The blood supply of the central nervous system (CNS) is of special interest because of the metabolic demands of nervous tissue. The brain depends on aerobic metabolism of glucose and is one of the most metabolically active organs of the body. Although composing only 2% of body weight, the brain receives about 17% of the cardiac output and consumes about 20% of the oxygen used by the entire body. Unconsciousness occurs after cessation of cerebral circulation in about 10 seconds. Lesions of vascular origin are responsible for more neurological disorders than any other category of disease process.
Arterial Supply of the Brain
The brain is supplied by the paired internal carotid and vertebral arteries through an extensive system of branches. Descriptions of the arteries follow, with some notes on their clinical significance. Later in this chapter, summaries are provided of cortical areas and deeper parts of the brain, indicating the arteries by which they are supplied.
INTERNAL CAROTID SYSTEM
The internal carotid artery, a terminal branch of the common carotid artery, traverses the carotid canal in the base of the skull and enters
the middle cranial fossa beside the dorsum sellae of the sphenoid bone. Beyond this point, the artery undergoes the following sequence of bends that constitute the carotid siphon in a cerebral angiogram (Fig. 25-1). The internal carotid artery first runs forward in the cavernous venous sinus and then turns upward on the medial side of the anterior clinoid process. At this point, the artery enters the subarachnoid space by piercing the dura mater and arachnoid, courses backward below the optic nerve, and finally turns upward immediately lateral to the optic chiasma. This brings the artery under the anterior perforated substance, where it divides into the middle and anterior cerebral arteries (Fig. 25-2).
Arterial occlusion by an embolus or a thrombus is usually followed by infarction of a portion of the region supplied. Anastomotic channels are present between branches of the major arteries on the surface of the brain. There are also communications at the arteriolar level, and the capillary bed is continuous throughout the brain. These anastomoses, however, are usually insufficient to sustain the circulation in the region normally supplied by a major artery. The size of an infarction depends on the caliber of the occluded artery, existing anastomoses, and the time elapsing before complete obstruction. In addition to intracranial occlusions, impairment of the cerebral circulation is often caused by stenosis of a carotid or vertebral artery in the neck.
The slender, thin-walled arteries that penetrate the ventral surface of the brain to supply the internal capsule and adjacent gray masses are especially prone to rupture. Hypertension and degenerative changes in these arteries are major factors that lead to cerebral hemorrhage.An aneurysm usually occurs at the site of branching of one of the larger arteries at the base of the brain. An aneurysm may leak or rupture, and there is bleeding into the subarachnoid space. In some cases, adhesion of the aneurysmal sac to adjacent structures can give rise to hemorrhage that is intracerebral or into a cranial nerve.
FIGURE 25-1 Carotid an giogram (lateral view). A, carotid siphon; B, branches of the middle cerebral artery; C, anterior cerebral artery. (Courtesy of Dr. J. M. Allcock.)
The following branches arise from the internal carotid artery before its terminal bifurcation.
FIGURE 25-2 Arteries that supply the brain, as seen from the ventral surface. The right cerebellar hemisphere and the tip of the right temporal lobe have been removed.
The posterior hypophysial arteries supply the neural (posterior) lobe of the pituitary gland, and the anterior hypophysial arteries enter the median eminence of the hypothalamus. The latter blood vessels break up into capillary loops, into which hypothalamic releasing factors gain access, and the capillary loops drain through small hypophysial portal veins into the capillaries of the anterior lobe. This constitutes the system through which the hypothalamus controls the output of anterior pituitary hormones (see also Chapter 11).
This branch comes off immediately after the internal carotid artery enters the subarachnoid space. The ophthalmic artery passes through the optic foramen into the orbit, supplying the eye and other orbital contents, frontal area of the scalp, frontal and ethmoid paranasal sinuses, and parts of the nose.
Posterior Communicating Artery
This slender artery arises from the internal carotid artery close to its terminal bifurcation and runs backward to join the proximal part of the posterior cerebral artery, thereby forming part of the arterial circle (circle of Willis). Some of the posteromedial central arteries, described later, are branches of the posterior communicating artery.
