Pathophysiology of Traumatic Brain Injury, Chronic Traumatic Encephalopathy, and Neuropsychiatric Clinical Expression - 07/08/21

Doi : 10.1016/j.psc.2021.04.003

Sharon Baughman Shively, MD, PhD ^a, David S. Priemer, MD ^b,^c, Murray B. Stein, MD, MPH ^d,^e, Daniel P. Perl, MD ^f,^⁎
^a Independent Researcher, Potomac, MD, USA
^b F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, USA
^c Henry M. Jackson Foundation for the Advancement of Military Medicine, Bethesda, MD, USA
^d University of California San Diego, La Jolla, CA, USA
^e Veterans Affairs San Diego Healthcare System, La Jolla, CA, USA
^f Department of Pathology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Room B-3138, Bethesda, MD 20814, USA

^∗Corresponding author.

Résumé

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.

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