Affiliations: [a] Department of Pathology, Anatomy, and Laboratory Medicine, Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV, USA
| [b] Department of Pathology, Western Michigan University Homer Stryker MD School of Medicine, Kalamazoo, MI, USA
| [c] College of Sciences, University of Texas, San Antonio, San Antonio, TX, USA
Correspondence:
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Correspondence to: Rudy J. Castellani, MD, 64 Medical Center Drive, 2289 HSC-S, MS 9203, Morgantown, WV 26506-9203, USA. Tel.: +1 304 293 1625; Fax: +1 304 293 1627; E-mail: Rudolph.castellani@hsc.wvu.edu.
Abstract: Traumatic brain injury (TBI) is widely assumed to be causal in neurodegenerative disease, based on epidemiological surveys demonstrating an increased risk of Alzheimer disease (AD) following TBI, and on recent theories surrounding repetitive head movement. We tested this assumption by evaluating 30 consecutive forensic examinations in which neuropathology consultation was sought, and in which a history of remote TBI was uncovered during the course of the investigation. In this series, there was a high frequency of psychiatric co-morbidities (100%), remote contusion (90%), and seizures (63%). Extent of proteinopathy showed no differences with age-matched controls. A subset of the cases showed focal geographic tauopathy that correlated with older age at autopsy, but had no correlation with clinical signs, and was minimal in comparison with the encephalomalacia secondary to trauma. The results suggest that cerebral contusion and post-traumatic epilepsy may be over-represented in civilian TBI, while structural brain damage from trauma is the predominant cause of morbidity following TBI. We found no evidence that TBI initiates a progressive proteinopathy.