Anterior Choroidal Artery
This branch has a wider distribution than its name suggests. The artery passes back along the optic tract and the choroid fissure at the medial edge of the temporal lobe. The anterior choroidal artery sends branches to the optic
tract, uncus, amygdala, hippocampus, globus pallidus, lateral geniculate body, and ventral part of the internal capsule. Branching is variable, and this artery sometimes supplies the subthalamus, ventral parts of the thalamus, and the rostral part of the midbrain. The terminal branches of the anterior choroidal artery supply the choroid plexus in the temporal horn of the lateral ventricle and anastomose there with branches of the posterior choroidal artery.
Internal Carotid Occlusion
Occlusion of the internal carotid artery has serious consequences. Blindness of the ipsilateral eye (supplied by the ophthalmic artery) and the contralateral half of the visual field of the other eye (from infarction of the optic tract and lateral geniculate body, supplied by the anterior choroidal artery) are added to the effects of occlusion of the middle and anterior cerebral arteries (principally a contralateral hemiplegia and hemianopsia, with global aphasia if the affected hemisphere is the dominant one for language).
Occlusion of the anterior choroidal artery alone can be asymptomatic, or it may have a variety of effects, depending on the site of the obstruction and the efficiency of the anastomoses with the posterior choroidal artery. Symptoms can include contralateral hemiplegia and sensory abnormalities (internal capsule) and contralateral homonymous hemianopia (optic tract and lateral geniculate body).
Middle Cerebral Artery
Of the terminal branches of the internal carotid artery, the middle cerebral artery is the larger and more direct continuation of the parent vessel (see Fig. 25-2). This artery runs deep in the lateral sulcus between the frontal and temporal lobes. Central arteries arise from the proximal part of the middle cerebral artery, lateral to the optic chiasma. They enter the base of the hemisphere and supply internal structures, including the internal capsule. Frontal, parietal, and temporal branches emerge from the lateral sulcus of the cerebral hemisphere (Fig. 25-3) to supply a large area of cortex and subcortical white matter in the three corresponding lobes of the cerebrum.
FIGURE 25-3 Distribution of the middle cerebral artery on the lateral surface of the left cerebral hemisphere. Terminal branches of the anterior and posterior cerebral arteries are also visible.
The territory of distribution of the middle cerebral artery includes most of the primary motor and premotor cortex, the frontal eye field, and the primary somatosensory area. The motor and sensory cortex for the lower limb and the perineum are excluded (compare Figs. 15-3
and 25-3). The left middle cerebral artery (in most people) supplies all the cortical areas concerned with language. These are the receptive language areas in the temporal and parietal lobes and Broca's expressive speech area in the inferior frontal gyrus (see Fig. 25-3 and Chapter 15). The white matter underlying the parietal cortex contains the geniculocalcarine tract.
Middle Cerebral Artery Occlusion
Loss of function of the cortical areas supplied by the middle cerebral artery results in contralateral paralysis most noticeable in the lower part of the face and in the arm, together with general somatic sensory deficits of the cortical type. Involvement of the geniculocalcarine tract results in hemianopia of the contralateral visual fields of both eyes (see Chapter 20). The auditory cortex is included in the area of distribution, but a unilateral lesion causes no demonstrable impairment of hearing because of the bilateral cortical projection from the organ of Corti (see Chapter 21). Occlusion of the middle cerebral artery of the hemisphere dominant for language causes global aphasia (seeChapter 15).
Fragments of the complete syndrome, such as monoplegia or receptive aphasia, are seen when individual cortical branches of the artery are blocked. Obstruction of the central branches can cause hemiplegia attributable to infarction of motor fibers in the internal capsule. A lesion in the internal capsule does not cause aphasia because the connections of the language areas with the contralateral hemisphere are intact.
Anterior Cerebral Artery
The smaller terminal branch of the internal carotid artery is the anterior cerebral artery, which is first directed medially above the optic nerve (see Fig. 25-2). The two anterior cerebral arteries almost meet at the midline where they are joined together by the anterior communicating artery. A special branch of the anterior cerebral artery is given off just proximal to the anterior communicating artery. This is the medial striate artery (also called recurrent artery of Heubner), which penetrates the anterior perforated substance to supply the ventral part of the head of the caudate nucleus, the adjacent part of the putamen, and the anterior limb and genu of the internal capsule.
