Description Module
The Description Module contains narrative descriptions of the clinical trial, including a brief summary and detailed description. These descriptions provide important information about the study's purpose, methodology, and key details in language accessible to both researchers and the general public.
Description Module path is as follows:
Study -> Protocol Section -> Description Module
Description Module
Ignite Creation Date:
2025-12-25 @ 3:16 AM
Ignite Modification Date:
2025-12-25 @ 3:16 AM
NCT ID:
NCT07252505
Brief Summary:
Subarachnoid hemorrhage (SAH) is a clinical phenomenon caused by the abrupt rupture and bleeding of blood vessels at the surface or base of the brain, which can occur for a number of reasons. As a result, the subarachnoid membrane receives direct blood flow. SAH is a debilitating neurological disorder with high morbidity and mortality. Despite advancements in medicine and surgical care, patients who survive their first bleeding event are at high risk for secondary sequelae, including delayed cerebral ischemia (DCI) and cerebral vasospasm (CV)
CV denotes a temporary, self-resolving constriction of the intracranial arteries that occurs several days after an SAH. This phenomenon is closely linked to clinical deterioration resulting from DCI, affecting up to 30% to 40% of patients. DCI is a significant clinical event that typically manifests 3 to 14 days after the initial bleeding and is characterized by subsequent neurological deterioration. These complications can lead to poor functional outcomes and long-term disability
Subarachnoid hemorrhage is classified into aneurysmal subarachnoid hemorrhage (aSAH) and Traumatic SAH (tSAH). TSAH has been described as an adverse prognostic factor leading to progressive neurological deterioration and increased morbidity and mortality. Traumatic subarachnoid hemorrhage is caused by head injuries from events like falls, motor vehicle crashes, and blows to the head, which damage blood vessels within the skull. The injury itself is the primary cause, leading to the brain being hit against the skull and tearing these blood vessels
Detailed Description:
Magnesium is a noncompetitive calcium antagonist with several important vascular and potentially neuro-protective effects. For instance, magnesium can lead to vasodilatation by blocking the voltage-dependent calcium channel and decreasing glutamate release and block the influx of calcium ions, inhibiting blood vessel contraction and preventing CV.In addition, magnesium also attenuates the effect of various potent vasoconstrictors, such as endothelin 1, and blocks the formation of reactive oxygen species These potentially helpful effects of magnesium on vasodilation and consequent neuro-protection has led some investigators to study the ability of magnesium to prevent of cerebral vasospasm and delayed cerebral ischemia after subarachnoid hemorrhage (SAH). Limited data exist for tSAH. Early intravenous Magnesium Sulfate (MgSO₄)application within 24 hours after diagnosis may prevent or attenuate vasospasm and improve neurological recovery and outcome
Study:
NCT07252505
Study Brief:
Protocol Section:
NCT07252505