The cerebral blood supply is derived from the internal carotid artery (ICA) and vertebral arteries. The ICA on either side delivers blood to the brain through its major branches, the middle and anterior cerebral arteries (ACAs), and the anterior choroidal artery (anterior circulation). The two vertebral arteries unite in the midline at the caudal border of the pons to form the basilar artery, which delivers blood to the brainstem and cerebellum, as well as to part of the cerebral hemispheres through its terminal branches, the posterior cerebral arteries (PCAs; posterior circulation). The anterior and posterior circulations communicate with each other through the arterial circle of Willis. There are also many other anastomotic connections among the arteries supplying the brain, and between the intracranial and extracranial circulations; thus, occlusion of a major vessel does not necessarily lead to stroke, because the brain tissue distal to the occlusion may be adequately perfused by collateral vessels.
Protracted interruption of blood flow to a part of the brain causes loss of function and, finally, ischemic necrosis of brain tissue (cerebral infarction or, synonymously, ischemic stroke). Cerebral ischemia generally presents with the sudden onset of a neurological deficit (hence the term stroke), due to loss of function of the affected part of the brain. Sometimes, however, the deficit appears gradually rather than suddenly. The most common causes of ischemia on the arterial side of the cerebral circulation are emboli (usually arising from the heart or from an atheromatous plaque, e.g., in the aorta or carotid bifurcation) and direct occlusion of small or middle-sized vessels by arteriolosclerosis (cerebral microangiopathy, usually due to hypertension). Cerebral ischemia can also be due to impairment of venous drainage (cerebral venous or venous sinus thrombosis).
Another cause of the stroke syndrome is intracranial hemorrhage, which may be either into the brain parenchyma itself (intracerebral hemorrhage) or into the neighboring meningeal compartments (subarachnoid, subdural, and epidural hemorrhage and hematoma).
The blood supply of the spinal cord is mainly provided by the unpaired anterior spinal artery and the paired posterolateral spinal arteries. The anterior spinal artery receives contributions from many segmental arteries. Like the brain, the spinal cord can be damaged by hemorrhage or by ischemia of arterial or venous origin.
Four great vessels supply the brain with blood: the right and left ICAs and the right and left vertebral arteries. The ICAs are of the same caliber on both sides, but the two vertebral arteries are often of very different sizes in a single individual. All of the arteries supplying the brain are anastomotically interconnected at the base of the brain through the arterial circle of Willis. They are also interconnected extracranially through small branches in the muscles and connective tissue, which may become important in certain pathological processes affecting the vasculature, but which are normally too small to be demonstrated.
The structures of the anterior and middle cranial fossae are mainly supplied by the ICAs (the so-called anterior circulation), while the structures of the posterior fossa and the posterior portion of the cerebral hemispheres are mainly supplied by the vertebral arteries (the so-called posterior circulation).
Common carotid artery. The ICA is one of the two terminal branches of the common carotid artery, which, on the right side, arises from the aortic arch in a common (brachiocephalic) trunk that it shares with the right subclavian artery (▶Fig. 11.1). The left common carotid artery usually arises directly from the aortic arch, but there are frequent anatomical variants. In 20% of individuals, the left common carotid artery arises from a left brachiocephalic trunk.
The internal carotid artery originates at the bifurcation of the common carotid artery at the level of the thyroid cartilage and ascends to the skull base without giving off any major branches. It passes through the carotid canal of the petrous bone, where it is separated from the middle ear only by a thin, bony wall, and then enters the cavernous sinus (▶Fig. 11.1). For its further intracranial course, see ▶Arteries of the Anterior and Middle Cranial Fossae.
Anastomotic connections of the arteries of the brain with the external carotid artery. The second branch of the common carotid artery, the external carotid artery, supplies the soft tissues of the neck and face. It makes numerous anastomotic connections with the opposite external carotid artery, as well as with the vertebral arteries (see ▶Fig. 11.11) and the intracranial territory of the ICA (e.g., through the ophthalmic artery [▶Fig. 11.11] or the inferolateral trunk, see ▶Collateral Circulation in the Brain). These connections can dilate in the setting of slowly progressive stenosis or occlusion of the ICA, thereby assuring continued delivery of blood to the brain.
