Stroke disease

Stroke disease

P. Langhorne

Clinical examination in stroke disease


Cerebrovascular disease is the third most common cause of death in high-income countries after cancers and ischaemic heart disease, and the most common cause of severe physical disability. It includes a range of disorders of the central nervous system (Fig. 27.1). Stroke is the most common clinical manifestation of cerebrovascular disease, and results in episodes of brain dysfunction due to focal ischaemia or haemorrhage. Subarachnoid haemorrhage (SAH) and cerebral venous thrombosis (CVT) will be discussed separately, since their pathophysiology, clinical manifestations and management are distinct from those of stroke. Vascular dementia is described in Chapters 10 and 26.

Functional anatomy and physiology

The main arterial supply of the brain comes from the internal carotid arteries, which supply the anterior brain, and the vertebral and basilar arteries (vertebrobasilar system), which provide the posterior circulation. The anterior and middle cerebral arteries supply the frontal and parietal lobes, while the posterior cerebral artery supplies the occipital lobe. The vertebral and basilar arteries perfuse the brain stem, mid-brain and cerebellum (Fig. 27.2). The functions of each of these areas of the brain are described on page 1141. Communicating arteries provide connections between the anterior and posterior circulations and between left and right hemispheres, creating protective anastomotic connections that form the circle of Willis. In health, regulatory mechanisms maintain a constant cerebral blood flow across a wide range of arterial blood pressures to meet the high resting metabolic activity of brain tissue; cerebral blood vessels dilate when systemic blood pressure is lowered and constrict when it is raised. This autoregulatory mechanism can be disrupted after stroke. The venous collecting system is formed by a collection of sinuses over the surface of the brain, which drain into the jugular veins (Fig. 27.3).


A range of investigations may be required to answer specific questions about brain structure and function and about the function of the vascular system.


Computed tomography (CT) scanning is the mainstay of stroke imaging. It allows the rapid identification of intracerebral bleeding and stroke ‘mimics’ (i.e. pathologies other than stroke that have similar presentations), such as tumours. Magnetic resonance imaging (MRI) is used when there is diagnostic uncertainty or delayed presentation, and when more information on brain structure and function is required (Fig. 27.4). Contraindications to MRI include cardiac pacemakers and claustrophobia on entering the scanner. These techniques are described on page 1149.

Vascular imaging

Various techniques are used to obtain images of extracranial and intracranial blood vessels (Fig. 27.5). The least invasive is ultrasound (Doppler or duplex scanning), which is used to image the carotid and the vertebral arteries in the neck. In skilled hands, reliable information can be provided about the degree of arterial stenosis and the presence of ulcerated plaques. Blood flow in the intracerebral vessels can be examined using transcranial Doppler. While the anatomical resolution is limited, it is improving and many centres no longer require formal angiography before proceeding to carotid endarterectomy (see below). Blood flow can also be detected by specialised sequences in MR angiography (MRA) but the anatomical resolution is still not comparable to that of intra-arterial angiography, which outlines blood vessels by the injection of radio-opaque contrast intravenously or intra-arterially. The X-ray images obtained can be enhanced by the use of computer-assisted digital subtraction or spiral CT. Because of the significant risk of complications, intra-arterial contrast angiography is reserved for patients in whom non-invasive methods have provided a contradictory picture or incomplete information, or in whom it is necessary to image the intracranial circulation in detail: for example, to delineate a saccular aneurysm, an arteriovenous malformation or vasculitis.

Lumbar puncture

Lumbar puncture (p. 1153) is largely reserved for the investigation of SAH.

Cardiovascular investigations

Electrocardiography (ECG; p. 532) and echocardiography (p. 537) may reveal abnormalities that may cause cardiac embolism in stroke.

Presenting problems

Most vascular lesions develop suddenly within a matter of minutes or hours, and so should be considered in the differential diagnosis of patients with any acute neurological presentation.


Unilateral weakness is the classical presentation of stroke and, much more rarely, of cerebral venous thrombosis. The weakness is sudden, progresses rapidly and follows a hemiplegic pattern (see Fig. 26.18, p. 1163). There is rarely any associated abnormal movement. Reflexes are initially reduced but then become increased with a spastic pattern of increased tone (see Box 26.20, p. 1162). Upper motor neuron weakness of the face (7th cranial nerve) is often present.

