Cerebrovascular disease

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35 Cerebrovascular disease

Chapter Summary

Introduction
Anterior circulation of the brain

Internal capsule
Posterior circulation of the brain
Transient ischemic attacks
Clinical anatomy of vascular occlusions
CLINICAL PANELS

Anterior choroidal artery occlusion
Anterior cerebral artery occlusion
Middle cerebral artery occlusion
Internal carotid artery occlusion
Occlusions within the posterior circulation
Posterior cerebral artery occlusion
Subarachnoid hemorrhage
Motor recovery after stroke

Study Guidelines

1 This final chapter touches upon a large range of neurological symptoms and signs, because it deals with vascular damage to every part of the brain. The great majority of the symptoms and signs have been already been mentioned, individually, in other contexts.
2 The Clinical Panels may convey the impression that clinical diagnosis is rather straightforward. However, following vascular insults, patients are seldom alert and cooperative.
3 An objective of this chapter is to demonstrate the value of understanding the regional as well as the systems anatomy of the brain, because cerebrovascular accidents cause injury to regions, with consequent effects on multiple systems.
4 The increasing range of diagnostic aids does not shrink the need for clinical acumen. The more accurate the tentative diagnosis, the more likely the most appropriate technology will be selected for further elucidation.
5 Perhaps refresh the blood supply (Ch. 5).

Introduction

Cerebrovascular disease is the third leading cause of death in adults, being superseded only by heart disease and cancer. The most frequent expression of cerebrovascular disease is that of a stroke, which is defined as a focal neurological deficit of vascular origin which lasts for more than 24 hours if the patient survives. The most frequent example is a hemiplegia caused by a vascular lesion of the internal capsule. However, it will be seen that many varieties of stroke symptomatologies are recognized, based upon place and size.

The chief underlying disorders are atherosclerosis within the large arteries supplying the brain, heart disease, hypertension, and ‘leaky’ perforating arteries.

• Atherosclerosis signifies fatty deposits in the intimal lining of the internal carotid and vertebrobasilar system – most notably in the internal carotid trunk or in one of the vertebral arteries. The deposits pose a dual threat: in situ enlargement may cause progressive occlusion of a main artery; and breakaway deposits may form emboli (plugs) blocking distal branches within the brain. However, gradual occlusion is often redeemed by routing of blood through alternative channels. For example, an internal carotid artery (ICA) may be progressively occluded over a period of 10 years or more without apparent brain damage; the contralateral ICA utilizes the circle of Willis to perfuse both pairs of anterior and middle cerebral arteries; and it is not unusual in such cases for external carotid blood to assist, by retrograde flow from the facial artery through the ophthalmic artery on the affected side. Similarly, occlusion of the stem of one of the three cerebral arteries may be compensated for through small (<0.5 mm) anastomotic arteries in the depths of cortical sulci, perfused by the other two cerebrals. The number of such small arteries varies greatly between individuals. The crescent-shaped anastomotic region is known as the border zone (Figure 35.1). On the other hand, all arteries penetrating the brain substance are end arteries, i.e. their communications with neighboring penetrating arteries are too fine to save brain tissue in the event of blockage.
• Many cerebral emboli originate as blood clots in the left side of the heart, in association with coronary or valvular disease.
• Hypertension is obviously associated with cerebral hemorrhage, which may be so massive as to rupture into the ventricular system and cause death within minutes or hours.
• Less obvious are lacunae (’small pools’) up to 2 cm in diameter, in the white matter adjacent to one or more perforating end-arteries. The souce is now believed to be a ‘leakiness’ of the vascular endothelium (blood–brain barrier) permitting extravasation of plasma into the perivascular space. The fundamental cause is not understood: there is only a marginal association with hypertension and none with atherosclerosis or stenosis. Lacunar strokes are the most likely to recur, and such recurrence has a high association with a state of multi-infarct dementia. An infarct is an area of brain destruction produced by vascular occlusion, hemorrhage or extravasation.
image

Figure 35.1 Border zone of anastomotic overlap between the middle cerebral artery (MCA) and the anterior and posterior cerebral arteries (ACA, PCA).

Cerebral infarcts become swollen after a few days because of osmotic activity. Some become large enough to produce distance effects by causing subfalcal or tentorial herniation of the brain in the manner of a tumor (Ch. 4).

It is usually easy to distinguish the symptoms/signs of vascular disease from those of a tumor. A vascular stroke takes up to 24 hours to evolve, whereas the time frame for tumors is usually several months or more. However, hemorrhage into a tumor may cause it to expand suddenly and to mimic the effects of a stroke. Very often, the hemorrhage is into a metastatic tumor, notably from lung, breast, or prostate; in fact, a stroke may be the first manifestation of a cancer in one of those organs.

