Posttraumatic Cerebral Arterial Spasm

Abstract

Posttraumatic cerebral arterial spasm (vasospasm) has been demonstrated in the past by angiography, and recently by transcranial Doppler ultrasonography. Posttraumatic vasospasm is a delayed complication that involves the large basal intracranial arteries (e.g., internal carotid, middle cerebral, basilar) and occurs in 25-40% of head trauma patient. The time course of posttraumatic vasospasm resembles that of vasospasm associated with aneurysmal subarachnoid hemorrhage with onset occurring 2 or more days after injury. A study of the relationship of admission CT scan findings to the incidence of vasospasm suggests that intradural bleeding, which extends into the CSF (subarachnoid, intraventricular, and subdural hemorrhage), plays a role in the pathogenesis of posttraumatic arterial spasm. The preliminary results of a large prospective study of head trauma patients suggest that vasospasm may be an important determinant of outcome from severe head injury.

The evolution of the treatment of traumatic cerebrovascular injury during wartime

“…While previous studies characterized the formation of vasospasm following trauma, 19,20,22,23,29,31,32,36,37 few were able to correlate delayed ischemic deficits and outcomes with its presence, 15,31,32,37 and even fewer described the safety or efficacy of endovascular interventions in this setting. 12 In addition, while not specifically correlated with vasospasm occurrence, there was a considerable predominance of blast-induced head injury in our population.…”

Posttraumatic Vasospasm Detected by Continuous Brain Tissue Oxygen Monitoring: Treatment with Intraarterial Verapamil and Balloon Angioplasty

“…For example, Hadani et al [8] found the incidence of PTV in the anterior or posterior circulation increased from 43% to 58% if traumatic subarachnoid hemorrhage (tSAH) was present. Romner et al [15] found anterior circulation PTV incidence increased from 28% to 41% with tSAH, a correlation that has been further supported by other authors as well [12,24,31,32]. Some studies, however, have correlated PTV with subdural or epidural hematoma [12,13,24,42], and found no relationship with presence of tSAH [13,42].…”

“…PTV typically develops between 12 h and 5 days after injury and lasts anywhere between 12 h and 30 days [7, 10-13, 15, 16, 19-21]. Although PTV is an independent predictor of permanent neurological deficit and poor outcome in many studies [3,4,6,7,10,[22][23][24][25], it continues to be an under-recognized source of secondary injury following TBI and guidelines for screening and treatment of PTV do not currently exist [26].…”

“…Intermittent trans-cranial Doppler (TCD) ultrasonography, CT angiography, and digital subtraction angiograms can be effectively used to screen for PTV but are limited in their ability to provide continuous, real-time monitoring [10,11,14,19,21,24,25,[27][28][29][30][31][32][33]. Since early diagnosis and treatment of vasospasm is critical to prevent its ischemic consequences, a continuous monitor has the potential of improving neurological outcome.…”

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“…[24,33,50] This discrepancy may result, in part, from other factors not reflected in either ICP or CPP, such as disturbed autoregulation, [2,14,34] traumatic vasospasm, [29] or neurochemical changes such as elevated excitatory amino acids, [1] which may adversely influence cerebral blood flow (CBF) or tissue oxygenation and contribute to infarction.…”