Clinical Neuroanatomy, 27 ed.

CHAPTER 12. Vascular Supply of the Brain

The brain and spinal cord are critically dependent on an uninterrupted supply of oxygenated blood, and thus are dependent on unimpeded flow through the cerebral vessels. About 18% of the total blood volume in the body circulates in the brain, which accounts for about 2% of the body weight. The blood transports oxygen, nutrients, and other substances necessary for proper functioning of the brain and carries away metabolites. Loss of consciousness occurs in less than 15 seconds after blood flow to the brain has stopped, and irreparable damage to the brain tissue occurs within 5 minutes.

Cerebrovascular disease, or stroke, occurs as a result of vascular compromise or hemorrhage and is one of the most frequent sources of neurologic disability. Because the cerebral vessels each tend to irrigate specific territories in the brain, their occlusion results in highly stereotyped syndromes that, even prior to imaging studies, can suggest the site of the vascular lesion.

Nearly half of the admissions to many busy neurologic services are because of strokes. Cerebrovascular disease is the third most common cause of death in industrialized societies. Because thrombolysis—if accomplished in the initial hours after a stroke occurs—can sometimes restore blood flow and improve clinical status, early recognition and treatment of stroke are essential.


Circle of Willis

The circle of Willis (named after the English neuroanatomist Sir Thomas Willis) is a hexagon of vessels that gives rise to all of the major cerebral arteries. It is fed by the paired internal carotid arteries and the basilar artery. When the circle is complete, it contains a posterior communicating artery on each side and an anterior communicating artery. The circle of Willis shows many variations among individuals. The posterior communicating arteries may be large on one or both sides (embryonic type); the posterior cerebral artery may be thin in its first stretch (embryonic type); and the anterior communicating artery may be absent, double, or thin. Despite these variations, occlusion of each of the major cerebral arteries usually produces a characteristic clinical picture.

Characteristics of the Cerebral Arteries

The course of the large arteries (at least in their initial stretches) is largely ventral to the brain in a relatively small region. The arteries course in the subarachnoid space, often for a considerable distance, before entering the brain itself; rupture of a vessel (eg, from an aneurysm that has burst) tends to cause a subarachnoid hemorrhage.

Each major artery supplies a certain territory, separated by border zones (watershed areas) from other territories; sudden occlusion in a vessel affects its territory immediately, sometimes irreversibly.

Principal Arteries

The arterial blood for the brain enters the cranial cavity by way of two pairs of large vessels (Figs 12–1 and 12–2): the internal carotid arteries, which branch off the common carotids, and the vertebral arteries, which arise from the subclavian arteries. The vertebral arterial system supplies the brain stem, cerebellum, occipital lobe, and parts of the thalamus, and the carotids normally supply the remainder of the forebrain. The carotids are interconnected via the anterior cerebral arteries and the anterior communicating artery; the carotids are also connected to the posterior cerebral arteries of the vertebral system by way of two posterior communicating arteries, part of the circle of Willis.


FIGURE 12–1 Major cerebral arteries.


FIGURE 12–2 Circle of Willis and principal arteries of the brain stem.

Vertebrobasilar Territory

After passing through the foramen magnum in the base of the skull, the two vertebral arteries form a single major midline vessel, the basilar artery (Figs 12–2 and 12–3; see also Fig 7–10). This vessel terminates in the interpeduncular cistern in a bifurcation as the left and right posterior cerebral arteries. These may be thin, large, or asymmetric depending on retention of the embryonic pattern (in which the carotid supplies the posterior cerebral arteries).


FIGURE 12–3 Principal arteries on the floor of the cranial cavity (brain removed).

Several pairs of small circumferential arteries arise from the vertebral arteries and their fused continuation, the basilar artery. These are the posterior and anterior inferior cerebellar arteries, the superior cerebellar arteries, and several smaller branches, such as the pontine and internal auditory arteries. These arteries can show asymmetry and variability but, in general, they irrigate critically important parts of the brain. The small penetrating arteries, which branch off the basilar artery, supply vital centers in the brain stem (Fig 12–4).