Some 10% of vascular strokes are caused by rupture of a ‘berry’ aneurysm into the brain. As explained later, berry aneurysms usually bleed directly into the subarachnoid space because they originate in or near the circle of Willis, but some arise at an arterial bifurcation point within the brain. A ruptured aneurysm is always a prime suspect when a stroke comes ‘out of the blue’ in someone less than 40 years old.

Anterior Circulation of the Brain

Clinicians refer to the ICA and its branches as the anterior circulation of the brain, and the vertebrobasilar system (including the posterior cerebral arteries) as the posterior circulation. The anterior and posterior circulations are connected by the posterior communicating arteries (Figure 35.2).

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Figure 35.2 Circle of Willis and its branches. This is an magnetic resonance (MR) angiogram based on the principle that flowing blood generates a different signal to that of stationary tissue, without injection of a contrast agent. Conventional angiograms, e.g. those in Chapter 5, require arterial perfusion with a contrast agent. The vessels shown here are contained within a single thick MR ‘slice’. Some, e.g. the calcarine branch of the posterior cerebral artery, could be followed further in adjacent slices. ACA, anterior cerebral artery; ICA, internal carotid artery; MCA, middle cerebral artery; PCA, posterior cerebral artery.

(From a series kindly provided by Professor J. Paul Finn, Director, Magnetic Resonance Research, Department of Radiology, David Geffen School of Medicine at UCLA, California, USA.)

About 75% of cerebrovascular accidents (CVAs) originate in the anterior circulation.

Internal capsule

The following details supplement the account of the arterial supply of the internal capsule in Chapter 5.

The blood supply of the internal capsule is shown in Figure 35.3. The three sources of supply are the anterior choroidal, a direct branch of the internal carotid; the medial striate, a branch of the anterior cerebral, and lateral striate (lenticulostriate) branches of the middle cerebral artery.

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Figure 35.3 Internal capsule.

(A) Pathways. Lateral view of the right cerebral hemisphere, showing the oval depression in the white matter following removal of the lentiform nucleus. The internal capsule occupies the floor of the depression. CNF, corticonuclear fibers; COF, cortico-oculomotor fibers; CPF, corticopontine fibers; CRF, corticoreticular fibers; CSF, corticospinal fibers; TCF, thalamocortical fibers. Other abbreviations as in Figure 35.4.

(B) Blood supply. The medial striate branch of the anterior cerebral artery is the recurrent artery of Heubner. Only two of the six lateral striate branches of the middle cerebral artery shown are labeled. *Indicates arterial supply from the anterior choroidal artery to the inferolateral part of the lateral geniculate body.

The contents of the internal capsule are shown in Figure 35.4. The anterior choroidal branch of the internal carotid artery supplies the lower part of the posterior limb and the retrolentiform part of the internal capsule, and the inferolateral part of the lateral geniculate body. Some of its branches (not shown) supply a variable amount of the temporal lobe of the brain and the choroid plexus of the inferior horn of the lateral ventricle.

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Figure 35.4 Horizontal section of the internal capsule at the level indicated (based on Figure 2.11), depicting its boundaries and parts (left) and stroke-relevant motor contents (right). SC, superior colliculus; LGB, lateral geniculate body; IC, internal capsule.

The medial striate branch of the anterior cerebral artery (recurrent artery of Heubner) supplies the lower part of the anterior limb and genu of the internal capsule.

The lateral striate arteries penetrate the lentiform nucleus and give multiple branches to the anterior limb, genu, and posterior limb of the internal capsule.

Posterior Circulation of the Brain

Additional information is confined to the stem branches of the posterior cerebral artery shown in Figure 35.5.

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Figure 35.5 Central branches of the posterior cerebral artery (PCA). Although only two arteries are shown, each in fact comprises several branches from the PCA. The thalamoperforating artery shown pierces the posterior perforated substance and supplies the anterior one-third of the thalamus. The thalamogeniculate artery shown supplies the geniculate bodies and the posterior two-thirds of the thalamus. ACA, anterior cerebral artery; ICA, internal carotid artery; LGB, MGB, lateral, medial geniculate bodies.

Transient Ischemic Attacks

Transient ischemic attacks (TIAs) are episodes of vascular insufficiency that cause temporary loss of brain function, with total recovery within 24 hours. Most TIAs last for less than half an hour, with no residual signs at the time of clinical examination. Diagnosis is therefore usually based upon reported symptoms alone.

Most attacks follow lodgment of fibrin clots or detached atheromatous tissue at an arterial branch point, with subsequent dissolution.