Vertebral artery. The vertebral arteries arise from the subclavian arteries on either side and are often of different caliber on the two sides. The left vertebral artery rarely arises directly from the aortic arch. The vertebral artery travels up the neck in the bony canal formed by the transverse foramina of the cervical vertebrae (▶Fig. 11.1), which it enters at the C6 level (i.e., it does not pass through the transverse foramen of C7). At the level of the atlas (C1), it leaves this bony canal and curves around the lateral mass of the atlas dorsally and medially, sitting in the sulcus of the vertebral artery on the upper surface of the posterior arch of C1. It then runs ventrally between the occiput and the atlas and passes through the atlanto-occipital membrane. It usually penetrates the dura mater at the level of the foramen magnum.
In the subarachnoid space, the vertebral artery curves ventrally and cranially around the brainstem, and then joins the contralateral vertebral artery in front of the caudal portion of the pons to form the basilar artery. The vertebral artery gives off many branches to the muscles and soft tissues of the neck; its major intracranial branches are the posterior inferior cerebellar artery (PICA) and the anterior spinal artery (▶Fig. 11.2). The origin of the PICA (see ▶Arteries of the Posterior Fossa) is just distal to the point where the vertebral artery enters the subarachnoid space; a ruptured aneurysm at the origin of the PICA may, therefore, be extracranial and nonetheless produce an SAH. The branches of the vertebral artery to the spinal cord have a variable anatomy. They supply blood to the upper cervical spinal cord and form anastomoses with segmental spinal arteries arising from the proximal portion of the vertebral artery, and with the nuchal arteries.
After exiting the carotid canal, the ICA courses rostrally, next to the clivus and beneath the dura mater, to the cavernous sinus. It curves upward and backward within the cavernous sinus, forming a loop that is open posteriorly (the carotid siphon, ▶Fig. 11.1). Fine extradural branches of the ICA supply the floor of the tympanic cavity, the dura mater of the clivus, the semilunar ganglion, and the pituitary gland.
Injury or rupture of the ICA within the cavernous sinus produces a “short-circuit” connection between its arterial blood and the venous blood of the sinus (carotid-cavernous fistula). If an intracavernous aneurysm of the ICA ruptures, exophthalmos develops but there is no SAH, because the aneurysm is extradural. The patient’s vision in the ipsilateral eye deteriorates thereafter because of outflow obstruction and congestion of the retinal veins.
Ophthalmic artery. The ICA enters the subarachnoid space medial to the anterior clinoid process. The ophthalmic artery arises at this point from the ICA; it is thus already intradural at its site of origin (▶Fig. 11.1). It enters the orbit together with the optic nerve and supplies not only the contents of the orbit, but also the sphenoid sinus, the ethmoid air cells, the nasal mucosa, the dura mater of the anterior cranial fossa, and the skin of the forehead, root of the nose, and eyelids. The cutaneous branches of the ophthalmic artery form anastomoses with branches of the external carotid artery, which can be an important path for collateral circulation around a stenosis or occlusion of the ICA (ophthalmic collaterals). Ruptured aneurysms or injuries of the ICA distal to the origin of the ophthalmic artery cause SAH.
Posterior communicating artery. The next angiographically visible artery arising from the ICA along its intradural course is the posterior communicating artery (▶Fig. 11.1 and ▶Fig. 11.2), often abbreviated PCommA. In the early stages of embryonic development, this artery is the proximal segment of the PCA, which is at first a branch of the ICA and only later comes to be supplied by the basilar artery. In some 20% of cases, the posterior communicating artery remains the main source of blood for the PCA; this is equivalent to a direct origin of the PCA from the ICA, or fetal origin of the PCA, as it is traditionally called. The fetal pattern, if present, is usually seen only on one side, while the contralateral PCA arises from an asymmetric basilar tip. Sometimes, however, both PCAs arise directly from the ICA through unusually large posterior communicating arteries. In such cases, the basilar tip is smaller than usual, and the basilar artery appears to terminate where it gives off the two superior cerebellar arteries.