FIGURE 12–4 Arterial supply of the brain stem. A: Midbrain. The basilar artery gives off paramedian branches that supply the oculomotor (III) nerve nucleus and the red nucleus (RN). A larger branch, the posterior cerebral artery, courses laterally around the midbrain, giving off a basal branch that supplies the cerebral peduncle (CP) and a dorsolateral branch supplying the spinothalamic tract (ST), medial lemniscus (ML), and superior cerebellar peduncle. The posterior cerebral artery continues (upper arrows) to supply the thalamus, occipital lobe, and medial temporal lobe. B: Pons. Paramedian branches of the basilar artery supply the abducens (VI) nucleus and the medial lemniscus (ML). The anterior inferior cerebellar artery gives off a basal branch to the descending motor pathways in the basis pontis (BP) and a dorsolateral branch to the trigeminal (V) nucleus, the vestibular (VIII) nucleus, and the spinothalamic tract (ST) before passing to the cerebellum (upper arrows). C: Medulla. Paramedian branches of the vertebral arteries supply descending motor pathways in the pyramid (P), the medial lemniscus (ML), and the hypoglossal (XII) nucleus. Another vertebral branch, the posterior inferior cerebellar artery, gives off a basal branch to the olivary nuclei (ON) and a dorsolateral branch that supplies the trigeminal (V) nucleus, the vestibular (VIII) nucleus, and the spinothalamic tract (ST) on its way to the cerebellum (upper arrows). (Reproduced, with permission, from Simon RP, Aminoff MJ, Greenberg DA: Clinical Neurology, 4th ed. Appleton & Lange, 1999.)

Carotid Territory

The internal carotid artery passes through the carotid canal of the skull and then curves forward within the cavernous sinus and up and backward through the dura, forming the carotid siphon before reaching the brain (see Fig 12–1). The first branch is usually the ophthalmic artery. In addition to their links with the vertebral system, the carotids branch into a large middle and a smaller anterior cerebral artery on each side (Fig 12–5). The two anterior cerebral arteries usually meet over a short distance in midplane to form a short but functionally important anterior communicating artery. This vessel forms an anastomosis between the left and right hemispheres, which is especially important when one internal carotid becomes occluded. The anterior choroidal artery, directly off the internal carotid, carries blood to the choroid plexus of the lateral ventricles as well as to adjacent brain structures.


FIGURE 12–5 Magnetic resonance image of a horizontal section at the level of the circle of Willis.

Cortical Supply

The middle cerebral artery supplies many deep structures and much of the lateral aspect of the cerebrum; it breaks up into several large branches that course in the depth of the lateral fissure, over the insula, before reaching the convexity of the hemisphere. Because it supplies cortical areas essential for speech in the left hemisphere, the left middle cerebral artery is sometimes called the “artery of speech”. The anterior cerebral artery and its branches course around the genu of the corpus callosum to supply the anterior frontal lobe and the medial aspect of the hemisphere; they extend quite far to the rear. The posterior cerebral artery curves around the brain stem, supplying mainly the occipital lobe and the choroid plexuses of the third and lateral ventricles and the lower surface of the temporal lobe (Figs 12–6and 12–7).


FIGURE 12–6 Arterial supply of the primary motor and sensory cortex (coronal view). Notice the location of the homunculus with respect to the territories of the cerebral arteries. (Reproduced, with permission, from Simon RP, Aminoff MJ, Greenberg DA: Clinical Neurology, 4th ed. Appleton & Lange, 1999.)


FIGURE 12–7 Arterial supply of the primary motor and sensory cortex (lateral view). (Reproduced, with permission, from Simon RP, Aminoff MJ, Greenberg DA: Clinical Neurology, 4th ed. Appleton & Lange, 1999.)

By comparing the territories irrigated by the anterior, middle, and posterior cerebral arteries on the one hand and the homunculus on the other, the student can predict the deficits caused by a stroke affecting the territories irrigated by each of these arteries (see Fig 12–6):

In a stroke affecting the territory of the middle cerebral artery, weakness and sensory loss are most severe in the contralateral face and arm, but the leg may be only mildly affected or unaffected.

In contrast, in a stroke affecting the territory irrigated by the anterior cerebral artery, weakness is most pronounced in the contralateral leg.

Cerebral Blood Flow and Autoregulation

Many physiologic and pathologic factors can affect the blood flow in the arteries and veins of the brain. Under normal conditions of autonomic regulation, the pressure in the small cerebral arteries is maintained at 450 mm H2O. This ensures adequate perfusion of the cerebral capillary beds despite changes in systemic blood pressure. Increased activity in one cortical area is accompanied by a shift in blood volume to that area.


Types of Channels

The venous drainage of the brain and coverings includes the veins of the brain itself, the dural venous sinuses, the dura’s meningeal veins, and the diploic veins between the tables of the skull (Figs 12–8 to 12–10). Emissary veins drain from the scalp, through the skull, into the larger meningeal veins and dural sinuses. Communication exists between most of these channels. Unlike systemic veins, cerebral veins have no valves and seldom accompany the corresponding cerebral arteries.


FIGURE 12–8 Organization of veins and sinuses of the brain. Figure 12–11 provides a frontal view, cut along the plane shown by the vertical line.


FIGURE 12–9 Three-dimensional view of veins and sinuses of the brain, left posterior lateral view.


