Post-traumatic vasospasm: Epidemiology, specificities, risk factors, and therapeutics

Post-traumatic vasospasm (PTV) of intracranial arteries is a serious complication of traumatic brain injury (TBI) that can lead to significant neurological deficits and ischemic brain lesions. Despite its clinical relevance, the pathogenesis of PTV is not fully understood, and effective management strategies remain a challenge. This review aims to synthesize the current knowledge on pathophysiology, risk factors, detection, prevention, and treatment of PTV. Early detection of PTV is made difficult by the complexity of TBI and its management. The gold standard for vasospasm detection remains digital subtraction angiography (DSA). However, noninvasive techniques such as transcranial Doppler (TCD) and S100 protein monitoring may assist in detecting PTV. Compared with vasospasm associated with aneurysmal subarachnoid hemorrhage (aSAH), PTV appears to occur earlier and to resolve more quickly. Several risk factors have been identified, including the severity of TBI, younger age, SAH, or the presence of other hematomas. Treatment options include nimodipine and endovascular therapies, such as angioplasty and milrinone, though these require careful management due to their invasive nature and potential hypotensive effect. PTV represents a critical complication of TBI, requiring early detection and timely intervention to prevent secondary brain injuries. Although current strategies, such as nimodipine and intra-arterial therapies, have shown promise, further research is needed to refine these approaches and improve outcomes. Enhanced understanding of PTV’s pathophysiology, along with the development of more effective diagnostic and therapeutic tools, is essential for advancing patient care in TBI.