Appendix C: Circulation of the Brain

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

• The Cerebral Vessels Have Unique Physiological Responses

• A Stroke Is the Result of Disease Involving Blood Vessels

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

  • Infarction Can Occur in the Middle Cerebral Artery Territory

  • Infarction Can Occur in the Anterior Cerebral Artery Territory

  • Infarction Can Occur in the Posterior Cerebral Artery Territory

  • The Anterior Choroidal and Penetrating Arteries Can Become Occluded

  • The Carotid Artery Can Become Occluded

  • The Brain Stem and Cerebellum Are Supplied by Branches of the Vertebral and Basilar Arteries

  • Infarcts Affecting Predominantly Medial or Lateral Brain Stem Structures Produce Characteristic Syndromes

  • Infarction Can Be Restricted to the Cerebellum

  • Infarction Can Affect the Spinal Cord

  • Diffuse Hypoperfusion Can Cause Ischemia or Infarction

  • Cerebrovascular Disease Can Cause Dementia

  • The Rupture of Microaneurysms Causes Intraparenchymal Stroke

  • The Rupture of Saccular Aneurysms Causes Subarachnoid Hemorrhage

• Stroke Alters the Vascular Physiology 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.

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).

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.

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 thalamoperforate 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).

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.

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.

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.

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. Para-spinal 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 quadrantanopia, 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.

Infarction Can Occur in the Anterior Cerebral Artery Territory

Infarction in the territory of the anterior cerebral artery (Figure C–5) causes weakness and sensory loss qualitatively similar to that of convexity lesions, but infarction in this territory affects mainly the distal contralateral leg. Urinary incontinence may be present, but it is uncertain whether this is because of a lesion of the paracentral lobule (medial hemispheric motor and sensory cortices) or a more anterior region necessary for the inhibition of bladder emptying. Damage to the supplementary motor cortex disturbs speech. Involvement of the anterior corpus callosum causes apraxia of the left arm (sympathetic apraxia), which is attributed to disconnection of the left (language-dominant) hemisphere from the right motor cortex.

Bilateral infarction in the territory of the anterior cerebral artery (occurring, for example, when both arteries arise anomalously from a single trunk) causes abulia, a severe behavioral disturbance consisting of profound apathy, motor inertia, and muteness, and attributable to destruction of the inferior frontal lobes (orbitofrontal cortex), deeper limbic structures, supplementary motor cortices, and cingulate gyri.

Infarction Can Occur in the Posterior Cerebral Artery Territory

Infarction in the territory of the posterior cerebral artery (Figure C–6) causes contralateral homonymous hemianopsia by destroying the medial occipital cortex. Macular (central) vision tends to be spared because the occipital pole, where macular vision is represented, receives anastomotic blood supply from the middle cerebral artery. If the lesion is on the left and the posterior corpus callosum is affected, alexia—the inability to read—may be present without aphasia or agraphia. A possible explanation for the alexia is the disconnection of the right occipital cortex (visual processing) from the language-dominant left hemisphere. If infarction is bilateral (eg, following thrombosis at the point where both posterior cerebral arteries arise from the basilar artery), there may be cortical blindness that is not recognized by the patient (Anton syndrome), or memory disturbance as a result of bilateral damage to the inferomedial temporal lobes.

If the posterior cerebral artery occlusion is proximal, the following structures may be damaged: the thalamus, causing contralateral hemisensory loss and sometimes dysesthesia (altered touch sensation) and spontaneous pain (thalamic pain syndrome); the subthalamic nucleus, causing contralateral severe proximal chorea (hemiballism); or even the midbrain, with ipsilateral oculomotor palsy and contralateral hemiparesis or ataxia from involvement of the corticospinal tract or the crossed superior cerebellar peduncle (dentato- thalamic tract).

The Anterior Choroidal and Penetrating Arteries Can Become Occluded

Anterior choroidal artery occlusion can cause contralateral hemiplegia and sensory loss from involvement of the posterior limb of the internal capsule and homonymous hemianopia from involvement of the thalamic lateral geniculate nucleus.

