Traumatic brain injury in later life increases risk for Parkinson disease.
OBJECTIVE
Traumatic brain injury (TBI) is thought to be a risk factor for Parkinson 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) International Classification of Disease, Ninth Revision code data for California hospitals from 2005-2006, we identified patients aged ≥55 years 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, health care use, and 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 nonfall) 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% vs 1.1%, p < 0.001, adjusted hazard ratio [HR] = 1.44, 95% confidence interval [CI] = 1.31-1.58). Risk of PD was similar for TBI sustained via falls versus nonfalls (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.


CONCLUSIONS
Among patients aged ≥55 years presenting to inpatient/ED settings with trauma, TBI is associated with a 44% increased risk of developing PD over 5 to 7 years that is unlikely to be due to confounding or reverse causation.
Department of Neurology, University of California, San Francisco, San Francisco, CA.|San Francisco Veterans Affairs Medical Center, San Francisco, CA.
Raquel C
RC
Gardner
Department of Neurology, University of Michigan and Department of Veterans Affairs, VA Center for Clinical Management and Research, Ann Arbor VA Healthcare System, Ann Arbor, MI.
James F
JF
Burke
San Francisco Veterans Affairs Medical Center, San Francisco, CA.|Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, CA.
Jasmine
J
Nettiksimmons
Department of Neurology, University of California, San Francisco, San Francisco, CA.|San Francisco Veterans Affairs Medical Center, San Francisco, CA.
Sam
S
Goldman
Department of Neurology, University of California, San Francisco, San Francisco, CA.|San Francisco Veterans Affairs Medical Center, San Francisco, CA.
Caroline M
CM
Tanner
Department of Neurology, University of California, San Francisco, San Francisco, CA.|San Francisco Veterans Affairs Medical Center, San Francisco, CA.|Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, CA.|Department of Psychiatry, University of California, San Francisco, San Francisco, CA.
Kristine
K
Yaffe
D000368:Aged; D000369:Aged, 80 and over; D001930:Brain Injuries / Q000150:complications* / Q000453:epidemiology; D002140:California / Q000453:epidemiology; D005260:Female; D005500:Follow-Up Studies; D050723:Fractures, Bone / Q000150:complications* / Q000453:epidemiology; D006801:Humans; D053208:Kaplan-Meier Estimate; D008297:Male; D008875:Middle Aged; D010300:Parkinson Disease / Q000453:epidemiology / Q000209:etiology*; D016016:Proportional Hazards Models; D012189:Retrospective Studies; D012307:Risk Factors; D013997:Time Factors; D015599:Trauma Severity Indices