Question:

Describe the pathophysiology of cerebral vasospasm in aneurysmal sub-arachnoid hemorrhage.

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Early detection and treatment of vasospasm in aneurysmal SAH is crucial to prevent permanent brain injury and neurological deficits.
Updated On: Dec 12, 2025
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Solution and Explanation

Cerebral vasospasm is a significant complication in patients with aneurysmal sub-arachnoid hemorrhage (SAH) and is the leading cause of delayed cerebral ischemia and neurological deterioration. It involves the constriction of cerebral arteries and is typically observed within 3 to 14 days following the hemorrhage.
Step 1: Mechanism of Vasospasm:
1. Subarachnoid Blood Irritation: Blood from the aneurysm irritates the smooth muscle cells of the cerebral arteries, causing inflammation and endothelial dysfunction.
2. Release of Vasoconstrictive Substances: The presence of blood products, particularly oxyhemoglobin, leads to the release of vasoconstrictive substances such as endothelin-1.
3. Decreased Nitric Oxide Availability: Blood products also reduce nitric oxide (NO) availability, which normally promotes vasodilation, further contributing to the vasospasm.
Step 2: Pathological Effects of Vasospasm:
1. Reduced Cerebral Blood Flow: Vasospasm causes narrowing of the arteries, reducing cerebral blood flow (CBF) and leading to ischemia.
2. Delayed Ischemic Deficits: The ischemia caused by vasospasm can result in delayed neurological deficits, including weakness, cognitive dysfunction, or even permanent brain injury.
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