Traumatic Brain Injury Linked to Parkinson's, Lewy Body Pathology

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Traumatic Brain Injury Linked to Parkinson's, Lewy Body Pathology
Traumatic Brain Injury Linked to Parkinson's, Lewy Body Pathology

Traumatic brain injury (TBI) with loss of consciousness (LOC) was found to be associated with the development of Parkinson's disease and Lewy body accumulation – but not dementia – in a study of pooled prospective data.

The results provide further evidence of the possible long-term consequences of TBI and chronic traumatic encephalopathy.

Paul Crane, MD, MPH, of the Department of Medicine at the University of Washington in Seattle, and colleagues, analyzed pooled data from 3 prospective cohorts to assess the association between TBI with LOC and the long-term risk of Alzheimer's disease, Parkinson's disease, and other dementias. The cohort studies included the Memory and Aging Project (MAP), the Religious Orders Study (ROS), and the Adult Changes in Thought study (ACT).

The study included 7130 participants with a history of head injury. The cohort was 59.6% female with a mean age of 79.9 years.

The researchers identified 1537 cases of incident dementia and 117 cases of incident Parkinson's over 45 190 person-years. For all 3 cohorts, there did not appear to be an association between TBI with LOC and dementia or Alzheimer's.

However, there was an association between incident Parkinson's in the ACT group after excluding participants with prevalent Parkinson's at the start of the study (TBI with LOC ≥ 1 hour, HR 3.56, 95% CI: 1.52-8.28). Likewise, an association between Parkinson's progression was found in the ROS and MAP cohorts (TBI with LOC ≤ 1 hour, OR: 1.65, 95% CI: 1.23-2.21 and TBI with LOC ≥ 1 hour, OR: 2.23, 95% CI: 1.16-4.29).

Autopsy data was available for 525 participants in ACT and 1064 in ROS and MAP along with TBI data. In the ROS and MAP cohorts, TBI with LOC of ≤ 1 hour was associated with Lewy bodies in the temporal or frontal cortex (RR: 1.64, 95% CI: 1.00-2.70). TBI with LOC ≥ 1 hour was associated with cortical cerebral microinfarcts (RR 2.2, 95% CI: 1.12-4.01) in ROS and MAP and Lewy bodies (RR 2.64, 95% CI: 1.40-4.99) and hippocampal sclerosis (RR 2.34, 95% 1.02-5.30) in ACT.

Pooled analyses demonstrated a similar association between TBI with LOC ≤ 1 hour and risk for frontal and temporal cortex Lewy bodies (RR 1.59, 95% 1.06-2.39). Similarly, TBI with LOC ≥ 1 hour in participants younger than 25 was also found to be associated with Lewy bodies in the temporal and frontal cortex (RR 2.53, 95% CI: 1.02-6.24) and microinfarcts (RR 1.66, 95% CI: 1.19-2.32).

The authors noted that the study was limited by a lack of data on smoking and alcohol intake, body mass index and physical activity, and occupational history. Further, the original studies were not designed to assess TBI-related neuropathy.

“Traumatic brain injury with LOC sustained early in life is not innocuous and appears to be associated with neurodegenerative conditions, although not AD,” the authors concluded.

Reference

Crane PK, Gibbons LE, Dams-O'Connor K. Association of Traumatic Brain Injury With Late-Life Neurodegenerative Conditions and Neuropathologic Findings. JAMA Neurol. 2016; doi:10.1001/jamaneurol.2016.1948. 

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