FIGURE 12–10 Magnetic resonance image of a midsagittal section through the head showing venous channels.

Internal Drainage

The interior of the cerebrum drains into the single midline great cerebral vein (of Galen), which lies beneath the splenium of the corpus callosum. The internal cerebral veins (with their tributaries, the septal, thalamostriate, and choroidal veins) empty into this vein, as do the basal veins (of Rosenthal), which wind (one right and one left) around the side of the midbrain, draining the base of the forebrain. The precentral vein from the cerebellum and veins from the upper brain stem also empty into the great vein, which turns upward behind the splenium and joins the inferior sagittal sinus to form the straight sinus. The venous drainage of the base of the cerebrum is also into the deep middle cerebral vein (coursing in the lateral fissure) and then to the cavernous sinus.

Cortical Veins

Venous drainage of the brain surface is generally into the nearest large vein or sinus, from there to the confluence of the sinuses, and ultimately to the internal jugular vein (see Fig 12–8).

The veins of the cerebral convex surfaces are divided into superior and inferior groups. The 6 to 12 superior cerebral veins run upward on the hemisphere’s surface to the superior sagittal sinus, generally passing under any lateral lacunae. Most of the inferior cerebral veins end in the superficial middle cerebral vein. The inferior cerebral veins that do not end in this fashion terminate in the transverse sinus. Anastomotic veins can be found; these connect the deep middle cerebral vein with the superior sagittal sinus or transverse sinus.

Venous Sinuses

Venous channels lined by mesothelium lie between the inner and outer layers of the dura; they are called intradural (or dural) sinuses. Their tributaries come mostly from the neighboring brain substance. All sinuses ultimately drain into the internal jugular veins or pterygoid plexus. The sinuses may also communicate with extracranial veins via the emissary veins. These latter veins are important for two reasons: The blood can flow through them in either direction, and infections of the scalp may extend by this route into the intracranial structures.

Of the venous sinuses, the following are considered most important:

Superior sagittal sinus: between the falx and the inside of the skull cap.

Inferior sagittal sinus: in the free edge of the falx.

Straight sinus: in the seam between the falx and the tentorium.

Transverse sinuses: between the tentorium and its attachment on the skull cap.

Sigmoid sinuses: S-curved continuations of the transverse sinuses into the jugular veins; a transverse and a sigmoid sinus together form a lateral sinus.

Sphenoparietal sinuses: drain the deep middle cerebral veins into the cavernous sinuses.

Cavernous sinuses: on either side of the sella turcica. The cavernous sinuses receive drainage from multiple sources, including the ophthalmic and facial veins. Blood leaves the cavernous sinuses via the petrosal sinuses (see Fig 12–8). The cavernous sinuses are convoluted, with different chambers separated by fibrous trabeculae; thus, they have the appearance of a cavern. A number of important arteries and cranial nerves are embedded within the cavernous sinus and its walls. The internal carotid artery runs through the cavernous sinus (Fig 12–11). In addition, the oculomotor, trochlear, and abducens nervesrun through the cavernous sinus, as does the ophthalmic division of the trigeminal nerve, together with the trigeminal ganglion.


FIGURE 12–11 The cavernous sinus and associated structures. A: Relationship to skull and brain. B: The cavernous sinus wraps around the pituitary. Several important structures run through the cavernous sinus: the internal carotid artery; the oculomotor, trochlear, and abducens nerves; and the ophthalmic branch of the trigeminal nerve and trigeminal ganglion.

Inferior petrosal sinuses: from the cavernous sinus to the jugular foramen.

Superior petrosal sinus: from the cavernous sinus to the beginning of the sigmoid sinus.

The pressure of the cerebrospinal fluid varies directly with acute changes in venous pressure.


Cerebrovascular disease is the most common cause of neurologic disability in adults and the third most common cause of death in our society. About 500,000 people are disabled or killed by cerebrovascular disease each year in the United States.

Most authorities classify cerebrovascular disease into ischemic and hemorrhagic disorders.

Ischemic Cerebrovascular Disease

As a result of its high metabolic rate and limited energy reserves, the central nervous system (CNS) is uniquely sensitive to ischemia. Ischemia results in rapid depletion of adenosine triphosphate (ATP) stores in the CNS. Because Na+–K+-AT-Pase function is impaired, K+ accumulates in the extracellular space, which leads to neuronal depolarization (see Chapter 3). According to the excitotoxic hypothesis, within gray matter of the CNS, there is an ensuing avalanche of neurotransmitter release (including inappropriate release of excitatory transmitters such as glutamate). This leads to an influx of calcium via glutamate-gated channels as well as voltage-gated calcium channels that are activated as a result of depolarization. Within white matter of the CNS, where synapses are not present, calcium is carried into nerve cells via other routes, including the Na+–Ca2+ exchanger, a specialized molecule that exchanges calcium for sodium. It is generally thought that increased intracellular calcium represents a “final common pathway” leading to irreversible cell injury (the calcium hypothesis of neuronal cell death) because calcium activates a spectrum of enzymes, including proteases, lipases, and endonucleases that damage the neuronal cytoskeleton and plasma membrane.

