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Citation
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Gardner RC, Burke JF, Nettiksimmons J, Goldman S, Tanner CM, Yaffe KC. Ann. Neurol. 2015; 77(6): 987-995. |
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Abstract
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OBJECTIVE: Traumatic brain injury (TBI) is thought to be a risk factor for Parkinson's disease (PD) but results are conflicting. Many studies do not account for confounding or reverse-causation. We sought to address these concerns by quantifying risk of PD after TBI compared to non-TBI trauma (NTT, defined as fractures).
METHODS: Using inpatient/emergency department (ED) ICD-9 code data for California hospitals from 2005-2006, we identified patients age ≥55 with TBI (n=52,393) or NTT (n=113,406) and without baseline PD or dementia who survived hospitalization. Using Kaplan-Meier estimates and Cox proportional hazards models (adjusted for age, sex, race/ethnicity, income, comorbidities, healthcare use, trauma severity), we estimated risk of PD after TBI during follow-up ending in 2011. We also assessed interaction with mechanism of injury (fall vs. non-fall) and effect of TBI-severity (mild vs. moderate/severe) and TBI-frequency (1 TBI vs. >1 TBI).
RESULTS: TBI patients were significantly more likely to be diagnosed with PD compared to NTT patients (1.7% versus 1.1%, p<0.001, adjusted hazard ratio (HR) 1.44, 95% CI 1.31-1.58). Risk of PD was similar for TBI sustained via falls versus non-falls (interaction p=0.6). Assessment by TBI-severity (mild TBI HR 1.24, 95% CI 1.04-1.48; moderate/severe TBI HR 1.50, 95% CI 1.35-1.66) and TBI-frequency (1 TBI HR 1.45, 95% CI 1.30-1.60; >1 TBI HR 1.87, 95% CI 1.58-2.21) revealed a dose-response.
INTERPRETATION: Among patients age ≥55 presenting to inpatient/ED settings with trauma, TBI is associated with a 44% increased risk of developing PD over 5-7 years that is unlikely due to confounding or reverse-causation. This article is protected by copyright. All rights reserved.
Language: en |