Cerebral Vasospasm: Pathophysiology, Risk Factors, Diagnosis, and Modern Therapeutic Strategies
Cerebral vasospasm refers to the constriction of cerebral arteries, often following subarachnoid hemorrhage, leading to reduced blood flow and potential ischemic brain injury. It is a major complication of aneurysmal rupture and traumatic brain injury, with onset typically between 3–14 days after hemorrhage. Pathophysiology involves endothelial dysfunction,
inflammatory cascades, oxidative stress, and smooth muscle contraction within arterial walls.
Risk factors include the amount of subarachnoid blood, patient age, hypertension, smoking, and delayed intervention. Early diagnosis is crucial to prevent cerebral ischemia, permanent neurological deficits, or death. Diagnostic tools include transcranial Doppler ultrasonography, CT angiography, MR angiography, and digital subtraction angiography. Clinical monitoring for changes in consciousness, focal neurological deficits, and headaches complements imaging studies.
Therapeutic strategies encompass pharmacological and interventional approaches. Calcium channel blockers, such as nimodipine, reduce the risk of ischemic injury. Endovascular techniques like balloon angioplasty and intra-arterial vasodilators treat severe vasospasm. Supportive measures, including blood pressure management, fluid therapy, and careful ICU monitoring, optimize cerebral perfusion. Ongoing research explores neuroprotective agents, anti-inflammatory drugs, and predictive biomarkers to improve outcomes.
FAQs
Q1: What is cerebral vasospasm?Constriction of cerebral arteries after subarachnoid hemorrhage, reducing blood flow to the brain.Q2: How is it diagnosed?Through transcranial Doppler, CT/MR angiography, and clinical monitoring.Q3: How is it treated?Calcium channel blockers, endovascular interventions, and supportive care.