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(Continued from page 94)
POST-TRAUMATIC VASOSPASMS
We have rediscovered with the use of transcranial Doppler that vasospasm occurs after a head injury. Vasospasms following subarachnoid hemorrhage most commonly affects the basilar cerebral artery and also affects the distal cerebral vasculature (Newell, et. al., "Neurosurgery," 1990, 27:574-577). This is something that was known when cerebral angiography was the standard diagnostic test used in head trauma. A number of groups demonstrated vasospasm in trauma patients years ago. With transcranial Doppler we have identified it even in a larger number of patients. Correlation between angiographic narrowing and transcranial Doppler velocity elevation has been demonstrated by Sloan, et. al., "Neurosurgery," 1989, 25:1514-1518; Lindegaard, et. al., "Stroke," 1987, 18:1025-1030; Aaslid, et. al., "Stroke," 1991, 22:1148-1154; Newell, "Cerebral Vasospasms," Tokyo, 1990, 3-8. Vasospasm after a head injury is very similar to vasospasm after subarachnoid hemorrhage. There is biphasic vasospastic response. The first and clinically unimportant phase occurs in the first hours and has no apparent significance. The time course of the second phase has been described. This phase is clinically significant. Onuma, et. al., "No Shinkei Geka," 1991, 19:435-442, demonstrated delayed traumatic vasospasm in individuals with an admission Glasgow coma scale of 9 to 15. Subarachnoid hemorrhage in the sylvian cistern was observed in all of the patients. There were brain contusions in the majority of the patients. The patients experienced ischemic changes between day 5 and 13. All ischemic changes were documented by cerebral angiographic vasospasms. Vasospasm appears to have an influence on the outcome of patients with traumatic brain injury. Traumatic subarachnoid hemorrhage is definitely a predictor of delayed ischemic symptoms. Taneda, et. al., "Journal of Neurosurgery," 1996, 84:762-8, prospectively studied 130 patients with closed head trauma who exhibited subarachnoid blood on admission. 10 patients developed delayed ischemic symptoms between days 4 and 16. In each of the 10 patients severe vasospasms were demonstrated by angiography performed after the development of symptoms. In 7 of the 10 patients follow up CT scans demonstrated focal ischemic areas in the cerebral territories corresponding to the vasospastic arteries. El Gindi, et. al., reported an incidence of angiographic vasospasms in 1.1% in their series of 2,000 patients, (El Gindi, et. al., "Acta Neurochirurgica," 1979, 48:237-244). Wilkens, et. al., "Journal of Neurosurgery," 1970, 32:626-633, estimated that 5 to 10% of his patients had clinical evidence of cerebral vasospasm after traumatic head injury. McPherson, "Journal of Neurology, Neurosurgery, and Psychiatry," 1973, 36:1069-1072, noted 57.5% incidence of cerebral vasospasms in patients suffering fatal head injury. This evidence is from the pre-CT era when angiography was used as the diagnostic modality of choice. The clinical deterioration leading to angiography occurred as early as a few hours after injury in a study (Continued on page 96)
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