The posterior communicating artery ends where it joins the proximal segment of the PCA some 10 mm lateral to the basilar tip. It is a component of the circle of Willis and the most important anastomotic connection between the anterior and posterior circulations.
The origin of the posterior communicating artery from the ICA is a preferred site for the formation of aneurysms. Such so-called posterior communicating artery aneurysms usually arise from the side wall of the ICA, and only rarely from the posterior communicating artery itself.
Anterior choroidal artery. This artery arises from the ICA immediately distal to the posterior communicating artery (▶Fig. 11.2), runs toward the occiput parallel to the optic tract, and then enters the choroidal fissure to supply the choroid plexus of the temporal horn of the lateral ventricle. Along its course, it gives off branches to the optic tract, uncus, hippocampus, amygdala, part of the basal ganglia, and part of the internal capsule. It is clinically significant that the anterior choroidal artery also supplies part of the pyramidal tract. It has anastomotic connections with the lateral posterior choroidal artery (see ▶Fig. 11.10).
The MCA is the largest branch of the ICA (▶Fig. 11.2). After its origin from the ICA above the anterior clinoid process, it travels laterally in the sylvian fissure (lateral sulcus). The main trunk of the MCA gives off numerous perforating branches to the basal ganglia and to the anterior limb and genu of the internal capsule, as well as to the external capsule and claustrum (▶Fig. 11.3).
Major branches of the middle cerebral artery. These are (▶Fig. 11.4): the orbitofrontal (I), prerolandic (II), rolandic (III), anterior parietal (IV), and posterior parietal (V) arteries, the artery of the angular gyrus (VI), and the temporo-occipital, posterior temporal (VII), and anterior temporal (VIII) arteries. The cortical areas supplied by the MCA include, among others, the primary sensory and motor cortices (except for their parasagittal and medial portions), the language areas of Broca and Wernicke, the primary auditory cortex, and the primary gustatory cortex.
Fig. 11.4 Territory and branches of the middle cerebral artery on the dorsolateral convexity of the brain. I: orbitofrontal artery, II: prerolandic artery, III: rolandic artery, IV: anterior parietal artery, V: posterior parietal artery, VI: artery of the angular gyrus, VII: posterior temporal artery, VIII: anterior temporal artery.
The ACA originates from the bifurcation of the ICA and then courses medially and rostrally. The ACAs of the two sides come to lie adjacent to each other across the midline in front of the lamina terminalis; from this location, the two arteries course in parallel upward and posteriorly. This is also the site of the anastomotic connection between the two ACAs through the anterior communicating artery, a further important component of the circle of Willis (see ▶Fig. 11.12). The anterior communicating artery and the neighboring segments of the ACAs are preferred sites for the formation of aneurysms (so-called AComm aneurysms, see ▶Subarachnoid Hemorrhage).
Branches of the anterior cerebral artery. The proximal (basal) segment of the ACA gives off numerous small perforating branches that supply the paraseptal region, rostral portion of the basal ganglia and diencephalon, and the anterior limb of the internal capsule (▶Fig. 11.3). The recurrent artery of Heubner is a large branch of the proximal segment of the ACA that supplies the basal ganglia; it is sometimes visible on an angiogram (see ▶Fig. 11.12).
In their further course, the ACAs wind around the genu of the corpus callosum and then course posteriorly until they reach the central region, where they make anastomotic connections with the PCAs. Along the way, they give off branches to the corpus callosum, the medial surfaces of the cerebral hemispheres, and the parasagittal region. Areas of the brain receiving their blood supply from the ACA include the leg areas of the primary sensory and motor cortices and the cingulate gyrus. The ACA makes anastomotic connections with the MCA as well as the PCA.
Major cortical branches. The major cortical branches of the ACA (▶Fig. 11.5) are the orbital (I), frontopolar (II), frontal, pericallosal (III), callosomarginal (IV), and internal parietal (V) arteries.
Fig. 11.5 Territories and branches of the anterior cerebral, posterior cerebral, and middle cerebral arteries on the medial surface of the brain. I, orbital a; II, frontopolar artery; III, pericallosal artery; IV, callosomarginal artery; V, internal parietal artery; I’, anterior temporal artery; II’, posterior temporal artery; III’, posterior occipital artery; IV’, calcarine artery; V’, parieto-occipital artery.
