Blood supply of the brain

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5 Blood supply of the brain

1 On simple outline drawings of the lateral, medial, and inferior surfaces of a cerebral hemisphere, learn to shade in the territories of the three cerebral arteries.

2 Identify the main sources of arterial supply to the internal capsule.

3 Become familiar with carotid and vertebral angiograms.

4 Be able to list the territories supplied by the vertebral and basilar arteries.

5 Identify the two blood–brain barriers. Be able to understand why, for example, shallow breathing following abdominal surgery may tip a patient into coma.

Because interpretation of the symptoms caused by cerebrovascular accidents requires prior understanding of brain function, Clinical Panels on this subject are placed in the final chapter.

A Clinical Panel on blood–brain barrier pathology is placed in the present chapter because the symptoms are of a general nature.

Introduction

The brain is absolutely dependent on a continuous supply of oxygenated blood. It controls the delivery of blood by sensing the momentary pressure changes in its main arteries of supply, the internal carotids. It controls the arterial oxygen tension by monitoring respiratory gas levels in the internal carotid artery and in the cerebrospinal fluid (CSF) beside the medulla oblongata. The control systems used by the brain are exquisitely sophisticated, but they can be brought to nothing if a distributing artery ruptures spontaneously or is rammed shut by an embolus.

Arterial Supply of the Forebrain

The blood supply to the forebrain is derived from the two internal carotid arteries and from the basilar artery (Figure 5.1).

Figure 5.1 (A) Brain viewed from below, showing background structures related to the circle of Willis. Part of the left temporal lobe (to right of picture) has been removed to show the choroid plexus in the inferior horn of the lateral ventricle. (B) The arteries comprising the circle of Willis. The four groups of central branches are shown; the thalamoperforating artery belongs to the posteromedial group, and the thalamogeniculate artery belongs to the posterolateral group. ACA, MCA, PCA, anterior, middle, posterior cerebral arteries; ICA, internal carotid artery.

Each internal carotid artery enters the subarachnoid space by piercing the roof of the cavernous sinus. In the subarachnoid space, it gives off ophthalmic, posterior communicating, and anterior choroidal arteries before dividing into the anterior and middle cerebral arteries.

The basilar artery divides at the upper border of the pons into the two posterior cerebral arteries. The cerebral arterial circle (circle of Willis) is completed by a linkage of the posterior communicating artery with the posterior cerebral on each side, and by linkage of the two anterior cerebrals by the anterior communicating artery.

The choroid plexus of the lateral ventricle is supplied from the anterior choroidal branch of the internal carotid artery and by the posterior choroidal branch from the posterior cerebral artery.

Dozens of fine central (perforating) branches are given off by the constituent arteries of the circle of Willis. They enter the brain through the anterior perforated substance beside the optic chiasm and through the posterior perforated substance behind the mammillary bodies. They have been classified in various ways but can be conveniently grouped into short and long branches. Short central branches arise from all the constituent arteries and from the two choroidal arteries. They supply the optic nerve, chiasm, and tract, and the hypothalamus. Long central branches arise from the three cerebral arteries. They supply the thalamus, corpus striatum, and internal capsule. They include the striate branches of the anterior and middle cerebral arteries.

Anterior cerebral artery (Figure 5.2)

The anterior cerebral artery passes above the optic chiasm to gain the medial surface of the cerebral hemisphere. It forms an arch around the genu of the corpus callosum, making it easy to identify in a carotid angiogram (see later). Close to the anterior communicating artery, it gives off the medial striate artery, also known as the recurrent artery of Heubner (pron.‘Hoibner’), which contributes to the blood supply of the internal capsule. Cortical branches of the anterior cerebral artery supply the medial surface of the hemisphere as far back as the parietooccipital sulcus (Table 5.1). The branches overlap on to the orbital and lateral surfaces of the hemisphere.

Figure 5.2 Medial view of the right hemisphere, showing the cortical branches and territories of the three cerebral arteries. ACA, PCA, anterior, posterior cerebral arteries.

