Chapter 8
A Survey of the Cerebrovascular System
Cerebral Arteries and Watershed Infarcts
Veins and Venous Sinuses of the Brain
Internal Veins of the Hemisphere
About 50% of the problems that occur inside the cranial cavity and result in neurologic deficits are vascular in origin. Consequently, a detailed understanding of cerebrovascular patterns is absolutely essential to establish an accurate diagnosis of the neurologically compromised patient. The brain is a voracious consumer of oxygen and therefore requires a great deal of oxygenated blood. Although it makes up only about 2% of total body weight in adults, the brain receives 15% to 17% of the total cardiac output and consumes about 20% of the oxygen used by the entire body.
An ongoing flow of oxygenated blood is essential for continued brain function. The average person will lose consciousness if the brain is deprived of blood for 10 to 12 seconds; after 3 to 5 minutes, irreparable brain damage or death may result. There are exceptions, however. Individuals who become hypothermic with a subsequent decrease in arterial blood flow to the brain, as in a winter near-drowning, may be revived after 10, 15, or even 20 minutes with little or no permanent damage. In these cases, the reduction in body temperature protects the brain against the consequences of reduced blood flow.
OVERVIEW
Blood is supplied to the brain by the internal carotid and vertebral arteries. The internal carotid arteries enter the skull and then divide into the anterior and middle cerebral arteries. The vertebral arteries pass through the foramen magnum and join to form the basilar artery; hence, the term vertebrobasilar is frequently applied to this part of the cerebral circulation. The basilar artery branches into right and left posterior cerebral arteries.
Venous outflow from the brain travels through superficial and deep veins, which drain into the dural venous sinuses. Blood in the sinuses, in turn, enters the internal jugular vein. Superficial veins in the scalp and veins in the orbit also may communicate with the dural sinuses, but these are not major conduits for venous drainage from the brain.
This chapter presents an overview of the cerebrovascular system, with particular emphasis on the distribution pattern of vessels on the surface of the brain and spinal cord. Details of the distribution of blood vessels to internal structures are covered in later chapters.
CAUSES OF VASCULAR COMPROMISE
Intracranial hemorrhage originates from arteries or veins and may result from diseases, trauma, developmental defects, or infections. Such bleeding is classified according to its location. Meningeal hemorrhages are found in relation to the coverings of the brain, whereas bleeding into the subarachnoid space is called subarachnoid hemorrhage. Hemorrhage may occur into the ventricular spaces (intraventricular) or into the substance of the brain (parenchymatous). Although many events can lead to cerebrovascular problems with resultant dysfunction, only three examples—aneurysm, cerebral embolism, and arteriovenous malformation—are considered here.
Aneurysm
An aneurysm is the dilation of a vessel wall (Fig. 8-1A), usually an artery, that extends from the lumen to the vessel surface. Aneurysms located inside the skull, cerebral aneurysms, may range from small (berry or saccular aneurysms) to very large (giant aneurysms are more than 2 cm in diameter), or they may involve an elongated portion of the vessel (fusiform aneurysm). Larger aneurysms may cause signs or symptoms by compression of adjacent structures such as cranial nerve roots. The second most common cause of blood in the subarachnoid space (subarachnoid hemorrhage) is rupture of an aneurysm, the first most common cause being trauma.
Figure 8-1. Representation of an aneurysm (A), an embolism (B), and an arteriovenous malformation (C).
Most intracranial (or cerebral) aneurysms (about 85%) are found on the branches of the internal carotid artery system (Fig. 8-2). On this portion of the vascular tree, aneurysms are most frequent on the anterior communicating artery or at its junction with the anterior cerebral artery (30% to 35%), on the internal carotid artery or at its junction with the posterior communicating artery (25% to 30%), or at the bifurcation of the M1 segment of the middle cerebral artery (20%) (Fig. 8-2). About 10% to 15% of intracranial aneurysms are located on branches of the vertebrobasilar system (Fig. 8-2). When aneurysms are present on these vessels, they are more likely to be located at the bifurcation of the basilar artery (5% to 10%), on the basilar artery, or on the posterior inferior cerebellar artery or at its junction with the vertebral artery. Regardless of where they may occur, intracranial aneurysms are frequently located at branch points of vessels or at points where the vessels may make a sharp abrupt turn in their course. The treatment of choice is to clip the stalk of the aneurysm to separate its friable sac from the cerebral circulation.
