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. 1. Introduction Traumatic brain injury (TBI) bears a heavy societal burden [1]. With an incidence rate of approximately 1.5 million new cases per year, TBI is the leading cause of death in the USA between the ages of one and forty-five [1]. Primary TBI management focuses on patient stabilization and treatment of elevated intracranial pressure (ICP). Surgical decompression and/or clot evacuation can decrease mass effect and cerebral edema, thus mitigating progressive neurological decline [2, 3]. The frequency of SAH following head trauma is estimated at 39%–65% [4–9], and its presence is an independent predictor of poor functional outcome [4, 7, 10, 11]. Severity of hemorrhage on CT scan has been shown to correlate with clinical status [12]. Although significant morbidity and mortality are attributable to the inciting trauma, deleterious sequelae of secondary injury are considerable and remain a critical focus of medical therapies. Vasospasm is a delayed, secondary consequence that can profoundly impact neurological recovery and functional outcome after TBI. Although vasospasm may result from traumatic subarachnoid hemorrhage (tSAH), other mechanisms such as blast-induced neurotrauma are increasingly recognized as causative factors [13–16]. This paper reviews the epidemiology, diagnosis, pathophysiology, prevention, and treatment of vasospasm
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