CPP (cerebral perfusion pressure) is the major factor determining the pressure flow characteristics in the cerebral vascular bed. Aaslid proposed that the CPP index could be estimated by combining information about arterial blood pressure and the Doppler flow velocity waveform of the intracranial arteries. The characteristics of pressure wave transmission in the intracranial cavity were determined by coherency. Sixteen cats were used to measure the ICP increase induced by hydrostatic pressure loading. BP and ICP were monitored using a Camino Digital Pressure Monitor 420 by catheterization into the abdominal aorta through the femoral artery and by Rt-fronter subarachnoid space catheterization, respectively. The intracranial blood flow Doppler signals were measured transorbitally using MF-20. The CPP index decreased as the ICP increased, indicating a correlation between CPP (BP-ICP) and CPP index. The slope of the straight line determined by coherency was greater between 45 and 70 mmHg than between 10 and 45 mmHg. This suggests that there is a point, located between 45 and 70 mmHg, where the increase in coherency values is accelerated. This is caused by the increase in intracranial elastance, as well as the increase in cerebrovascular compliance due to the reduced vascular transmural pressure.

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Transcranial Doppler ultrasonography (TCD) provides useful information on cerebral ischemia associated with increased intracranial pressure (ICP) . This paper summarizes our previous paper, which described an in vivo model that approximates cerebral pulsatile flow and illustrates the application of this model to the study of changes that occur in Doppler spectral waveforms in intracranial hypertension.

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Neurosonological evaluations of both adult and child cases of brain death were reviewed. Also, the current status of Doppler examinations in confirmatory tests of brain death was compared among the European, North American, and Japanese criteria.
There are three unsolved problems related to cerebral circulation and metabolism in the pathophysiology of brain death. First, does persisting intracranial circulation demonstrated by neuroradiological (angiography, contrast CT, MRI, etc.) and color duplex examination indicate complete cerebral circulatory arrest? Second, does intracranial circulatory arrest continue after confirmation of brain death? (Does intracranial reperfusion occur after cessation of intracranial circulation?) Third, there are discrepancies between neuronal function data and cerebral circulation and metabolism (e.g., persisting cerebral circulation and glucose metabolism were identified in an infant case of clinical brain death and electrocerebral silence) .
Also, equivocal Doppler findings of cerebral circulatory arrest have been reported by Hassler et al. (1989) . Intracranial arteries are visualized clearly by color flow imaging despite evidence of cerebral circulatory arrest, such as oscillating flow or systolic spikes, by Doppler sonography. Continuous Doppler sonograms, with or without early systolic reverse flow, can be obtained for the cervical common carotid and internal carotid arteries, even if there is Doppler cerebral circulatory arrest in the intracranial arteries. Doppler findings in infants with open fontanelle probably differ from those of adults in the extra- and intracranial arteries, with regard to features such as diastolic tailing and late diastolic reversal.
Doppler examination as a confirmatory test of brain death is accepted in only two European countries and Canada. This is probably because of the above-mentioned reliability problems of Doppler tests, difficulty of insonation via temporal windows, the technical skill required by attending physicians or technologists, and the availability of neurosonological equipment in intensive care units.
Neurophysiological tests demonstrating cessation of cerebral circulation and metabolism, including Doppler examination, basically are subsided by clinical determination of brain death. Pathophysiological evaluations in cases of impending brain death are, however, extremely important and a promising research field in neurosonology.

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This study was conducted to evaluate the effects of probucol and pravastatin on intima-media thickness (IMT) in patients with hypercholesterolemia. Alterations of IMT (ΔIMT) at carotid bif urcations were measured after treatment with probucol or pravastatin during a mean follow-up period of 23 months in 20 patients. ΔIMT was significantly lower in the 10 patients treated with probucol (-0.128±0.121mm/y) than in the 10 patients treated with pravastatin (0.091±0.043mm/y) (p<0.0001) . There was a significant correlation between serum levels of HDL cholesterol and ΔIMTs after treatment with probucol (r=0.720, p=0.0190) . These results suggest the inhibitory as well as regressive effects of probucol on carotid atherosclerosis in comparison with pravastatin.

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Transcranial Doppler ultrasound (TCD) can detect circulating cerebral emboli, which may be a risk factor for embolic stroke. We examined the relationship between the results of a TCD study and some of the hematological markers of coagulation. 15 patients with cerebral embolism receiving anticoagulation therapy were evaluated by continuous monitoring over the middle cerebral artery for 30 min, and the number of high-intensity transient signals (HITS) were recorded.
We were able to demonstrate HITS in two of the patients by TCD. Thrombin-antithrombin III complex (TAT) and D-dimer had no influence on the number of HITS. International normalized ratio (INR) intensity was not correlated with the number of HITS, but high-intensity anticoagulation of INR was shown to reduce the frequency of HITS. HITS are not a common phenomenon in patients with cerebral embolism.

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An attempt was made to evaluate the findings of color Doppler flow imaging (CDFI) of the superior ophthalmic vein (SOV) in relation to clinical features and angiographic findings in 20 patients with intracranial dural arteriovenous fistula (DAVF) .
CDFI studies provided information about the size, flow direction and pulsed Doppler wave curve (waveform) of the SOV in each case. The mean diameter of the SOV was 3.13 mm which was significantly (p<0.05) wider than in normal controls. The flow direction was reversed in one patient, and was normal in the other 19 patients. A reversed pulsatile waveform was observed in one patient, a normograde inverse pulsatile waveform in four and a normal waveform in 15. The patients with clinical symptoms or angiographically retrograde cortical venous filling showed dilatation of the SOV. There was no significant difference in SOV CDFI findings according to the location of the lesion. Surgical removal was performed in 14 patients. Postoperatively, the abnormal SOV CDFI findings improved significantly.
The SOV CDFI findings in the DAVFs correlated well with the clinical symptoms, angiographic findings and surgical results, and these data were useful for evaluation of intracranial venous hemodynamics and also follow-up studies. DAVFs indicating a dilated SOV with an abnormal flow direction and abnormal waveform in SOV CDFI studies were seen in patients with clinical symptoms or retrograde cortical venous filling on angiography.

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Recently the lateral-frontal bone window has been used to determine MCA insonation rates. In this study we analyzed the insonation rates of 48 healthy Japanese subjects (male 28, female 20) using TC-CFI through this window.
Using a HP SONOS 5500 with a cardiac probe (1.8 MHz) . We examined the MCA bilaterally with TC-CFI through a temporal window and a lateral-frontal bone window. The MCA insonation rate through the temporal bone window was 83% for all subjects, 84% for males, and 77% for females. The MCA insonation rate through the lateral-frontal bone window was 34% for all subjects, 27% for males, and 45% for females. The MCA insonation rates through the lateral-frontal bone window were lower than those through the temporal bone window. We conclude that TC-CFI performed through a lateral-frontal bone window is not as effective for MCA scanning as that performed through a temporal bone window.

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