Search

Object The aim of the present study was to evaluate the time course for cerebral autoregulation (AR) recovery following severe traumatic brain injury (TBI) Methods Thirty-six patients (27 males and 9 females, mean ± SEM age 33 ± 15.1 years) with severe TBI underwent serial dynamic AR studies with leg cuff deflation as a stimulus, until recovery of the AR responses was measured. Results The AR was impaired (AR index < 2.8) in 30 (83%) of 36 patients on Days 3–5 after injury, and in 19 individuals (53%) impairments were found on Days 9–11 after the injury. Nine (25%) of 36 patients exhibited a poor AR response (AR index < 1) on postinjury Days 12–14, which eventually recovered on Days 15–23. Fifty-eight percent of the patients with a Glasgow Coma Scale score of 3–5, 50% of those with diffuse brain injury, 54% of those with elevated intracranial pressure, and 40% of those with poor outcome had no AR recovery in the first 11 days after injury. Conclusions Autoregulation recovery after severe TBI can be delayed, and failure to recover during the 2nd week after injury occurs mainly in patients with a lower Glasgow Coma Scale score, diffuse brain injury, elevated ICP, or unfavorable outcome. The finding suggests that perfusion pressure management should be considered in some of the patients for a period of at least 2 weeks.

✓ Intracranial pressure (ICP) and continuous transcranial Doppler ultrasound signals were monitored in 20 head-injured patients and simultaneous synchronous fluctuations of middle cerebral artery (MCA) velocity and B waves of the ICP were observed. Continuous simultaneous monitoring of MCA velocity, ICP, arterial blood pressure, and expired CO2 revealed that both velocity waves and B waves occurred despite a constant CO2 concentration in ventilated patients and were usually not accompanied by fluctuations in the arterial blood pressure. Additional recordings from the extracranial carotid artery during the ICP B waves revealed similar synchronous fluctuations in the velocity of this artery, strongly supporting the hypothesis that blood flow fluctuations produce the velocity waves. The ratio between ICP wave amplitude and velocity wave amplitude was highly correlated to the ICP (r = 0.81, p < 0.001). Velocity waves of similar characteristics and frequency, but usually of shorter duration, were observed in seven of 10 normal subjects in whom MCA velocity was recorded for 1 hour. The findings in this report strongly suggest that B waves in the ICP are a secondary effect of vasomotor waves, producing cerebral blood flow fluctuations that become amplified in the ICP tracing, in states of reduced intracranial compliance.

The aim of the present study was to evaluate the time course for cerebral autoregulation (AR) recovery following severe traumatic brain injury (TBI).Thirty-six patients (27 males and 9 females, mean +/- SEM age 33 +/- 15.1 years) with severe TBI underwent serial dynamic AR studies with leg cuff deflation as a stimulus, until recovery of the AR responses was measured.The AR was impaired (AR index2.8) in 30 (83%) of 36 patients on Days 3-5 after injury, and in 19 individuals (53%) impairments were found on Days 9-11 after the injury. Nine (25%) of 36 patients exhibited a poor AR response (AR index1) on postinjury Days 12-14, which eventually recovered on Days 15-23. Fifty-eight percent of the patients with a Glasgow Coma Scale score of 3-5, 50% of those with diffuse brain injury, 54% of those with elevated intracranial pressure, and 40% of those with poor outcome had no AR recovery in the first 11 days after injury.Autoregulation recovery after severe TBI can be delayed, and failure to recover during the 2nd week after injury occurs mainly in patients with a lower Glasgow Coma Scale score, diffuse brain injury, elevated ICP, or unfavorable outcome. The finding suggests that perfusion pressure management should be considered in some of the patients for a period of at least 2 weeks.

✓ A transcranial ultrasonic method for the recording of murmurs from cerebral vessels is described. Using the new approach the authors have observed musical murmurs of pure tone quality in 15 patients with increased flow velocities in the cerebral arteries after spontaneous subarachnoid hemorrhage (SAH). The frequency range of the pure tones was from 140 to 820 Hz, corresponding to flow velocities between 73 and 215 cm/sec. The musical murmurs occurred as a transitional state between silent flow and the well known phenomenon of bruit. They were observed between the 4th and the 20th day after SAH. The most likely cause of the musical murmur is a periodic shedding of vortices in the cerebral arteries, commonly referred to as “a von Kármán vortex street.” Clinically the presence of musical murmurs indicated that pathologically increased blood velocities were present in the artery under investigation. This probably reflected the degree of spasm.