• Transient symptoms originating in the anterior circulation include: motor weakness (a ‘heavy feeling’) in an arm or leg, hemisensory deficit (a ‘numb feeling’), dysphasia, and monocular blindness from occlusion of the central artery of the retina.
• Transient symptoms originating in the posterior circulation include: vertigo, diplopia, ataxia, and amnesia.

Recognition of TIAs involving the anterior circulation is important because they serve notice of impending major illness. Without treatment, one patient in four will die from a heart attack within 5 years, and one in six will suffer a stroke.

Clinical Anatomy of Vascular Occlusions

In the Clinical Panels, the term occlusion encompasses all causes of regional arterial failure other than aneurysms. Symptoms of occlusions within the anterior circulation are summarized in Clinical Panels 35.1–35.4, within the posterior circulation in Clinical Panel 35.5, specifically within the terrirory of the posterior cerebral artery in Clinical Panel 35.6. Subarachnoid hemmorrhage is considered in Clinical Panel 35.7.

Clinical Panel 35.1 Anterior choroidal artery occlusion

A complete anterior choroidal artery syndrome is produced by occlusion of the proximal part of the artery, compromising the lower part of the posterior limb and retrolentiform part of the internal capsule. The clinical picture is one of contralateral hemiparesis, hemisensory loss of cortical type (Ch. 29), and hemianopia. Damage to the (crossed) cerebellothalamocortical pathway may add evidence of intention tremor in the contralateral upper limb, yielding so-called ataxic hemiparesis.

Isolated occlusion of the branch to the lateral geniculate body results in a contralateral upper quadrant hemianopia.

Clinical Panel 35.2 Anterior cerebral artery occlusion

Complete interruption of flow in the proximal anterior cerebral artery (ACA) is rare because the opposite artery has direct access to its distal territory through the anterior communicating artery. However, branch occlusions are well recognized, with corresponding variations in the clinical picture:

• Orbital or frontopolar branch. The usual result is an apathetic state with some memory loss.
• Medial striate artery (recurrent artery of Heubner) occlusion may result in dysarthria owing to compromise of the motor supply to the contralateral nuclei supplying the muscles of the mandible (V), lips (VII) and tongue (XII). Hoarseness and dysphagia are also present if the supranuclear supply to the nucleus ambiguus is interrupted.
• Callosomarginal. This branch supplies the dorsomedial prefrontal cortex, the supplementary motor area (SMA) and the lower limb and perineal areas of the sensorimotor cortex and the supplementary sensory area (SSA). The commonest manifestation of occlusion is motor weakness and some cortical-type sensory loss in the contralateral lower limb, as a result of infarction within the paracentral lobule. Urinary incontinence may occur for some days owing to contralateral weakness of the pelvic floor. Damage to the prefrontal cortex results in abulia (lack of initiative). A left-sided infarct of the SMA may produce mutism because SMA normally collaborates with Broca’s area in the initiation of speech. Finally, damage to the SSA may result in inability to reach with the contralateral arm toward the side of the lesion.
• Pericallosal. Infarction of the anterior part of the corpus callosum may result in ideomotor apraxia. (The lesion would be comparable to lesion 1 in Figure 32.7). Infarction of the midregion may cause tactile anomia owing to blocked transfer of tactile information from right to left parietal lobe.

Reference

Kang SY, Kim JS. Anterior cerebral artery infarction. Neurology. 2008;70:2386-2393.

Clinical Panel 35.3 Middle cerebral artery occlusion

Embolic and lacunar infarcts are frequent in late middle life and in the elderly. Hemorrhage from one of the striate branches is also a frequent event.

Embolism

An embolus may lodge in the stem of the artery, in the upper division, in the lower division, or in a cortical branch of either division.

Stem

Occlusion of the stem affects the central as well as the cortical branches. The complete picture includes contralateral hemiplegia, severe contralateral sensory loss, contralateral homonymous hemianopia, and drifting of the eyes toward the side of the infarct. Left-sided lesions are usually accompanied by global aphasia, right-sided ones with contralateral sensory neglect. Many patients die in coma following midbrain compression by a swollen infarct.

The condition of some patients with stem occlusion improves markedly within days, as explained in Clinical Panel 35.8.

Upper division

An embolus occluding the upper division gives rise to contralateral paresis (weakness) and cortical-type sensory loss in the face and arm, together with dysarthria arising from damage to supranuclear pathways involved in speech articulation. Left-sided lesions are usually accompanied by Broca’s aphasia, right-sided lesions by contralateral neglect.

Lower division

Embolism of the lower division produces contralateral homonymous hemianopia, and sometimes a confused, agitated state attributed to involvement of limbic pathways in the temporal lobe. Left-sided lesions are also accompanied by Wernicke’s aphasia, alexia, and sometimes by ideomotor apraxia (corresponding to lesion 3 in Figure 32.7).

