Abstract

Background:Musician’s dystonia (MD) is a task-specific movement disorder characterized by muscle cramps and impaired voluntary motor-control whilst playing a musical instrument. Recent studies suggest an involvement of adverse childhood experiences (ACEs) in the development of MD.Objectives:By investigating the prevalence of ACEs in MD patients with perfectionism as possible mediating factor this study aims to gain further insights into the etiology of MD.Methods:The Adverse Childhood Experiences Scale (ACE-S), the Childhood Trauma Questionnaire (CTQ) and Frost’s Multidimensional Perfectionism Scale (FMPS) were answered by 128 MD patients and 136 healthy musicians. Regression and mediator analyses were conducted to identify relevant predictors of MD and to investigate the role of perfectionism.Results:The CTQ total score (OR: 1.04; 95% CI [1.01, 1.08]) and the sub-score “emotional neglect” (OR: 1.13; 95% CI [1.02, 1.25]) were identified as two predictors of MD. Patients scored significantly higher on the sub-score emotional neglect, but no significant differences were observed for other forms of ACEs. Perfectionism had no mediating function on the association between ACEs and MD.Discussion:Though only slight differences between both groups were found, there is a trend towards higher rates of emotional neglect among dystonic musicians. A possible explanation for the association between musician’s dystonia and emotional neglect could be a lower stress resilience in musicians with a history of ACEs, which increases vulnerability to acquire dysfunctional movement patterns.These tendencies should be further investigated in future studies in which the MD and HM groups are more evenly matched in sex and age.HighlightsWe investigated the role of Adverse Childhood Experiences in the development of musician’s dystonia, comparing a large sample of healthy musicians and dystonia patients. Our findings suggest that experiencing emotional neglect might increase the probability to acquire musician’s dystonia. The findings offer new implications for etiology and treatment of dystonia.

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