Citation

Iacono D, Shively SB, Edlow BL, Perl DP. Phys. Med. Rehabil. Clin. N. Am. 2017; 28(2): 301-321.

Affiliation

Brain Tissue Repository & Neuropathology Core, Center for Neuroscience and Regenerative Medicine (CNRM), Uniformed Services University of the Health Sciences (USUHS), 4301 Jones Bridge Road, Bethesda, MD 20814, USA; Department of Pathology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences (USUHS), 4301 Jones Bridge Road, Bethesda, MD 20814, USA. Electronic address: daniel.perl@usuhs.edu.

Copyright

(Copyright © 2017, Elsevier Publishing)

DOI

10.1016/j.pmr.2016.12.007

PMID

28390515

Abstract

Chronic traumatic encephalopathy (CTE) is a neuropathologic diagnosis typically made in human brains with a history of repetitive traumatic brain injury (rTBI). It remains unknown whether CTE occurs exclusively after rTBI, or whether a single TBI (sTBI) can cause CTE. Similarly, it is unclear whether impact (eg, motor vehicle accidents) and non-impact (eg, blasts) types of energy transfer trigger divergent or common pathologies. While it is established that a history of rTBI increases the risk of multiple neurodegenerative diseases (eg, dementia, parkinsonism, and CTE), the possible pathophysiologic and molecular mechanisms underlying these risks have yet to be elucidated.

Published by Elsevier Inc.

Language: en

Keywords

Acute and long-term effects; Chronic traumatic encephalopathy; Diffuse axonal injury; Neurodegeneration; Neuropsychiatric disorders; Tau; Traumatic brain injury; β-Amyloid