain parenchyma sonography (BPS) is highly characteristic for idiopathic PD. We studied 7 symptomatic and 7 asymptomatic parkin mutation carriers (PMC) from a large kindred with adult‐onset parkinsonism. BPS revealed larger SN echogenic sizes in PMC with parkin mutations on both alleles (homozygous, compound‐heterozygous), compared to PMC with only one mutated allele (Mann–Whitney U test, P = 0.007). In symptomatic PMC, larger SN echogenic size was correlated with younger age at onset of the disease (Spearman rank correlation, Rho = −0.937, P = 0.002) but not with age, disease duration, or disease severity. BPS demonstrated SN hyperechogenicity, in concordance with abnormal nigrostriatal 18F‐dopa positron emission tomography (PET), in all symptomatic and 3 asymptomatic PMC. In 2 asymptomatic PMC, PET and BPS were normal. However, in another 2 asymptomatic PET‐normal PMC, SN hyperechogenicity could be detected. Data suggest SN hyperechogenicity as an early marker to detect preclinical parkinsonism. © 2004 Movement Disorder Society

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DOI: 10.1002/mds.20232


Affiliations:


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<div type="abstract" xml:lang="en">Substantia nigra (SN) hyperechogenicity on brain parenchyma sonography (BPS) is highly characteristic for idiopathic PD. We studied 7 symptomatic and 7 asymptomatic parkin mutation carriers (PMC) from a large kindred with adult‐onset parkinsonism. BPS revealed larger SN echogenic sizes in PMC with parkin mutations on both alleles (homozygous, compound‐heterozygous), compared to PMC with only one mutated allele (Mann–Whitney U test, P = 0.007). In symptomatic PMC, larger SN echogenic size was correlated with younger age at onset of the disease (Spearman rank correlation, Rho = −0.937, P = 0.002) but not with age, disease duration, or disease severity. BPS demonstrated SN hyperechogenicity, in concordance with abnormal nigrostriatal 18F‐dopa positron emission tomography (PET), in all symptomatic and 3 asymptomatic PMC. In 2 asymptomatic PMC, PET and BPS were normal. However, in another 2 asymptomatic PET‐normal PMC, SN hyperechogenicity could be detected. Data suggest SN hyperechogenicity as an early marker to detect preclinical parkinsonism. © 2004 Movement Disorder Society</div>
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