Citation

Shively SB, Priemer DS, Stein MB, Perl DP. Psychiatr. Clin. North Am. 2021; 44(3): 443-458.

Copyright

(Copyright © 2021, Elsevier Publishing)

DOI

10.1016/j.psc.2021.04.003

PMID

unavailable

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.

Language: en

Keywords

Dementia; Traumatic brain injury (TBI); Chronic traumatic encephalopathy (CTE); Posttraumatic stress disorder (PTSD); Tauopathy