Conclusions And Future Directions

The pathophysiology of cerebral vasospasm is a complex and poorly understood phenomenon. Spasmogens released from the subarachnoid clot activate multiple overlapping pathways that result in abnormal vasoconstriction and SMC proliferation. Other factors released from the clot result in endothelial dysfunction and injury, further disrupting the delicate balance between cerebral vasodilatation and constriction. Changes in VSMC growth, death, and migration, and in cellular matrix result in vascular remodeling, altering vessel lumen and compliance. Cerebral oxygen delivery is ultimately compromised regionally or globally. New therapeutic approaches to the prevention and treatment of cerebral vasospasm will evolve as our understanding of the underlying pathophysiologic mechanisms improves.

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