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An ultrasonic Doppler method was used to monitor flow velocities in basal cerebral arteries in 21 patients with spontaneous subarachnoid hemorrhage (SAH). The time course of vasospasm as evaluated by this technique was similar to that reported in angiographic studies. In 82% of the patients an increase in intracranial velocities to 120 cm/s or more was found during the second or third week after hemorrhage. (Normal value 62 cm/s). Arterial narrowing giving rise to velocities above 200 cm/s was classified as severe spasm. This occurred in 42% of the cases, and a significant decrease in flow velocity in the extracranial carotid artery was found in this group.

Pulsed wave 2 MHz Doppler with acoustical focusing was used to obtain blood flow velocity recordings through the intact cranium in 11 patients with occlusive disease of major intracranial arteries. Increased blood flow velocities were recorded from stenoses of the carotid siphon and of the middle cerebral, anterior cerebral and basilar arteries. A clear, inverse relationship existed between angiographical residual lumen diameter and flow velocity. The Kendall rank correlation coefficient (Tau) was -0.89 (p = 0.0001). Transcranial Doppler is a useful means for evaluating patients with this disorder.

The dynamics of the metabolic mechanism that regulates cerebral blood flow was studied in 10 normal human subjects using a noninvasive transcranial ultrasonic Doppler method. Flow volume in the posterior cerebral artery, supplying the visual cortex, increased 20.2% in response to light stimulation of the retina, while flow velocity in the same artery increased 16.4%. The regulation of blood flow was very rapid; only 2.3 seconds elapsed from application of the light stimulus to 50% of full response. Full regulation (90% of full response) took 4.6 seconds. The blood flow response adapted slightly after about 10 seconds. Flow velocity in the middle cerebral artery increased significantly, by 3.3%, while flow in the superior cerebellar artery showed no significant change in response to this stimulus. These findings suggest the mechanism of very fast metabolic regulation of cerebral blood flow in humans.

The pulsative inflow of blood to the brain causes fluctuations in the cerebral blood volume, and this is considered to be the main cause of the pulsations of the intracranial pressure (ICP). This statement allows discrimination between two different factors that influence the pulse amplitude of the ICP: 1. The pulsatile pattern of the cerebral arterial blood flow. 2. The slope of the intracranial pressure-volume curve. In order to clarify the relative contributions of the two factors we have developed a simulation model of the intracranial pressure-volume curve and the cerebral blood flow. Measurements from clinical practice and data from other authors can be interpreted with reference to this model. The increase in the pulse amplitude due to a moderate increase in the ICP is mainly explained by the decrease of the intracranial compliance. However, it is recognized that, when the ICP approaches the arterial blood pressure, the ICP amplitude increases disproportionally with increasing ICP. In this situation the transmural pressure of the cerebral arteries approaches zero, and the compliance relevant to the arterial flow system is no longer that of the vessel wall but the compliance of the craniospinal compartment.

Five patients undergoing cardiopulmonary bypass (CPB) procedures were extensively monitored because of anticipated high risk for neurological complications. Arterial blood pressure (BP), central venous pressure, and epidural intracranial pressure (EDP) were continuously recorded throughout CPB; thus, information on the cerebral perfusion pressure (CPP) was also continuously available (CPP = BP – EDP). Cerebral electrical activity was recorded by a cerebral function monitor. The flow velocity in the middle cerebral artery (MCA) was recorded using a transcranial Doppler technique. During steady-state CPB (constant hematocrit, constant temperature, and constant flow from the heart-lung machine) partial pressure of arterial carbon dioxide (PaCO 2 ) was repeatedly changed to study the effect of changes in this variable on MCA flow velocity during nonpulsatile bypass. During CPB with constant temperature, hematocrit, and PaCO 2 , the effect of changes in CPP on MCA flow velocity was recorded and analyzed. During nonpulsatile, moderately hypothermic (28° to 32°C), low-flow (1.5 L/min/m 2 ) CPB, there was no evidence of cerebral autoregulation, with CPP levels ranging from 20 to 60 mm Hg. The CO 2 reactivity, however, was clearly present and in the range of 1.9 to 4.1%/mm Hg, indicating that there was a dissociation between cerebral autoregulation and CO 2 reactivity under these circumstances.

