Cerebral Vasospasm after Head Injury

Abstract

Cerebral vasospasm occurs frequently after head injury. Correlation between neurological deterioration and vasospasm has been reported previously, but delayed neurological deterioration secondary to vasospasm in head injury is a rare occurrence. We report the case of a 57-year-old man who, after a motorcycle accident, developed an acute subdural hematoma and a thick subarachnoid deposition of blood in the left sylvian-insular cistern. After surgical evacuation of the hematoma, the patient improved until the 10th postoperative day, when he developed aphasia and a right hemiparesis. Angiography demonstrated multitapering spasm, and a computed tomographic (CT) scan showed persistence of the cisternal deposition of blood. Despite therapy with hypervolemia, the patient improved only slightly. The association of head injury with substantial subarachnoid hemorrhage producing vasospasm has been considered rarely. Delayed posttraumatic vasospasm secondary to blood degradation products seems to play some role in the vasospasm after head injury. CT scanning may be useful in predicting vasospasm in such patients, and digital subtraction angiography might be useful in demonstrating it.

Cerebral Vasospasm in Traumatic Brain Injury

“…Still, the anatomic region of greatest hemorrhage density often correlates with the location of vasospasm following tSAH [11, 31, 56, 60], thus suggesting that blood breakdown products may be responsible for the vessel narrowing. The same mechanisms proposed in aSAH, with blood breakdown products and irritation, would exist in both instances.…”

“…The same mechanisms proposed in aSAH, with blood breakdown products and irritation, would exist in both instances. However, this could represent an epiphenomenon, as the traumatic focus and resultant maximal vessel manipulation would also likely coincide with the region of greatest hemorrhage [11, 31, 56, 60]. …”

Traumatic subarachnoid hemorrhage: our current understanding and its evolution over the past half century

“…Early investigators intuitively hypothesized and showed that similar phenomena may take place following traumatic SAH 36,50 . In fact, post-mortem 40 , angiographies 36,40,41,50,51 and more recently transcranial Doppler (TCD) study 37,41,42,44,47,[52][53][54][55][56][57] have demonstrated evidence of anatomic or radiologic vasospasm following head injury and based on association it can be concluded that neurological deficits following TBI may in part be related to this ischemic phenomenon 40,51,58,59 . Vasospasm in TBI is reported to occur in 2-41% of patients with head injury by angiography 40,47 and as high as 60% by TCD.…”

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

“…Although there is significant data suggesting that PTV is significantly correlated with ischemia, neurological deficits [3,4,6,7,10,[22][23][24][25] and/or death [8,[69][70][71], there are no published guidelines for its detection and treatment. Both 133 Xe CBF [11] and SPECT [15] studies have shown that middle cerebral artery spasm is strongly associated with cerebral ischemia and PTV of the basilar artery is strongly associated with worse outcome [3,18,20].…”

“…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].…”