The anterior cerebral artery ascends in the longitudinal fissure and bends backward around the genu of the corpus callosum (Fig. 25-4). Branches given off just distal to the anterior communicating artery supply the medial part of the orbital surface of the frontal lobe, including the olfactory bulb and olfactory tract. The artery continues along the upper surface of the corpus callosum as the pericallosal artery, and a large branch, the callosomarginal artery, follows the cingulate sulcus. The anterior cerebral artery supplies the medial surfaces of the frontal and parietal lobes and the corpus callosum. In addition, branches extend over the dorsomedial border of the hemisphere and supply a strip on the lateral surface (see Fig. 25-3). The supplementary and cingulate motor areas and the dorsal parts of the primary motor and primary somatosensory areas are included in its territory.
The vertebral artery, a branch of the subclavian artery, ascends in the foramina of the transverse processes of the upper six cervical vertebrae. On reaching the base of the skull, the artery winds around the lateral mass of the atlas, pierces the posterior atlanto-occipital membrane, and enters the subarachnoid space at the level of the foramen magnum by piercing the dura and arachnoid. The artery then runs forward with a medial inclination, giving off small branches that deeply penetrate the medial parts of the medulla. The left and right vertebral arteries join at the caudal border of the pons to form the basilar artery. The latter vessel runs rostrally in the midline of the pons and divides into the posterior cerebral arteries (see Fig. 25-2).
Branches of the Vertebral Artery
The rostral segments of the cervical cord receive blood through spinal branches of the vertebral arteries. A single anterior spinal artery is formed by a contribution from each vertebral artery. A posterior spinal artery arises on each side as a branch
of either the vertebral or the posterior inferior cerebellar artery (see Fig. 25-2). The anterior and posterior spinal arteries continue throughout the length of the spinal cord. These are small vessels, however, and most of their blood comes from reinforcements by the anterior and posterior radicular arteries, which are described later.
FIGURE 25-4 Distribution of the anterior and posterior cerebral arteries on the medial surface of the left cerebral hemisphere.
Posterior Inferior Cerebellar Artery
The posterior inferior cerebellar artery (PICA) is the largest branch of the vertebral artery. It pursues an irregular course between the medulla and cerebellum. Branches are distributed to the posterior part of the cerebellar hemisphere, inferior vermis, central nuclei of the cerebellum, and choroid plexus of the fourth ventricle. There are also importantmedullary branches to the dorsolateral region of the medulla.
Anterior Cerebral Artery Occlusion
Occlusion of the anterior cerebral artery causes paralysis and sensory deficits in the contralateral leg and perineum. Commonly, affected patients have urinary incontinence caused by inadequate perineal sensation and defective cortical control of the pelvic floor musculature. If the obstruction is in the proximal part of the vessel, blocking the medial striate artery, patients also have contralateral upper motor neuron weakness of the face, tongue, and upper limb because of corticofugal motor fibers that are in or near the genu of the internal capsule before they pass into its posterior limb (see Chapter 16). A proximal occlusion may also cause ipsilateral anosmia attributable to infarction of the olfactory bulb and tract.
Anterior cerebral artery syndromes often are associated with mental confusion and dysphasia, perhaps attributable to loss of functions of the prefrontal cortex, the cingulate gyrus, and the supplementary motor area.
Branches of the Basilar Artery
The basilar artery gives off the following branches before dividing into the posterior cerebral arteries at the rostral border of the pons.
Anterior Inferior Cerebellar Artery
Arising from the caudal end of the basilar artery, the anterior inferior cerebellar artery (AICA) supplies the cortex of the inferior surface of the cerebellum anteriorly and the underlying white matter; it assists in the supply of the central cerebellar nuclei. In addition, slender twigs from the artery penetrate the upper medulla and the tegmentum of the lower pons.
This vessel is a branch of the basilar artery (see Fig. 25-2) or, more frequently, the AICA. The labyrinthine artery traverses the internal acoustic meatus and ramifies throughout the membranous labyrinth of the internal ear.
