Cerebrovascular disease

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35 Cerebrovascular disease

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Cerebrovascular disease is the third leading cause of death in adults, being superseded only by heart disease and cancer.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.

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).

image

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.

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.

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 35.135.4, 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 35.2 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:

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.

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.

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.

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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 35.5 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:

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).

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.

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

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.

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.

Core Information

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 35.135.4.

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.