Background: Evidence does not support the view that Parkinson disease (PD) rep resents an accelerated aging process; however, the additional contribution of ag ing to the severity of different motor signs in patients ...Background: Evidence does not support the view that Parkinson disease (PD) rep resents an accelerated aging process; however, the additional contribution of ag ing to the severity of different motor signs in patients with PD is not known. T his knowledge may have implications for clinical trials of neuroprotective agent s in PD. Objective: To investigate the contribution of aging to the severity of the different motor signs of idiopathic PD. Setting: Center for Parkinson Diseas e and Other Movement Disorders of the Columbia University Medical Center and a n eurology clinic that primarily served individuals from the Washington Heights-I nwood community in New York City. Patients: Sample of patients with a wide range of disease duration and age. Design: Cross-sectional clinic-based study. Pati ents with PD were evaluated using the Unified Parkinson Disease Rating Scale (UP DRS). The total UPDRS motor score was divided into 6 motor domains (tremor, rigi dity, bradykinesia, facial expression, speech, and axial impairment) and 2 subsc ores 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 o f disease duration in the models, adjusting for sex, years of education, levodop a dosage, and use of other antiparkinsonian medications, was calculated. The add itional 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 UPDR S. Results: A total of 451 patients participated in the study. Mean age at exami nation 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; rang e, 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 explai ned 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 nondopa minergic subcortical structures.展开更多
文摘Background: Evidence does not support the view that Parkinson disease (PD) rep resents an accelerated aging process; however, the additional contribution of ag ing to the severity of different motor signs in patients with PD is not known. T his knowledge may have implications for clinical trials of neuroprotective agent s in PD. Objective: To investigate the contribution of aging to the severity of the different motor signs of idiopathic PD. Setting: Center for Parkinson Diseas e and Other Movement Disorders of the Columbia University Medical Center and a n eurology clinic that primarily served individuals from the Washington Heights-I nwood community in New York City. Patients: Sample of patients with a wide range of disease duration and age. Design: Cross-sectional clinic-based study. Pati ents with PD were evaluated using the Unified Parkinson Disease Rating Scale (UP DRS). The total UPDRS motor score was divided into 6 motor domains (tremor, rigi dity, bradykinesia, facial expression, speech, and axial impairment) and 2 subsc ores 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 o f disease duration in the models, adjusting for sex, years of education, levodop a dosage, and use of other antiparkinsonian medications, was calculated. The add itional 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 UPDR S. Results: A total of 451 patients participated in the study. Mean age at exami nation 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; rang e, 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 explai ned 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 nondopa minergic subcortical structures.