The deeper cerebral white matter and diencephalon are supplied by small penetrating arteries, which arise from the circle of Willis or the proximal portions of the middle, anterior, and posterior cerebral arteries. Occlusion of these end-arteries causes small infarcts (less than 1.5 cm in diameter) called lacunes with characteristic syndromes. For example, lacunes in the pyramidal tract area of the internal capsule cause pure hemiparesis, with face, arm, and leg weakness of equal severity but little or no sensory loss, visual field disturbance, aphasia, or spatial disruption. Lacunes in the ventral posterior nucleus of the thalamus produce pure hemisensory loss, with involvement of pain, temperature, proprioceptive, and discriminative modalities and with little motor, visual, language, or spatial disturbance. Most lacunes occur in redundant areas (eg, nonpyramidal corona radiata) and so are not symptomatic. If bilateral and numerous, however, they may cause a characteristic syndrome (état lacunaire) of progressive dementia, shuffling gait, and pseudobulbar palsy (spastic dysarthria and dysphagia, with lingual and pharyngeal paralysis and hyperactive palate and gag reflexes, plus lability of emotional response, with abrupt crying or laughing out of proportion to mood).

Infarction restricted to structures supplied by the recurrent artery of Heubner or other deep penetrating branches of the anterior cerebral artery (the anterior caudate nucleus and, less predictably, the anterior putamen and anterior limb of the internal capsule) results in varying combinations of psychomotor slowing, dysarthria, agitation, contralateral neglect, and, when left hemispheric, language disturbance.

The Carotid Artery Can Become Occluded

Atherothrombotic vessel occlusion often occurs in the internal carotid artery rather than the intracranial vessels. Particularly in a patient with an incomplete circle of Willis, infarction may include the territories of both the middle and anterior cerebral arteries, with arm and leg weakness and sensory loss equally severe. Alternatively, infarction may be limited to the distal shared territory (border zones) of these vessels, destroying motor cortex at the upper cerebral convexity and producing weakness limited to the arm or the leg.

The Brain Stem and Cerebellum Are Supplied by Branches of the Vertebral and Basilar Arteries

Branches of the vertebral and basilar arteries consist of three groups: (1) paramedian branches, including the anterior spinal artery, supply midline structures; (2) short circumferential branches supply more lateral structures, including the inferior, middle, and superior cerebellar peduncles; and (3) long circumferential arteries—the posterior inferior, anterior inferior, and superior cerebellar arteries—also supply lateral brain stem structures and the cerebellar peduncles, as well as the cerebellum itself. Most of the midbrain is supplied by branches of the posterior cerebral artery. The interpeduncular branches, the most medial branches located between the basilar artery bifurcation and the posterior communicating arteries, supply paramedian midbrain structures. Lateral to this group are the thalamoperforate branches, which supply the inferior, medial, and anterior thalamus and the subthalamic nucleus. Further laterally are the thalamogeniculate branches, which supply lateral and dorsal structures in the midbrain and thalamus. In some people the midbrain also receives blood from the superior cerebellar, posterior communicating, and anterior choroidal arteries. After passing around the midbrain, the posterior cerebral artery enters the middle fossa to supply the occipital and inferior temporal lobes. It does not supply the cerebellum.

Damage to specific brain stem structures produces a variety of syndromes (Figure C–7). With the exception of the lateral medullary syndrome of Wallenberg, however, most original descriptions of these syndromes were based on patients with neoplasms. Brain stem in- farction more often follows occlusion of the vertebral or basilar arteries themselves rather than their medial or lateral branches; resulting syndromes and signs tend to be less stereotyped than originally described.

Generally speaking, a lesion of the posterior fossa is suggested by (1) bilateral long tract (motor or sensory) signs, (2) crossed (eg, left face and right limb) motor or sensory signs, (3) cerebellar signs, (4) stupor or coma (from involvement of the ascending reticular activating system), (5) disconjugate eye movements or nystagmus, and (6) involvement of cranial nerves not usually affected by unilateral hemispheric infarcts (eg, unilateral deafness or pharyngeal weakness). Sometimes a lesion involving only a single tiny structure can be localized accurately by symptomatology. For example, internuclear ophthalmoplegia implicates a lesion of the median longitudinal fasciculus. Other lesions produce more ambiguous symptoms. For example, in-farction limited to the upper pontine corticospinal tract can produce contralateral face, arm, and leg weakness indistinguishable from that caused by a small infarct in the internal capsule.

