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Impact of ataxia aetiology on self-reported mental health, fatigue, cognition and ataxia symptom severity
Impact of ataxia aetiology on self-reported mental health, fatigue, cognition and ataxia symptom severity
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Impact of ataxia aetiology on self-reported mental health, fatigue, cognition and ataxia symptom severity
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Impact of ataxia aetiology on self-reported mental health, fatigue, cognition and ataxia symptom severity
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Impact of ataxia aetiology on self-reported mental health, fatigue, cognition and ataxia symptom severity
Impact of ataxia aetiology on self-reported mental health, fatigue, cognition and ataxia symptom severity
Journal Article

Impact of ataxia aetiology on self-reported mental health, fatigue, cognition and ataxia symptom severity

2024
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Overview
Introduction It has been increasingly recognised that the impact of Ataxia extends beyond physical and motor symptomology. However, it is less known whether self-reported non-motor and ataxia symptom severity varies across ataxias of differing aetiology, which would have important implications for providing more targeted treatment. Aim This study aimed to investigate the impact of ataxia aetiology (hereditary, acquired or idiopathic) on self-reported depression, anxiety, fatigue, cognitive deficits, and ataxia symptom severity. Comparisons were also made between the ataxia sample as a whole and a neurologically healthy control group. Method Responses were collected using a cross-sectional online survey to recruit a national UK sample of people with ataxia. Results The study recruited 110 participants with ataxia (hereditary = 51, acquired = 16, idiopathic = 43) and 32 healthy controls. No significant differences were found across study variables for different causes of ataxia. However, participants with ataxia did report significantly higher levels of depression, anxiety, fatigue, cognitive deficits, and ataxia symptom severity compared to healthy controls. Conclusion This study found that participants with ataxia self-reported increased non-motor symptoms compared to healthy controls, which was a generally homogenous experience across different causes of ataxia. There was also considerable comorbidity of symptoms which requires further exploration. This study highlights the need for early assessment and intervention to address these non-motor symptoms in ataxia populations.