Branch embolism

The following isolated deficits are attributable to an embolus lodged in one of the cortical branches:

• Orbitofrontal: elements of a prefrontal syndrome (Ch. 32) may be present.
• Precentral (prerolandic): Broca’s aphasia (left lesion); monotone speech (right lesion).
• Central (rolandic): contralateral loss of motor and/or sensory function in the face and arm.
• Inferior parietal: contralateral hemineglect (especially with right lesion); tactile anomia.
• Angular: contralateral homonymous hemianopia; alexia with left lesion.
• Posterior/middle temporal: Wernicke’s aphasia (left lesion); sensory aprosodia (right lesion).

Lacunar infarcts

Lacunar infarction is suspected where the clinical evidence suggests a small lesion. Well-recognized are the following:

• pure motor hemiparesis, caused by a lacuna in the corona radiata or internal capsule (see also pons, later). The weakness is mainly in the lower face and arm and there are no sensory or higher cortical disturbances.
• pure sensory syndrome, produced by a lacuna in the ventral posterior nucleus of the thalamus. There is severe impairment of tactile discrimination (Ch. 15) in the contralateral limbs, together with sensory ataxia.
• dysarthria–clumsy hand syndrome, produced by a lacuna among fibers descending to, or within, the genu of the internal capsule, containing (a) corticonuclear fibers descending to contralateral motor nuclei of pons and medulla oblongata, and (b) fibers from the premotor cortex involved in contralateral manual control. The most apparent results are dysarthria owing to paresis of lip, tongue and jaw musculature, and clumsiness of hand movement.

Hemorrhage

The commonest source of a cerebral hemorrhage is one of the lateral striate branches of the middle cerebral artery. The commonest location is the putamen, with spread into the anterior and posterior limbs of the internal capsule. The usual cause is a pre-existing systemic hypertension. The hematoma may be as small as a pea or as big as a golf ball. Large hemorrhages rupture into the lateral ventricle and are usually fatal within 24 hours.

A typical clinical case is one in which a sudden, severe headache is followed by unconsciousness within a few minutes. The eyes tend to drift toward the side of the lesion, as noted in Chapter 29. With recovery of consciousness, there is a complete, flaccid hemiplegia (apart from the upper part of the face). Tendon reflexes are absent on the hemiplegic side and a Babinski sign is present.

Following any kind of stroke involving the left internal capsule, right-handers often notice some initial clumsiness in the left hand. Functional magnetic resonance imaging studies indicate that in healthy right-handers the left motor cortex is more active during movements of the left hand than the right motor cortex is during movements of the right hand. In other words, the left motor cortex has a greater degree of bilateral control.

The end result of capsular stroke is often one of ambulatory spastic hemiparesis with hemihypesthesia (reduced sensation). Figure CP 35.3.1 shows the typical posture during walking: the elbow and fingers are flexed and the leg has to be circumducted during the swing phase (unless an ankle brace is worn) because of the antigravity tone of the musculature. During the early rehabilitation period an arm sling is required in order to protect the shoulder joint from downward subluxation (partial dislocation) This is because the supraspinatus muscle is normally in continuous contraction when the body is upright, preventing slippage of the humeral head.

Figure CP 35.3.2 is from a magnetic resonance (MR) study of a patient who had suffered a right hemiplegia with sensory loss 11 days previously. The picture shows extensive infarction of the white matter on the left side, at the junctional region between the corona radiata and internal capsule, with compression of the lateral ventricle.

Internal carotid artery

In addition to being a source of cerebral emboli, atheromatous plaques may cause partial or complete occlusion of the internal carotid artery itself (see Clinical Panel 35.4).

Reference

Mohr JP, Lazar RM. Middle cerebral artery disease. In: Mohr JP, Choi DW, Grotta JC, Weir B, Wolf PA, editors. Stroke pathophysiology, diagnosis and management. ed 4. Philadelphia: Churchill Livingstone; 2004:123-166.

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Figure CP 35.3.1 Hemiplegic gait. The patient’s right side is affected.

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Figure CP 35.3.2 Contrast-enhanced MR image taken from a patient 11 days after an embolic stroke (see text).

(From Sato A et al, Radiology 178:433–439, 1991, with kind permission of Dr S. Takahashi, Department of Radiology, Tohoku University School of Medicine, Sendai, Japan, and the editors of Radiology.)