Infarcts Affecting Predominantly Medial or Lateral Brain Stem Structures Produce Characteristic Syndromes

Medullary and pontine syndromes are conveniently viewed as lateral or medial (Figure C–7). Infarction of the lateral medulla follows occlusion of the vertebral artery or less often the posterior inferior cerebellar artery. Symptoms and signs include (1) vertigo, nausea, vomiting, and nystagmus (from involvement of the vestibular nuclei); (2) ataxia of gait and ipsilateral limbs (inferior cerebellar peduncle or the cerebellum itself); (3) decreased pain and temperature (but not touch) sensation on the ipsilateral face (spinal tract and nucleus of the trigeminal nerve) and the contralateral body (spinothalamic tract); (4) dysphagia, hoarseness, ipsilateral weakness of the palate and vocal cords, and ipsilaterally decreased gag reflex (nucleus ambiguus, or glossopharyngeal and vagus outflow tracts); and (5) ipsilateral Horner syndrome (descending sympathetic fibers). Involvement of the nucleus solitarius can cause ipsilateral loss of taste, and hiccups are often present. The symptoms and signs for infarcts affecting different levels of the brain stem are listed in Table C–1.

Infarction of the medial medulla causes contralateral hemiparesis (from involvement of the corticospinal tract), ipsilateral tongue weakness with dysarthria and deviation toward the paretic side (hypoglossal nucleus or outflow tract), and contralateral impaired proprioception and discriminative sensation with preserved pain and temperature sensation (medial lemniscus).

Infarction of the lateral pons affects caudal structures when the anterior inferior cerebellar artery is occluded and rostral structures when the superior cerebellar artery is occluded (Figure C–8). Symptoms of caudal damage resemble those of lateral medullary infarction, with vertigo, nystagmus, gait and ipsilateral limb ataxia, crossed face-and-body pain and temperature loss, Horner syndrome, and ipsilateral loss of taste. There is also unilateral tinnitus and deafness (from involvement of the cochlear nuclei). Involvement of more medial structures can cause ipsilateral gaze paresis or facial weakness. Symptoms of rostral damage include gait and ipsilateral limb ataxia, Horner syndrome, and crossed sensory loss, which at this level includes touch as well as pain and temperature sensation on the ipsilateral face (from involvement of the primary sensory nucleus or entering sensory fibers of the trigeminal nerve). There may also be ipsilateral jaw weakness with deviation to the paretic side (trigeminal motor nucleus and outflow tract). Vertigo, deafness, and face weakness are not present.

Infarction of the medial pons, whether caudal or rostral, causes contralateral hemiparesis (from involvement of the corticospinal tract). Caudal lesions affecting the facial nucleus or outflow tract cause ipsilateral facial weakness. Rostral lesions result in contralateral facial weakness. There may also be ipsilateral gaze paresis (paramedian pontine reticular formation or abducens nucleus, together comprising the pontine gaze center) or abducens paresis (sixth nerve outflow tract); internuclear ophthalmoplegia and limb and gait ataxia are often present. Contralateral impairment of proprioception and discriminative touch is most prominent with caudal lesions. Rapid involuntary movements of the palate—so-called palatal myoclonus —has been attributed to involvement of the central tegmental tract; the involuntary movements may spread to include the pharynx, larynx, face, eyes, or respiratory muscles.

Midbrain syndromes are viewed as ventral (or peduncle), tegmental, and dorsal (including the collicular, pretectal, and tectal areas) (Figure C–9). Because the vertebral and basilar arteries themselves are usually the site of occlusion, pure forms of these stereotypic syndromes are infrequently encountered clinically. Unilateral ventral lesions cause Weber syndrome, characterized by ipsilateral paresis of adduction and vertical gaze and pupillary dilation (involvement of oculomotor nerve outflow tract) and contralateral face, arm, and leg paresis (corticospinal and cortico-bulbar tracts). Unilateral tegmental lesions cause Claude syndrome, characterized by oculomotor paresis (oculomotor nucleus) and contralateral ataxia and tremor (often referred to as rubral tremor but probably the result of damage to projections from the cerebellum to the thalamus). Lesions affecting both the peduncle and tegmentum produce combinations of oculomotor paresis, ataxia, and weakness (Benedikt syndrome). Dorsal midbrain lesions, which are infrequently vascular and rarely unilateral, cause Parinaud syndrome, characterized by impaired vertical gaze—especially upward (posterior commissure and the rostral interstitial nucleus of the median longitudinal fasciculus)—and loss of the pupillary light reflex (pretectal structures).

