What causes vertebrobasilar artery spasm?

Vertebrobasilar artery spasm—also referred to as vertebrobasilar vasospasm—is a transient, reversible narrowing of the vertebral or basilar arteries, which together constitute the vertebrobasilar circulation supplying blood to the brainstem, cerebellum, thalamus, and occipital lobes. While less commonly discussed than cerebral vasospasm following subarachnoid hemorrhage, vertebrobasilar spasm can arise from several underlying mechanisms. Primary causes include acute vascular irritation—most notably from subarachnoid hemorrhage (SAH), particularly when blood accumulates in the posterior fossa or around the basilar artery. Other important contributors are severe systemic hypotension or shock, which may trigger autoregulatory vasoconstriction; acute migraine with aura, especially in patients with underlying vascular susceptibility; and exposure to potent vasoconstrictive agents such as ergot alkaloids, certain stimulants (e.g., amphetamines, cocaine), or serotonin-receptor agonists like triptans in predisposed individuals. Less common but clinically relevant etiologies include vasculitides (e.g., granulomatosis with polyangiitis, primary angiitis of the CNS), reversible cerebral vasoconstriction syndrome (RCVS), carotid or vertebral artery dissection with secondary reflex spasm, and metabolic disturbances such as severe hyponatremia or hypercalcemia. Importantly, isolated vertebrobasilar spasm without an identifiable structural or systemic cause warrants thorough neurovascular evaluation—including high-resolution vessel wall MRI, CT or MR angiography, and lumbar puncture when SAH is suspected—to exclude mimics such as acute ischemic stroke, posterior circulation stenosis, or inflammatory arteriopathy.