Clinical Panel 35.4 Internal carotid artery occlusion

The lumen of the internal carotid artery may become progressively obstructed by atheromatous deposits. Common sites of obstruction are the point of commencement in the neck, and the cavernous sinus. A slowly progressive obstruction may be compensated for by the opposite internal carotid artery, through the circle of Willis. Additional blood may also be provided through the orbit from the facial artery. At the other extreme, sudden occlusion may cause death from infarction of the entire anterior and middle cerebral territories, and sometimes the posterior cerebral also.

Warning signs of carotid occlusion take the form of transient ischemic attacks (TIAs) lasting for up to a few hours. As with TIAs elsewhere, the physician is unlikely to be present during an attack and must interpret the account given by the patient or relative. The territory of the middle cerebral artery is most often affected. Individual symptoms tend to occur in isolation and include any of the following: a feeling of heaviness/weakness/numbness/tingling in one arm or leg, halting or slurring of speech. Disturbance of flow in the ophthalmic artery may cause transient monocular blindness (one eye may be perceived as filled with fog or white steam).

Clinical Panel 35.5 Occlusions within the posterior circulation

The clinical phrase long tract signs is most often used in the context of brainstem lesions. It refers to evidence of a lesion in one or more of the three long tracts: namely, the pyramidal tract, the posterior column–medial lemniscal pathway, and the spinothalamic pathway. All of the long tract signs occur in the limbs on the side opposite to the lesion.

Small brainstem infarcts may yield the following features:

• Midbrain. Ipsilateral third nerve paralysis and/or bilateral cerebellar ataxia caused by damage to the decussation of the superior cerebellar peduncles; ‘crossed’ third nerve paralysis featuring ipsilateral paralysis combined with contralateral hemiplegia.
• Pons. A tegmental infarct may cause ipsilateral facial and/or abducens and/or mandibular nerve paralysis and/or anesthesia of the face. A basilar infarct may produce a contralateral pure motor hemiplegia whose brainstem origin may be indicated by transient ipsilateral functional impairment of the abducens, facial or mandibular nerve passing through the tegmentum.
• Medulla oblongata. Most characteristic is the lateral medullary syndrome, described in Chapter 19, caused by occlusion of the posterior inferior cerebellar artery. Occlusion of the labyrinthine branch of the anterior inferior cerebellar artery causes immediate destruction of the inner ear; sudden deafness in that ear is accompanied by vertigo with a tendency to fall to that side.

Large brainstem infarcts in pons or medulla oblongata are usually fatal because of damage to the vital centers of the reticular formation. In the midbrain, they may produce a permanent state of coma.

Cerebellar ataxia of the limbs on one side, without brainstem damage, is more often due to occlusion of the top end of the vertebral artery on that side than to occlusion of one of the three cerebellar arteries.

The posterior cerebral arteries are usually perfused through the basilar bifurcation. Occlusion is more common in branches than in either main stem (Clinical Panel 35.6).

Reference

Savitz I, Caplan LR. Vertebrobasilar disease. N Eng J Med. 2005;352:2618-2626.

Clinical Panel 35.6 Posterior cerebral artery occlusion

A variety of effects may follow occlusion of branches of the posterior cerebral artery. Usually the occlusion is limited to a branch to the midbrain, or to the thalamus, or to the subthalamic nucleus, or to the cerebral cortex.

Midbrain

The classic picture of a unilateral infarct of the midbrain is that of a crossed third nerve palsy, i.e. a complete oculomotor paralysis on one side with a hemiplegia on the other side (Weber’s syndrome). The hemiplegia is due to infarction of the crus cerebri, which contains corticospinal and corticonuclear fibers in its mid-portion. The hemiplegia usually shows early improvement, but ataxia may appear on that side because of damage to dentatothalamic fibers bypassing the red nucleus.

Thalamus

Occlusion of a thalamogeniculate branch may cause infarction of the posterior lateral nucleus of the thalamus (which receives the spinothalamic tract and medial lemniscus), and sometimes of the lateral geniculate nucleus also. The usual result is a contralateral sense of numbness, perhaps with hemianopia. The rare and unpleasant thalamic syndrome (Ch. 27) may supervene.

The term central poststroke pain (CSSP) is now more often used. Up to 10% of patients with diminished tactile sensitivity develop spontaneous pain on the affected side during the ensuing months or even years. The most likely explanation at the moment is that the stroke disables tonically active GABAergic neurons projecting from the thalamic reticular nucleus to the ventral posterior nucleus where it receives the spinothalamic tract.

Subthalamic nucleus

Occlusion of a thalamoperforating branch may destroy the small subthalamic nucleus and give rise to ballism on the contralateral side, usually affecting the arm (Ch. 33).

Corpus callosum

Infarction of the splenium of the corpus callosum blocks transfer of written information from the right visual association cortex to the left. The result of infarction is alexia for written material presented to the left visual field.

