Circulation of the Brain

THE BRAIN IS HIGHLY VULNERABLE to disturbance of its blood supply. Anoxia lasting only seconds causes neurological symptoms; when it lasts minutes it can cause irreversible neuronal damage. Blood flow to the central nervous system must efficiently deliver oxygen, glucose, and other nutrients and remove carbon dioxide, lactic acid, and other metabolites. The cerebral vasculature has special anatomical and physiological features that protect the brain. However, when these mechanisms fail, the result is a stroke. Broadly defined, the term stroke, or cerebrovascular accident, refers to the neurological symptoms or signs that result from diseases involving blood vessels. These are usually focal and acute.

The Blood Supply of the Brain Can Be Divided into Arterial Territories

Each cerebral hemisphere is supplied by an internal carotid artery, which arises from the common carotid artery beneath the angle of the jaw, enters the cranium through the carotid foramen, traverses the cavernous sinus (giving off the ophthalmic artery), penetrates the dura, and then divides into the anterior and middle cerebral arteries (Figure C–1).

Figure C-1 The blood vessels of the brain. The circle of Willis is made up of the proximal posterior cerebral arteries, posterior communicating arteries, internal carotid arteries just before their bifurcations, proximal anterior cerebral arteries, and anterior communicating artery. Black areas are common sites of atherosclerosis and occlusion.

The large surface branches of the anterior cerebral artery supply the cortex and white matter of the inferior frontal lobe, the medial surface of the frontal and parietal lobes, and the anterior corpus callosum (Figure C–2). Smaller penetrating branches—including the so-called recurrent artery of Heubner—supply the deeper cerebrum and diencephalon, including limbic structures, the head of the caudate, and the anterior limb of the internal capsule.

Figure C-2 Cerebral arterial areas.

The large surface branches of the middle cerebral artery supply most of the cortex and white matter of the hemisphere’s convexity, including the frontal, parietal, temporal, and occipital lobes, and the insula (Figure C–2). Smaller penetrating branches (the lenticulostriate arteries) supply the deep white matter and diencephalic structures, such as the posterior limb of the internal capsule, putamen, outer globus pallidus, and body of the caudate. After the internal carotid emerges from the cavernous sinus, it also gives off the anterior choroidal artery, which supplies the anterior hippocampus and, at a caudal level, the posterior limb of the internal capsule.

Left and right vertebral arteries arise from the subclavian arteries and enter the cranium through the foramen magnum. Each gives off an anterior spinal artery and a posterior inferior cerebellar artery. The vertebral arteries join at the junction of the pons and medulla to form the basilar artery, which at the pontine level gives off the anterior inferior cerebellar artery and the internal auditory artery and at the midbrain level the superior cerebellar artery. The basilar artery then divides into the two posterior cerebral arteries, which supply the inferior temporal and medial occipital lobes and the posterior corpus callosum (Figure C–2). The smaller penetrating branches of these vessels (the thalamoperfo-rate and thalamogeniculate arteries) supply diencephalic structures, including the thalamus and the subthalamic nuclei, as well as parts of the midbrain.

Interconnections between blood vessels (anastomoses) protect the brain when part of its vascular supply is blocked (Figure C–3). At the circle of Willis, which provides an overlapping blood supply, the two anterior cerebral arteries are connected by the anterior communicating artery, and the posterior cerebral arteries are connected to the internal carotid arteries by the posterior communicating arteries. Other important anastomoses include connections between the ophthalmic artery and branches of the external carotid artery through the orbit, and connections at the brain surface between branches of the middle, anterior, and posterior cerebral arteries (sharing border zones or watersheds). The small penetrating vessels arising from the circle of Willis and proximal major arteries tend to lack anastomoses. The deep brain regions they supply are therefore referred to as end zones (no source of overlapping blood supply).

Figure C-3 Angiograms demonstrate the importance of anastomoses in allowing retrograde filling after occlusion of the middle cerebral artery. (Reproduced, with permission, from Margaret Whelan and Sadek K. Hilal.)

A. Occlusion of the middle cerebral artery results in no filling in the middle cerebral distribution.

B. Retrograde filling of the middle cerebral artery has begun via distal anastomotic branches of the anterior cerebral artery.