Transient ischemia, if brief enough, may produce reversible signs and symptoms of neuronal dysfunction. If ischemia is prolonged, however, death of neurons (infarction) occurs and is usually accompanied by persistent neurologic deficits. Because of this time-dependence, ischemic cerebral disease is a medical emergency.

Surrounding the area of infarction, there is often a penumbra, in which neurons have been metabolically compromised and are electrically silent but are not yet dead. Neurons within the penumbra may be salvageable, and various neuroprotective strategies that interfere with calcium influx are being experimentally studied.


Diseases involving vessels of the brain and its coverings have characteristic clinical profiles and can be classified as follows (Table 12–1).

TABLE 12–1 Clinical Profile of Cerebrovascular Disorders.


Occlusive cerebrovascular disorders: These result from arterial or venous thrombosis, or embolism, and can lead to infarction of well-defined parts of the brain. Because each artery irrigates a specific part of the brain, it is often possible, on the basis of the neurologic deficit, to identify the vessel that is occluded.

Transient cerebral ischemia: Transient ischemia, if brief enough, can occur without infarction. Episodes of this type are termed transient ischemic attacks (TIAs). As with occlusive cerebrovascular disease, the neurologic abnormalities often permit the clinician to predict the vessel that is involved.

Hemorrhage: The rupture of a blood vessel is often associated with hypertension or vascular malformations or with trauma.

Vascular malformations and developmental abnormalities: These include aneurysms or arteriovenous malformations (AVMs), which can lead to hemorrhage. Hypoplasia or absence of vessels occurs in some brains.

Degenerative diseases of the arteries: These can lead to occlusion or to hemorrhage.

Inflammatory diseases of the arteries: Inflammatory diseases, including systemic lupus erythematosus, giant cell arteritis, and syphilitic arteritis, can result in occlusion of cerebral vessels, which, in turn, can produce infarction.

The neurologic deficits in cerebral infarcts or hemorrhages—cerebrovascular accidents (CVAs)—develop rapidly (hence the term “stroke”). Patients have sudden, severe focal disturbances of brain function (ie, hemiplegia, aphasia). The deficits appear rapidly (over minutes) or can develop with a stuttering course, over hours. The term stroke is a general one, and further determination of the site (where is the lesion?) and type of disease (what is the lesion?) are essential for correct diagnosis and treatment.

Occlusive Cerebrovascular Disease

Insufficient blood supply to portions of the brain leads to infarction and swelling with necrosis of brain tissue (Figs 12–12 to 12–14A, B; see Table 12–1). Most infarcts are caused by atherosclerosis of the vessels, leading to narrowing, occlusion, or thrombosis; a cerebral embolism, that is, occlusion caused by an embolus (a plug of tissue or a foreign substance) from outside the brain; or other conditions such as prolonged hypotension, drug action, spasm, or inflammation of the vessels. Venous infarction is less common, but may occur when a venous channel becomes occluded.


FIGURE 12–12 Schematic illustration of stages of occlusion of the internal carotid artery. (Modified and reproduced, with permission, from Poirer J, Gray F, Escourolle R: Manual of Basic Neuropathology. 3rd ed. WB Saunders, 1990.)


FIGURE 12–13 Coronal section through the cerebrum showing a large infarct caused by occlusion of the internal carotid artery.


FIGURE 12–14 A. Computed tomography image of a horizontal section of the head showing an infarct caused by middle cerebral artery occlusion. B. Magnetic resonance image of horizontal section of the head from another patient who also sustained an infarct in the distribution of the left middle cerebral artery. This patient presented with sudden onset of aphasia and right-sided weakness. (Courtesy of Joseph Schindler, MD, Yale Medical School.)

The extent of an infarct depends on the presence or absence of adequate anastomotic channels. The extent of the infarct will often confirm to the territory supplied by the occluded artery, as shown in Figure 14A, B. Capillaries from adjacent vascular territories and corticomeningeal capillaries at the surface may reduce the size of the infarct. When arterial occlusion occurs proximal to the circle of Willis, collateral circulation through the anterior communicating artery and posterior communicating arteries may permit sufficient blood flow to prevent infarction. Similarly, in some cases in which the internal carotid artery is occluded in the neck, anastomotic flow in the retrograde direction via the ophthalmic artery, from the external carotid artery, may provide adequate circulation, thus preventing infarction.