Cortex

Occlusion of the stem of the posterior cerebral artery behind the midbrain gives rise to a homonymous hemianopia in the contralateral field. Macular vision may be spared. One view of macular sparing is that it signifies bilateral representation of the fovea in the primary visual cortex. Another view is that the occipital pole is supplied by a long branch from the middle cerebral artery supplying the angular gyrus.

Occlusion of the left artery also produces alexia, the left visual field being the only area detectable by the patient.

A pure alexia, without agraphia, may follow a lesion of the left lingual gyrus.

Bilateral occlusion

Partial or complete cortical blindness may result from a thrombus arrested where the lumen of the basilar artery normally narrows below the basilar bifurcation, with consequent blockage of both posterior cerebral arteries. It has also been recorded following cardiac arrest with resuscitation.

Temporary cessation of flow in both posterior cerebral arteries sometimes affects only the anterior parts of their territories. If damage is confined to the occipitotemporal junctions, prosopagnosia (inability to identify faces) may occur alone. (Prosopagnosia has been recorded with purely right-sided perfusion failure.) If the entorhinal cortex/hippocampus is compromised on both sides, anterograde and/or retrograde amnesia may follow.

Clinical Panel 35.7 Subarachnoid hemorrhage

Blister-like ‘berry’ aneurysms 5–10 mm in diameter are a routine autopsy finding in about 5% of people. Most are in the anterior half of the circle of Willis. Spontaneous rupture of an aneurysm into the interpeduncular cistern usually occurs in early or late middle age. The characteristic presentation is a sudden blinding headache, with collapse into semiconsciousness or coma within a few seconds. On physical examination, a diagnostic feature (absent in one-third of cases) is nuchal (neck) rigidity. This is caused by movement of blood into the posterior cranial fossa, where the dura mater is supplied by cervical nerves 2 and 3 (Ch. 4). The term meningismus is sometimes used for this sign.

The massive rise in intracranial pressure may be fatal within a few hours or days. Recovery may be impeded by a secondary elevation of intracranial pressure caused by blood clot obstruction of cerebrospinal fluid circulation through the tentorial notch or even within the arachnoid granulations.

About a quarter of all cases develop a neurological deficit 4 to 12 days after the initial attack. The deficit is fatal in a quarter of those who get it. The immediate cause is spasm of the main, conducting segments of the cerebral arteries. The amount of spasm is proportionate to the size of the surrounding blood clot in the interpeduncular cistern.

It is usual practice to define the aneurysm by means of carotid angiography, and to ligate it surgically. Without operation, most aneurysms will leak again at some future date.

It should be emphasized that the majority of strokes originate in the territory of the middle cerebral artery.

Finally, recovery of motor function after a stroke is discussed in Clinical Panel 35.8.

Clinical Panel 35.8 Motor recovery after stroke

Very early recovery – up to 24 hours

Within hours of a stroke associated with severe hemiplegia, caused by embolic occlusion of a major artery of supply to the corona radiata or internal capsule, some patients show remarkable recovery of motor function, to a level where only a moderate weakness of an arm or leg may persist. One or both of two explanations are possible:

• The embolus has undergone fragmentation, freeing up some or all of the primary branches of the artery.
• Collapse of the blood pressure within the territory of the blocked artery has permitted retrograde filling of the peripheral branches through the small-artery anastomoses along the border zone illustrated in Figure 35.1.

Early recovery – the first few days

A more limited improvement, during a period of a week or more, is attributable to resolution of the surrounding edema, permitting resumption of oxygen and glucose supply to viable neurons.

Later recovery

During the ensuing months, slow but progressive recovery of motor function is the rule, especially with the assistance of remedial exercises supervised by a physical therapist. Because the majority of strokes result from damage to white matter rather than cortex, attention has been directed bilaterally to all areas of the cortex known to influence corticospinal output. (The parietal lobe contribution is not considered relevant here, being concerned only with sensory modulation.)

A consistent feature on functional magnetic resonance imaging (fMRI) scans is a widespread hyperexcitability of cortical areas connected to the lesion site. The hyperexcitability, accociated with reduced local activity of inhibitory, smooth stellate (GABA) neurons, appears within days and gradually diminishes over a period of up to a year or even more.