Just after it enters the dura mater, the vertebral artery gives off branches to the cervical spinal cord. The vascular anatomy in this area is variable, but the anterior spinal artery almost always arises from the intradural portion of the vertebral artery.
Posterior inferior cerebellar artery (PICA). The PICA is the largest branch of the vertebral artery (▶Fig. 11.1, ▶Fig. 11.2, ▶Fig. 11.6, ▶Fig. 11.7, and ▶Fig. 11.8) and likewise arises from its intradural portion, just before the vertebral artery joins its counterpart from the opposite side to form the basilar artery. The PICA supplies the basal portion of the cerebellar hemispheres, the lower portion of the vermis, part of the cerebellar nuclei, and the choroid plexus of the fourth ventricle, as well as the dorsolateral portion of the medulla. It makes numerous anastomotic connections with the remaining cerebellar arteries.
The size of the PICA territory is inversely related to that of the anterior inferior cerebellar artery (AICA) territory; furthermore, the PICA and its territory may be of very different sizes on the two sides. If one PICA is particularly small, the basal portion of the cerebellum will be supplied by the AICA ipsilaterally and the larger PICA contralaterally. A congenitally small (“hypoplastic”) vertebral artery may terminate as the PICA and give off no contribution to the basilar artery, which, in such cases, is simply a continuation of the contralateral vertebral artery. This is a fairly common normal variant.
The basilar artery arises from the union of the right and left vertebral arteries in front of the brainstem at a lower pontine level (▶Fig. 11.2). Its major branches are the two pairs of cerebellar arteries and the PCAs. The basilar artery also gives off numerous small perforating branches to the brainstem—the paramedian branches as well as the short and long circumferential branches (▶Fig. 4.58). Occlusions of these branches produce the brainstem syndromes described in ▶Chapter 4.
Anterior inferior cerebellar artery (AICA). The first major branch of the basilar artery is the AICA (▶Fig. 11.1, ▶Fig. 11.2, ▶Fig. 11.6, ▶Fig. 11.7, and ▶Fig. 11.8), which supplies the flocculus and the anterior portion of the cerebellar hemisphere. Its territory is inversely related in size to the ipsilateral PICA territory: in some individuals, part of the cerebellar hemisphere that is usually supplied by the PICA is actually supplied by the AICA. The AICA also gives off the labyrinthine artery to the inner ear.
Superior cerebellar artery. The superior cerebellar artery (▶Fig. 11.1, ▶Fig. 11.2, ▶Fig. 11.6, ▶Fig. 11.7, and ▶Fig. 11.8) arises from the basilar artery below its tip and supplies the rostral portion of the cerebellar hemisphere and the upper portion of the vermis. As it curves around the midbrain, it gives off branches to the tegmentum.
Basilar tip. The basilar tip (end of the basilar artery) is the site where the artery divides into the two PCAs (▶Fig. 11.2).
The PCA has connections to both the anterior and posterior circulation. Most of the blood flowing within it is usually derived from the basilar tip, but there is also a smaller contribution from the ICA by way of the posterior communicating artery (▶Fig. 11.1; see also posterior communicating artery). At an earlier stage in ontogenetic development, the PCA is a branch of the ICA (as discussed in Posterior communicating artery). The posterior communicating artery joins the PCA some 10 mm distal to the basilar tip. The segment of the PCA proximal to this point is called the precommunicating segment, or, in Fischer’s terminology, the P1 segment, while the segment distal to this point is the postcommunicating or P2 segment. Both the PCA and the posterior communicating artery give off perforating branches to the midbrain and thalamus (▶Fig. 11.3).
The PCA originates at the basilar bifurcation and then curves around the midbrain and enters the ambient cistern, where it has a close spatial relation to the tentorial edge (▶Fig. 11.9). Within the ambient cistern, the PCA divides into its major cortical branches, including the calcarine and occipitotemporal arteries and the temporal branches (▶Fig. 11.5).
