Stroke



Stroke


Stroke follows heart disease and cancer as the third leading cause of death in developed countries, accounting for 10% of overall mortality in the UK. It is defined clinically as an acute neurological deficit of vascular origin that lasts more than 24 hours or causes death.



Types of stroke


Stroke is caused by inadequate tissue perfusion or ischaemia (Greek: isch-, restriction; haema, blood). The brain is particularly sensitive to ischaemia because neurons have a high metabolic rate and can only survive a few minutes without oxygen and glucose. Tissue death as a result of inadequate blood flow (e.g. due to an occluded blood vessel) is called infarction (Latin: infarctus, stuffed). The area of dead tissue is referred to as ‘an infarct’. There are two main types of stroke (Figs 10.1 and 10.2):





In both types of stroke the brain tissue normally supplied by the vessel is suddenly deprived of blood and its function is lost. This causes focal neurological deficits that develop very rapidly (e.g. sudden weakness or loss of speech) and abrupt onset is the clinical hallmark of stroke. In haemorrhagic stroke, there may also be mechanical damage, such as tearing and compression of brain tissue, caused by blood escaping under arterial pressure.




Ischaemic stroke


Ischaemic stroke can be divided into five groups based on cause: (i) large-artery atherosclerosis; (ii) cardioembolism; (iii) small vessel occlusion; (iv) other defined cause; and (v) unknown cause (cryptogenic stroke). This classification is derived from a multicentre trial of acute stroke treatment (‘TOAST’) in the 1990s and continues to be widely used in UK stroke trials. The ‘other defined cause’ category incorporates many uncommon and rare causes of stroke including abnormalities of blood coagulation, infectious diseases, arterial damage and inflammatory disorders.



Large vessel and cardioembolic stroke


Cerebral blood vessels may be occluded by an embolus (Greek: embolos, wedge or plug). This is a small piece of coagulated blood (or occasionally some other material such as fat) that travels in the circulation and lodges in the vascular tree of the brain. Emboli often originate from the heart (cardioembolic stroke) in association with valve disease or an abnormal heart rhythm (Clinical Box 10.1). Disease in the neck vessels or aortic arch may also give rise to emboli.



Some ischaemic strokes are caused by coagulation of blood within a cerebral vessel, termed in situ thrombosis (Greek: thrombos, blood clot) or large artery intracranial occlusive disease. This is more common in people of Asian and African origin, but is increasingly recognized in Caucasians.



Small vessel disease


Small vessel disease is particularly common in patients with arterial hypertension together with other vascular risk factors (e.g. diabetes, cigarette smoking, elevated cholesterol). High blood pressure damages the arterial wall and its smooth muscle is gradually replaced by collagen, termed hyaline arteriosclerosis. In some cases there is vessel wall necrosis with accumulation of lipid-laden foam cells, which is referred to as lipohyalinosis.


Both types of pathology cause arteriosclerosis or ‘hardening’ of the arteries (Greek: sklerōs, hard). Sclerotic vessels are unable to dilate in response to reduced flow, leading to lacunar infarcts (see Ch. 12, Figs 12.18 and 12.19). These are small areas of ischaemic tissue damage (often in the basal ganglia or internal capsule) measuring less than 1 cm in diameter (Latin: lacūna, hole or gap). Small vessel disease is also an important cause of vascular cognitive impairment and dementia (Ch. 12).





Haemorrhagic stroke


Spontaneous intracerebral haemorrhage is more common in people with high blood pressure and frequently occurs in the basal ganglia, cerebellum or pons (Fig. 10.2A). However, the incidence of hypertensive intracerebral haemorrhage is declining in the UK and USA and an increasingly important cause is cerebral amyloid angiopathy, particularly in the elderly (see Ch. 12, Clinical Box 12.5). This is caused by deposition of amyloid beta peptide in the walls of cortical and meningeal arteries, leading to atypical (or lobar) haemorrhages that are close to the cortical surface (Fig. 10.2B).


Up to a third of spontaneous intracranial haemorrhages are caused by rupture of an aneurysm (a dilatation in the wall of an artery). Since the cerebral blood vessels travel and branch within the subarachnoid space, this results in subarachnoid haemorrhage (Clinical Box 10.2). Aneurysms that rupture in the substance of the brain may cause devastating brain damage or sudden death.





Blood supply to the brain


The brain is supplied by two pairs of arteries that arise from branches of the aortic arch (Fig. 10.4):




The arteries at the base of the brain are linked by communicating vessels to form the circle of Willis. This gives rise to anterior, middle and posterior cerebral arteries on each side, which supply most of the cerebral hemisphere. The cerebral blood supply can be divided into anterior and posterior circulations (Fig. 10.5A).




Anterior circulation


The internal carotid artery divides at the base of the brain, giving rise to the middle cerebral artery (MCA) and the anterior cerebral artery (ACA). The MCA is the larger of the two and receives 80% of the internal carotid blood flow. For this reason, cardiogenic emboli are much more likely to enter the MCA than the ACA. The middle cerebral artery continues laterally between the frontal and temporal lobes and emerges from the lateral sulcus to supply most of the hemispheric convexity (Figs 10.6A and 10.7).




The anterior cerebral artery passes forward and medially to meet its partner between the cerebral hemispheres. It winds around the corpus callosum and supplies the medial aspect of the hemisphere as far back as the parieto-occipital sulcus (Figs 10.6 and 10.8). Posterior to this point the posterior cerebral artery takes over to supply the occipital lobe. Perforating branches of the anterior circulation supply the optic radiations, so that anterior circulation strokes may cause a contralateral visual field defect.





Circle of Willis


The circle of Willis is a polygonal arrangement of blood vessels surrounding the optic chiasm and pituitary stalk. It connects the anterior and posterior circulations via the single anterior communicating artery and the paired posterior communicating arteries (Figs 10.5B and 10.9). The circle of Willis shows considerable anatomical variation and is incomplete in 50% of people. It is an example of a collateral circulation, an arrangement of interconnected vascular channels permitting blood flow via an alternative route in the event of an obstruction. Interconnections between vessels exist elsewhere (e.g. between the distal territories of the three main cerebral blood vessels) but are not always effective, particularly in the elderly. Some structures do not have a collateral blood supply (e.g. the internal capsule and basal ganglia) and are therefore more vulnerable to stroke.



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Jun 19, 2016 | Posted by in NEUROLOGY | Comments Off on Stroke

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