Reorganization within the affected M1

• Cell columns adjacent to those inactivated by the infarct, now liberated from lateral (surround) inhibition, become especially active. Previously silent hand-specific columns within the arm and shoulder representations are likely to become active. Existence of outlying hand-specific columns would be analagous to the cortical representation of the tongue, which in the homunculus is shown entirely below that for the face, although outlying tongue-specific columns extend halfway up the motor cortex.
• Change of allegiance. In monkeys, a significant contribution to recovery from paralysis (e.g. of the hand) produced by excising a patch of motor cortex, arises from neighboring (e.g. arm-related) cortical cell columns activating hand rather than arm motor neurons in the cord. This phenomenon is easily explained by the extensive overlap of cortical motor territories in the spinal cord, the focusing factor normally being the recurrent (Renshaw cell) inhibitory shield surrounding the zone of maximal activation. Suspended activation of spinal cell columns includes loss of surround inhibition, thereby rendering the silent motor neurons accessible to excitation by collateral branches of nearby corticospinal fibers.

Contributions originating outside the affected M1

• Active secondary motor areas contributing to the contralesional (left) corticospinal tract include premotor cortex, SMA (supplementary motor area) and anterior cingulate cortex, and the arm/shoulder area of the left M1 (Figure CP 35.8.1). All three are active during the recovery period. fMRI monitoring indicates that, in those patients with greatest damage to the corticospinal tract, there is greatest reliance on secondary motor areas to generate some motor output. Their recruitment is often bilateral, presumably because of bilateral hand representations.

Opinions differ concerning the contribution of the hand area of the left M1 to motor recovery, although some contribution would be expected in view of its 10% contribution to the left lateral corticospinal tract.

• The cerebellum and motor thalamus (ventrolateral nucleus) are also active bilaterally throughout and share the progressive reduction of activity during later stages. Cerebellar activity during motor learning was touched upon in Chapter 23, whereby an ‘efference copy’ of pyramidal tract activity is sent to the cerebellar cortex via red nucleus and inferior olivary nucleus, representing intended movements. Sensory feedback during movement enables the cerebellum to detect any discrepancy between intention and execution, leading to adjustment of the cerebellar discharge via thalamus to motor cortex. As accuracy improves, cerebellar corrective activity declines.

Sensory system contributions

Visual and tactile areas of the cortex show above-normal activation during the recovery period; so too does the dorsolateral prefrontal cortex. These activities suggest a heightened level of sensory attention, with the objective of optimizing task performance.

Collectively, fMRI observations reveal the recruitment of alternative pathways capable of activating the anterior horn cells that have been functionally deprived by the stroke.

References

Brozici M, van der Zwan A, Hillen B. Anatomy and functionality of leptomeningeal anastomoses: a review. Stroke. 2003;34:2750-2758.

Cramer SC. Repairing the human brain after stroke: I. Mechanisms of spontaneous recovery. Ann Neurol. 2008;63:272-287. II. Restorative therapies, Ann Neurol 63:549–560, 2008

Giles MF, Rothwell PM. Transient ischaemic attack: clinical revelance, risk prediction and urgency of secondary prevention. Curr Opin Neurol. 2009;22:46-53.

Henry JL, Lalloo C, Yashpal K. Central poststroke pain: an abstruce outcome. Pain Res Manage. 2008;13:41-49.

Losseff L, Browne M, Grieve J. Stroke and cerebrovascular disease. In: Clarke C, Howard R, Rossor M, Shorvon S, editors. Queen Square Textbook of Neurology. London: Wiley-Blackwell; 2009:109-154.

Schaechter JD. Motor rehabilitation and brain plasticity after hemiparetic stroke. Progr Neurobiol. 2004;73:61-72.

Ward NS, Brown MM, Thompson AJ, Frockowiak RSJ. Neural correlates of motor recovery after stroke. Brain. 2003;126:2476-2496.

Ward NS, Cohen LG. Mechanisms underlying recovery of motor function after stroke. Arch Neurol. 2004;61:1844-1848.

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Figure CP 35.8.1 Areas of cortical activity revealed by fMRI during recovery from stroke caused by an embolus within the white matter containing the right corticospinal tract.

(A) The ‘manipulandum’ used by Ward et al. to register the squeezing power of the affected hand.

(B) Depiction of embolic compromise of the right corticospinal tract.

(C) Lateral view of areas of increased cortical activity in the left (contralesional) cortex of cerebrum and cerebellum.

(D) Corresponding view of the right (lesional) side.

(E) Medial view of the left side.

(F) Medial view of the right side.

(Assistance of Dr. Nick Ward, Honorary Consultant Neurologist, National Hospital for Neurology and Neurosurgery, Queen Square, London is gratefully acknowledged.)

Core Information

Etiology of cerebrovascular accidents

The three chief underlying disorders are atherosclerosis of the internal carotid artery or vertebrobasilar system, thrombi issuing from the left side of the heart, and hypertension. Hypertension may lead either to sudden hemorrhage into the white matter or to production of small lacunae there. Hemorrhage into a tumor may mimic the effects of a vascular stroke. Some 10% of vascular strokes are caused by rupture of a ‘berry’ aneurysm.