Because the vertebral and basilar arteries themselves are usually the site of occlusion, pure forms of these stereotypic syndromes are infrequently encountered clinically.

Bilateral brain stem lesions can be devastating. Paramedian infarction of the upper brain stem can destroy the reticular activating system and cause stupor or coma. Bilateral infarction of the rostral basis pontis destroys descending corticospinal and cortico-bulbar fibers, causing paralysis of all muscles except eye movements; if the tegmentum is spared such patients remain awake and communicate with their eyes (the locked-in state).

Infarction Can Be Restricted to the Cerebellum

Infarcts of the inferior cerebellum, which has extensive vestibular connections, can cause vertigo, nausea, and nystagmus without other symptoms, suggesting disease of the inner ear or vestibular nerve. More superior cerebellar infarcts produce gait and ipsilateral limb ataxia.

Infarction Can Affect the Spinal Cord

Vascular anatomy explains the characteristic pattern of spinal cord infarction (Figure C–10). Vessel occlusion is usually in a proximal segmental artery. Because of the anastomotic continuity of the posterior spinal arteries, infarction tends to be limited to the anterior spinal artery territory. Thus paraparesis or quadriparesis (corticospinal tracts), loss of bladder and bowel control, and loss of pain and temperature sensation below the lesion (spinothalamic tracts) are common; but proprioception and discriminative touch (dorsal columns) are spared.

If the cervical or lumbar spinal cord is involved, atrophic weakness of upper or lower extremity muscles (anterior horns) can occur. Because the anterior spinal artery gives off sulcal arteries that alternately enter the left and right halves of the spinal cord, in-farction can sometimes produce a Brown-Séquard syndrome, with ipsilateral weakness and contralateral loss of pain and temperature sensation.

Diffuse Hypoperfusion Can Cause Ischemia or Infarction

Brain ischemia or infarction may accompany diffuse hypoperfusion (shock). In such circumstances the most vulnerable regions are often the border zones between large arterial territories and the end zones of deep penetrating vessels. Whatever the cause of reduced cerebral perfusion, signs tend to be bilateral. Paralysis and sensory loss may be present in both arms (from bilateral infarction of the cortex at the junction of the middle and anterior arterial supply, affecting the arm control area of the motor and sensory cortex).

Disturbed vision or memory may result (from in-farction of the occipital or inferior temporal lobes at the junction of the middle and posterior cerebral arterial supply). There may also be ataxia (from cerebellar border zone infarction) or abnormal movements such as chorea or myoclonus (presumably from involvement of the basal ganglia). Such signs may exist alone or in combination and may be accompanied by aphasia or other cognitive disturbances.

Hypotension can also cause spinal cord infarction, most often upper thoracic, affecting either the territory of the anterior spinal artery or the border zone between the anterior and posterior spinal arteries.

Cerebrovascular Disease Can Cause Dementia

Cerebral infarction causes dementia by a number of mechanisms:

1. Infarcts may be critically located. For example, thalamic or inferomedial temporal damage (posterior cerebral artery, usually bilateral) can cause amnesia; hemispheric convexity damage (middle cerebral artery) can cause cognitive or behavioral impairment not explained by disruption of language or spatial discrimination; and bilateral inferomedial frontal lobe damage (anterior cerebral artery) can cause abulia and impaired memory.

2. Multiple scattered infarcts, none sufficient to cause significant cognitive loss, can produce additive effects culminating in dementia. In such patients at least 100 cc of brain volume has usually been destroyed.

3. Small vessel disease, affecting especially the deep cerebral white matter, can cause either scattered lacunes or more diffuse ischemic lesions. When such lesions are severe enough to cause dementia, there is often altered behavior, pseudobulbar palsy, pyramidal signs, disturbed gait, and urinary incontinence.