C. Retrograde filling of the middle cerebral artery continues at a time when little contrast material is seen in the anterior cerebral artery.

The Cerebral Vessels Have Unique Physiological Responses

Although the human brain constitutes only 2% of total body weight, it receives approximately 15% of the cardiac output and consumes approximately 20% of the oxygen used by the entire body. These values reflect the high metabolic rate and oxygen requirements of the brain. The total blood flow to the brain is 750 to 1000 mL/min; approximately 350 mL of this amount flows through each carotid artery and approximately 100 to 200 mL flow through the vertebrobasilar arterial system. Flow per unit mass of gray matter (somata and dendrites) is approximately four times that of white matter (axons).

Cerebral vessels are capable of altering their own diameter and can respond to altered physiological conditions. Two main types of autoregulation exist. Brain arterioles constrict when the systemic blood pressure is raised and dilate when it is lowered. These adjustments help maintain optimal cerebral blood flow. The result is that normal people have a constant cerebral blood flow between mean arterial pressures of 60 to 150 mm Hg. Above or below these pressures cerebral blood flow rises or falls linearly.

The second type of autoregulation involves blood or tissue gases and pH. When arterial carbon dioxide (CO₂) is raised, brain arterioles dilate and cerebral blood flow increases; with hypocarbia, vasoconstriction results and cerebral blood flow decreases. The response is sensitive: Inhalation of 5% CO₂ increases blood flow by 50%; 7% CO₂ doubles it. Changing arterial O₂ causes an opposite and less pronounced response. Breathing pure O₂ lowers blood flow by approximately 13%; 10% O₂ raises it by 35%. The mechanism of these responses is uncertain. The vasodilatory action of arterial CO₂ is probably mediated by alterations in extracellular pH. Local concentrations of K⁺, and adenosine, both of which cause vasodilation, may play a role.

Whatever the mechanism, these responses protect the brain by increasing the delivery of oxygen and the removal of acidic metabolites under conditions of hypoxia, ischemia, or tissue damage. They also allow nearly instantaneous adjustments of regional cerebral blood flow to meet the demands of rapidly changing oxygen and glucose metabolism that accompany normal brain activities. For example, viewing a complex scene increases oxygen and glucose consumption in the visual cortex of the occipital lobes. The resulting increased CO₂ concentration and lowered pH in the area rapidly increase local blood flow.

A Stroke Is the Result of Disease Involving Blood Vessels

Diseases of blood vessels are among the most frequent serious neurological disorders, ranking third as a cause of death in the adult population in the United States and probably first as a cause of chronic functional incapacity. Approximately two million Americans today are impaired by the neurological consequences of cerebrovascular disease, many between 25 and 64 years of age.

Strokes are either occlusive (closure of a blood vessel) or hemorrhagic (bleeding from a vessel). Insufficiency of blood supply is termed ischemia; if it is temporary, symptoms and signs may clear with little or no pathological evidence of tissue damage. Ischemia results in more than simply anoxia, because a reduced blood supply deprives tissue not only of oxygen but also of glucose. In addition, it prevents the removal of potentially toxic metabolites such as lactic acid. When ischemia is sufficiently severe and prolonged, neurons die; this condition is called infarction.

Hemorrhage may occur at the surface of the brain (extraparenchymal), for example from rupture of saccular aneurysms at the circle of Willis, causing subarachnoid hemorrhage. Alternatively, hemorrhage may be intraparenchymal, for example from rupture of vessels damaged by chronic hypertension—and may cause a blood clot or hematoma within the cerebral hemispheres, brain stem, or cerebellum. Hemorrhage may result in ischemia or infarction. Because of its mass, an intracerebral hematoma may limit the blood supply of adjacent brain tissue. By mechanisms that are not understood, subarachnoid hemorrhage may cause reactive vasospasm of cerebral surface vessels, leading to further ischemic brain damage.

Although most occlusive strokes are caused by atherosclerosis and thrombosis and most hemorrhagic strokes are associated with hypertension or aneurysms, strokes of either type may occur at any age from many other causes, including cardiac disease, trauma, infection, neoplasm, blood dyscrasia, vascular malformation, immunological disorder, and exogenous toxins.

