Stroke is the third commonest cause of death in developed countries. The incidence of strokes is 1-2 per 1000 population per annum in Europe and the USA but is higher in the Afro-Caribbean population. It is uncommon below the age of 40 years and is slightly more common in males. However, 16% of women compared with 8% of men die of a stroke. This difference is due to the higher mean age of stroke onset and the greater life expectancy in women. The incidence of stroke is decreasing in the age range 30-60 years as hypertension is recognized and treated. In the elderly population, stroke remains a major cause of morbidity and mortality.
Cerebrovascular disease comprises:
• Thromboembolic infarction
• Primary intracranial haemorrhage
• Subarachnoid haemorrhage
• Subdural and extradural haemorrhage and haem atom a
• Cortical venous and dural venous sinus thrombosis
STROKE. This is a focal neurological deficit due to a vascular lesion. It is usually of rapid onset and, by definition, lasts longer than 24 hours if the patient survives. Hemiplegia due to middle cerebral arterial thromboembolism is a common example.
A COMPLETED STROKE is when the neurological deficit has reached its maximum, usually within 6 hours of onset.
A STROKE ‘IN-EVOLUTION’ is when symptoms and signs are getting worse, usually within 24 hours of onset.
A MINOR STROKE. These patients recover without a significant deficit usually within 1 week.
TRANSIENT ISCHAEMIC ATTACK (TIA). This is a focal deficit lasting less than 24 hours. There is complete clinical recovery. The attack is usually of sudden onset. TIAs have a tendency to recur.
These definitions, although valuable, clinically are arbitrary. The clinical picture of ‘stroke’ may also be caused by tumour, abscess, subdural haematoma or, rarely, by demyelination.
Difficulties occur in the diagnosis of cerebrovascular disease because similar clinical events can be caused by different pathological processes.
COMPLETED STROKE. A completed stroke is caused by three processes:
1 Embolism from a distant site and subsequent braininfarction
2 Thrombosis of a cerebral vessel and subsequent brain infarction
3 Haemorrhage into the brain
The underlying risk factors and predisposing pathology are shown in Table 18.25.
TRANSIENT ISCHAEMIC ATTACKS. TIAs are usually caused by the passage of micro emboli into the brain. Less commonly, they may be caused by a fall in cerebral perfusion (e.g. due to a cardiac dysrhythmia, postural hypotension or decreased flow through atheromatous vertebral arteries) but this is usually prevented by autoregulation. Small areas of brain infarction following thrombosis or even haemorrhage may occasionally cause a clinical TIA. Thromboembolism from vascular disease outside the brain is the cause of:
• 70% of all strokes and
• 90% of TIAs
The principal sources of emboli are atheromatous plaques within the great vessels, the carotid and vertebral systems, or from the heart. The latter are associated with atrial fibrillation often secondary to valvular disease, or mural thrombi formed after myocardial infarction.
Heart disease, e.g. mitral stenosis
Low cerebral perfusion, e.g. hypotension
Hyperviscosity, e.g. polycythaemia
Arteritis, e.g. SLE
Metabolic diseases, e.g. homocystinuria (very rare)
An understanding of normal arterial anatomy and the likely sites of atheromatous plaques and stenotic lesions is important.
The circle of Willis is supplied by the two internal carotid arteries and by the basilar artery, which is formed by the union of the two vertebral arteries. Proximal to the circle, atheromatous plaques and stenoses are common at the following five sites:
1 The origins of the common carotid arteries
2 The origins of the internal carotid arteries
3 Within the carotid syphon (in the cavernous sinus)
4 Within the subclavian vessels
5 The origins of vertebral arteries
The distribution of the anterior, middle and posterior cerebral arteries, which supply the cerebrum.
AUTOREGULATION. The smooth muscle of small intracerebral arteries responds directly to changes in pressure gradient across the vessel wall. In the normal situation, constant cerebral blood flow (CBF) can be maintained with systolic blood pressures between 80 and 170 mmHg (i.e. the CBF is independent of perfusion pressure). In disease states, CBF autoregulation may fail. The contributory causes are:
SEVERE HYPOTENSION (systolic blood pressure <75 mmHg)
SEVERE HYPERTENSION (systolic blood pressure >180 mmHg)
INCREASE IN BLOOD VISCOSITY (polycythaemia, hyperviscosity syndromes)
RAISED INTRACRANIAL PRESSURE CHANGES IN ARTERIAL P02 and Pco,
TRANSIENT ISCHAEMIC ATTACKS SYMPTOMS TIAs cause sudden loss of function in one region of the brain. Symptoms usually reach their peak in seconds and last for minutes or hours (but by definition <24 hours). The general site of the cerebral lesion is often suggested by the clinical pattern of the attack.
The diagnosis of a TIA is often based upon the description of the event. During an attack the loss of function can be demonstrated. Consciousness is usually preserved. There may be clinical evidence of a source of embolus, such as:
• Carotid artery stenosis (arterial bruit)
• Atrial fibrillation (or other dysrhythmia)
• Valvular heart disease or endocarditis
• Recent myocardial infarction
• Difference between right and left brachial blood pressure (subclavian stenosis)
There may be other clinical evidence of associated disease, such as:
• Postural hypotension
• Bradycardia or low cardiac output
• Diabetes mellitus
• Rare-arteritis, polycythaemia
SPECIFIC TYPES OF TRANSIENT ISCHAEMIC ATTACK
The clinical features of many of the forms of TIA are given in Table 18.26. Hemiparesis, vertigo or aphasia are the commonest complaints. Two examples are mentioned briefly here. Amaurosis fugax This is a sudden transient loss of vision in one eye due to the passage of emboli through the retinal arteries. The emboli are sometimes visible through an ophthalmoscope. Amaurosis fugax is suggestive of a TIA in the anterior circulation and is often the first clinical evidence of carotid stenosis. It may also herald a hemiparesis.
Transient global amnesia
pisodes of amnesia with confusion lasting for several hours are probably caused by ischaemia in the posterior circulation.
TIAs must be distinguished (usually on wholly clinical grounds) from other causes of transient loss of function. Focal epilepsy is usually accompanied by ‘irritative phenomena’ (e.g. jerking of the limbs) and characteristically here is a ‘march’ of events, with some progression. In a TIA the maximum deficit is usually apparent immediately.
Migraine, with a focal prodrome, sometimes causes diagnostic confusion. Headache is distinctly unusual in a TIA and there are usually no visual disturbances suggestive of migraine.
A TIA is an important prognostic event. Prospective studies have shown that 5 years after the TI A:
• One out of six patients will have suffered a stroke
• One out of four patients will have died (usually from heart disease or stroke)
A TIA in the anterior circulation is generally of more serious prognostic significance than a TIA in the posterior circulation.