Implicit in discussions of ischemic stroke and its treatment is the existence of a “penumbra” zone that is marginally perfused and contains at-risk but viable neurons. Presumably this zone exists at the margins of an infarction, which at its core has irrevocably damaged tissue that is destined to become necrotic. Using various methods, such a penumbra can be demonstrated in association with some infarctions but not all, and the degree of reversible tissue damage has been difficult to determine but is more recently being demonstrated with imaging techniques. The neurons in the penumbra are considered to be physiologically “stunned” by moderate ischemia and subject to salvage if blood flow is restored in a certain period of time. Olsen and colleagues demonstrated hypoperfused penumbral zones but, interestingly, found that regions just adjacent to them are hyperperfused. These concepts find a parallel in attempts to demonstrate by imaging matching of perfusion and infarction (detected by diffusion-weighted images on MRI) in patterns with acute stroke as discussed in the section on treatment. Elevating the systemic blood pressure or improving the rheologic flow properties of blood in small vessels by hemodilution improves flow in the penumbra; however, attempts to use that techniques in clinical work has met with mixed success. Reperfusion of the penumbral area by removal of the occluding clot has, however, been successful in improving outcome after stroke.
The effects of a focal arterial occlusion on brain tissue vary depending on the location of the occlusion and on available collateral and anastomotic channels. In occlusion of the internal carotid artery in the neck, there may be anastomotic flow through the anterior and posterior communicating arteries of the circle of Willis from the external carotid artery through the ophthalmic artery or via other smaller external-internal connections (Fig. 33-1). With blockage of the vertebral artery, the anastomotic flow may be via the deep cervical, thyrocervical, or occipital arteries or retrograde from the other vertebral artery and again through the posterior communicating arteries. If the occlusion is in the stem portion of one of the cerebral arteries, that is, distal to the circle of Willis, a series of meningeal interarterial anastomoses may carry sufficient blood into the compromised territory to lessen ischemic damage (Fig. 33-2). There is also a capillary anastomotic system between adjacent arterial branches, and although it may reduce the size of an ischemic territory, it is usually not adequate to prevent infarction. Thus, in the event of occlusion of a major arterial trunk, the extent of infarction ranges from none at all to the entire vascular territory of that vessel. Between these two extremes are all degrees of variation in the extent of infarction and its degree of completeness, including a penumbral zone in some cases.
The phenomenon of cerebrovascular autoregulation is appropriately introduced here. Over a range of mean blood pressures of approximately 50 to 150 mm Hg, the small pial vessels are able to dilate and to constrict in order to maintain cerebral blood flow (CBF) in a relatively narrow range. This accommodation eventually fails at the extremes of blood pressure, after which CBF follows systemic pressure passively, either falling precipitously or rising to levels that damage the walls of small vessels. The conditions in which the limits of autoregulation are exceeded are at the extremes of hypertensive encephalopathy at one end and circulatory failure at the other, both of which are discussed in later sections of the chapter.
If brain tissue is observed in experimental circumstances at the time of arterial occlusion, the venous blood is first seen to darken, owing to an increase in deoxygenated hemoglobin. The viscosity of the blood and resistance to flow both increase, and there is sludging of formed blood elements within vessels. The tissue becomes pale. Arteries and arterioles become narrowed. Upon reestablishing flow in the occluded artery, the sequence is reversed and there may be a slight hyperemia.