Intracranial hemodynamics were studied in 36 patients with diffuse (n=16) and focal brain injuries (n=20) and also in experimental animals, with extradural balloon inflation, by use of TCD ultrasound. The mean flow velocities in the basal cerebral arteries commonly decreased on the side of hematoma depending on intracranial pressure (ICP) elevation and cerebral perfusion pressure (CPP) reduction in focal brain injury. The pulsatility amplitude between the systolic and diastolic flow velocities (S/D ratio) was then increased significantly. The decrease of the flow velocities and increase of S/D ratio returned to normal after treatment. The mean flow velocity of the middle cerebral artery and blood flow in the internal carotid artery exhibited the flow patterns which change correlatively depending on ICP and CPP in monkey models of acute intracranial hypertension. The flow velocities transiently increased bilaterally within several days after injury and there was no difference between the right and left side in diffuse brain injury. The velocities remained high even when the ICP increased and the CPP decreased. The result in focal brain injury therefore represents compression ischemia in the hemisphere due to increased cerebrovascular resistance. In patients with diffuse brain injury, however, hemodynamic events are more complex than those in focal brain injury. The flow velocities in diffuse brain injury may represent hyper or hypoperfusion states or arterial narrowing due to associated diffuse axonal injury, diffuse cerebral swelling or traumatic subarachnoid hemorrhage. Noninvasive study by use of TCD ultrasound can thus provide valuable informations on variant hemodynamic phenomena in patients with diffuse and focal brain injuries. But many complicated factors must be considered in the interpretation of TCD data in diffuse brain injury.
Hemodynamics of Intracranial vessels were evaluated by Transcranial Doppler Sonography (TCD) . In 30 healthy subjects and 12 patients (AVM 4, Moyamoya disease 3, cerebral tumor 3, giant aneurysm 2) . Blood flow velocity and S/D ratio were measured. CO2reactivity during hyperventilation was also studied. TCD obtained abnormal velocity waveform in 8 out of 12 cases with Intracranial abnormal vessels. As to screening test method of intracranial abnormal vessels, TCD has some problems such as angle between ultrasonic beam and vessel, narrow acuostic window and sampling volume. But TCD is feasible for evaluation of cerebrovascular reactivity.
To clarify diagnostic significance of intracranial circulatory arrest monitored by TCD, its temporal relationship with loss of cerebral and/or brainstem function was evaluated in 66 cases of impending brain death. We introduced a continuous, multimodal neuromonitoring system of somatosensory evoked potentials (SEP) and compressed spectral arrays (CSA) for assessing cerebral function, brainstem auditory evoked potentials (BAEP) and SEP for evaluating brainstem function, and TCD for measuring supratentorial circulation. Neurological brain function was preserved after supratentorial circulatory arrest in 44% of cases, and supratentorial circulation persisted in 21% after loss of all neurological brain functions. In relation to cerebral function: supratentorial circulation persisted after loss of SEP N20; loss of CSA activity significantly correlated with supratentorial circulatory arrest. In correlations with brainstem function: SEP P13/14 (58% cases) was more persistent than BAEP beyond wave II (42%) particularly regarding supratentorial lesions. Time interval to loss of cerebral function was shorter than to loss of brainstem function. These time intervals were shorter, mainly less than 24 hours, with complete signal loss than with persistent diastolic reverse or systolic flow. Loss of brain functions after supratentorial circulatory arrest progress rostro-caudally and are nearly complete within 24 hours.
Indication and limits of TCD for diagnosis and treatment were evaluated in 20 normal subjects and 15 patients with arteriovenous malformations 5 (AVM), Blood flow velocity of AVM supplying arteries (feeders), namely the middle cerebral artery and others were measured, and pulsatility index (PI) and resistance index (R) were calculated. To see pCO2 reactivity, hyperventilation was perfarmed (deep breath, twice/5s for 30s) . In patients, flow velocity increased remarkably and both of PI and R decreased significantly. Reactivity against hypocapnia also showed significant decrease. These changes varied according to the relationship between the artery and the nidus, and cases were divided into three groups, namely: main (Group A), partial (Group B) and poor (Group C) angioma supplying arteries. Significant changes were seen in Group A. Postoperatively, these changes recovered to the normal range. After removal of the AVM, flow velocity and vascular reactivity were closely related with the condition of the brain tissue which surrounded the nidus before the removal. NPPB tends to occur in such areas especially in Group A. As a conclusion, characteristic changes were recognized in hemodynamics and pCO2 reactivity of feeders, especially on mainly angioma supplying arteries. In such cases, care should be taken to guard against the normal perfusion pressure breakthrough phenomenon during and after surgery.
To investigate the effect of cigarette smoking on human circulatory systems, five healthy male smokers were assigned to smoke a high nicotine cigarette for 5 minutes. Before, during and after smoking we recorded blood pressure, heart rate, respiratory rate and expiratory Pco2, and also measured the blood flow velocity of cerebral and peripheral arteries continuously using the Multi-Doppler-System. Change of blood flow velocity was checked statistically in each artery for 1 minute before and 1 minute after the beginning of smoking. Significant increases of blood flow velocities were observed in all 5 cerebral arteries (5 subjects) for 1 minute after the beginning of smoking. Of 5 peripheral arteries (5 subjects), 3 showed significant decrease and the other 2 showed no significant change. No remarkable change of blood pressure or heart rate was observed in all 5 subjects. The level of Pco2 decreased during smoking in all 4 subjects measured. We concluded that the smoking of a high nicotine cigarette resulted in an increase of cerebral blood flow even with the decrease of Pco2. The effect of smoking seems unclear for the flow of the peripheral artery.