A 5-Year Longitudinal Clinical and Magnetic Resonance Imaging Study in Spinocerebellar Ataxia Type 3.


Journal

Movement disorders : official journal of the Movement Disorder Society
ISSN: 1531-8257
Titre abrégé: Mov Disord
Pays: United States
ID NLM: 8610688

Informations de publication

Date de publication:
09 2020
Historique:
received: 20 12 2019
revised: 16 04 2020
accepted: 01 05 2020
pubmed: 10 6 2020
medline: 28 4 2021
entrez: 10 6 2020
Statut: ppublish

Résumé

The natural history of neurodegeneration in spinocerebellar ataxia type 3/Machado Joseph disease is still unclear. Here, we built a long-term longitudinal clinical and neuroimaging study to address this point. Twenty-three patients with spinocerebellar ataxia type 3/Machado Joseph disease and 22 healthy controls underwent 3T MRI twice 5.0 years apart. T1 and diffusion tensor imaging sequences were obtained. We used T1 multiatlas, diffusion tensor imaging multiatlas, SpineSeg, and CERES-SUIT for cerebral gray and white matter, spinal cord and cerebellar analyses, respectively. Clinical severity was assessed with scale for assessment and rating of ataxia. Analysis of covariance evaluated longitudinal between-group changes. Effect sizes were calculated for each significant result. Progressive volumetric abnormalities were most evident in the cerebellum (Lobule X and Crus II; effect size, 2.0), followed by the basal ganglia (effect size, 0.7). The cerebellar peduncles had the largest white-matter diffusivity changes (effect size, 1.29). Scale for assessment and rating of ataxia-related effect size was 0.82. We failed to identify progressive spinal cord abnormalities. Longitudinal changes in spinocerebellar ataxia type 3/Machado Joseph disease are more evident in the cerebellum and connections, followed by the basal ganglia. © 2020 International Parkinson and Movement Disorder Society.

Sections du résumé

BACKGROUND
The natural history of neurodegeneration in spinocerebellar ataxia type 3/Machado Joseph disease is still unclear. Here, we built a long-term longitudinal clinical and neuroimaging study to address this point.
METHODS
Twenty-three patients with spinocerebellar ataxia type 3/Machado Joseph disease and 22 healthy controls underwent 3T MRI twice 5.0 years apart. T1 and diffusion tensor imaging sequences were obtained. We used T1 multiatlas, diffusion tensor imaging multiatlas, SpineSeg, and CERES-SUIT for cerebral gray and white matter, spinal cord and cerebellar analyses, respectively. Clinical severity was assessed with scale for assessment and rating of ataxia. Analysis of covariance evaluated longitudinal between-group changes. Effect sizes were calculated for each significant result.
RESULTS
Progressive volumetric abnormalities were most evident in the cerebellum (Lobule X and Crus II; effect size, 2.0), followed by the basal ganglia (effect size, 0.7). The cerebellar peduncles had the largest white-matter diffusivity changes (effect size, 1.29). Scale for assessment and rating of ataxia-related effect size was 0.82. We failed to identify progressive spinal cord abnormalities.
CONCLUSIONS
Longitudinal changes in spinocerebellar ataxia type 3/Machado Joseph disease are more evident in the cerebellum and connections, followed by the basal ganglia. © 2020 International Parkinson and Movement Disorder Society.

Identifiants

pubmed: 32515873
doi: 10.1002/mds.28113
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1679-1684

Informations de copyright

© 2020 International Parkinson and Movement Disorder Society.

Références

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Auteurs

Camila Callegari Piccinin (CC)

School of Medical Sciences, University of Campinas, Campinas, Brazil.
Brazilian Institute of Neuroscience and Neurotechnology (BRAINN), Campinas, Brazil.

Thiago Junqueira Ribeiro Rezende (TJR)

Brazilian Institute of Neuroscience and Neurotechnology (BRAINN), Campinas, Brazil.
Department of Neurology, University of Campinas, Campinas, Brazil.

Jean Levi Ribeiro de Paiva (JLR)

School of Medical Sciences, University of Campinas, Campinas, Brazil.

Pedro Cury Moysés (PC)

School of Medical Sciences, University of Campinas, Campinas, Brazil.
Brazilian Institute of Neuroscience and Neurotechnology (BRAINN), Campinas, Brazil.

Alberto Rolim Muro Martinez (ARM)

Brazilian Institute of Neuroscience and Neurotechnology (BRAINN), Campinas, Brazil.
Department of Neurology, University of Campinas, Campinas, Brazil.

Fernando Cendes (F)

Brazilian Institute of Neuroscience and Neurotechnology (BRAINN), Campinas, Brazil.
Department of Neurology, University of Campinas, Campinas, Brazil.

Marcondes Cavalcante França (MC)

Brazilian Institute of Neuroscience and Neurotechnology (BRAINN), Campinas, Brazil.
Department of Neurology, University of Campinas, Campinas, Brazil.

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