Pathophysiology of Traumatic Brain Injury, Chronic Traumatic Encephalopathy, and Neuropsychiatric Clinical Expression.

Abstract

This article focuses on neuropsychiatric clinical expression and neuropathology associated with chronic traumatic encephalopathy (CTE), which is thought to develop years after traumatic brain injury. The incidence, prevalence, additional risk factors, and pathophysiology remain largely unknown. CTE is considered a tauopathy because the endogenous brain protein tau, in its hyperphosphorylated state (p-tau), defines the predominant neuropathological findings and may underlie aspects of cell toxicity, synapse and circuit dysfunction, and clinical signs and symptoms. We discuss pathophysiological mechanisms possibly affecting p-tau accumulation. Finally, we interweave how clinical features and neuroanatomical sites associated with CTE potentially intersect with posttraumatic stress disorder.

• Authors: Sharon Baughman Shively, David S Priemer, Murray B Stein, Daniel P Perl
• Journal: The Psychiatric clinics of North America (Psychiatr Clin North Am) Vol. 44 Issue 3 Pg. 443-458 (09 2021) ISSN: 1558-3147 [Electronic] United States
• PMID: 34373000 (Publication Type: Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Review)
• Copyright: Copyright © 2021 Elsevier Inc. All rights reserved.

Chemical References

• tau Proteins

Topics

• Brain
• Brain Injuries, Traumatic (complications)
• Chronic Traumatic Encephalopathy
• Humans
• Stress Disorders, Post-Traumatic
• tau Proteins (metabolism)