Table 5.1 Named cortical ^a branches of the anterior cerebral artery

Branch	Territory
Orbitofrontal	Orbital surface of frontal lobe
Polar frontal	Frontal pole
Callosomarginal	Cingulate and superior frontal gyri; paracentral lobule
Pericallosal	Corpus callosum

^a The term cortical is conventional. Terminal is better, because these arteries also supply the underlying white matter.

Middle cerebral artery (Figure 5.3)

The middle cerebral artery is the main continuation of the internal carotid, receiving 60–80% of the carotid blood flow. It immediately gives off important central branches, then passes along the depth of the lateral fissure to reach the surface of the insula. There it usually breaks into upper and lower divisions. The upper division supplies the frontal lobe, the lower division supplies the parietal and temporal lobes and the midregion of the optic radiation. Named branches and their territories are listed in Table 5.2. Overall, the middle cerebral supplies two-thirds of the lateral surface of the brain.

Figure 5.3 Lateral view of right cerebral hemisphere, showing the cortical branches and territories of the three cerebral arteries.

Table 5.2 Cortical branches of the middle cerebral artery

Origin	Branch(es)	Territory
Stem	Frontobasal	Orbital surface of frontal lobe
Stem	Anterior temporal	Anterior temporal cortex
Upper division	Prefrontal	Prefrontal cortex
	Precentral	Premotor areas
	Central	Pre- and postcentral gyri
	Postcentral	Postcentral and anterior parietal cortex
	Parietal	Posterior parietal cortex
Lower division	Middle temporal	Midtemporal cortex
	Temporooccipital	Temporal and occipital cortex
	Angular	Angular and neighboring gyri

The central branches of the middle cerebral include the lateral striate arteries (Figure 5.4). These arteries supply the corpus striatum, internal capsule, and thalamus. Occlusion of one of the lateral striate arteries is the chief cause of classic stroke, where damage to the pyramidal tract in the posterior limb of the internal capsule causes hemiplegia, a term denoting paralysis of the contralateral arm, leg, and lower part of face.

Figure 5.4 Distribution of perforating branches of the middle cerebral, anterior choroidal, and posterior cerebral arteries (schematic). The anterior choroidal artery arises from the internal carotid.

Note: Additional information on the blood supply of the internal capsule is provided in Chapter 35.

Posterior cerebral artery (Figures 5.2 and 5.5)

The two posterior cerebral arteries are the terminal branches of the basilar. However, in embryonic life they arise from the internal carotid, and in about 25% of individuals the internal carotid persists as the primary source of blood on one or both sides, by way of a large posterior communicating artery.

Figure 5.5 View from below the cerebral hemispheres, showing the cortical branches and territories of the three cerebral arteries. ACA, MCA, PCA, anterior, middle, posterior cerebral arteries; ICA, internal carotid artery.

Close to its origin, each posterior cerebral artery gives branches to the midbrain and a posterior choroidal artery to the choroid plexus of the lateral ventricle. Additional, central branches are sent into the posterior perforated substance (Figure 5.1). The main artery winds around the midbrain in company with the optic tract. It supplies the splenium of the corpus callosum and the cortex of the occipital and temporal lobes. Named cortical branches and their territories are given in Table 5.3.

Table 5.3 Named cortical branches of the posterior cerebral artery

Branch	Artery	Territory
Lateral	Anterior temporal	Anterior temporal cortex
	Posterior temporal	Posterior temporal cortex
	Occipitotemporal	Posterior temporal and occipital cortex
Medial	Calcarine	Calcarine cortex
	Parietooccipital	Cuneus and precuneus
	Callosal	Splenium of corpus callosum

The central branches, called thalamoperforating and thalamogeniculate, supply the thalamus, subthalamic nucleus, and optic radiation.

Note: Additional information on the central branches is provided in Chapter 35.

Neuroangiography

The cerebral arteries and veins can be displayed under general anesthesia by rapid injection of a radiopaque dye into the internal carotid or vertebral artery, followed by serial radiography every 2 s. The dye completes its journey through the arteries, brain capillaries, and veins in about 10 s. The arterial phase of the journey yields either a carotid angiogram or a vertebrobasilar angiogram. Improved vascular definition in radiographs of the arterial phase or of the venous phase can be procured by a process of subtraction, whereby positive and negative images of the overlying skull are superimposed on one another, thereby virtually deleting the skull image.