These are slender branches of variable length that arise from the basilar artery along its length. The short paramedian pontine arteries supply the basal part of the pons, including most of the bundles of corticospinal fibers, pontine nuclei, and transverse (pontocerebellar) fibers. These paramedian vessels extend dorsally to the floor of the fourth ventricle, supplying the medial parts of the pontine tegmentum. Longer circumferential pontine arteries pierce and supply the lateral parts of the pons and middle cerebellar peduncle and then turn medially to supply the lateral part of the tegmentum.
Vascular Lesions That Affect the Brain Stem
A substantial hemorrhage within the pons is instantly fatal. Thrombosis of the whole basilar artery causes coma and decerebrate rigidity (seeChapter 23), soon followed by death attributable to failure of the central control of respiration.
An embolus that passes through a vertebral artery typically lodges at the bifurcation of the basilar artery, bilaterally occluding the superior cerebellar and the posteromedial central arteries. The latter are the first branches of the posterior cerebral arteries. Infarction in the reticular formation of the rostral pons and caudal midbrain causes coma, and the associated destruction of the fibers of both oculomotor nerves results in bilateral divergence of the eyes with fixed, dilated pupils (see Chapter 8). This syndrome can resemble the end stage of compression of the oculomotor nerves and midbrain caused by herniation through the tentorial incisura (see Chapter 26), but the effects of an embolus are sudden, not gradual. A small embolus that lodges in one of the posteromedial central arteries can cause a small infarct in the midbrain, such as the lesion responsible for Weber's syndrome (see Chapter 7).
Many syndromes have been described as resulting from small infarcts caused by occlusion of individual branches of the vertebral and basilar arteries. The positions and levels of the lesions can be deduced from the effects of transection of tracts and destruction of nuclei or fibers of cranial nerves. A few examples are cited in Chapter 7. Of these, the most common is the lateral medullary (Wallenberg's) syndrome, typically caused by obstruction of the PICA. This syndrome may also occur after thrombosis of the vertebral artery.
Although a rare occurrence, occlusion of the labyrinthine artery (or of its usual parent vessel, the AICA) results in the expected deafness in the corresponding ear and vestibular dysfunction (vertigo, with a tendency to fall toward the side of the lesion).
Infarction of the ventral part of the pons transects motor tracts. This causes paralysis of all voluntary movement except that of the eyes (because the medial longitudinal fasciculus is spared). The general and special sensory pathways and the reticular formation are spared, and the patient is conscious but can communicate only by means of eye movements. This condition is called the locked-in syndrome. More dorsally located lesions in the rostral pons or caudal midbrain cause one of the two forms of akinetic mutism (see Chapter 23). In this form, consciousness is severely impaired.
Superior Cerebellar Artery
This branch arises close to the terminal bifurcation of the basilar artery, ramifies over the dorsal surface of the cerebellum, and supplies the cortex, white matter, and central nuclei. Branches from the proximal part of the superior cerebellar artery are distributed to the rostral pontine tegmentum, superior cerebellar peduncle, and inferior colliculus of the midbrain.
Posterior Cerebral Artery
The posteromedial central arteries arise at and near the bifurcation of the basilar artery. Each posterior cerebral artery then curves around the midbrain, above the tentorium, and reaches the medial surface of the cerebral hemisphere beneath the splenium of the corpus callosum (see Fig. 25-4). The artery gives off temporal branches, which ramify over the inferior surface of the temporal lobe and calcarine and parieto-occipital branches, which run along the corresponding sulci. All these arteries send branches around the border of the cerebral hemisphere to supply a peripheral strip on the lateral surface (see Fig. 25-3). The calcarine branch is of special significance because it supplies all the primary and some of the association cortex for vision. Much of the parahippocampal gyrus is supplied by the temporal branches, along with parts of the hippocampus.
The posterior choroidal artery (not seen in Fig. 25-4) comes off the posterior cerebral artery in the region of the splenium and runs forward in the transverse fissure beneath the corpus callosum. The posterior choroidal artery supplies the choroid plexus of the central part of the lateral ventricle, the choroid plexus of the third ventricle, the posterior part of the thalamus, the fornix, and the tectum of the midbrain. Its terminal branches anastomose with those of the anterior choroidal artery within the choroid plexus of the lateral ventricle.