Although sudden occlusion can lead to irreparable damage, slowly developing local ischemia may be compensated for by increased flow through anastomoses involving one or more routes: the circle of Willis, the ophthalmic artery (whose branches communicate with external carotid vessels), or corticomeningeal anastomoses from meningeal vessels.

Atherosclerosis of the Brain

The principal pathologic change in the arteries of the brain occurs in the vasculature of the neck and brain, although similar changes may also be present in other systemic vessels. Disturbances in metabolism, especially of fats, are believed to be a prominent associated change. Hypertension accelerates the progression of atherosclerosis and is a treatable risk factor for stroke.

Atheromatous changes in the arterial system are found relatively frequently at postmortem examination among those who have reached middle age (Fig 12–15). They are particularly common in patients with untreated hypertension or with unfavorable lipid profiles. Vessels of all sizes may be affected. A combination of degenerative and proliferative changes can be seen microscopically. The muscularis is the main site of proliferation; the intima may be absent. The areas most often involved are near branchings or confluences of vessels (Fig 12–16 and Table 12–2). The most common and severe atherosclerotic lesions are in the carotid bifurcation. Others occur at the origin of the vertebral arteries, in the upper and lower parts of the basilar artery, and in the internal carotid artery at its trifurcation, the first third of the middle cerebral artery, and the first part of the posterior cerebral artery. Narrowing of vessels severe enough to cause vascular insufficiency is more frequent in older persons.


FIGURE 12–15 Atherosclerosis in arteries at the base of the brain.


FIGURE 12–16 Distribution of degenerative lesions in large cerebral arteries of the circle of Willis. The severity of the lesions is illustrated by the intensity of the shaded areas; the darkest areas show the most severe lesions.

TABLE 12–2 Frequency Distribution (in %) of Arterial Lesions Causing Cerebrovascular Insufficiency.


Cerebral Embolism

The sudden occlusion of a brain vessel by a blood clot, a piece of fat, a tumor, a clump of bacteria, or air abruptly interrupts the blood supply to a portion of the brain and can result in infarction (see Figs 12–13 and 12–14 and Table 12–1). One of the most common causes of cerebral embolism is atrial fibrillation. Other common causes include endocarditis and mural thrombus after myocardial infarction. Atheromatous material can break off from a plaque in the carotid artery and, after being carried distally, occlude smaller arteries.

Transient Cerebral Ischemia

Focal cerebral ischemic attacks, especially in middle- aged and older persons, can be caused by transient occlusion of an already narrow vessel. The cause is thought to be a vasospasm, a small embolus that is later carried away, or thrombosis of a diseased vessel (and subsequent lysis of the clot, or anastomosis). Such TIAs result in reversible ischemic neurologic deficits, such as sudden vertigo or sudden focal weakness, loss of cranial nerve function, or even brief loss of consciousness. These episodes are usually due to ischemia in the territory of an artery within the carotid or vertebrobasilar system. There is usually full recovery from a TIA in less than 24 hours (commonly within 30 minutes). These attacks are considered warning signs of future, or imminent, occlusion and merit a rapid workup as shown in Clinical Illustration 12–1.

Localization of the Vascular Lesion in Stroke Syndromes

The cerebral vessels tend to irrigate particular, well-defined parts of the brain, in patterns that are reproducible from patient to patient. Thus, it is often possible, in stroke syndromes, to identify the affected blood vessel on the basis of the neurologic signs and symptoms, even before imaging studies are carried out.

Carotid artery disease is often accompanied by contralateral weakness or sensory loss. If the dominant hemisphere is involved, there may be aphasia or apraxia. Transient blurring or loss of vision (amaurosis fugax) may occur if there is retinal ischemia. In practice, after occlusion of the internal carotid artery, ischemia is often limited to the territory of the middle cerebral artery, so that weakness predominantly affects the contralateral face and arm. This is because the anterior and posterior cerebral artery territories are nourished via collateral flow from the contralateral circulation via the anterior communicating and posterior communicating arteries. Clinical Illustration 12–1 provides an example.

As predicted from its position with respect to the motor and sensory homunculi, unilateral occlusion of the anterior cerebral artery results in weakness and sensory loss in the contralateral leg (Fig 12–17). In some patients, after bilateral occlusion of the anterior cerebral arteries, there is damage to the frontal lobes, resulting in a state of akinetic mutism, in which the patient is indifferent and apathetic, moving little, and not speaking even though there is no paralysis of the immobile limbs.


FIGURE 12–17 Computed tomography image of a horizontal section of the head, showing an infarct caused by a right-sided anterior cerebral artery occlusion (arrows). Notice the location of the infarct (compare with Figs 12–6 and 12–7). The patient had weakness and numbness of the left leg.

