Vasospasm Delayed hemiplegia and other deficits because of focal vasospasm usually appear 3 to 10 days after rupture and rarely before or after this period. Fisher and coworkers (1980) demonstrated that the most severe vasospasm occurs in arteries that are surrounded by collections of clotted subarachnoid blood after 24 h. These same authors devised a widely used scale that rates the extent and location of remaining clot. The reduction in the caliber of blood vessels (vasospasm) appears to be a direct effect of some blood product on the adventitia of the adjacent artery but which component of blood or another mechanism has eluded study for many decades. Areas of ischemic infarction in the territory of the vessel bearing the aneurysm, without thrombosis or other intraluminal changes in the vessel, is the usual finding in such cases. The mechanism is presumed to be purely a reduction in blood flow distal to the area of vasospasm but therefore influenced by systemic blood pressure and by collateral circulation in the cortex. The ischemic lesions are often multiple and had in the past occurred with great frequency than they do currently according to Hijdra and associates, perhaps as a result in overall management of hemorrhage in ICUs.
After a few days, arteries in chronic spasm undergo a series of morphologic changes. The smooth muscle cells of the media become necrotic, and the adventitia is infiltrated with neutrophilic leukocytes, mast cells, and red blood corpuscles, some of which have migrated to a subendothelial position. One current notion is that these changes are caused by products of hemolyzed blood seeping inward from the pia-arachnoid into the muscularis of the artery.
The clinical features of delayed cerebral vasospasm depend on the affected blood vessel but typically include a fluctuating hemiparesis or aphasia and increasing confusion that must be distinguished from the effects of hydrocephalus (see below). In the past, an arteriogram was required to verify the diagnosis, although it is not often performed now because of the slight associated risk of worsening vascular spasm and the ease with which the condition can be recognized by its clinical presentation. Severe vasospasm is also visualized with MRA and CT techniques (Fig. 33-28). Transcranial Doppler ultrasonography measurements provide an indirect way of following, by observations of blood flow velocity, the caliber of the main vessels at the base of the brain but they are somewhat imprecise for this purpose. Almost all patients have a greatly increased velocity of blood flow in the affected vessel that can be detected by ultrasound in the days after hemorrhage. However, progressive elevation of flow velocity in any one vessel (especially if over 175 cm/s) suggests that focal vasospasm is occurring. There is a reasonable correlation between these findings and the radiographic appearance of vasospasm, but the clinical manifestations of ischemia depend on additional factors such as collateral blood supply and the cerebral perfusion pressure.
Hydrocephalus If a large amount of blood ruptures into the ventricular system or floods the basal subarachnoid space, it may find its way into the ventricles through the foramina of Luschka and Magendie. The patient then becomes confused or unconscious as a result of acute hydrocephalus. The clinical signs are reversed by draining the ventricles, either by external ventriculostomy or, in selected cases, by lumbar puncture, but the routine use of ventricular drainage after subarachnoid hemorrhage is not uniformly agreed upon.
Delayed and subacute hydrocephalus as a result of blockage of the CSF pathways by blood may appear after 2 to 4 weeks and is managed similarly. Many of these latter cases improve. There are further instances of long-delayed hydrocephalus that present as normal-pressure hydrocephalus (NPH) months or years after subarachnoid hemorrhage, as described in Chap. 29.
Anatomic–Clinical Correlations of Aneurysms