Clinical Vascular Syndromes May Follow Vessel Occlusion, Hypoperfusion, or Hemorrhage

Infarction Can Occur in the Middle Cerebral Artery Territory

Infarction in the territory of the middle cerebral artery (Figure C–4) causes the most frequently encountered stroke syndrome, with contralateral weakness, sensory loss, and visual field impairment (homonymous hemianopia), and, depending on the hemisphere involved, either language disturbance (left) or impaired spatial perception (right). Weakness and sensory loss affect the face and arm more than the leg because of the somatotopy of the motor and sensory cortex (pre- and postcentral gyri). The face- and arm-control areas are on the convexity of the hemisphere, whereas the leg-control area is on the medial surface.

Figure C-4 Computed tomography scan showing infarction (dark area) in the territory of the middle cerebral artery. (Reproduced, with permission, from Allan J. Schwartz.)

Motor and sensory loss are greatest in the hand because the more proximal limbs and the trunk tend to have greater representation in both hemispheres. Paraspinal muscles, for example, are rarely weakened in unilateral cerebral lesions. Similarly, the facial muscles of the forehead and the muscles of the pharynx and jaw are represented in both hemispheres and therefore are usually spared. Tongue weakness is variable. If weakness is severe (plegia), muscle tone is usually decreased at first but gradually increases over days or weeks to spasticity with hyperactive tendon reflexes. A Babinski sign, reflecting upper motor neuron disturbance, is usually present. When weakness is mild, or during recovery, there may be clumsiness or slowness of movement out of proportion to loss of strength; such motor disability may resemble parkinsonian bradykinesia or even cerebellar ataxia.

Acute paresis of contralateral conjugate gaze often occurs as a result of damage to the convexity of the frontal cortex anterior to the motor cortex (the frontal eye field). For reasons that are unclear, this gaze palsy persists for only one or two days, even when other signs remain severe.

Sensory loss tends to involve discriminative and proprioceptive modalities more than affective modalities (pain and temperature sensation), which may be impaired or altered but are usually not lost completely. Joint position sense may be severely disturbed, causing limb ataxia, and there may be loss of two-point discrimination, astereognosis (inability to recognize an object by tactile sensation alone), or extinction (failure to appreciate a touch stimulus if a comparable stimulus is delivered simultaneously to the unaffected side of the body).

Homonymous hemianopia is the result of damage to the optic radiations, the deep fiber tracts connecting the thalamic lateral geniculate nucleus to the visual (calcarine) cortex. If the parietal radiation is primarily affected, the visual field loss may be an inferior quad-rantanopia, whereas in temporal lobe lesions quadrantanopia may be superior.

In more than 95% of right-handed persons and most of those who are left handed, the left hemisphere is dominant for language. Destruction of left frontal, parietal, or temporal opercular (perisylvian) cortex in left-dominant people causes aphasia, which takes several forms depending on the degree and distribution of the damage. Frontal opercular lesions tend to produce particular difficulty with speech output and writing while preserving at least partially language comprehension (Broca aphasia). Infarction of the posterior superior temporal gyrus tends to cause severe difficulty in speech comprehension and reading (Wernicke aphasia). When damage to the opercular cortex is widespread, a severe disturbance of mixed type occurs (global aphasia). Left-hemisphere convexity damage, especially parietal, also causes motor apraxia, a disturbance of learned motor acts not explained by weakness or incoordination.

Right-hemisphere convexity infarction, especially parietal, causes disturbances of spatial perception. Patients may have difficulty in copying simple diagrams (constructional apraxia), interpreting maps or finding their way about (topographagnosia), or putting on their clothing properly (dressing apraxia). Awareness of space and the patient’s own body on the side contralateral to the lesion may be particularly impaired (hemi-inattention or hemineglect). Patients also fail to acknowledge their hemiplegia (anosognosia), left arm (asomatognosia), or any external object to the left of their own midline.

Particular types of language or spatial dysfunction tend to result from occlusion of one of the several main pial branches of the middle cerebral artery, not the proximal stem. In these circumstances other signs (eg, weakness or visual field defect) may be absent. Similarly, occlusion of the rolandic branch of the middle cerebral artery causes motor and sensory loss affecting the face and arm without disturbing vision, language, or spatial perception.