Vertebrobasilar artery disease often presents with vertigo, ataxia (impaired coordination), dysarthria (slurred speech), and dysphasia (impaired swallowing). Vertigo, nausea, and vomiting may be present, and if the oculomotor complex is involved, there may be diplopia (double vision). The brain stem syndromes are discussed in Chapter 7, and those arising from arterial occlusion are summarized in Table 12–3.

TABLE 12–3 Brain Stem Syndromes Resulting from Vascular Occlusion.



A 48-year-old attorney was told he was hypertensive but did not take his blood pressure medications. He was apparently well until 4 days after his birthday, when he had several episodes of blurred vision, “like a shade coming down,” involving his left eye. These attacks each lasted less than an hour. He was referred for neurologic evaluation but canceled the appointment because of a busy schedule. Several weeks later, he complained to his wife of a left-sided headache. She found him a half hour later slumped in a chair, apparently confused and paralyzed on the right side. Neurologic examination in the hospital revealed total paralysis of the right arm and severe weakness of the right face. The leg was only mildly affected. Deep tendon reflexes were initially depressed on the right side but within several days became hyperactive; there was a Babinski response on the right. The patient was globally aphasic; he was unable to produce any intelligible speech and appeared to understand only very simple phrases. A computed tomography (CT) scan revealed an infarct in the territory of the middle cerebral artery of the left side (see Fig 4–3). Angiography revealed occlusion of the internal carotid artery. The patient recovered only minimally.

This tragic case illustrates several points. Although the carotid artery on the left was totally occluded, the patient’s cerebral infarct was limited to the territory of the middle cerebral artery. Even though the anterior cerebral artery arises (together with the middle cerebral artery) from the carotid, the anterior cerebral artery’s territory was spared, probably as a result of collateral flow from other vessels (eg, via the anterior communicating artery). The patient’s functional deficit was nevertheless devastating because much of the motor cortex and the speech areas in the left hemisphere were destroyed by the infarction.

This case reminds us that hypertension represents an important risk factor for stroke, and all patients with hypertension should be carefully evaluated and treated if appropriate. It is not enough to prescribe medication; the physician must follow up and make sure the patient takes the medicine. This patient exhibited several episodes of amaurosis fugax, or transient monocular blindness. These episodes, which are due to ischemia of the retina, often occur in the context of atherosclerotic disease of the carotid artery. Indeed, angiography after this patient’s stroke revealed occlusion of the carotid artery. It has become clear that, in patients with significant stenosis of the carotid artery, endarterectomy (removal of the atherosclerotic material within the artery) may prevent stroke. The probability of a stroke appears to be highest in the period after TIA onset. Any patient with TIAs of recent onset should be evaluated on an urgent basis.

The recent advent of thrombolysis with tPA has made acute stroke a treatble entity if therapy is begun early enough. Strokes, and suspected strokes, should be regarded as “brain attacks,” and patients should be transported to the emergency room without delay.

Newer methods of MRI permit the area of ischemic brain damage (the area of infarction, where neurons have died and are not salvageable) to be distinguished from the area of the brain where perfusion is impaired. Within this region of impaired cerebral perfusion, an ischemic penumbra (at-risk tissue that is ischemic due to impaired blood flow, but not yet in-farcted) can sometimes be seen. Visualization of a salvageable ischemic penumbra can be clinically helpful in identifying patients who are candidates for thrombolysis and/or stenting, and can guide therapy (Fig 12–18).




FIGURE 12–18A, B A: A 41-year-old male experienced sudden onset of right facial droop, right arm and right leg numbness, as well as right hemiplegia. Initial CT head without contrast (left) ruled out intracerebral hemorrhage. CT angiography (right) showed absence of arterial filling due to thrombus in a major segment of the middle cerebral artery (arrow). In addition, a moderate-to-severe stenosis of the origin of the right vertebral artery was found (not shown). B: CT-perfusion maps of time to peak (TTP), cerebral blood flow (CBF), mean transit time (MTT), and cerebral blood volume (CBV) for this patient are shown in the top row. There is a significant mismatch between the area of abnormality on the MTT and CBV maps. Red denotes the ischemic core (not salvageable) and green denotes the tissue at-risk (the ischemic penumbra, in which brain tissue is potentially salvageable). C: The patient was taken to angiography where he received stenting of the right vertebral artery as well as thrombolysis by selective intraarterial tPA (not shown). A follow up CT 24 hours after initial presentation demonstrated the expected ischemic infarct in the cortical and subcortical substance of the left insular region and adjacent frontal and temporal lobes. The originally identified tissue at risk on CT-perfusion maps was salvaged (arrows). The patient’s neurological status continued to improve after intervention and he was left with only mild right facial droop and mild right upper extremity pronator drift two days after initial presentation. (Courtesy of Nils Henninger, M.D.)

