Cerebrovascular disease

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35 Cerebrovascular disease

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Cerebrovascular disease is the third leading cause of death in adults, being superseded only by heart disease and cancer.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

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).

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.

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.

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.

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.

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