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Dr. Dan Miulli

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which demonstrated increased concentrations of endothelin I, endothelin III, and big endothelin I in cerebrospinal fluid of patients with aneurysmal subarachnoid hemorrhage vasospasms.  The volume of the hematoma in the basal cisterns was predictive of the concentrations of the endothelins in the CSF.
When angiography was the gold standard for studying mass lesions in head trauma patients, a number of groups observed narrowing of intracranial arteries.  The percentage was as high as 31% (Martin et. al., "Neurotrauma," 1995, 12:897-901).  More recently Dr. Weber (Weber, et. al., "Neurosurgery," 1990, 27: 106-112) and also Dr. Martin's group have demonstrated that post-traumatic vasospasms can be demonstrated by transcranial Doppler in as many as 30 to 40% of the patients.  It definitely occurs in head trauma.  For example in severe head trauma such as a motorcycle accident patient without using a helmet had a CT scan that demonstrated minor subarachnoid hemorrhage around the brain stem and in the suprasellar region, had transcranial Doppler results which showed vasospasm. 
Transcranial Doppler insinates intracranial blood vessels by using a very low frequency Doppler signal.  By the Bernouli effect when the artery becomes narrowed, flow velocity which one measures goes up in the vessel.  This is also seen when you put your finger over the end of a garden hose and it makes the water come out much quicker.  In the example of the patient in a motorcycle accident, the flow velocity in the two middle cerebral arteries demonstrated profound increases in velocity bilaterally.  The normal flow velocity in a young patient is about 80 and in this patient the flow velocities went up very high, above 200 bilaterally.  Levels above 200 have been associated with patients with ruptured aneurysm with post-hemorrhage delayed ischemic deficits.  In this example concomitant measure by the Xenon 133 technique demonstrated a significant decrease in cerebral blood flow, which was consistent with the increase in flow velocity by transcranial Doppler.  The angiogram in this patient demonstrates profound internal carotid artery spasm, as well as middle cerebral artery spasm.  If one measures the daily flow velocities in patients with middle cerebral artery vasospasms that have had closed head injury and compares it with the daily cerebral blood flows in those same patients, one sees changes in the first 72 hours, blood flow beginning low and then climbing at the same time that the transcranial Doppler velocities climb.  Flow velocity increases when volume increases; it is simply a flow volume effect.  At one point the graphs become dissociate at the higher levels when we are in the hyperemic phase, then have their blood flow drop to a lower level while their flow velocities increase for approximately two weeks before they start coming down again.  This can only be vasospasms.  It is not hyperemia because they have their blood flows measured and they are not hyperemic.  The vasospasm begin around day three or four, peak around day 10 or 11, just as it does in

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