Hemorrhagic Cerebrovascular Disease: Hypertensive Hemorrhage

Chronic high blood pressure may result in the formation of small areas of vessel distention—microaneurysms—mostly in small arteries that arise from much larger vessels. A further rise in blood pressure then ruptures these aneurysms, resulting in an intracerebral hemorrhage (see Table 12–3). In order of frequency, the most common sites are the lentiform nucleus, especially the putamen, supplied by the lenticulostriate arteries (Fig 12–19); the thalamus, supplied by posterior perforating arteries off the posterior cerebrobasilar artery bifurcation (Fig 12–20); the white matter of the cerebral hemispheres (lobar hemorrhages); the pons, supplied by small perforating arteries from the basilar artery; and the cerebellum, supplied by branches of the cerebellar arteries. The blood clot compresses and may destroy adjacent brain tissue; cerebellar hemorrhages may compress the underlying fourth ventricle and produce acute hydrocephalus. Intracranial hemorrhages are thus medical emergencies and require prompt diagnosis and treatment.


FIGURE 12–19 Computed tomography image of a horizontal section through the head, showing a hematoma (arrows) in the putamen.


FIGURE 12–20 Hemorrhage in the right posterior thalamus and internal capsule in a 64-year-old woman.

Subarachnoid Hemorrhage

Subarachnoid hemorrhages usually derive from ruptured aneurysms or vascular malformations (Figs 12–21 to 12–23; see Table 12–1). Aneurysms (abnormal distention of local vessels) may be congenital (berry aneurysm) or the result of infection (mycotic aneurysm). One complication of subarachnoid hemorrhage, arterial spasm, can lead to infarcts.


FIGURE 12–21 Computed tomography image of a horizontal section through the head, showing high densities, representing a subarachnoid hemorrhage (arrows) in the sulci.


FIGURE 12–22 A: Computed tomography image of a horizontal section through the head, showing a large aneurysm of the anterior communicating artery. (Reproduced, with permission, from deGroot J: Correlative Neuroanatomy of Computed Tomography and Magnetic Resonance Imaging. Lea & Febiger, 1984.) B: Corresponding angiogram showing the partially thrombosed aneurysm (arrows).


FIGURE 12–23 Magnetic resonance image of a horizontal section through the head, demonstrating an arteriovenous malformation (arrows).


A 44-year-old woman was admitted after a seizure. She was lethargic, with a right facial droop, right hemiparesis, and right hyperreflexia. She complained of headache and a painful neck. A few days later, she seemed slightly more alert and made purposeful movements with her left hand but not her right hand. She was still unresponsive to spoken commands and had a rigid neck. Other findings included papilledema, a right pupil that was smaller than the left, incomplete extraocular movements on the left side (nerve VI function was normal), decreased right corneal reflex, and right nasolabial droop. The patient’s right arm was hypertonic and paretic, but the other extremities were normal. Reflexes appeared normal. The right plantar extensor response was equivocal, but the left was normal.

The blood pressure was 120/85; pulse rate, 60; and temperature, 38 °C (100.4 °F). The white blood count was 11,200/μL, and the erythrocyte sedimentation rate was 30 mm/h.

Where is the lesion? What is the cause of the lesion? What is the differential diagnosis?

A CT scan showed a high-density area in the cisterns, especially on the right side. What is the diagnosis now? Would you request a lumbar puncture with analysis of the cerebrospinal fluid?

Congenital berry aneurysms are seen most frequently in the circle of Willis or in the middle cerebral trifurcation; they are especially common at sites of arterial branching. Aneurysms are seen infrequently in vessels of the posterior fossa. A ruptured aneurysm generally bleeds into the subarachnoid space or, less frequently, into the brain substance itself.

Vascular malformations, especially AVMs, often occur in younger persons and are found on the surface of the brain, deep in the brain substance, or in the meninges (dural AVMs). Bleeding from such malformations can be intracerebral, subarachnoid, or subdural.


A 55-year-old salesman exhibiting signs of confusion was brought to the hospital. The history elicited from his landlady indicated that he drank alcohol excessively. His landlady had entered the apartment on the day of admission because he did not respond to her calls. She found him lying on the floor, incontinent and appearing bewildered; he had also bitten his lip. The landlady remembered that he had been involved in a bar fight 2 months earlier, and 3 weeks previously he had fractured his wrist falling down stairs.

On examination, the patient was unconcerned and disheveled. Bruises on his head and legs were consistent with recent trauma. The liver was palpable 4 cm below the right costal margin. The patient appeared to fall asleep when left alone. Neurologic examination showed normal optic fundi, normal extraocular movements, and no abnormalities that would result from dysfunction of other cranial nerves. When the left hand was extended, it showed a slow downward drift. The reflexes were normal and symmetric, and there was a left-sided plantar extensor response.

