Muscle MRI in periodic paralysis shows myopathy is common and correlates with intramuscular fat accumulation.


Journal

Muscle & nerve
ISSN: 1097-4598
Titre abrégé: Muscle Nerve
Pays: United States
ID NLM: 7803146

Informations de publication

Date de publication:
10 2023
Historique:
revised: 05 07 2023
received: 03 11 2022
accepted: 08 07 2023
medline: 22 9 2023
pubmed: 29 7 2023
entrez: 29 7 2023
Statut: ppublish

Résumé

The periodic paralyses are muscle channelopathies: hypokalemic periodic paralysis (CACNA1S and SCN4A variants), hyperkalemic periodic paralysis (SCN4A variants), and Andersen-Tawil syndrome (KCNJ2). Both episodic weakness and disabling fixed weakness can occur. Little literature exists on magnetic resonance imaging (MRI) in muscle channelopathies. We undertake muscle MRI across all subsets of periodic paralysis and correlate with clinical features. A total of 45 participants and eight healthy controls were enrolled and underwent T1-weighted and short-tau-inversion-recovery (STIR) MRI imaging of leg muscles. Muscles were scored using the modified Mercuri Scale. A total of 17 patients had CACNA1S variants, 16 SCN4A, and 12 KCNJ2. Thirty-one (69%) had weakness, and 9 (20%) required a gait-aid/wheelchair. A total of 78% of patients had intramuscular fat accumulation on MRI. Patients with SCN4A variants were most severely affected. In SCN4A, the anterior thigh and posterior calf were more affected, in contrast to the posterior thigh and posterior calf in KCNJ2. We identified a pattern of peri-tendinous STIR hyperintensity in nine patients. There were moderate correlations between Mercuri, STIR scores, and age. Intramuscular fat accumulation was seen in seven patients with no fixed weakness. We demonstrate a significant burden of disease in patients with periodic paralyses. MRI intramuscular fat accumulation may be helpful in detecting early muscle involvement, particularly in those without fixed weakness. Longitudinal studies are needed to assess the role of muscle MRI in quantifying disease progression over time and as a potential biomarker in clinical trials.

Identifiants

pubmed: 37515374
doi: 10.1002/mus.27947
doi:

Substances chimiques

NAV1.4 Voltage-Gated Sodium Channel 0
SCN4A protein, human 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

439-450

Subventions

Organisme : Medical Research Council
ID : MR/V037838/1
Pays : United Kingdom
Organisme : Department of Health
Pays : United Kingdom

Commentaires et corrections

Type : ErratumIn

Informations de copyright

© 2023 The Authors. Muscle & Nerve published by Wiley Periodicals LLC.

Références

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Auteurs

Vinojini Vivekanandam (V)

Queen Square Centre for Neuromuscular Diseases, UCL Queen Square Institute of Neurology, London, UK.

Karen Seutterlin (K)

Queen Square Centre for Neuromuscular Diseases, UCL Queen Square Institute of Neurology, London, UK.
AGE Research Group, NIHR Newcastle Biomedical Research Centre, Newcastle upon Tyne Hospitals NHS Foundation Trust and Newcastle University, Newcastle upon Tyne, UK.

Emma Matthews (E)

Atkinson-Morley Neuromuscular Centre, Department of Neurology, St George's University Hospitals NHS Foundation Trust, and Molecular and Clinical Sciences Research Institute, St George's University of London, London, UK.

John Thornton (J)

Neuroradiological Academic Unit, UCL Queen Square Institute of Neurology, UCL, London, UK.

Dipa Jayaseelan (D)

Queen Square Centre for Neuromuscular Diseases, UCL Queen Square Institute of Neurology, London, UK.

Sachit Shah (S)

Neuroradiological Academic Unit, UCL Queen Square Institute of Neurology, UCL, London, UK.

Jasper M Morrow (JM)

Queen Square Centre for Neuromuscular Diseases, UCL Queen Square Institute of Neurology, London, UK.

Tarek Yousry (T)

Neuroradiological Academic Unit, UCL Queen Square Institute of Neurology, UCL, London, UK.

Michael G Hanna (MG)

Queen Square Centre for Neuromuscular Diseases, UCL Queen Square Institute of Neurology, London, UK.

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