The Rupture of Microaneurysms Causes Intraparenchymal Stroke

The two most common causes of hemorrhagic stroke, hypertensive intraparenchymal hemorrhage and rupture of a saccular aneurysm, tend to occur at particular sites and to cause recognizable syndromes. Hypertensive intracerebral hemorrhage is the result of damage to the same small penetrating vessels that, when occluded, cause lacunes; in the case of hemorrhage the damaged vessels develop weakened walls (Charcot-Bouchard microaneurysms) that eventually rupture. The most common sites are the putamen, thalamus, pons, internal capsule and corona radiata, and cerebellum. Large diencephalic hemorrhages tend to cause stupor and hemiplegia and have a high mortality rate.

With putamenal hemorrhage (Figure C–11) the eyes are usually deviated ipsilaterally (because of disruption of capsular pathways descending from the frontal eye field), whereas with thalamic hemorrhage (Figure C–12) the eyes tend to be deviated downward and the pupils may not react to light (because of involvement of midbrain pretectal structures essential for upward gaze and pupillary light reactivity). Small hemorrhages may not impair alertness, and with small thalamic hemorrhages sensory loss may exceed weakness. Moreover, computerized tomography reveals that small thalamic hemorrhages can cause aphasia when on the left and hemineglect when on the right.

Pontine hemorrhage, unless quite small, usually causes coma (by disrupting the reticular activating system) and quadriparesis (by transecting the cortico-spinal tracts). Eye movements, spontaneous or reflex (eg, to ice water in either external auditory canal) are absent, and pupils are pinpoint in size, reflecting transection of descending sympathetic pathways. Pupillary light reactivity is usually preserved, however, for the pathway mediating this reflex, from retina to midbrain, is intact. Respirations may be irregular, presumably because the caudal reticular formation is involved. These strokes are nearly always fatal.

Cerebellar hemorrhage, which tends to occur in the region of the dentate nucleus, typically causes a sudden inability to stand or walk (astasia-abasia), with ipsilateral limb ataxia. There may be ipsilateral abducens palsy, or horizontal gaze palsy, or facial weakness, presumably from pontine compression. Long-tract motor and sensory signs are usually absent, however. As swelling increases, further brain stem damage may cause coma, ophthalmoplegia, miosis, and irregular respiration, with fatal outcome.

The Rupture of Saccular Aneurysms Causes Subarachnoid Hemorrhage

Saccular aneurysms (not to be confused with hypertensive Charcot-Bouchard microaneurysms) are most often found at the junction of the anterior communicating artery with an anterior cerebral artery, the junction of a posterior communicating artery with an internal carotid artery, and the first bifurcation of a middle cerebral artery in the sylvian fissure. Each aneurysm, upon rupture, tends to cause not only sudden severe headache but also a characteristic syndrome. By producing a hematoma directly over the oculomotor nerve as it traverses the base of the brain, a ruptured posterior communicating artery aneurysm often causes ipsilateral pupillary dilation with loss of light reactivity. A middle cerebral artery aneurysm may, by either hematoma or secondary infarction, cause a clinical picture resembling that of middle cerebral artery occlusion. After rupture of an anterior communicating artery aneurysm, there may be no focal signs but only decreased alertness or behavioral changes.

Posterior fossa aneurysms most often occur at the rostral bifurcation of the basilar artery or at the origin of the posterior inferior cerebellar artery. They cause a variety of cranial nerve and brain stem signs. Rupture of an aneurysm at any site may cause abrupt coma; the reason is uncertain but may be related to sudden increased intracranial pressure and functional disruption of vital pontomedullary structures.

After a stroke, cerebral blood flow and cerebrovascular responses to changes in blood pressure or arterial gases are altered. There may be vasomotor paralysis with loss of autoregulation in response to blood pressure changes and then blunted responses to alterations in arterial O₂ or CO₂. This kind of physiological abnormality is especially likely in brain areas that are ischemic but not yet infarcted; such an area often surrounds acutely infarcted brain tissue and is called the ischemic penumbra. Lowered blood pressure in this setting can, by critically reducing perfusion in the penumbra, convert ischemia to infarction. The use of cerebral vasodilators can also produce an unintended response, increasing cerebral blood flow in regions distant from the ischemic region without affecting vessels within the ischemic region. Blood may therefore be shunted from ischemic to normal brain.

Strategies for restoring cerebral perfusion in patients with acute ischemic stroke (for example, giving recombinant tissue-type plasminogen activator to degrade the clot causing the infarction) are based on the assumption that an ischemic penumbra represents salvageable tissue, even if infarction within it does not.