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Cerebral vasospasm is a well-recognized complication following subarachnoid hemorrhage (SAH) and is primarily responsible for the delayed onset of ischemic neurological deficits. After SAH, blood is present in the subarachnoid space, which leads to local irritation of the cerebral vessels. This irritation can cause the smooth muscle in these vessels to contract, leading to vasospasm.

The clinical manifestations of vasospasm typically present 5 to 14 days after the initial hemorrhage and include confusion, focal neurological deficits, and changes in consciousness, all of which indicate impaired cerebral blood flow and ischemia. The process disrupts normal brain autoregulation, meaning that the brain's ability to maintain stable blood flow despite changes in systemic blood pressure is compromised.

The other complications associated with SAH, such as hypertension, hyponatremia, and hydrocephalus, can indeed occur, but they do not specifically match the scenarios of confusion and focal neurological deficits linked directly to cerebral ischemia as vasospasm does. While hypertension may exacerbate the risk of further bleeding or complications, it does not directly cause ischemic damage like vasospasm does. Hyponatremia can lead to neurological symptoms