Arterial supply of internal capsule

The anterior choroidal artery supplies the posterior limb and the retrolentiform portion. The medial striate artery supplies the anterior limb and genu. Lateral striate branches supply anterior limb, genu, and posterior limb.

Transient ischemic attacks

Transient ischemic attacks (TIAs) are episodes of vascular insufficiency causing temporary loss of brain function with complete recovery within 24 hours. Anterior circulation TIAs may cause motor and/or sensory deficit and/or dysphasia, sometimes monocular blindness. Posterior circulation TIAs may cause vertigo, diplopia, ataxia, or amnesia.

Arterial occlusion within the anterior circulation

Anterior choroidal artery syndrome results from occlusion of the anterior choroidal artery. The complete syndrome comprises contralateral hemiparesis with upper limb ataxia (‘ataxic hemiparesis’), hemihypesthesia and hemianopia.

Clinical effects of anterior, middle and posterior cerebral artery branch occlusion are summarized in Tables 35.1–35.4.

Table 35.1 Clinical effects of anterior cerebral artery branch occlusion

Branch Clinical effects
Orbital/frontopolar Apathy with some memory loss
Medial striate Paresis of face and arm
Callosomarginal Paresis and hypesthesia of face and arm ± abulia ± mutism ± inability to reach across
Pericallosal Ideomotor apraxia (anterior lesion), tactile anomia (posterior lesion)

Table 35.2 Clinical effects of middle cerebral artery occlusion

Segment Clinical effects
Left temporal Wernicke aphasia
Either stem Hemiplegia, hemihypesthesia, hemianopia
Left stem Same + global aphasia
Right stem Same + sensory neglect
Either upper division Paresis and hypesthesia of face and arm, dysarthria
Left upper division Same + Broca’s aphasia
Right upper division Same + hemineglect or expressive aprosodia
Either lower division Hemianopia ± agitated state
Left lower division Same ± Wernicke’s aphasia, alexia, ideomotor apraxia
Branches  
Orbitofrontal Prefrontal syndrome
Left precentral Broca’s aphasia
Right precentral Motor aprosodia
Central Loss of motor ± sensory function in face and arm
Inferior parietal Hemineglect
Either angular Hemianopia
Left angular Alexia
Right temporal Receptive aprosodia

Table 35.3 Clinical effects of three common lacunar infarcts

Location Clinical effects
Genu of internal capsule Dysarthria-clumsy hand syndrome ± dysphagia
Posterior limb of internal capsule Pure motor hemiparesis
Ventral posterior nucleus of thalamus Pure sensory syndrome ± sensory ataxia

Table 35.4 Clinical effects of posterior cerebral artery occlusion

Stem Clinical effects
Either Homonymous hemianopia
Left Alexia in visible field
Both Cortical blindness ± amnesia
Branch  
Midbrain Ipsilateral third nerve palsy + contralateral hemiplegia
Thalamus Contralateral numbness ± hemianopia ± thalamic syndrome
Subthalamic nucleus Contralateral ballism
Corpus callosum Alexia in contralateral visual field

The effects of middle cerebral artery occlusion are shown in Table 35.2.

Small lacunar infarcts are commonly associated with chronic hypertension. Typical examples are in Table 35.3.

Cerebral hemorrhage most often spreads from the putamen into the internal capsule; contralateral severe, flaccid hemiplegia results. Sufficient recovery may eventually permit stick-supported spastic ambulation.

Clinical effects of vertebrobasilar arterial occlusion have been summarized in the main text.

Aneurysms

Subarachnoid hemorrhage follows spontaneous rupture of a berry aneurysm at the base of the brain. A typical sequence of clinical effects, in those who survive, is sudden, blinding headache followed by collapse into unconsciousness and development of neck rigidity. About a quarter of cases develop a neurological deficit within 2 weeks.

References

De Ruck J, de Groote L, Van Maele G. The classic lacunar syndromes: clinical and neuroimaging correlates. Eur J Neurol. 2008;15:681-684.

Lee JS, Han M-K, Kim SH, Kwon H-K, Kim JH. Fiber tracking by diffusion tensor imaging in corticospinal tract stroke: topographical correlation with clinical symptoms. Neuroimage. 2005;26:771-776.

Losseff N, Brown M, Grieve J. Stroke and cerebrovascular diseases. In: Clarke C, Howard R, Rossor M, Shorvon S, editors. Neurology: A Queen Square Textbook. London: Wiley-Blackwell; 2009:109-194.

Wardlaw JM. What causes lacunar stroke? J Neurol Neurosurg Psychiatry. 2005;76:617-619.

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