A relatively recent technique, three-dimensional angiography, is based on simultaneous angiography from two slightly separate perspectives.

Arterial phases of carotid angiograms are shown in Figures 5.6–5.8.

Figure 5.6 Arterial phase of a carotid angiogram, lateral view. Contrast medium injected into the left internal carotid artery is passing through the anterior and middle cerebral arteries (ACA, MCA). The base of the skull is shown in hatched outline. ICA, internal carotid artery.

(From an original series kindly provided by Dr. Michael Modic, Department of Radiology, The Cleveland Clinic Foundation.)

Figure 5.7 Arterial phase of a right carotid angiogram, anteroposterior view. Note some perfusion of left anterior cerebral artery (ACA) territory (via the anterior communicating artery). ICA, internal carotid artery; MCA, middle cerebral artery. (Angiogram kindly provided by Dr. Pearse Morris, Director, Interventional Neuroradiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.)

Figure 5.8 (A) Excerpt from a conventional carotid angiogram, anteroposterior view, showing an aneurysm attached to the middle cerebral artery. (B) Excerpt from a three-dimensional image of the same area. ACA, MCA, anterior and middle cerebral arteries; ICA, internal carotid artery.

(Originals kindly provided by Dr. Pearse Morris, Director, Interventional Neuroradiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.)

Figure 5.9 was taken at the parenchymal phase, when the dye is filling a web of minute terminal branches of the anterior and middle cerebral arteries, some of these anastomosing on the brain surface but most occupying the parenchyma, i.e cortex and subjacent white matter.

Figure 5.9 Parenchymal phase of a carotid angiogram, anteroposterior view. ACA, MCA, anterior and middle cerebral arteries; ICA, internal carotid artery.

(Angiogram kindly provided by Dr. Pearse Morris, Director, Interventional Neuroradiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.)

Arterial Supply to Hindbrain

The brainstem and cerebellum are supplied by the vertebral and basilar arteries and their branches (Figure 5.10).

Figure 5.10 Arterial supply of hindbrain.

The two vertebral arteries arise from the subclavian arteries and ascend the neck in the foramina transversaria of the upper six cervical vertebrae. They enter the skull through the foramen magnum and unite at the lower border of the pons to form the basilar artery. The basilar artery ascends to the upper border of the pons and divides into two posterior cerebral arteries (Figures 5.11 and 5.12).

Figure 5.11 Vertebrobasilar angiogram, lateral view. Contrast medium was injected into the left vertebral artery. Basilar supply to the upper half of the cerebellum is somewhat obscured by overlying posterior parietal branches of the posterior cerebral artery. PCA, posterior cerebral artery; PICA, posterior inferior cerebellar artery.

(From an original series kindly provided by Dr. Michael Modic, Department of Radiology, The Cleveland Clinic Foundation.)

Figure 5.12 Vertebrobasilar angiogram, Townes’s view (from above and in front), showing the vertebrobasilar arterial system. Note the large aneurysm arising from the bifurcation point of the basilar artery and accounting for the patient’s persistent headache. AICA, anterior inferior cerebellar artery; PICA, posterior inferior cerebellar artery.

(Angiogram kindly provided by Dr. Pearse Morris, Director, Interventional Neuroradiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.)

All primary branches of the vertebral and basilar arteries give branches to the brainstem.

Vertebral branches

The posterior inferior cerebellar artery supplies the side of the medulla before giving branches to the cerebellum. Anterior and posterior spinal arteries supply the ventral and dorsal medulla, respectively, before descending through the foramen magnum.

Basilar branches

The anterior inferior cerebellar and superior cerebellar arteries supply the side of the pons before giving branches to the cerebellum. The anterior inferior cerebellar usually gives off the labyrinthine artery to the inner ear.

About a dozen pontine arteries supply the full thickness of the medial part of the pons.

The midbrain is supplied by the posterior cerebral artery, and by the posterior communicating artery linking the posterior cerebral to the internal carotid.

