Cerebrovascular Disease

Chapter Summary
Anterior circulation of the brain
- Internal capsule
Posterior circulation of the brain
Transient ischaemic attacks
Clinical anatomy of vascular occlusions
CLINICAL PANELS

Study guidelines

1.

This final chapter touches upon a large range of neurologic symptoms and signs, because it deals with vascular damage to every part of the brain. The great majority of the symptoms and signs have 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 your understanding of the blood supply ( Chapter 5 ).

Cerebrovascular disease is the second leading cause of death in adults, superseded only by heart disease. The most frequent expression of cerebrovascular disease is a stroke , which is defined clinically as a focal neurologic deficit of ischaemic vascular origin, involving the central nervous system (CNS) or retina and lasting for more than 24 hours if the patient survives. An 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 recognised, based upon location and size.

The chief underlying pathophysiology is 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 may be progressively occluded over a period of 10 years or more without apparent brain damage; the contralateral internal carotid artery utilises the circle of Willis to perfuse both pairs of the 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 by small (less than 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—that is, their communications with neighbouring penetrating arteries are too fine to save brain tissue in the event of blockage.

Figure 35.1

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

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 haemorrhage, 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 aetiology is believed to be an occlusion by microatheromas or lipohyalinosis. Lacunar strokes can recur, and such recurrence has a high association with a state of vascular subcortical dementia ( multi-infarct dementia ). An infarct is an area of ischaemic injury produced by vascular occlusion, haemorrhage, or extravasation.

Cerebral infarcts become swollen after a few days because of osmotic activity. Some become large enough to produce distance effects by causing subfalcine or tentorial herniation of the brain in the manner of a tumour ( Chapter 6 ).

It is usually easy to distinguish the symptoms/signs of vascular disease from those of a tumour. A vascular stroke takes up to 24 hours to evolve, whereas the time frame for tumours is usually several months or more. However, haemorrhage into a tumour may cause it to expand suddenly and to mimic the effects of a stroke. Very often the haemorrhage is into a metastatic tumour, notably from lung, breast, or prostate; in fact, a stroke may be the first manifestation of a cancer in one of those organs, but some types of highly vascular malignant metastases are more likely to be associated with haemorrhage (e.g. choriocarcinoma, melanoma, or hypernephroma).

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’, there is associated severe headache and loss of consciousness, and the individual is less than 40 years old.

Anterior circulation of the brain

Clinicians refer to the internal carotid artery 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 ).

About 75% of strokes 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.

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 .

Transient ischaemic attacks

Transient ischaemic attacks (TIAs) are episodes of vascular insufficiency that cause temporary loss of brain function and are not associated with evidence of infarction. Most TIAs last for less than half an hour, with no residual signs at the time of clinical examination. Diagnosis is suggested based upon reported symptoms and confirmed by neuroimaging.

Most attacks follow lodgement 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’), aphasia, 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 or posterior 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 summarised in Clinical Panels 35.1 to 35.4 , within the posterior circulation in Clinical Panel 35.5 , and specifically within the territory of the posterior cerebral artery in Clinical Panel 35.6 . Subarachnoid haemorrhage 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 the cortical type ( Chapter 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 is rare because the opposite artery has direct access to its distal territory through the anterior communicating artery. However, branch occlusions are well recognised, 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 the SMA normally collaborates with the Broca area in the initiation of speech. Finally, damage to the SSA may result in inability to reach with the contralateral arm towards 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.