Anterior and posterior thalamoperforating arteries. The anterior thalamoperforating artery is a branch of the posterior communicating artery that mainly supplies the rostral portion of the thalamus. The posterior thalamoperforating artery arises from the PCA proximal to the insertion of the posterior communicating artery and supplies the basal and medial portions of the thalamus, as well as the pulvinar (▶Fig. 11.10). The posterior thalamoperforating arteries of the two sides may share a common trunk, called the artery of Percheron; this is often seen in association with unilateral hypoplasia of the P1 segment and fetal origin of the PCA. An alternative nomenclature is sometimes used for the anterior and posterior thalamoperforating arteries, in which the former is called the thalamotuberal artery, and the latter is called the thalamoperforating artery.
Thalamogeniculate artery. This artery arises from the PCA distal to the origin of the posterior communicating artery (▶Fig. 11.10). It supplies the lateral portion of the thalamus.
Medial and lateral posterior choroidal arteries. These also arise distal to the origin of the posterior communicating artery (▶Fig. 11.9 and ▶Fig. 11.10). They supply the geniculate bodies, medial and posteromedial thalamic nuclei, and pulvinar. The medial posterior choroidal artery gives off branches to the midbrain and supplies the choroid plexus of the third ventricle. The lateral posterior choroidal artery supplies the choroid plexus of the lateral ventricle and has an anastomotic connection with the anterior choroidal artery.
Cortical branches of the posterior cerebral artery. The territories of the PCA and MCA vary widely in extent. In some cases, the PCA territory is delimited by the sylvian fissure; in others, the MCA supplies the entire convexity of the brain all the way back to the occipital pole. The visual cortex of the calcarine sulcus is always supplied by the PCA. The optic radiation, however, is often supplied by the MCA, so that homonymous hemianopsia does not always imply an infarct in the territory of the PCA. The PCA supplies not only the occipital lobe but also the medial temporal lobe through its temporal branches.
When the ICA is stenotic, blood is diverted from branches of the external carotid artery into the ICA distal to the stenosis, enabling continued perfusion of the brain. The facial or superficial temporal artery, for example, can form an anastomotic connection with the ophthalmic artery by way of the angular artery; retrograde flow in the ophthalmic artery then takes the blood back into the carotid siphon (▶Fig. 11.11). Collaterals to the ophthalmic artery can also be fed by the buccal artery. Further external-to-internal anastomotic connections exist between the ascending pharyngeal artery and meningeal branches of the ICA. These arteries, usually too small to be seen by angiography, are known collectively as the inferolateral trunk.
Fig. 11.11 Anastomoses of the arteries of the brain. The following collateral pathways are shown: collaterals from the external to the internal carotid circulation: 1, external carotid artery—facial artery—angular artery—internal carotid artery; 2, external carotid artery—superficial temporal artery—angular artery—internal carotid artery. 3, collaterals from the external to the vertebral circulation: external carotid artery—occipital artery—vertebral artery. 4, circle of Willis. 5, leptomeningeal collaterals between the anterior, middle, and posterior cerebral arteries. (Reproduced with permission from Poeck K, Hacke W. Neurologie. 11th ed. Berlin/Heidelberg: Springer: 2001.)
The branches of the external carotid artery and vertebral artery that supply the cervical and nuchal muscles are anastomotically connected at multiple points. The most important branch of the external carotid artery in this respect is the occipital artery. Collaterals can form in either direction (▶Fig. 11.11): proximal occlusion of the vertebral artery can be compensated by blood from nuchal branches of the occipital artery, while occlusion of the common carotid artery or proximal occlusion of the ICA can be compensated by blood entering the anterior circulation from the muscular branches of the vertebral artery by way of the occipital artery. As another example, if a proximal occlusion of the common carotid artery has cut off both the internal and the external cerebral arteries from the circulation, then blood from the vertebral artery can flow in the external carotid artery in retrograde fashion down to the carotid bifurcation, and then up again in the ICA, restoring perfusion in the ICA territory.