Speech disturbance

Dysphasia and dysarthria are the most common presentations of disturbed speech in stroke (p. 1168). Dysphasia indicates damage to the dominant frontal or parietal lobe (see Box 26.2, p. 1142), while dysarthria is a non-localising feature reflecting weakness or incoordination of the face, pharynx, lips, tongue or palate.


Stroke causing damage to the cerebellum and its connections can present as an acute ataxia (p. 1168) and there may be associated brainstem features such as diplopia (p. 1170) and vertigo (p. 1167). The differential diagnosis includes vestibular disorders (p. 1186).


Stroke is a common medical emergency. The incidence rises steeply with age, and in many lower- and middle-income countries it is rising in association with less healthy lifestyles. About one-fifth of patients with an acute stroke die within a month of the event and at least half of those who survive are left with physical disability.


Of the 180–300 patients per 100 000 population presenting annually with a stroke, 85% sustain a cerebral infarction due to inadequate blood flow to part of the brain, and most of the remainder have an intracerebral haemorrhage (see Fig. 27.1).

Cerebral infarction

Cerebral infarction is mostly caused by thromboembolic disease secondary to atherosclerosis in the major extracranial arteries (carotid artery and aortic arch). About 20% of infarctions are due to embolism from the heart, and a further 20% are due to thrombosis in situ caused by intrinsic disease of small perforating vessels (lenticulostriate arteries), producing so-called lacunar infarctions. The risk factors for ischaemic stroke reflect the risk factors for the underlying vascular disease (Box 27.1). About 5% are due to rare causes, including vasculitis (p. 1115), endocarditis (p. 625) and cerebral venous disease (see below). Cerebral infarction takes some hours to complete, even though the patient’s deficit may be maximal shortly after the vascular occlusion. After the occlusion of a cerebral artery, infarction may be forestalled by the opening of anastomotic channels from other arterial territories that restore perfusion to its territory. Similarly, reduction in perfusion pressure leads to compensatory homeostatic changes to maintain tissue oxygenation (Fig. 27.6). These compensatory changes can sometimes prevent occlusion of even a carotid artery from having any clinically apparent effect.

However, if and when these homeostatic mechanisms fail, the process of ischaemia starts, and ultimately leads to infarction unless the vascular supply is restored. As the cerebral blood flow declines, different neuronal functions fail at various thresholds (Fig. 27.7). Once blood flow falls below the threshold for the maintenance of electrical activity, neurological deficit develops. At this level of blood flow, the neurons are still viable; if the blood flow increases again, function returns and the patient will have had a transient ischaemic attack (TIA). However, if the blood flow falls further, a level is reached at which irreversible cell death starts. Hypoxia leads to an inadequate supply of adenosine triphosphate (ATP), which leads to failure of membrane pumps, thereby allowing influx of sodium and water into the cell (cytotoxic oedema) and the release of the excitatory neurotransmitter glutamate into the extracellular fluid. Glutamate opens membrane channels, allowing the influx of calcium and more sodium into the neurons. Calcium entering the neurons activates intracellular enzymes that complete the destructive process. The release of inflammatory mediators by microglia and astrocytes causes death of all cell types in the area of maximum ischaemia. The infarction process is worsened by the anaerobic production of lactic acid (Fig. 27.8) and consequent fall in tissue pH. There have been attempts to develop neuroprotective drugs to slow down the processes leading to irreversible cell death but so far these have proved disappointing.

The final outcome of the occlusion of a cerebral blood vessel therefore depends upon the competence of the circulatory homeostatic mechanisms, the metabolic demand, and the severity and duration of the reduction in blood flow. Higher brain temperature, as occurs in fever, and higher blood sugar have both been associated with a greater volume of infarction for a given reduction in cerebral blood flow. Subsequent restoration of blood flow may cause haemorrhage into the infarcted area (‘haemorrhagic transformation’). This is particularly likely in patients given antithrombotic or thrombolytic drugs, and in patients with larger infarcts.

Radiologically, a cerebral infarct can be seen as a lesion that comprises a mixture of dead brain tissue that is already undergoing autolysis, and tissue that is ischaemic and swollen but recoverable (the ‘ischaemic penumbra’). The infarct swells with time and is at its maximal size a couple of days after stroke onset. At this stage, it may be big enough to exert mass effect both clinically and radiologically; sometimes, decompressive craniectomy is required (see below). After a few weeks, the oedema subsides and the infarcted area is replaced by a sharply defined fluid-filled cavity.

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Apr 9, 2017 | Posted by in GENERAL SURGERY | Comments Off on Stroke disease

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