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A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage
Published on: July 28, 2018
Cerebral Vasospasm After Traumatic Subarachnoid Hemorrhage: A Narrative Review
Urška Hržič1, Andreja Möller Petrun1,2
1Department of Anesthesiology, Intensive Care and Pain Management, University Medical Centre Maribor, 2000 Maribor, Slovenia.
Traumatic subarachnoid hemorrhage (tSAH) is a common complication of traumatic brain injury (TBI) and represents an important predictor of poor functional outcome. One of the most serious secondary complications is cerebral vasospasm. The pathophysiology of vasospasm is complex, involving the effects of blood breakdown products, inflammatory mediators, and direct mechanical injury to the cerebral vessels. Compared to aneurysmal subarachnoid hemorrhage (aSAH), vasospasm in tSAH typically occurs earlier, lasts for a shorter duration, and presents mostly with a milder clinical course. Due to its atypical clinical presentation and the presence of concurrent injuries, vasospasm is often not recognized in time and may manifest as neurological deterioration or new ischemic lesions on CT imaging. Timely recognition and appropriate management can significantly improve neurological outcomes. This paper presents key characteristics and differences between tSAH and aSAH, available diagnostic approaches, and treatment options, including nimodipine, milrinone, and stellate ganglion block. Owing to the lack of specific clinical guidelines for tSAH, current management strategies often rely on recommendations and experiences from aSAH. Further research is needed to better define risk factors for vasospasm following tSAH, optimize diagnostic pathways, and evaluate targeted treatment strategies.
Traumatic subarachnoid hemorrhage (tSAH) is a common complication of traumatic brain injury (TBI) and represents an important predictor of poor functional outcome. One of the most serious secondary complications is cerebral vasospasm. The pathophysiology of vasospasm is complex, involving the effects of blood breakdown products, inflammatory mediators, and direct mechanical injury to the cerebral vessels. Compared to aneurysmal subarachnoid hemorrhage (aSAH), vasospasm in tSAH typically occurs earlier, lasts for a shorter duration, and presents mostly with a milder clinical course. Due to its atypical clinical presentation and the presence of concurrent injuries, vasospasm is often not recognized in time and may manifest as neurological deterioration or new ischemic lesions on CT imaging. Timely recognition and appropriate management can significantly improve neurological outcomes. This paper presents key characteristics and differences between tSAH and aSAH, available diagnostic approaches, and treatment options, including nimodipine, milrinone, and stellate ganglion block. Owing to the lack of specific clinical guidelines for tSAH, current management strategies often rely on recommendations and experiences from aSAH. Further research is needed to better define risk factors for vasospasm following tSAH, optimize diagnostic pathways, and evaluate targeted treatment strategies.
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