The cerebral arteries are connected to each other through a wreathlike arrangement of blood vessels at the base of the brain known as the circle of Willis (after Thomas Willis, an English anatomist of the seventeenth century). This interconnection enables continued perfusion of brain tissue even if one of the great vessels is stenotic or occluded. The circle itself consists of segments of the great vessels and the so-called communicating arteries linking them to one another. Traveling around one side of the circle from anterior to posterior, we find the anterior communicating artery, the proximal (A1) segment of the ACA, the distal segment of the ICA, the posterior communicating artery, the proximal (P1) segment of the PCA, and the basilar tip (▶Fig. 11.12). Decreased blood flow in a great vessel due to slowly progressive stenosis below the circle of Willis can usually be compensated by increased collateral flow around the circle, so that hemodynamic infarction will not occur. There are, however, frequent anatomical variants of the circle of Willis in which one or more of its constituent arterial segments may be hypoplastic or absent. The unlucky combination of a stenotic great vessel with an anatomical variant of the circle of Willis preventing adequate collateral flow can result in hemodynamic infarction (see ▶Case Presentation 11.1 and ▶Fig. 11.2).
The anterior and posterior cerebral circulations are anastomotically connected through the callosal arteries (▶Fig. 11.1). Thus, when the ACA is occluded, blood from the PCA may continue to supply the central region.
Furthermore, the branches of the anterior, posterior, and middle cerebral arteries are anastomotically linked to each other through the arteries of the pia mater and arachnoid (▶Fig. 11.11). There are also leptomeningeal anastomoses linking the branches of the three main cerebellar arteries.
The veins of the brain, unlike those of the rest of the body, do not run together with its arteries. The territories of the cerebral arteries do not coincide with the drainage areas of the cerebral veins. Venous blood from the brain parenchyma crosses the subarachnoid and subdural spaces in short cortical veins whose anatomy is relatively invariable: these include the superior anastomotic vein (of Trolard), the dorsal superior cerebral vein, the superficial middle cerebral vein, and the inferior anastomotic vein (of Labbé) on the lateral surface of the temporal lobe (▶Fig. 11.13).
Venous blood from deep regions of the brain, including the basal ganglia and thalamus, drains into the paired internal cerebral veins and the paired basal veins of Rosenthal. The internal cerebral veins are created by the confluence of the vein of the septum pellucidum (septal vein) with the thalamostriate vein. These four veins, coming from the two sides, join behind the splenium to form the great vein of Galen. From here, venous blood drains into the straight sinus (sinus rectus) and then into the confluence of the sinuses (confluens sinuum, torcular Herophili), which is the junction of the straight sinus, the superior sagittal sinus, and the transverse sinuses of the two sides (▶Fig. 11.14, ▶Fig. 11.15, and ▶Fig. 11.16).
The superficial and deep veins of the brain drain into the cranial venous sinuses formed by double folding of the inner dural membrane (▶Fig. 11.17). Most of the venous drainage from the cerebral convexities travels from front to back in the superior sagittal sinus, which runs in the midline along the attachment of the falx cerebri. At the point in the back of the head where the falx cerebri merges with the tentorium, the superior sagittal sinus is joined by the straight sinus, which runs in the mid-line along the attachment of the tentorium and carries blood from deep regions of the brain. Venous blood from the superior sagittal sinus and straight sinus is then distributed to the two transverse sinuses in the torcular Herophili (“winepress of Herophilus,” after Herophilus of Alexandria); from each transverse sinus, blood drains into the sigmoid sinus, which then continues below the jugular foramen as the internal jugular vein. The sinuses are often asymmetric, and there are a number of anatomical variants of the venous drainage pattern in the region of the torcular.
Blood from the brain drains not only into the internal jugular system, but also, by way of the pterygoid plexus, into the venous system of the viscerocranium. The cavernous sinus, formed by a double fold of dura mater at the base of the skull, also drains some of the venous blood from basal regions of the brain. It mainly receives blood from the temporal lobe and from the orbit (by way of the superior and inferior ophthalmic veins). It drains into a variety of venous channels. One of these is the sigmoid sinus, to which it is connected by the superior and inferior petrosal sinuses. Some of its blood also enters the pterygoid plexus.
Pathologically elevated venous pressure in the cavernous sinus, caused, for example, by the intracavernous rupture of an aneurysm of the ICA, causes reversal of flow in these veins, resulting in chemosis and exophthalmos.
