Cerebral Vasospasm in Traumatic Brain Injury

Abstract

Vasospasm following traumatic brain injury (TBI) may dramatically affect the neurological and functional recovery of a vulnerable patient population. While the reported incidence of traumatic vasospasm ranges from 19%–68%, the true incidence remains unknown due to variability in protocols for its detection. Only 3.9%–16.6% of patients exhibit clinical deficits. Compared to vasospasm resulting from aneurysmal SAH (aSAH), the onset occurs earlier and the duration is shorter. Overall, the clinical course tends to be milder, although extreme cases may occur. Traumatic vasospasm can occur in the absence of subarachnoid hemorrhage. Surveillance transcranial Doppler ultrasonography (TCD) has been utilized to monitor for radiographic vasospasm following TBI. However, effective treatment modalities remain limited. Hypertension and hypervolemia, the mainstays of treatment of vasospasm associated with aSAH, must be used judiciously in TBI patients, and calcium-channel blockers have offered mixed clinical results. Currently, the paucity of large prospective cohort studies and level-one data limits the ability to form evidence-based recommendations regarding the diagnosis and management of vasospasm associated with TBI.

Traumatic brain injury and intracranial hemorrhage–induced cerebral vasospasm: a systematic review

“…37 However, clinical evidence shows that PTV can occur without the presence of blood in the subarachnoid space. 14,25 Mechanical factors have been implicated in the pathogenesis of PTV, with in vitro studies showing that vasospasm can occur from mechanical manipulation or irritation, although experimentally it is sustained for a shorter time than is seen clinically. 5,42 Stretching of cerebral vessels during blast injuries has also been proposed as a cause of PTV without cisternal or subarachnoid blood.…”

“…5,42 Stretching of cerebral vessels during blast injuries has also been proposed as a cause of PTV without cisternal or subarachnoid blood. 14 Although the pathophysiology of cerebral vasospasm continues to be a topic of debate, there is a general consensus that spasmogenic and neuroinflammatory substances generated from lysis of subarachnoid blood propagate the process. 27 Molecular models focus around endothelin-1 protein and its effect on endothelin receptor A. CSF and serum obtained in patients who have sustained a TBI show increased levels of endothelin-1, supporting its involvement in TBI and subsequent vasospasm in these patients.…”

“…Current literature shows that PTV typically occurs earlier [after TBI] than does aneurysmal vasospasm (2-3 days posttrauma vs 3-5 days post-aneurysmal vasospasm). 12,14 Rarely does PTV occur as late as 6 days posttrauma. The range of PTV onset times makes it difficult for clinicians to effectively assess a patient for PTV.…”

“…41 Triple-H therapy can cause or worsen cerebral edema, which may be more severe in trauma than in aneurysmal rupture and may worsen neurological function. 14 Currently, nimodipine is the most efficacious and widely used medication in the setting of PTV .…”

Prospective Evaluation of Post-Traumatic Vasospasm and Post-Injury Functional Outcome Assessment: Is Cerebral Ischemia Going Unrecognized in Patients with Traumatic Brain Injury?

“…Cerebral vasospasm can profoundly impact neurological recovery and functional outcome [6]. Vasospasm has been described as a sustained arterial narrowing and is classified as either angiographic or clinical [7].…”