Vasospasmen

Vasospasmen, or vasospasm, are a reversible narrowing of blood vessels caused by contraction of vascular smooth muscle. This reduces blood flow to the supplied tissue and can cause ischemia if the constriction is prolonged or severe. Vasospasm can affect the cerebral, coronary, or peripheral circulation and may occur with or without an underlying disease.

Vasospasm most commonly occurs in several contexts: cerebral vasospasm after aneurysmal subarachnoid hemorrhage, coronary vasospasm producing variant angina, and peripheral vasospasm such as Raynaud phenomenon. Drug-induced vasospasm (for example, from cocaine or certain vasoactive medications) and vasospasm associated with cold exposure are also recognized. The clinical impact depends on the affected vascular bed.

Pathophysiology involves dysregulated vascular tone driven by factors such as endothelin-1, reduced nitric oxide, inflammation, and autonomic influences. In cerebral vasospasm after subarachnoid hemorrhage, breakdown products in the subarachnoid space promote sustained constriction and can lead to delayed cerebral ischemia.

Symptoms reflect the territory involved: focal neurologic deficits or altered consciousness with cerebral vasospasm, chest pain or ischemic changes with coronary vasospasm, and color change, numbness, or sensitivity to cold with peripheral vasospasm. Diagnosis combines clinical assessment with imaging, including transcranial Doppler for intracranial vessels and CT/MR angiography; coronary angiography may be used for suspected coronary involvement.

Treatment targets the underlying cause and perfusion. Nimodipine is standard to prevent delayed cerebral ischemia after subarachnoid hemorrhage. Other calcium channel blockers, nitrates, and supportive measures may be used. Prognosis varies; timely recognition and management reduce the risk of lasting ischemic damage.