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Determinants of autonomic dysfunction in idiopathic Parkinson’s disease

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Abstract

Objectives

To determine demographic or disease-related factors that may influence the severity of autonomic dysfunction in idiopathic Parkinson’s disease (IPD).

Methods

532 patients with IPD aged between 55 and 75 years were included. Severity of autonomic dysfunction was assessed using a 9-item autonomic dysfunction score (ADS). In addition, several demographic factors (e. g. age, gender, comorbidities) and disease- related (e. g. motor stage, disease duration, antiparkinsonian therapy) factors were recorded. A group of 67 age-matched healthy volunteers served as a control group. Demographic and clinical data of this cross-sectional survey were analyzed by a logistic stepwise regression model to determine independent predictors of autonomic dysfunction.

Results

IPD patients showed significantly higher ADS values than controls, even in the youngest age groups and in mild disease stages. Hoehn&Yahr (H&Y) stage, disease duration, age at onset and various therapy combinations all showed significant correlations with ADS. However, stepwise logistic regression revealed that age (OR 10.71; CI 7.17–16.0) and arterial hypertension (OR 3.05; CI 1.66–5.58) were the only independent risk factors associated with autonomic dysfunction. Linear regression indicated that ADS increases with age in controls as well as in patients, but with a significantly steeper slope in the latter.

Conclusions

Autonomic dysfunction as an inherent feature of IPD is present already in early disease stages. According to a logistic regression model, the severity of autonomic dysfunction in IPD is primarily related to demographic but not to disease-related factors. This and the differences in predictors for motor versus autonomic decline may indicate at least partly independent neurodegenerative processes.

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Correspondence to Alexei Korchounov MD.

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Korchounov, A., Kessler, K.R., Yakhno, N.N. et al. Determinants of autonomic dysfunction in idiopathic Parkinson’s disease. J Neurol 252, 1530–1536 (2005). https://doi.org/10.1007/s00415-005-0909-6

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  • DOI: https://doi.org/10.1007/s00415-005-0909-6

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