Posterior Cerebral Artery Occlusion
Infarction of the cortical areas and subcortical white matter supplied by the posterior cerebral artery causes blindness in the contralateral fields of vision of both eyes (homonymous hemianopia; see Chapter 20). Ischemia of the hippocampal formation can result in a disturbance of memory after the arterial occlusion, but patients recover from this because lesions in the limbic system must be bilateral to cause lasting disability. If the infarct is located in the hemisphere dominant for language (usually the left) and extends into the splenium of the corpus callosum, the contralateral (intact) visual cortex is disconnected from the language areas of the dominant hemisphere. This causes alexia (see Chapter 15) in addition to the homonymous hemianopia.
Herniation of the uncus and midbrain through the tentorial incisura, caused by an expanding space-occupying lesion in the supratentorial compartment of the cranial cavity, can stretch and compress one or both posterior cerebral arteries over the rigid anterior edge of the tentorium (see Chapter 26). Even if the cause is treated surgically, necrosis of the areas supplied by the compressed arteries may develop. Cortical blindness results, and the patient may also have permanent impairment of the ability to form new memories (see Chapter 18) because of bilateral hippocampal involvement. Intracranial hemorrhage caused by head injury can lead to these consequences of bilateral ischemia in the territory of the posterior cerebral artery.
ANASTOMOSES BETWEEN CORTICAL ARTERIES
Anastomoses between branches of the anterior, middle, and posterior cerebral arteries are concealed in the sulci. The caliber of an anastomotic vessel may be sufficient to sustain part of the territory of another artery if the latter is occluded. The cerebral arteries are also interconnected through an arteriolar network in the pia mater. Whereas short cortical branches from the pial plexus supply the rich capillary network of the cortex, longer branches of arteries in the subarachnoid space penetrate into the white matter and form a less profuse capillary network.
ARTERIAL CIRCLE (CIRCLE OF WILLIS)
The major arteries that supply the cerebrum are joined to one another at the base of the brain in the circle of Willis (see Fig. 25-2). Starting from the midline in front, the circle consists of the anterior communicating, anterior
cerebral, internal carotid (a short segment), posterior communicating, and posterior cerebral arteries; then it continues to the starting point in reverse order. Normally, little exchange of blood takes place between the main arteries through the slender communicating vessels. The arterial circle provides alternative routes, however, when one of the major arteries leading into it is occluded. Frequently, these anastomoses are inadequate, especially in elderly people in whom the large vessels and communicating arteries may be narrowed by atheroma.
Aneurysms often develop at sites of branching of arteries in and near the arterial circle, and they can rupture or leak, causing subarachnoid hemorrhage. The most common sites for such aneurysms are the terminal part of the internal carotid artery, the anterior communicating artery, the proximal part of the middle cerebral artery, and the posterior communicating artery. A subarachnoid hemorrhage causes a severe headache of sudden onset, with a stiff neck and other signs of meningeal irritation.
Many variants of the conventional configuration of the arterial circle exist. Each posterior cerebral artery starts out as a branch of the internal carotid artery. In later embryonic development, the posterior cerebral arteries become the terminal branches of the basilar arteries, leaving the left and right posterior communicating arteries as vestiges of the earlier condition. About one in three people has one posterior cerebral artery as a major branch of the internal carotid artery. This type of connection of the posterior cerebral artery seldom occurs bilaterally. Often one anterior cerebral artery is unusually small in the first part of its course, in which case the anterior communicating artery has a larger-than-usual caliber, and one carotid artery provides blood for the medial surfaces of both cerebral hemispheres.
Branches of striate arteries in the claustrum and external capsule are the most common site of cerebral hemorrhage caused by hypertension. The escaping blood destroys the surrounding brain tissue and may eventually occupy a substantial proportion of the volume of the cerebral hemisphere. Blood also commonly enters the ventricular system of the brain. A large hemorrhage of this kind causes contralateral hemiplegia, which is likely to be followed by coma and death.
Some hypertensive cerebral hemorrhages originate in Charcot-Bouchard aneurysms, which are dilatations of arterioles attributed to degenerative changes in the vessel wall. These microaneurysms probably develop much less frequently than was formerly believed, however, even in hypertensive individuals.