✓ The use of an ultrasonic transcranial Doppler technique for noninvasive evalution of cerebral vasospasm is described. Middle cerebral arteries (MCA's), classified as spastic on angiography, demonstrated blood-flow velocity between 120 and 230 cm/sec. The flow velocities in these arteries had a clear inverse relationship to the diameter as measured from angiograms in 38 patients with recent subarachnoid hemorrhage. This relationship in the proximal anterior cerebral artery (ACA) was found to be more complicated to assess, due to the collateral channels in the anterior part of the circle of Willis. The authors conclude, however, that the new method of measuring vasospasm will also detect spasm in the ACA if it has a hemodynamically significant effect upon flow resistance.

✓Blood flow velocities in basal cerebral arteries were recorded noninvasively in 28 patients with cerebral arteriovenous malformations (AVM's) and were correlated with the angiographic findings. In normal arteries remote from the AVM, flow velocities ranged from 44 to 94 cm/sec (median 65 cm/sec) with pulsatility indexes from 0.65 to 1.10 (median 0.87). This is consistent with findings in normal individuals. Arteries feeding the AVM's were identified by the high flow velocities (ranging from 75 to 237 cm/sec, median 124 cm/sec). The pulsatility index ranged from 0.22 to 0.74 (median 0.48). The difference of these results from findings in normal remote arteries was highly significant (p < 0.001). Hyperventilation tests illustrated the hemodynamic difference between an AVM and normal cerebrovascular beds. Flow velocity measurements permitted noninvasive diagnosis of AVM's in 26 of the 28 patients. Furthermore, the identification of individual feeding arteries permitted good definition of the anatomical localization of individual AVM's. Flow velocity measurements combined with computerized tomography scans are useful in the diagnosis of AVM's. With the feeding artery's configuration identified on angiography, flow velocity measurements permit a new insight into the “hemodynamic dimension” of an AVM and its possible effects on adjacent normal brain-tissue perfusion in the individual patient.

✓ Noninvasive transcranial Doppler recordings were correlated to the angiographic findings in 77 patients with carotid artery disease. Stenoses reducing the luminal area of the internal carotid artery by 75% or more also reduced the pulsatility transmission index (PTI) of the ipsilateral middle cerebral artery (MCA). The PTI is the pulsatility index of the artery under study expressed as a percent of the pulsatility index of another intracranial artery with presumed unimpeded inflow in the same individual. For stenoses in the 75% to 89% category, PTI reduction was significantly greater in patients with bilateral carotid stenosis, indicating an impaired potential for collateral flow in these patients. The PTI reduction probably reflects both the pressure drop across the stenosis and the cerebral autoregulatory response. Two criteria proved useful in demonstrating collateral MCA supply through the circle of Willis. On the recipient side, retrograde flow in the proximal anterior cerebral artery was demonstrated in 29 of the 31 patients when this flow pattern was disclosed angiographically. In 26 of these patients, the anterior cerebral artery on the supplying side also had clearly increased flow velocity. Increased flow velocities in the proximal posterior cerebral artery were present in 26 of the 30 vessels that were acting as a collateral channel to the ipsilateral MCA.

✓ In 39 patients with a proven subarachnoid hemorrhage (SAH), the clinical status, the amount of subarachnoid blood on a computerized tomography scan obtained within 5 days after SAH, and the flow velocities (FV's) in both middle cerebral arteries (MCA's) measured by transcranial Doppler sonography were recorded daily and correlated. All patients had pathological FV's over 80 cm/sec between Day 4 and Day 10 after SAH. The side of the ruptured aneurysm showed higher FV's than did the unaffected side in cases of laterally localized aneurysms. Increase in FV preceded clinical manifestation of ischemia. A steep early increase of FV's portended severe ischemia and impending infarction. Maximum FV's in the range of 120 to 140 cm/sec were not critical and in no case led to brain infarction. Maximum FV's over 200 cm/sec were associated with a tendency for ischemia, but the patients may remain clinically asymptomatic. In cases of no or only a little blood in the basal cisterns, mean FV's in both MCA's increased only moderately whereas, with thick clots of subarachnoid blood, there was a steeper and higher increase of mean FV's.

✓ In this report the authors describe a noninvasive transcranial method of determining the flow velocities in the basal cerebral arteries. Placement of the probe of a range-gated ultrasound Doppler instrument in the temporal area just above the zygomatic arch allowed the velocities in the middle cerebral artery (MCA) to be determined from the Doppler signals. The flow velocities in the proximal anterior (ACA) and posterior (PCA) cerebral arteries were also recorded at steady state and during test compression of the common carotid arteries. An investigation of 50 healthy subjects by this transcranial Doppler method revealed that the velocity in the MCA, ACA, and PCA was 62 ± 12, 51 ± 12, and 44 ± 11 cm/sec, respectively. This method is of particular value for the detection of vasospasm following subarachnoid hemorrhage and for evaluating the cerebral circulation in occlusive disease of the carotid and vertebral arteries.