Cerebral Autoregulation and Cardiovascular Physiology Dysfunction in Traumatic Brain Injury Cases: A Brief Review

Introduction: Traumatic brain injury (TBI) is one of the leading causes of death and disability in the early years of life. Post-TBI physiological alterations vary across adult and pediatric patients and severity. This disease affects the quality of life of most people. Acute hemiparesis can cause cognitive impairments. It may also impact mood, memory, and decision-making. Furthermore, parasympathetic dysfunction and sympathetic activation appear to contribute to cardiac injury via modulation of the myocardial inflammatory response via acetylcholine receptors.

Purpose: This review aims to explain the neuronal response and cardiac dysfunction after traumatic brain injury cases.

Methods: The review used Pubmed and Google Scholar to search for articles on traumatic brain injury, neuronal response, and cardiac biomarkers. The articles were chosen for their language, publishing, content, exposure, and outcome. The main reference is obtained from up to 79 articles that meet the inclusion requirements.

Results: TBI can cause localized brain injury or diffuse brain injury from physical trauma such as diffuse axonal injury or brain edema. Repeated concussions raise the likelihood of chronic neurological, cognitive, and behavioral issues. Stress-induced catecholamine surges and inflammatory mediator production in response to trauma may also endanger cardiac disturbances. ECG changes in patients with severe traumatic brain injury are associated with cardiac dysfunction. Cardiac enzymes can be used as a diagnostic tool and indicate the patient's prognosis.

Conclusion: Cerebral autoregulation and cardiac physiological responses have a synergistic relationship in maintaining tissue homeostasis in patients with traumatic brain injury. Patients with TBI may experience cardiac dysfunction as a result of the body’s exaggerated systemic response to brain injury.