Cerebrovascular Disease

Ischaemic Strokes

While there are multiple potential aetiologies for a stroke, initial classification is ischaemic, comprising 85% of all strokes, and the remainder are haemorrhagic. For ischaemic stroke the underlying mechanism is either vessel pathology that leads to occlusion (e.g., atherothrombosis) or a source (e.g. the heart) generating a ‘particle’ that results in embolic occlusion of a vessel (e.g. cardiac). A third group of ischaemic stroke involves occlusion of cerebral small vessels that results in small subcortical infarctions within the territory of those perforating arterioles and on neuroimaging (and postmortem) the appearance of fluid-filled cavities called lacunes, hence the name lacunar strokes . There is a subgroup of these small-vessel arteriole strokes that, based on their clinical presentation, identify lacunar syndromes that reflect injury to specific white matter tracks or subcortical structures ( Clinical Panel 35.4 ). Historically chronic hypertension (a risk factor for cerebrovascular disease) was the assumed primary cause of these occlusions, but now the proposed aetiology is dysfunction in endothelial cells and disruption of the blood–brain barrier that eventually leads to arteriole injury, degeneration, and occlusion.

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. Embolic strokes can also arise from blood clots in the left side of the heart, in association with coronary or valvular disease.

The expected deficit from the gradual occlusion of a vessel may be minimised by routing of blood through alternative, collateral, blood vessels. 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. Or the external carotid can bypass the occlusion through collateral vessels that originate from branches of the facial artery and anastomose with 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 cerebral arteries. The number of such small arteries varies greatly between individuals and this ‘crescent-shaped’ anastomotic region is known as the watershed area ( Fig. 35.1 ). On the other hand, all arteries penetrating the brain substance are end arteries and their communications with neighbouring penetrating arteries are too fine to prevent ischaemic injury for most cerebral arterial occlusions.

Haemorrhagic Strokes

The remaining 15% of acute strokes are haemorrhagic, either intracerebral (10%) or from subarachnoid haemorrhage (5%). Most haemorrhagic strokes represent spontaneous rupture of a small cerebral vessel and hypertension is the most common aetiological factor. The remainder reflect bleeding from various vascular malformations or abnormalities of blood coagulation that predispose to bleeding.

Nontraumatic subarachnoid haemorrhage ( SAH ) is most frequently (80%) the result of rupture of an intracranial aneurysm (‘berry aneurysm’). A typical sequence of clinical events is the sudden onset of headache (‘worst headache of my life’) followed by altered mental status and signs of meningeal irritation (neck stiffness with pain on motion secondary to the irritative effects of blood). Morbidity is significant and mortality is up to 50%.

Intracranial aneurysms originate near the circle of Willis, but some arise at arterial bifurcation points within the brain. This location explains the fact that when these aneurysms rupture, blood directly enters the subarachnoid space and bleeding continues until the intracranial pressure increases and stops bleeding at the aneurysmal rupture site and thrombus forms. In up to 40% of cases there is an earlier rupture, less catastrophic, but serving as a warning or ‘ sentinel leak ’ weeks before the more serious event. This serves as the rationale for a high suspicion of SAH if an individual presents with a sudden, severe, and unusual headache.

The cranial cavity is a rigid structure and any increase in volume is associated with an increase in intracranial pressure. Cerebral infarcts (or haemorrhage) result in cytotoxic oedema that consists of an increase in intracellular water in the area of ischaemic injury. This causes an increase in intracranial pressure and displacement of cerebral structures that can result in effects at a distance by causing subfalcine or tentorial herniation of the brain in the manner of a tumour (see Chapter 5 ), and cerebral blood flow in initially unaffected vessels can also be affected. Cerebral oedema typically reaches its maximum in 72 to 120 hours and cytotoxic oedema does not respond to steroid administration (the oedema frequently encountered with brain tumours is extracellular, vasogenic oedema , and does respond to steroids).

Stroke Mimics

There are other clinical conditions that can mimic a stroke as they present with neurological impairment, but symptoms are often vague and lack the localising features seen in stroke syndromes. These include seizure, brain tumour, migraine with aura, metabolic derangements that result in dysfunction of the brain, and encephalopathy (e.g. hypoglycaemia, electrolyte disturbance, drugs) as the most frequent. When history, exam, and neuroimaging are inconclusive, such individuals may initially be evaluated and treated as a stroke until time allows further clarification.

Internal Capsule

The following details supplement the account of the arterial supply of the internal capsule in Chapter 4 .

The blood supply of the internal capsule is shown in Fig. 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 Fig. 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 of the internal capsule, genu of the internal capsule, and the head of the caudate.

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