Numerous central arteries arise from the region of the arterial circle as four groups (see Fig. 25-2). These slender, thin-walled blood vessels, also known as ganglionic, nuclear,striate, or thalamic perforating arteries, supply parts of the corpus striatum, internal capsule, diencephalon, and midbrain. The medial striate artery (recurrent artery of Heubner) is similar to the central arteries with respect to its distribution, as are the anterior and posterior choroidal arteries with respect to parts of their distributions. Table 25-1 summarizes the origins and distributions of the groups of central arteries.
DISTRIBUTION OF CENTRAL ARTERIES
Table 25-2 identifies the blood supply of structures within the regions of the brain that are supplied by the central arteries.
TABLE 25-1 Origin and Distribution of Central Arteries of the Brain
TABLE 25-2 Structures Supplied by Central Arteries
The calibers of small arteries in the brain are controlled by autoregulation, which means that their muscular walls contract if the pressure inside increases and relax if the pressure decreases, so that a constant rate of flow tends to be maintained. The increased blood flow in active areas of gray matter is probably caused by vasodilator metabolites, notably carbon dioxide. Noradrenergic axons (from the sympathetic system and from the locus coeruleus) are present in the walls of many cerebral blood vessels, but their functional importance has not yet been ascertained.
Cerebral Blood Flow and Intracranial Pressure
Venous Drainage of the Brain
The brain stem and cerebellum are drained by unnamed veins that empty into the dural venous sinuses adjacent to the posterior cranial fossa. The cerebrum has an external and an internal venous system. Whereas the external cerebral veins lie in the subarachnoid space on all surfaces of the hemispheres, the central core of the cerebrum is drained by internal cerebral veins situated beneath the corpus callosum in the transverse fissure (which is described in Chapter 13). Both sets of cerebral veins empty into dural venous sinuses, which are described in Chapter 26.
EXTERNAL CEREBRAL VEINS
The superior cerebral veins, of which there are eight to 12 in number, course upward over the lateral surface of the hemisphere. On nearing the midline, they pierce the arachnoid, run between the arachnoid and the dura mater for 1 to 2 cm, and empty into the superior sagittal sinus or into venous lacunae adjacent to the sinus.
Trauma to the head may tear a superior cerebral vein as it lies between the arachnoid and dura mater, resulting in a subdural hemorrhage.Owing to the low venous pressure, the blood may escape slowly, clotting as it accumulates in the subdural space and gradually pushing the cerebrum downward.
The superficial middle cerebral vein runs downward and forward along the lateral sulcus and empties into the cavernous sinus. Anastomotic channels allow for drainage in other directions (Fig. 25-5A). These are the superior anastomotic vein (vein of Trolard), which opens into the superior sagittal sinus and the inferior anastomotic vein (vein of Labbé), which opens into the transverse sinus.
The deep middle cerebral vein runs downward and forward in the depths of the lateral sulcus to the ventral surface of the brain. The anterior cerebral vein accompanies the anterior cerebral artery. These veins unite in the region of the anterior perforated substance to form the basal vein (vein of Rosenthal), which runs backward at the base of the brain, curves around the midbrain, and empties into the great cerebral vein (Fig. 25-5B; see also the section “Internal Cerebral Veins” in this chapter). The basal vein receives tributaries from the optic tract, hypothalamus, temporal lobe, and midbrain.
In addition to the veins just noted, numerous small vessels drain limited areas. These have no consistent pattern and empty into adjacent dural sinuses.
INTERNAL CEREBRAL VEINS
The internal venous system forms adjacent to each lateral ventricle and continues through the transverse cerebral fissure beneath the corpus callosum (see Chapter 13 and Fig. 25-5C). The thalamostriate vein (vena terminalis) begins in the region of the amygdaloid body in
the temporal lobe and follows the curve of the tail of the caudate nucleus on its medial side, receiving tributaries from the corpus striatum, internal capsule, thalamus, fornix, and septum pellucidum. The tortuous choroidal vein runs along the choroid plexus of the lateral ventricle. In addition to draining the choroid plexus, this vein receives tributaries from the hippocampus, fornix, and corpus callosum. The thalamostriate vein and choroidal vein unite immediately behind the interventricular foramen to form the internal cerebral vein.The paired internal cerebral veins run posteriorly in the transverse fissure, uniting beneath the splenium of the corpus callosum to form the great cerebral vein (vein of Galen). The latter vein, which is no more than 2 cm long, also receives the basal veins and tributaries from the cerebellum. The great cerebral vein empties into the straight sinus, which is in the midline of the tentorium cerebelli.