Venous Drainage of the Brain

The venous drainage of the brain is of great importance in relation to neurosurgical procedures. It is also important to the professional neurologist, because a variety of clinical syndromes can be produced by venous obstruction, venous thrombosis, and congenital arteriovenous communications. In general medical practice, however, problems (other than subdural hematomas, Ch. 4) caused by cerebral veins are rare in comparison with arterial disease.

The cerebral hemispheres are drained by superficial and deep cerebral veins. Like the intracranial venous sinuses, they are devoid of valves.

Superficial veins

The superficial cerebral veins lie in the subarachnoid space overlying the hemispheres. They drain the cerebral cortex and underlying white matter, and empty into intracranial venous sinuses (Figures 5.13A, 5.14, and 5.15).

Figure 5.13 Cerebral veins. (A) Superficial veins viewed from the right side; arrows indicate direction of blood flow. (B) Deep veins viewed from above.

Figure 5.14 Internal carotid angiogram, venous phase, lateral view. The dye is draining into the dural venous sinuses.

(Photograph kindly provided by Dr. James Toland, Department of Radiology, Beaumont Hospital, Dublin, Ireland.)

Figure 5.15 Internal carotid angiogram, venous phase, anteroposterior view. Same patient as in Figure 5.6; this picture taken circa 8 s later. The vascular pattern is unusual, in that the left rather than the right transverse sinus is dominant.

(Angiogram kindly provided by Dr. Pearse Morris, Director, Interventional Neuroradiology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA.)

The upper part of each hemisphere drains into the superior sagittal sinus. The middle part drains into the cavernous sinus (as a rule) by way of the superficial middle cerebral vein. The lower part drains into the transverse sinus.

Deep veins (Figure 5.13B)

The deep cerebral veins drain the corpus striatum, thalamus, and choroid plexuses.

A thalamostriate vein drains the thalamus and caudate nucleus. Together with a choroidal vein, it forms the internal cerebral vein. The two internal cerebral veins unite beneath the corpus callosum to form the great cerebral vein (of Galen).

A basal vein is formed beneath the anterior perforated substance by the union of anterior and deep middle cerebral veins. The basal vein runs around the crus cerebri and empties into the great cerebral vein.

Finally, the great cerebral vein enters the midpoint of the tentorium cerebelli. As it does so, it unites with the inferior sagittal sinus to form the straight sinus. The straight sinus empties in turn into the left (occasionally, right, as we shall see) transverse sinus.

Regulation of Blood Flow

Under normal conditions, cerebral blood flow (perfusion) amounts to 700–850 mL per minute, accounting for 20% of the total cardiac output. The blood flow is primarily controlled by autoregulation, which is defined as the capacity of a tissue to regulate its own blood supply.

The most rapid source of autoregulation is the intraluminal pressure within the arterioles. Any increase in pressure elicits a direct, myogenic response. When other factors are controlled (in animal experiments), the myogenic response is sufficient to maintain steady-state perfusion of the brain within a systemic blood pressure range of 80–180 mmHg (11–24 kPa).

A second powerful source of autoregulation in the central nervous system (CNS) is the H⁺ ion concentration in the extracellular fluid (ECF) surrounding the arterioles within the brain parenchyma. Generalized relaxation of arteriolar smooth muscle tone is produced by hypercapnia (excess plasma Pco₂). On the other hand, hypocapnia leads to arteriolar constriction.

Local blood flow increases within cortical areas and deep nuclei involved in particular motor, sensory or cognitive tasks. Local arteriolar relaxation can be accounted for by a rise in K⁺ levels caused by propagation of action potentials, and by a rise in H⁺ caused by increased cell metabolism.

The Blood–Brain Barrier

The nervous system is isolated from the blood by a barrier system that provides a stable and chemically optimal environment for neuronal function. The neurons and neuroglia are bathed in brain extracellular fluid (ECF), which accounts for 15% of total brain volume.

The extracellular compartments of the CNS are shown diagrammatically in Figure 5.16. As previously described (Ch. 4), CSF secreted by the choroid plexuses circulates through the ventricular system and the subarachnoid space before passing through the arachnoid villi into the dural venous sinuses. In addition, CSF diffuses passively through the ependyma–glial membrane lining the ventricles and enters the brain extracellular spaces. It adds to the ECF produced by the capillary bed and by cell metabolism, and it diffuses through the pia–glial membrane into the subarachnoid space. This ‘sink’ movement of fluid compensates for the absence of lymphatics in the CNS.

