The authors present the results of an investigation of the vasogenic type of brain edema using cold injury in cats as a model. Their findings indicate that bulk flow and not diffusion should be considered the main mechanism for the spread of edema through the white matter. This conclusion is based on: 1) comparison of the distances actually traveled by various substances during edema spread with those calculated theoretically for migration of the substances by diffusion; 2) coincidence in the speed of movement by two substances (sucrose and albumin) with widely different diffusion coefficients; 3) measurement of interstitial fluid pressure (IFP) at various distances from the lesion showing the presence of increased IFP in the lesion area and decreasing pressures along the edema pathway toward the normal tissue; and 4) the fact that spreading of edema can be significantly impeded by inducing before the cold lesion an intracellular type of brain edema that reduces the size of the extracellular space (ECS) and increases the resistance to flow of edema fluid. The pressure-volume curve of the brain ECS, as derived from determinations of IFP and tissue water content, indicates that initial steep slope in IFP probably represents the high resistance to fluid mobility through the small diameter extracellular channels and the counteracting resistance of the intermingled structures of brain parenchyma to be separated. Once the IFP exceeds these opposing forces, the ECS dilates, fluid mobility increases, and the edema front advances.
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 less than 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.
A total of 153 consecutive patients with proven aneurysmal subarachnoid hemorrhages (SAHs) admitted immediately after diagnosis regardless of clinical condition were managed according to the same protocol. The initial evaluation included computed tomography (CT), transcranial Doppler ultrasound (TCD), angiography-CT, and/or angiography. Intravenous nimodipine (2 mg/hour) was started after confirmation of the diagnosis. The timing of operation was determined individually according to age, clinical course, and CT and TCD findings. Twenty-one Grade V patients treated with intensive care and ventriculostomy died or did not improve within 24 hours after SAH. Three patients with life-threatening intracerebral hematomas underwent emergency operation. Operation was early in 55 good risk patients and late in 57 patients because of poor initial grade, late admission, or logistic reasons. Seventeen patients had no operation because of old age, persistent poor clinical condition, medical complication, or lethal rebleeding before operation. In the total series, 90 patients (59%) made a full recovery, the overall morbidity rate was 14% (21 of 153 cases), and the mortality rate was 27% (42 of 153). Postoperative mortality including emergency evacuation of hematomas was 7.8% and mortality after elective operation was 6.2%. The causes of disability and death were the initial effect of the hemorrhage in 25 patients (16.3%), rebleeding in 15 (9.8%), delayed cerebral infarction in 8 (5.2%), surgical complications in 7 (4.5%), hydrocephalus in 4 (2.6%), and medical complications in 4 (2.6%).
The flow conditions and the related stresses in glass and silastic model aneurysms located at bifurcations were quantitatively determined by means of laser-Doppler-anemometry. The flow velocities in straight terminal models with the aneurysm forming an extension of the afferent vessel were unstable if the outflow through the branches of the bifurcation was balanced. Average flow velocities in the fundus were small, but irregular flow fluctuations of high amplitudes were observed. Asymmetrical outflow through the branches of the bifurcation induced a rotatory intra-aneurysmal circulation from the dominant to the subordinate branch. The circulation in angled terminal aneurysms with the aneurysmal axis at a 45 degree angle to the plane of the bifurcation was a vortex caused by the eccentric inflow from the afferent vessel. Maximum flow velocities measured in the center plane of the angled terminal aneurysms were in the range 50%-80% of the axial velocity in the afferent vessel. The present results indicate that the geometrical relation between aneurysm and parent vessels is the primary factor governing the intra-aneurysmal flow pattern. The elasticity of the models did not affect the average flow velocities, but the intra-aneurysmal pulse wave was damped in elastic models. On the basis of the measured velocity gradients near the walls, maximum shear stresses on the wall of a typical human terminal aneurysm were estimated to be in the order of 50 dyne/cm2 (5 Pascal), a value that is similar to the shear stresses that occur at the flow divider of a cerebral artery bifurcation. This is based on absolute flow velocity measurements in patients [8, 13].
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