The spinal cord receives blood from an anastomotic network of arteries on its surface. There are three named longitudinal arteries, but these are multiply interconnected as they travel down the spinal cord, so that the vascular pattern resembles a chain of anastomoses rather than three distinct, independent vessels.
Anterior spinal artery. The unpaired (single) anterior spinal artery runs down the ventral surface of the spinal cord at the anterior edge of the anterior median fissure. It receives segmental contributions from a number of arteries (see below) and supplies the ventral part of the spinal gray matter through perforating vessels known as the sulcocommissural arteries. These arteries branch off segmentally from the anterior spinal artery and run transversely through the median fissure, from which they enter the parenchyma. Each sulcocommissural artery supplies one half of the spinal cord. Important structures supplied by the anterior spinal artery include the anterior horns, the lateral spinothalamic tract, and part of the pyramidal tract (▶Fig. 11.18).
Posterolateral spinal arteries. The posterolateral spinal arteries are the major longitudinal vessels on the dorsal side of the spinal cord; they run down the cord between the posterior roots and the lateral columns on either side. Like the anterior spinal artery, they arise from a confluence of segmental arteries; this confluence can be incomplete in places. The posterolateral spinal arteries supply the posterior columns, the posterior roots, and the dorsal horns (▶Fig. 11.18). The longitudinal axes are connected by radicular anastomoses. These supply the anterior and lateral columns through perforating branches.
The arteries of the spinal cord are interconnected by many anastomoses. Thus, proximal stenosis or occlusion of one of these arteries is usually asymptomatic. In the periphery, however, the arteries of the spinal cord are functional end arteries; intramedullary embolic occlusion of a sulcocommissural artery therefore causes infarction of the spinal cord.
The embryonic spinal cord receives its blood supply from segmental arteries, in accordance with the metameric segmentation of the spine. Over the course of development, many of these arteries regress, leaving only a few major ones to supply the cord. There is no way to know which of the original segmental arteries has persisted in the ature individual, except by angiography. Yet the blood supply of the spinal cord does receive relatively constant contributions from a number of segmental levels (▶Fig. 11.19).
In the upper cervical region, the anterior spinal artery receives most of its blood from the vertebral artery. In principle, both vertebral arteries may supply blood to the anterior spinal artery, but the vertebral artery of one side is usually dominant. Further down the cord, the anterior and posterior longitudinal vessels receive most of their blood either from the vertebral artery or from cervical branches of the subclavian artery (or both). Spinal cord arteries preferentially arise from the costocervical or thyrocervical trunk. From T3 downward, the anterior spinal artery is fed by aortic branches: the thoracic and lumbar segmental arteries, in addition to the branches that they give off to the musculature, connective tissue, and bones, also contribute a few branches to the anterior spinal artery or the posterolateral spinal artery. These spinal branches are the segmental spinal cord arteries that did not regress during embryonic development. Each one divides into an anterior and a posterior branch, which enter the spinal canal with the anterior and posterior root, respectively. Because the spinal cord elongates to a lesser extent than the vertebral column during development, each radicular artery enters the spinal cord some distance above its level of origin. There is usually one particularly large segmental artery supplying the lower spinal cord, arising at the level of the ninth thoracic vertebra, which is called the great radicular artery or, more commonly, the artery of Adamkiewicz after its original describer. This artery is often involved in arteriovenous fistulae. The developmental “ascent” of the spinal cord makes this artery join the anterior spinal artery at an acute angle (hairpin configuration).
The venous blood of the spinal cord drains into epimedullary veins that form a venous network in the subarachnoid space, called the internal spinal venous plexus or the epimedullary venous network. These vessels communicate via radicular veins with the epidural venous plexus (external venous plexus, anterior and posterior external vertebral venous plexus). The venous blood then drains from the epidural venous plexus into the large veins of the body. The venous drainage of the spinal cord is shown in detail in ▶Fig. 11.20.
The finite ability of the radicular veins to drain blood from the epimedullary veins may be exceeded in the presence of arteriovenous malformations, even when the shunt volume is relatively low. The result is a rapid increase of venous pressure. Even small pressure increases can damage spinal cord tissue (see section on impaired venous drainage, ▶Impaired Venous Drainage).