Vital signs, complete blood count, and urinalysis were within normal limits. A lumbar puncture showed an opening pressure of 180 mm H2O, xanthochromia, a protein level of 80 mg/dL, and a glucose level of 70 mg/dL. Cell counts in all tubes showed red blood cells, 800/μL; lymphocytes, 20/μL; and polymorphonuclear neutrophils, 4/mL. A CT scan of the head was obtained.

Over the next 36 hours, the patient became deeply obtunded, and a left-sided hemiparesis seemed to develop.

What is the differential diagnosis? What is the most likely diagnosis?

Questions and answers pertaining to Section IV (Chapters 7 through 12) can be found in Appendix D.

Cases are discussed further in Chapter 25.

Subdural Hemorrhage

Tearing of the bridging veins between brain surface and dural sinus is the most frequent cause of subdural hemorrhage (Figs 12–24 and 12–25; see Table 12–1). It can occur as the result of a relatively minor trauma, and some blood may be present in the subarachnoid space. Children (because they have thinner veins) and aged adults with brain atrophy (because they have longer bridging veins) are at greatest risk.


FIGURE 12–24 Magnetic resonance image of a horizontal section through the head, showing a left subdural hematoma (arrows) causing a midline shift.


FIGURE 12–25 Schematic illustration of a subdural hemorrhage.

Epidural Hemorrhage

Bleeding from a torn meningeal vessel (usually an artery) may lead to an extradural (outside the dura) accumulation of blood that can rapidly compress the brain, progressing to herniation or death if not surgically evacuated. Fracture of the skull can cause this type of epidural, or extradural, hemorrhage (Figs 12–26 and 12–27; see Table 12–1). Uncontrolled arterial bleeding may lead to compression of the brain and subsequent herniation. Immediate diagnosis and surgical drainage are essential.


FIGURE 12–26 Schematic illustration of an epidural hemorrhage.


FIGURE 12–27 Computed tomography image of a horizontal section through the head, showing an extradural hematoma and intracerebral contrecoup lesion. (Reproduced, with permission, from deGroot J: Correlative Neuroanatomy of Computed Tomography and Magnetic Resonance Imaging. 21st ed. Appleton & Lange, 1991.)

AVMs and Shunts

AVMs, in which cerebral arteries and veins form abnormal tangles or webs, can occur as developmental anomalies. Whereas some AVMs are clinically silent, others tend to bleed or cause infarction in nearby parts of the brain. Trauma can also cause the rupture of adjacent vessels, allowing arterial blood to flow into nearby veins. For example, in a carotid-cavernous fistula, the internal carotid drains into the cavernous sinus and jugular vein, causing ischemia in the cerebral arteries. There is often pulsating exophthalmos (forward protrusion of the eye in the orbit), and there may be extraocular palsies because of pressure on the oculomotor, trochlear, and abducens nerves, which run through the cavernous sinus. Interventional methods, which involve inserting a balloon or other instrumentation into the shunt via a catheter or surgery, may correct the problem.


Barnett HJ, Mohr JP, Stein BM, Yatsu FM: Stroke—Pathophysiology, Diagnosis, and Management, 3rd ed. Churchill Livingstone, 1998.

Batjer HH, Caplan LR, Friberg L, Greenlee RG, Kopitnik TA, Young WL: Cerebrovascular Disease. Lippincott-Raven, 1997.

Choi DW: Neurodegeneration: Cellular defenses destroyed. Nature 2005;433:696.

Del Zoppo G: TIAs and the pathology of cerebral ischemia. Neurology 2004;62:515.

Felberg RA, Burgin WS, Grotta JC: Neuroprotection and the ischemic cascade. CNS Spectr 2000;5:52.

Fisher CM: Lacunar strokes and infarcts: A review. Neurology 1982;32:871.

Hemmen TM, Zivin JA: Molecular mechanisms in ischemic brain disease. In: Molecular Neurology, Waxman SG (editor). Elsevier, 2007.

Kogure K, Hossmann KA, Siesjo B: Neurology of Ischemic Brain Damage. Elsevier, 1994.

Mohr JP, Choi D, Grotta J, Weir B, Wolf PA: Stroke: Pathophysiology, diagnosis, and management. Lippincott, 2004.

Salamon G: Atlas of the Arteries of the Human Brain. Sandoz, 1973.

Waxman SG, Ransom BR, Stys PK: Nonsynaptic mechanisms of calcium-mediated injury in the CNS white matter. Trends Neurosci 1991;14:461.

If you find an error or have any questions, please email us at Thank you!