Cerebral Embolism
A cerebral embolism is the occlusion of a cerebral vessel by some extraneous material (such as a clot, tumor cells, a clump of bacteria, air, or plaque fragments). This occlusion leads to ischemia (a localized anemia) and, if prolonged, ultimately to infarction (a localized vascular insufficiency resulting in necrosis) of the area served by the vessel (Fig. 8-1B). In many cases the deficits seen in the patient reflect the loss of function of the damaged area of the brain or spinal cord. An embolus made up exclusively of blood products is called a thrombus.
The size of the embolus determines where it lodges. Very small emboli may temporarily occlude small cerebral vessels and give rise to a transient ischemic attack, a sudden loss of neurologic function that usually resolves within a few minutes (about 70% of cases), a few hours (about 20% of cases), or in a minority of cases up to 24 hours. On the other hand, large emboli that suddenly occlude major vessels may cause sudden and catastrophic neurologic problems that result in permanent deficits or death.
One well-known cause of cerebral embolism is seen in patients with atherosclerotic disease. Plaques form at many locations, but those at the bifurcation of the common carotid into the external and internal carotid arteries (Fig. 8-1B) are especially problematic. Pieces of plaque may dislodge, pass into the cerebral circulation, and block distal branches of the internal carotid system; the deficits reflect the brain territory damaged. Septic emboli are composed of bacteria usually originating from an extracranial location. This type of embolus may cause an interruption of blood supply, with a consequent infarction, or result in an infection within the central nervous system (CNS) once the bacteria become lodged in a vessel. Septic emboli may also infect and weaken the vessel wall itself, resulting in a mycotic aneurysm. Air embolism may occur in surgical procedures in which a dural sinus is opened. Air may enter the sinus, and movement of blood through the sinus is compromised; if the air gets into the general vascular system and to the heart, other and equally serious problems may arise.
Penumbra
“Time is brain” is a phrase well known to physicians dealing with stroke. In the case of a stroke resulting from vascular occlusion (Fig. 8-1B), it may be described as an occlusive stroke or ischemic stroke; there are three brain areas of particular concern. If a central portion of the ischemic area is permanently lost, an immediately surrounding area, the penumbra, may be salvaged with appropriate and rapid treatment, and an area outside the penumbra will most likely survive (Fig. 8-3). For this type of stroke, treatment may be by the use of tPA (tissue plasminogen activator, infused within 3 to 4.5 hours after the onset of symptoms) or endovascular removal of the clot (within 8 hours). Successful treatment, if it is initiated early, may save the area of the penumbra, decrease brain loss, and result in fewer or less severe neurologic deficits. If treatment is not initiated quickly, the penumbra may be recruited into the area of permanent brain tissue loss, and the neurologic deficits will be accordingly greater. Hemorrhagic strokes cannot be treated with tPA.
Arteriovenous Malformation
An arteriovenous malformation (AVM) results when the communications between major arteries and veins do not develop normally (Fig. 8-1C). These lesions consist of masses of tortuous, interconnecting channels composed of large arteries connecting with large veins. The intervening capillary bed is missing, and there is little or no normal brain tissue in this vascular mass. An AVM may be located on the surface or within the substance of the brain (Fig. 8-4).
Whereas in the strict sense an AVM is not a neoplasm, an AVM shares important features with this type of lesion. Like neoplasms, AVMs are dynamic lesions that will grow, change in their configuration, and cause additional deficits by damaging adjacent brain areas in the process. Degenerative changes in the abnormal vessels within the AVM may lead to hemorrhage. Such hemorrhage may be into the substance of the brain, subarachnoid space, ventricles, or brainstem, depending on the location of the AVM.
The treatment of choice for AVMs is surgical removal. Superficially located lesions, with few feeding arteries and draining veins, are more easily removed, whereas those located deep within the hemisphere or within the brainstem are much more difficult to treat with surgery. However, newer interventional methods (endovascular embolization) now make it possible to pass a small cannula into an AVM to inject substances that occlude the larger channels. Embolization alone is usually inadequate to definitively treat the lesion. In some cases this method is used as a preparatory step to eventual surgical removal.