FIGURE 25-5 Internal cerebral system of veins, as seen from above after removal of the corpus callosum and fornix. Veins of the cerebrum. (A) Veins on the lateral aspect of the left hemisphere. (B) Veins of the right hemisphere, viewed from below. Part of the temporal lobe has been cut away, revealing the choroid plexus of the lateral ventricle. (C)Internal system of veins, as seen from above after removal of the corpus callosum and fornix.
Blood Supply of the Spinal Cord
The median anterior spinal artery and the paired posterior spinal arteries run longitudinally throughout the length of the spinal cord. The anterior spinal artery originates in a Y-shaped configuration from the vertebral arteries, as already described, and runs caudally along the ventral median fissure. Each posterior spinal artery is a branch of either the vertebral or the PICA and consists of multiple anastomosing channels along the line of attachment of the dorsal roots of the spinal nerves.
The blood received by the spinal arteries from the vertebral arteries is sufficient for only the upper cervical segments of the spinal cord. The arteries are therefore reinforced at intervals in the following manner. The vertebral artery in the cervical region, the posterior intercostal branches of the thoracic aorta, and the lumbar branches of the abdominal aorta give off segmental spinal arteries, which enter the vertebral canal through the intervertebral foramina. In addition to supplying the vertebrae, these segmental spinal arteries give rise to anterior and posterior radicular arteries, which run along the ventral and dorsal roots of the spinal nerves. Most of the radicular arteries are of small caliber, sufficient only to supply the nerve roots and contribute to a vascular plexus in the pia mater covering the spinal cord. A variable number of anterior radicular arteries of substantial size, about 12 including both sides, join the anterior spinal artery. Similarly, a variable number of posterior radicular arteries, about 14 including both sides, join the posterior spinal arteries. These larger radicular arteries are in the lower cervical, lower thoracic, and upper lumbar regions; the largest, an anterior radicular artery known as the spinal artery of Adamkiewicz, is usually situated in the upper lumbar region. The spinal cord is vulnerable to circulatory impairment if the important contribution by a major radicular artery is compromised by injury or by the placing of a surgical ligature.
Sulcal branches arise in succession from the anterior spinal artery and enter the right and left sides of the spinal cord alternately from the ventral median fissure. The sulcal arteries are least frequent in the thoracic part of the spinal cord. The anterior spinal artery supplies the ventral gray horns, part of the dorsal gray horns, and the ventral and lateral white funiculi. Penetrating branches from the posterior spinal arteries supply the remainder of the dorsal gray horns and the dorsal funiculi of white matter. A fine plexus (the vasocorona) derived from the spinal arteries is present in the pia mater on the lateral and ventral surfaces of the cord. Penetrating branches from the vasocorona supply a narrow zone of white matter beneath the pia mater.
Although the pattern of spinal veins is irregular, there are essentially six of them. Anterior spinal veins run along the midline and along the line of ventral rootlets. Posterior spinal veins are situated in the midline and along the line of dorsal rootlets. The spinal veins are drained at intervals by up to 12 anterior radicular veins and by a similar number ofposterior radicular veins. The radicular veins empty into an epidural venous plexus, which, in turn, drains into an external vertebral plexus through channels in the intervertebral foramina. Blood from the
external vertebral plexus empties into the vertebral, intercostal, and lumbar veins.
Imaging Cerebral Blood Vessels
In 1927, de Egas Moniz introduced the technique of cerebral angiography, which developed into a valuable diagnostic aid in the hands of neuroradiologists. The method consists of injecting a radiopaque solution into the artery, followed by serial radiographic photography at about 1-second intervals. The radiographs show the contrast medium in progressive stages of its passage through the arterial tree and the venous return. Injection into the common carotid artery or the internal carotid artery shows the distribution of the middle and anterior cerebral arteries (see Figs. 25-1 and 25-6). Similarly, injection of the vertebral artery permits visualization of the vertebral, basilar, and posterior cerebral arteries together with their branches (Fig. 25-7) The cerebral veins are seen in later pictures of a series. (The internal carotid and vertebral arteries are approached with a long catheter passed through a femoral artery and the aorta.)
