ArticleJournal of neural transmission (Vienna, Austria : 1996)2025
Atrophy of cerebellar lobule VI and primary motor cortex in cervical dystonia - a region of interest-based study.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Emotion-tremor coupling in Wilson's disease: EEG microstate C as a marker of salience network dysregulation.Orphanet journal of rare diseases · 2026Article
- Brain network topology and neural mechanisms in Sanda athletes: a comparative study across training levels.Frontiers in neuroscience · 2026Article
- Multimodal MRI reveals structural and functional alterations in isolated cervical dystonia: associations with motor severity and affective symptoms.Frontiers in neurologyArticle
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7 authors.
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Abstract
backgroundRecently, a network model of cervical dystonia (CD) has been adopted that implicates nodes and pathways involving cerebellar, basal-ganglia and cortico-cortical connections. Although functional changes in the cerebello-thalamo-cortical network in dystonia have been reported in several studies, structural information of this network remain sparse.
objectiveTo characterize the structural properties of the cerebellar motor network in isolated CD patients. This includes cerebellar lobules involved in motor processing, the dentate nucleus (DN), the thalamus, and the primary motor cortex (M1).
methodsMagnetic resonance imaging data of 18 CD patients and 18 healthy control subjects were acquired. In CD patients, the motor part of the Toronto Western Spasmodic Torticollis Rating Scale was assessed to evaluate motor symptom severity. The volume of cerebellar lobules I-VI and VIII, the DN and thalamus, and the cortical thickness (CT) of M1 were determined for a region of interest (ROI)-based quantitative analysis. Volumes/CT of these ROIs were compared between groups and associated with motor symptom severity in patients.
resultsThe volume of lobule VI and the CT of M1 were reduced in CD patients. The volumes of the other ROIs were not different between groups. No association was identified between the structural properties of lobule VI or M1 and the severity of CD motor symptoms.
conclusionAtrophy within the cerebellum and M1 contributes to CD's complex motor network pathology. Further investigations are needed to ascertain the mechanisms underlying the local volume loss.
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