AVMs (Fig. 8-4) are commonly identified in the second or third decade of life, although signs and symptoms (hemorrhage [into the brain, subarachnoid, ventricular], seizures, mass effect [cranial nerve signs], evidence of increased intracranial pressure, hydrocephalus) may be noted earlier. Bleeding from AVMs is common and may be “silent” or may result in obvious neurologic deficits. AVMs are a part of a larger category of vascular lesions found in the brain that fall under the general classification of vascular hamartomas. These include capillary telangiectases, cavernous angiomas, and venous malformations commonly called venous angiomas.
INTERNAL CAROTID SYSTEM
The internal carotid artery system consists of the internal carotid artery (ICA), as it enters the base of the skull, and its branches. There are several important branches of the ICA; its terminal branches are the anterior cerebral and the middle cerebral arteries.
Internal Carotid Artery
The ICA consists of a cervical part that ascends in the neck, a petrous part, a cavernous part, and a cerebral part (Fig. 8-5). The petrous part is located in the carotid canal and has no branches of consequence. The cavernous part passes through the cavernous sinus and gives rise to the inferior hypophysial and meningeal arteries.
The cerebral part of the internal carotid begins where this vessel penetrates the dura just anterior (ventral) to the optic nerve. Its branches are the ophthalmic, posterior communicating, anterior choroidal, and superior hypophysial arteries (Fig. 8-6).
Figure 8-6. Arteries on the base of the brain showing the relationship of vessels to structures and the arrangement of the circle of Willis (see Fig. 8-11).
The ophthalmic artery, after entering the orbit via the optic foramen, gives rises to the central artery of the retina just distal to the foramen. This latter vessel then passes along the ventral aspect of the optic nerve (it may be inside or outside the dura) to eventually enter the nerve about 10 to 15 mm behind the bulb of the eye to serve the retina. Occlusion of the ophthalmic artery may result in significant visual loss in the ipsilateral eye. Also, aneurysms at the ophthalmic-carotid intersection may cause visual loss because of direct pressure on the optic nerve.
The posterior communicating artery joins the posterior cerebral artery, and the anterior choroidal artery follows caudolaterally along the optic tract (Fig. 8-6). Occlusion of the anterior choroidal artery will result in a combination of visual deficits and weakness of the opposite upper and lower extremities; this is called the anterior choroidal artery syndrome. The ICA ends by dividing into the anterior and middle cerebral arteries.
Anterior Cerebral Artery
Taking its entire extent into consideration, from its origin at the internal carotid to its termination at about the parietooccipital sulcus, the anterior cerebral artery (ACA) is divided into five segments designated A1 to A5 (Fig. 8-7). The precommunicating segment, A1, extends from the internal carotid artery to the anterior communicating artery. A2, the infracallosal segment, extends from the anterior communicating artery to about where the rostrum and genu of the corpus callosum meet. The precallosal segment, A3, arches around the genu of the corpus callosum; this segment ends as the vessels turn sharply caudal. Segments A4, supracallosal, and A5, postcallosal, are located superior and caudal to the corpus callosum; A5 ends at about the level of the parietooccipital sulcus (Figs. 8-7 and 8-8).
Figure 8-8. Arteries on the medial surface of the cerebral hemisphere and on the inferior surface of the temporal lobe.
The A1 segment of the ACA passes superiorly over the optic chiasm and is joined to its counterpart by the anterior communicating artery (Fig. 8-6). The anterior communicating artery and the distal parts of the A1 segments are located in the cistern of the lamina terminalis and give rise to small branches that serve structures in the immediate area, such as parts of the anterior hypothalamus and the optic chiasm.
About 30% to 35% of all intracranial aneurysms are found either on the anterior communicating artery or where this vessel joins the ACA (Figs. 8-1A and 8-2). Patients with aneurysms at these locations may have visual deficits because of the proximity to the optic chiasm. Rupture of aneurysms in this area always results in blood in the interhemispheric fissure between the frontal lobes, and these patients frequently have hematomas in the brain itself or blood in the ventricles.
Distal to the anterior communicating artery, the A2