FIGURE 25-6 Carotid angiogram (anteroposterior view). A, carotid siphon; B, branches of the middle cerebral artery; C, anterior cerebral artery. (Courtesy of Dr. J. M. Allcock.)
The technique of cerebral angiography is especially useful in identifying vascular malformations and aneurysms. The method often provides valuable information concerning occlusive vascular disease and space-occupying lesions that displace blood vessels.
The larger cerebral vessels can be demonstrated by computed tomography after intravenous injection of a contrast medium and by nuclear magnetic resonance imaging (seeChapter 4). Ultrasound can provide information about the anatomy and blood flow in the carotid arteries. These less invasive techniques do not display the vascular anatomy in as much detail as angiography.
Certain substances fail to pass from capillary blood into the CNS, although the same substances
gain access to non-nervous tissues. They include dyes used in animal experimentation and some antibiotics and other drugs that would otherwise be of therapeutic value. In the blood, these substances are bound to plasma protein molecules, which are unable to leave normal cerebral blood vessels. The lumen of a capillary and the parenchyma of the brain and spinal cord are separated by endothelium, a basal lamina, and perivascular end feet of astrocytic processes. In mammals, the blood-brain barrier to proteins is formed by the internal plasma membranes of the endothelial cells and the tight junctions between them. The barrier properties of the endothelium are induced by the adjacent cells, principally astrocytes, of the CNS tissue. Small hydrophobic molecules, including oxygen, carbon dioxide, and ethanol, can diffuse through endothelial cell membranes and cytoplasm and are not excluded by the brain.
FIGURE 25-7 Vertebral angiogram (lateral view). This is a subtraction image, made by superimposing a positive plain radiograph of the patient's skull (i.e., with dark bones) on the angiogram and then photographing through the two films so that the contrast medium appears dark and the naturally radiopaque structures are largely eliminated. The contrast medium has flowed into the basilar artery and the contralateral vertebral artery, so the vertebrobasilar circuation is filled bilaterally. B, basilar artery; C, calcarine branch of a posterior cerebral artery; PICA, posterior inferior cerebellar arteries of both sides; Po, posterior cerebral arteries; SC, superior cerebellar arteries; Th, position of thalamus; To, position of cerebellar tonsil; V, vertebral arteries (superimposed). (Courtesy of Dr. D. M. Pelz.)
Tight junctions between cells of the choroid epithelium and arachnoid prevent diffusion of plasma proteins into the CSF from the extracellular spaces of the choroid plexus and dura mater, respectively. Molecules of all sizes can diffuse freely between the CSF and the extracellular spaces of the CNS.
The entry of small molecules into the brain is restricted by carrier mechanisms within the endothelial cells of the cerebral blood vessels. These regulate the transport of glucose (the GLUT-1 transporter), amino acids (the L-1 transporter), and other substances from the blood to the neurons and neuroglia. An efflux transporter (P-glycoprotein) returns unwanted hydrophobic substances from the endothelial cytoplasm to the blood. The composition of CSF is similarly controlled by the choroid epithelial cells.
In a few small regions known as circumventricular organs (e.g., the area postrema in the medulla, the subfornical organ, and the neurohypophysis), the blood-brain barrier is lacking. Sensory and autonomic ganglia are permeated by plasma proteins and so are spinal nerve roots. The capillaries within the endoneurium of a peripheral nerve are partly permeable to proteins, and the innermost layer of the perineurium (see Chapter 3) restricts diffusion of proteins from the epineurium, which has fully permeable blood vessels.
The blood-brain barrier is defective for 2 to 3 weeks after injury, and it also fails in various pathological states, such as inflammatory
and neoplastic diseases. It is possible to make images of sites of abnormal vascular permeability by administering an appropriate radioactive tracer and scanning the head for the emitted radiation. Other tracers (gadolinium compounds) make permeable regions visible in images produced by nuclear magnetic resonance imaging.
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