Traumatic brain injury persistently increases the incidence of both ischemic and hemorrhagic strokes: potential mechanisms.

Abstract

Traumatic brain injuries (TBI) significantly increase the risk of both ischemic and hemorrhagic strokes, with effects persisting for years after the initial injury. The mechanisms underlying this increased stroke risk are complex, multifactorial, and incompletely understood but likely include chronic cerebrovascular dysfunction, blood-brain barrier disruption, and inflammatory responses. Epidemiological studies consistently show that TBI is an independent risk factor for stroke, with more severe injuries associated with greater risk, especially for hemorrhagic strokes. Traditional risk factors for stroke, such as hypertension, poor diet, and sedentary lifestyle, further elevate the risk in TBI survivors. Modifiable lifestyle factors, such as improving sleep, increasing physical activity, and adopting heart-healthy diets, offer potential intervention points to mitigate stroke risk. Pharmacological considerations, including the use of antidepressants, anticoagulants, and statins, also influence stroke risk, particularly with regard to hemorrhagic complications. This review explores the pathophysiological mechanisms linking TBI and stroke, emphasizing the need for future research to identify specific biomarkers and imaging techniques to predict stroke vulnerability in TBI patients. Addressing the gaps in understanding, particularly regarding small vessel pathology will be essential to developing targeted therapies for reducing stroke incidence in TBI survivors.