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.
Figure 8-2. Stick drawing of the vertebrobasilar and internal carotid systems showing the locations where aneurysms are found on this vascular pattern. The larger balloons represent the positions from which aneurysms more frequently originate; the smaller balloons represent the less frequent points of origin.
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.
“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.
Figure 8-3. After an occlusive stroke, the penumbra is an interface between a region of permanent tissue damage and an area that will most likely survive. Rapid and appropriate treatment, with reperfusion of the penumbra, may salvage this region and reduce the neurologic deficits suffered by the patient.
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).
Figure 8-4. Sagittal magnetic resonance (T1-weighted) image near the midline showing an arteriovenous malformation in the frontal lobe. This lesion includes branches of the anterior cerebral artery and drains into the superior sagittal sinus.
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.
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.
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.
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).
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 segment passes through the cistern of the lamina terminalis rostrally toward the genu of the corpus callosum and usually gives rise to frontopolar and orbitofrontal branches (Figs. 8-7 and 8-8). The A3 segment arches around the genu and usually gives rise to the callosomarginal artery and to the more anterior and middle of the internal frontal branches. A4 and A5 segments of the ACA are composed of the pericallosal and callosomarginal arteries and their branches on the medial aspect of the cerebral hemisphere (Figs. 8-7 and 8-8). These distal portions of the ACA serve the lower extremity areas of the somatomotor and somatosensory cortex; damage to this vascular territory may result in hemimotor and hemisensory deficits of the lower extremity.
The main branches of A3 to A5 lie within the callosal cistern. When aneurysms occur on the more distal parts of the ACA, they are usually located at the branch points of the frontopolar and callosomarginal arteries.
The middle cerebral artery (MCA) is usually (70% of the time) the larger of the two terminal branches of the internal carotid artery (Figs. 8-5 and 8-6). The part of this vessel located between its origin from the internal carotid and the point where it branches at the ventromedial aspect of the insula (the limen insulae) is the M1 segment (Fig. 8-9A). Branches from M1 serve adjacent medial and rostral aspects of the temporal lobe and, via lenticulostriate arteries, structures located inside the hemisphere. Whereas it is common to refer to the lenticulostriate arteries (plural), in about 40% of patients, this vessel originates as a single trunk that immediately divides into a number of branches (the arteries) that penetrate the hemisphere. The other patterns are two main trunks (30%) that immediately divide and 10 to 15 small arteries (30%) arising directly from M1.
FIGURE 8-9. A, A representation of the hemisphere in coronal section showing the segments of the middle cerebral artery (M1 to M4). B, A computed tomography arteriogram showing the same vessels in a patient.
The M1 segment is located in medial portions of the sylvian cistern. On the ventromedial aspect of the insular cortex, the M1 segment usually bifurcates into superior and inferior trunks (Figs. 8-5, 8-6, and 8-9A). Aneurysms on the MCA frequently arise at the bifurcation of M1 into the superior and inferior trunks; the aneurysm represents the true position of the bifurcation in cases in which there may appear to be multiple bifurcations of M1. These trunks and their distal branches collectively serve the insular cortex, the inner aspects of the opercula, and the lateral surface of the cerebral hemisphere. Those branches on the insular cortex (insular part of the MCA) are the M2 segment (Figs. 8-5 and 8-9A, B). The larger vessels continue on to the inner aspects of the opercula (frontal, parietal, temporal), where they are designated M3, the opercular part of the MCA (Fig. 8-9A, B). Distal branches of the superior and inferior trunks exit the lateral fissure and serve, respectively, cortical areas located above and below this fissure. These cortical branches (cortical part of the MCA) collectively form the M4 segment (Figs. 8-5 and 8-9A, B). Most of these distal branches are named according to the general area or structure they serve; their distribution patterns are shown in Figure 8-10. M4 branches serve trunk, upper extremity, and face areas of the somatomotor and somatosensory cortex