Figure 5.16 Extracellular compartments of the brain. Arrows indicate circulation of cerebrospinal fluid.

Metabolic water is the only component of the CSF that does not pass through the blood–brain barrier. It carries with it any neurotransmitter substances that have not been recaptured following liberation by neurons, and it accounts for the presence in the subarachnoid space of transmitters and transmitter metabolites that could not penetrate the blood–brain barrier.

Relative contributions to the CSF obtained from a spinal tap are approximately as follow:

• choroid plexuses, 60%

• capillary bed, 30%

• metabolic water, 10%.

The blood–brain barrier has two components. One is at the level of the choroid plexus, the other resides in the CNS capillary bed.

Blood–CSF barrier (Figure 5.17)

The blood–CSF barrier resides in the specialized ependymal lining of the choroid plexuses. This choroidal epithelium differs from the general ependymal epithelium in three ways.

1 Cilia are almost completely replaced by microvilli.

2 The cells are bonded by tight junctions. These pericellular belts of membrane fusion are the actual site of the blood–CSF barrier.

3 The epithelium contains numerous enzymes specifically involved in transport of ions and metabolites.

Figure 5.17 (A) Diagram of blood–cerebrospinal fluid barrier. (B) Ultrastructure of choroidal epithelium. The epithelial cells are rich in mitochondria and granular endoplasmic reticulum. Apical regions of adjacent cells are bonded by a tight junction (arrow).

(From Pannese 1994, with permission of Thieme.)

Blood–ECF barrier (Figure 5.18)

The blood–ECF barrier resides in the CNS capillary bed, which differs from that of other capillary beds in three ways.

1 The endothelial cells are bonded by tight junctions.

2 Pinocytotic vesicles are rare, and fenestrations are absent.

3 The cells contain the same transport systems as those of the choroidal epithelium.

Figure 5.18 (A) Diagram of blood–extracellular fluid barrier. (Astrocytes are described in Ch. 6.) (B) Central nervous system capillary. In this transverse section, a single endothelial cell completely surrounds the lumen, its edges being sealed by a tight junction (inset). Outside its basement membrane, the capillary is invested with an astrocytic sheath.

(From Pannese 1994, with permission of Thieme.)

Roles of microvascular pericytes

Pericytes are in cytoplasmic continuity with the endothelial cells, by way of gap junctions. Tissue culture studies have provided strong evidence for their primary roles in capillary angiogenesis during development and in the production and maintenance of the tight junctions.

Pericytes express receptors for vasoactive mediators, including norepinephrine (noradrenaline), vasopressin, and angiotensin II, all indicative of a role in cerebrovascular autoregulation. In the presence of chronic hypertension, they strengthen the capillary bed by undergoing hypertrophy, hyperplasia, and internal production of cytoplasmic contractile protein filaments.

Pericytes are equipped for a hemostatic function, having an appropriate membrane surface for assembly of the prothrombin complex.

Pericytes are also phagocytic, and possess immunoregulatory cytokines.

The surface area of the brain capillary bed is about the size of a tennis court! This huge area accounts for the brain’s consumption of 20% of basal oxygen intake by the lungs. The density of the cortical capillary bed is demonstrated in the latex cast shown in Figure 5.19.

Figure 5.19 Latex injection cast of the blood vessels in human postmortem brain. The convoluted whitish threads represent cortical capillaries.

(From Duvernoy et al. 1981, with permission.)

Functions of the blood–brain barrier

• Modulation of the entry of metabolic substrates. Glucose, in particular, is a fundamental source of energy for neurons. The level of glucose in the brain ECF is more stable than that of the blood, because the specific carrier becomes saturated when blood glucose rises and becomes hyperactive when it falls.

• Control of ion movements. Na⁺–K⁺ ATPase in the barrier cells pumps sodium into the CSF and pumps potassium out of the CSF into the blood.

• Prevention of access to the CNS by toxins and by peripheral neurotransmitters escaping into the bloodstream from autonomic nerve endings.