Ischemic lesions of the brain parenchyma are caused by persistent disruption of the brain′s blood supply, usually either by blockage of the supplying (arterial) vessels or, more rarely, by an impediment to venous outflow leading to stasis of blood in the brain, with secondary impairment of the delivery of oxygen and nutrients.
The central nervous system has a very high demand for energy that can only be met by the continuous, uninterrupted delivery of metabolic substrates. Under normal conditions, this energy is derived exclusively from the aerobic metabolism of glucose. The brain has no way of storing energy to tide itself over potential interruptions of substrate delivery. If its neurons are not given enough glucose and oxygen, they can cease functioning within seconds.
Very different amounts of energy are needed to keep brain tissue alive (structurally intact) and to keep it functioning. Even under normal conditions, brain perfusion varies markedly from one region to another: values of 80 to 120 mL/100 g/min are normal for gray matter, while 20 to 40 mL/100 g/min sometimes suffices for white matter. The minimal blood flow requirement for maintenance of structure is about 5 to 8 mL per 100 g per minute (in the first hour of ischemia). In contrast, the minimal blood flow requirement for continued function is 20 mL per 100 g per minute. It follows that hypoperfusion may give rise to a functional deficit in the absence of death of tissue (infarction). If the endangered blood supply is rapidly restored, as by spontaneous or therapeutic thrombolysis or thrombectomy, the brain tissue remains undamaged and recovers its function as before, i.e., the neurological deficit regresses completely. This is the sequence of events in a TIA, which is clinically defined as a transient neurological deficit of no more than 24 hours’ duration. Eighty percent of all TIAs last less than 30 minutes. Their clinical manifestations depend on the particular vascular territory of the brain that is affected. TIAs in the territory of the MCA are common; patients report transient contralateral paresthesiae and sensory deficits, as well as transient contralateral weakness. Such attacks are sometimes hard to distinguish from focal epileptic seizures. Ischemia in the vertebrobasilar territory, on the other hand, causes transient brainstem symptoms and signs, including vertigo.
If hypoperfusion persists longer than the brain tissue can tolerate, cell death ensues. Ischemic stroke is not reversible. Cell death with collapse of the blood–brain barrier results in an influx of water into the infarcted brain tissue (accompanying cerebral edema). The infarct thus begins to swell within hours of the ischemic event, is maximally swollen a few days later, and then gradually contracts again.
In patients with large infarcts with extensive accompanying edema, clinical signs of life-threatening intracranial hypertension such as headache, vomiting, and disturbances of consciousness must be noted and treated appropriately (see below). The critical infarct volume needed for this situation to arise varies depending on the patient′s age and brain volume. Younger patients with normal-sized brains are at risk after extensive infarction in the territory of the MCA alone. In contrast, older patients with brain atrophy may not be in danger unless the infarct involves the territories of two or more cerebral vessels. Often, in such situations, the patient’s life can be saved only by timely medical treatment to lower the intracranial pressure, or by surgical removal of a large piece of the skull (hemicraniectomy) in order to decompress the swollen brain.
In the aftermath of infarction, the dead brain tissue liquefies and is resorbed. What remains is a cystic cavity filled with CSF, perhaps containing a few blood vessels and strands of connective tissue, along with reactive glial changes (astrogliosis) in the surrounding parenchyma. No scar is formed in the proper sense of the term (proliferation of collagenous tissue), but the reactive glia changes are also referred to as “glial scar” in the literature.
The importance of collateral circulation. The temporal course and extent of cerebral parenchymal edema depend not only on the patency of the blood vessel(s) that normally supply the brain region at risk, but also on the availability of collateral circulation through other pathways. In general, the arteries of the brain are functional end arteries: collateral pathways normally cannot provide enough blood to sustain brain tissue distal to a suddenly occluded artery. If an artery becomes narrow very slowly and progressively, however, the capacity of the collateral circulation can increase. Collaterals can often be “trained” by chronic, mild tissue hypoxia to the extent that they can meet the energetic needs of tissue even if the main arterial supply is blocked for relatively long periods of time. The infarct is then much smaller, and far fewer neurons are lost, than one would otherwise see if the same artery were suddenly occluded from a state of normal patency.