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rTMS for Cerebellar Ataxia in Children

The University of Hong Kong · 2025
ClinicalTrials.gov · Datasets · License: Public Domain · 2025
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childrennatms
Dysfunction of the cerebellum can result in cerebellar ataxia (CA), typically marked by symptoms such as movement incoordination, gait instability, articulation disorder, oculomotor and swallowing difficulties. Children affected by paediatric cerebellar ataxia (PCA) often suffer from an array of motor symptoms, affecting their quality of life and psychosocial well-being. It was estimated that PCA affects 26/100,000 children worldwide for both genetic and acquired causes. Epidemiological data on PCA, however, are absent in the Hong Kong population. PCAs comprise a varied group of cerebellar development disorders, marked by impaired balance and motor coordination (e.g., dysmetria and tremor) when performing voluntary movement. Clinical symptoms in children with PCA are related to lesioned localization - focal disorder of the cerebellar vermis leads to truncal instability, head titubation, and nystagmus; while lesioned cerebellar hemispheres results in ataxia gait (wide-staggering gait, tend to fall towards the affected side). These clinical symptoms result in functional difficulties involving balance and walking, reaching, grasping and manipulation, oculomotor and speech domains. Abnormalities of motor excitability have been reported in patients with cerebellar lesions - the motor threshold was found to be raised in the motor cortex contralateral to a hemi-cerebellar lesion. With no effective pharmacological treatments available, rehabilitation serves as the primary treatment approach. Even though adaptive learning is affected by cerebellar lesion, motor learning is still possible via exercise interventions. Interventions may include compensatory (educate strategies to compensate for impairment) or restorative approaches (improve functions through training). While exercise interventions have been explored as a potential therapeutic approach for paediatric patients with cerebellar lesions or degeneration, the current evidence lacks robust, high-quality randomized con
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