The aim of this study was to evaluate the relationship between antiparkinsonian treatments, especially dopamine agonist (DAs) and the development of postural disorders in patients with Parkinson's disease (PD).
We performed an exploratory case-control study. Cases were PD patients with camptocormia, Pisa syndrome, or anterocollis. Control subjects were PD patients without postural disorders matched by sex and age. Demographic and clinical data including pharmacologic treatments history were collected retrospectively. Characteristics of cases and control subjects were compared using parametric and nonparametric tests accordingly, and logistic regression models were used to analyze correlations.
We included 63 patients with PD and postural disorders and 63 control subjects. Cases were more exposed to DAs (74.60% vs 58.73%, P = 0.05) and amantadine (30.16% vs 7.94%, P < 0.05) than control subjects. Cases showed longer disease duration (7.63 ± 7.83 vs 4.27 ± 3.87 years, P < 0.05), higher Hoehn and Yahr stage (2.83 ± 0.80 vs 2.15 ± 0.73, P < 0.05), higher Movement Disorder Society Unified Parkinson's Disease Rating Scale part III score (29.61 ± 1.39 vs 20.76 ± 10.94, P = 0.05), and more dyslipidemia (28.57% vs 12.70%, P < 0.05) than control subjects, as well as lower prevalence of depression (46.03% vs 28.57%, P < 0.05). We found no clinical predictors for the development of postural disorders after multivariable adjusted regression.
Our results suggest a possible association between the use of DAs and amantadine and the development of postural disorders in PD and suggest potential risk factors including advanced disease and more severe motor symptoms. These results support the need of a cautious use of these medications in patients with advanced disease due to the possibility of increasing the risk-benefit ratio.
*Movement Disorders Section, Neuroscience Department, Raúl Carrea Institute for Neurological Research (FLENI), Buenos Aires, Argentina;
†Movement Disorders Program, Department of Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada; and
‡Argentine National Scientific and Technological Research Council (CONICET), Buenos Aires, Argentina.
Address correspondence and reprint requests to Lucía Ameghino, MD, Movement Disorders Section, Raul Carrea Institute for Neurological Research (FLENI), Montañeses 2325, Ciudad Autónoma de Buenos Aires (1428), Argentina; E-mail: email@example.com
L.A. and V.B. contributed equally to this study.
Conflicts of Interest and Source of Funding: The authors have no conflicts of interest to declare.
Author contributions: L.A. was involved in study concept and design, acquisition of data, and data analysis and interpretation. V.B. was involved in study concept and design and data analysis and interpretation. M.M. was involved in study concept and design, critical revision of the manuscript for important intellectual content, and study supervision.