For some clinical notes concerning the blood–brain barrier, see Clinical Panel 5.1. Clinical Panel 5.2 describes the knock-on effects of raised intracranial pressure.

Clinical Panel 5.1 Blood–brain barrier pathology

The following five conditions are associated with breakdown of the blood–brain barrier:

1 Patients suffering from hypertension are liable to attacks of hypertensive encephalopathy should the blood pressure exceed the power of the arterioles to control it. The pressure may then open the tight junctions of the brain capillary endothelium. Rapid exudation of plasma causes cerebral edema with severe headache and vomiting, sometimes progressing to convulsions and coma.

2 In patients with severe hypercapnia brought about by reduced ventilation of the lungs (as in pulmonary or heart disease, or after surgery), relaxation of arteriolar muscle may be sufficient to induce cerebral edema even if the blood pressure is normal. In this case, the edema may be expressed by mental confusion and drowsiness progressing to coma.

3 Brain injury, whether from trauma or spontaneous hemorrhage, leads to edema owing to the osmotic effects of tissue damage (and other factors).

4 Infections of the brain or meninges are accompanied by breakdown of the blood–brain barrier, perhaps because of the large-scale emigration of leukocytes through the brain capillary bed. The breakdown can be exploited because the porous capillary walls will permit the passage of non–lipid-soluble antibiotics.

5 The capillary bed of brain tumors is fenestrated. As a result, radioactive tracers too large to penetrate healthy brain capillaries can be detected within tumors.

Clinical Panel 5.2 Intracranial pressure curve

Figure CP 5.2.1 represents progressive ventricular expansion in an adult case of hydrocephalus. As noted in Clinical Panel 4.3, hydrocephalus can result from obstruction of the fourth ventricular outlets by leptomeningeal webs caused by meningitis. The same effect can be induced by accumulated blood around the base of the brain following spontaneous arterial hemorrhage into the subarachnoid space.

The lateral ventricles are expanding progressively (arrows). The rising intracranial pressure is being monitored by an intraparenchymal pressure monitor. The vascular perfusion pressure rises in parallel.

(1) The pressure–volume curve commences with a relatively flat part: interstitial fluid is displaced into the subarachnoid space; subarachnoid CSF is shifted into the spinal dural sac; and venous blood is squeezed through the intracranial sinuses into the internal jugular vein. (2) ICP rises with increasing speed during the steep part. (3) A critical pressure point is reached where decompensation takes place: the vascular circulation is completely blocked, the vital centers run out of oxygen, the patient loses consciousness and will die unless the CSF is urgently drained through a burr (drill) hole.

Reference

Bodkin PA, Hassan MF, Kane PJ, Brady N, Whittle IR. urgical’ causes of benign intracranial hypertension. J R Soc Med. 2008;101:250-261.

Figure CP 5.2.1 (A) Adult hydrocephalus. Arrows indicate compression of cerebral parenchyma by expanding lateral ventricles. IPM, intraparencymal pressure monitor. (B) Intracranial pressure–CSF volume curve. (Based on Steiner and Andrews 2006.)

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Blood supply of the brain

Introduction

Arterial Supply of the Forebrain

Anterior cerebral artery (Figure 5.2)

Middle cerebral artery (Figure 5.3)

Posterior cerebral artery (Figures 5.2 and 5.5)

Neuroangiography

Arterial Supply to Hindbrain

Vertebral branches

Basilar branches

Venous Drainage of the Brain

Superficial veins

Deep veins (Figure 5.13B)

Regulation of Blood Flow

The Blood–Brain Barrier

Blood–CSF barrier (Figure 5.17)

Blood–ECF barrier (Figure 5.18)

Roles of microvascular pericytes

Functions of the blood–brain barrier

Arteries

Veins

Autoregulation

Blood–brain barrier

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Blood supply of the brain

Anterior cerebral artery (Figure 5.2)

Middle cerebral artery (Figure 5.3)

Posterior cerebral artery (Figures 5.2 and 5.5)

Deep veins (Figure 5.13B)

Blood–CSF barrier (Figure 5.17)

Blood–ECF barrier (Figure 5.18)

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