The clinical significance of spontaneous intracranial pressure plateau waves (PW) has been shown by LUNDBERG (1), who has also discussed the mechanism causing this pressure pattern.

The end-tidal carbon dioxide partial pressure (PCO2) response curves for the flow velocity in the middle cerebral artery were studied in 31 normal subjects with transcranial Doppler techniques. An exponential curve with an exponent of 0.034 mm Hg−1 was found to be a good fit to the recorded data. By means of this relationship, recordings of flow velocity in cerebral arteries can be normalized to a standard value of PCO2. Physiological aspects of cerebrovascular reactivity to PCO2 and the clinical implications of the PCO2 response curve are discussed. The normal material provides a reference for assessing pathological responses.

✓ 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.

An arteriovenous malformation (AVM) is a development anomaly that results when the embryonic vascular network fails to evolve normally. Primarily normal arteries and veins are involved in conveying flow to and from the AVM [8]. Arteries leading to an AVM convey blood through the shunt and into the venous side. The size and flow rates of these arteries is far out of proportion to the low metabolism within an AVM. We therefore use the term “feeders” to distinguish these vessels from normal arteries purely conveying nutrient flow to neural tissues.

Tissue strength and stiffness of cerebral aneurysm walls obtained intraoperatively or at autopsy were evaluated by uniaxial strain/stress measurements. For comparison, corresponding measurements were also made on autopsy specimens of intracranial arteries. The maximum stress that the aneurysm tissue could tolerate, the yield stress, was found to be slightly lower than in arteries, which is likely due to the content of immature forms of collagen. The material stiffness, as determined by division of the yield stress by the corresponding strain, was also smaller in aneurysms than in arteries. The stress resistance of aneurysms and arterial tissue decreased over a period of several hours. The relaxation curves were found to be identical in aneurysms and arteries. The stress tolerated by aneurysm walls was found to be in the range of the stress that is imposed in vivo by the blood pressure. Arteries resisted stresses corresponding to pressures 5–10 times higher than physiological values. It is suggested that the balance of tissue strength and the stress imposed by the blood pressure is causally related to aneurysm growth.

✓ 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.

Greenfield and Tindall noted in 1965 that the diastolic component of the flow waveform in the internal carotid artery decreased and could even go to zero when the intracranial pressure (ICP) was increased to levels 25 to 35 mmHg below the arterial blood pressure (ABP). In patients with brain tamponade, Lindegaard et al. (1980) found reverberating flow velocity waveforms. These changes are gross and reflect extreme conditions for the brain circulation, nevertheless, they suggest that perhaps less obvious changes in the flow pattern may be detected by refined methods of waveform analyses and be used to obtain an estimate of ICP.

✓ 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.

A 2 MHz continuous waveform non-invasive ultrasound doppler system has been used in the present investigation. With the aid of the audio signals of the frequency shifts, the ultrasound probe was positioned on the external chest so that the axis of the incident ultrasonic beam coincided with the direction of the maximum velocity vectors of the mitral jet. The frequency shifts due to the mitral jet were frequency analyzed and the time course of the maximum frequency shift was determined. The time course of the maximum mitral jet velocity was then determined from the doppler equation and the time course of the mitral pressure gradient from an orifice equation. The usefulness of the technique was evaluated by studying 25 patients with mitral stenosis and 10 without heart disease. The patients with mitral stenosis were studied during cardiac catheterization and the ultrasound data, the pulmonary artery wedge pressure, and the left ventricular pressure were recorded simultaneously. A table is presented where the gradient determined with the ultrasound technique, deltaPU, is compared with the gradient determined from the pressure tracing, deltaPM. Averaged over the 25 patients studied, deltaPU was 1.7 mmHg smaller than deltaPM at 0.08 sec diastolic time and 1.8 mmHg smaller at 0.25 sec diastolic time. The findings in the patients without heart disease differed distinctly from those in the patients with mitral stenosis. The investigation demonstrated that the non-invasive ultrasound technique can be used with confidence to gain an impression of the magnitude of the mitral pressure gradient. The findings also suggest that deltaPU represents the actual pressure gradient more accurately than deltaPM. Another investigation is proposed to assess the accuracy of the technique more completely.