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Gilberto Levy, MD; Elan D. Louis, MD, MS; Lucien Cote, MD; Mario Perez, MD; Helen Mejia-Santana, MS; Howard Andrews, PhD; Juliette Harris, PhD, MS; Cheryl Waters, MD, FRCP; Blair Ford, MD, FRCP; Steven Frucht, MD; Stanley Fahn, MD; Karen Marder, MD, MPH

Arch Neurol. 2005;62:467-472.

Background  Evidence does not support the view that Parkinson disease (PD) represents an accelerated aging process; however, the additional contribution of aging to the severity of different motor signs in patients with PD is not known. This knowledge may have implications for clinical trials of neuroprotective agents in PD.

Objective  To investigate the contribution of aging to the severity of the different motor signs of idiopathic PD.

Setting  Center for Parkinson Disease and Other Movement Disorders of the Columbia University Medical Center and a neurology clinic that primarily served individuals from the Washington Heights–Inwood community in New York City.

Patients  Sample of patients with a wide range of disease duration and age.

Design  Cross-sectional clinic-based study. Patients with PD were evaluated using the Unified Parkinson Disease Rating Scale (UPDRS). The total UPDRS motor score was divided into 6 motor domains (tremor, rigidity, bradykinesia, facial expression, speech, and axial impairment) and 2 subscores that represented predominantly dopaminergic (subscore A: tremor, rigidity, bradykinesia, and facial expression) and nondopaminergic (subscore B: speech and axial impairment) deficiency. Analyses were performed using linear regression models with the UPDRS motor domains and subscores as the outcomes. The variation (adjusted R²) of the outcome variables explained by the inclusion of disease duration in the models, adjusting for sex, years of education, levodopa dosage, and use of other antiparkinsonian medications, was calculated. The additional variation explained by adding age at examination to the models was used to gauge the contribution of aging to each motor domain and subscore of the UPDRS.

Results  A total of 451 patients participated in the study. Mean age at examination was 62.0 years (SD, 12.6 years; median, 62.0 years; range, 18-93 years), and mean disease duration was 7.2 years (SD, 5.9 years; median, 5.6 years; range, 0.1-41.6 years). The additional variation of the outcome variable explained by including age in the models was higher for subscore B (14.3%; 95% confidence interval [CI], 9.9%-20.4%) than subscore A (4.7%; 95% CI, 2.0%-9.1%). Among the 6 motor domains, the additional variation of the outcome variable explained by including age in the models was highest for axial impairment (13.6%; 95% CI, 9.4%-19.6%).

Conclusion  Axial (gait and postural) impairment in PD may result from the combined effect of the disease and the aging process on nondopaminergic subcortical structures.

Author Affiliations: Statistical Analysis Center, Department of Biostatistics (Dr Levy), Departments of Neurology (Drs Louis, Cote, Harris, Waters, Ford, Frucht, Fahn, and Marder and Ms Mejia-Santana) and Psychiatry (Drs Andrews and Marder), G. H. Sergievsky Center (Drs Louis, Perez, Andrews, and Marder and Ms Mejia-Santana), and Taub Institute for Alzheimer’s Disease and the Aging Brain (Drs Louis and Marder), Columbia University, New York, NY.