Chapter: Medicine and surgery: Nervous system

Stroke - Cerebrovascular disease

A stroke is defined as a sudden onset of non-traumatic focal neurological defect of a vascular aetiology, that either causes death or lasts more than 24 hours. - Definition, Incidence, Age, Sex, Aetiology, Pathophysiology, Clinical features, Complications, Investigations, Management, Prognosis.

Cerebrovascular disease






A stroke is defined as a sudden onset of non-traumatic focal neurological defect of a vascular aetiology, that either causes death or lasts more than 24 hours.




Third commonest cause of death in Western World (1–2 per 1000 per year).



Uncommon under 40 years.




> F, but mortality twice as high in females.




Black community, Japanese more common.




·        20% of strokes are haemorrhagic and 80% are ischaemic, of which two-thirds arise from extracranial lesions and one-third arise from intracranial lesions. Strokes may also be due to subarachnoid haemorrhage. Risk factors for stroke can be divided into Intra- or extra-cranial atherosclerosis: In particular hypertension, smoking, hyperlipidaemia, family history of stroke or ischaemic heart disease and diabetes mellitus.


·        Heart disease: Valvular heart disease such as mitral stenosis, infective endocarditis, and any condition which predisposes to mural thrombus such as atrial fibrillation or myocardial infarction.


·        Less common causes: Hyperviscosity or prothrombotic states, e.g. polycythaemia, oral contraceptive pill; vasculitis; clotting disorders.




Haemorrhagic strokes are discussed elsewhere. Ischa-emic strokes are due to the interruption of arterial blood supply, and the clinical picture depends on the size of artery and hence extent of territory affected, the area affected, and whether there is temporary or permanent ischaemia and hence infarction.


Clinical features


Anterior circulation (carotid territory) strokes are the most common, in particular those involving a branch of the middle cerebral artery. This causes infarction of the motor pathways (at the level of the motor cortex or the internal capsule) and usually results in a contralateral hemiparesis. This is an upper motor neurone (UMN) deficit, i.e. increased tone, reduced power and brisk ten-don reflexes, although acutely there may be a flaccid, areflexic paralysis. The arm tends to be affected more than the leg (the motor cortex for the leg is supplied by the anterior cerebral artery).

Other features of an MCA territory infarct include an ipsilateral UMN lesion of the face (weakness of the lower facial muscles), hemianopic visual field loss and if the dominant hemisphere is affected dysphasia may occur due to infarction of areas governing speech (Wernicke’s and Broca’s areas).


Posterior circulation (the vertebral, basilar arteries and their branches) strokes affect the brainstem, cerebellum and occipital lobes. One characteristic but uncommon pattern is lateral medullary syndrome which can be caused by thromboembolism of the posterior inferior cerebellar artery (PICA) or the vertebral artery. It causes sudden vertigo and vomiting. On examination there is ipsilateral ataxia (loss of co-ordination), contralateral loss of pain and temperature sensation and there may be nystagmus, diplopia and an ipsilateral Horner’s syndrome.


·        If the pontine reticular formation is involved in brain-stem infarcts, important basic functions such as alertness, breathing and circulation may be affected leading

to coma and death.


Lacunar infarcts are small (<1 cm) often slit-shaped areas of infarction usually in the basal ganglia, internal capsule and pons caused by hyaline arteriosclerosis within the small fine perforating arteries of the brain. They are predisposed to by hypertension and diabetes, are often asymptomatic but may cause focal neurological defects such as weakness of a single limb, or limited ataxia.


·        Multiple lacunar or larger infarcts can result in a multiinfarct dementia with a picture of loss of intellect occurring in a step-wise pattern. The final picture may include dementia and a shuffling gait which resembles Parkinson’s Disease.


In clinical situations a full neurological examination should be performed and a careful cardiovascular examination in order to reveal any source of embolus or other predisposing disease.




In the first 24 hours, there is little macroscopic change. The tissue may look paler and lose differentiation between white and grey matter.


The normal pattern of tissue change within the brain following a stroke is liquifactive necrosis. Structural breakdown takes place, the infarcted tissue becomes soft and is at risk of reperfusion haemorrhage.

Macrophages enter the infarct and remove the dead tissue, whilst around the edges astrocytes proliferate and healing takes place by scarring (gliosis). Large infarcts cannot be completely replaced and heal as spaces surrounded by gliosis.




·        CT brain scanning is used to differentiate between haemorrhage, infarction and a space occupying lesion. The scan may be normal in the first 24–48 hours, although large infarcts normally show due to oedema and loss of differentiation between white and grey matter. MRI scans are more sensitive.


·        Investigation of underlying cause


Full blood count: Haemoglobin and platelets for polycythaemia, anaemia or thrombocytopenia/ thrombocytosis, ESR for vasculitis/arteritis.


Urinalysis and blood glucose for diabetes mellitus. Cardiac investigation: Blood pressure measurement,


chest X-ray, ECG for recent infarct/arrhythmia. Transthoracic is indicated and transoesophageal echocardiography may also be required.


Carotid doppler studies to examine for carotid vascular disease particularly in younger patients or if signs dictate. Further investigation such as carotid and vertebral angiography may be indicated.




Patients who present within 3 hours of onset of symptoms who have no evidence of haemorrhage or large infarct on CT head scan should be considered for thrombolysis.


Acutely, treat any exacerbating factors such as hypotension, hypoglycaemia, hyperglycaemia, or severe hypertension (with caution, to prevent sudden loss of perfusion pressure, particularly in the acute stages, when the brain is unable to autoregulate BP well). Prevent and treat any complications such as deep vein thrombosis due to immobility, aspiration pneumonia due to disordered swallow, pressure sores and limb contractures.


Inpatient or outpatient rehabilitation is used to regain maximal functional improvement, and so reduce the impact on the patient’s life, including physiotherapy, speech therapy, and occupational therapy. Patients who are admitted to a dedicated stroke unit have been shown to have improved functional outcome and reduced mortality.


Prevention of recurrence: Any risk factors present should be treated. All patients with ischaemic (not haemorrhagic) stroke should ideally be on an antiplatelet agent such as aspirin. Cholesterol-lowering agents (statins) and anti-hypertensive agents have also been shown to reduce recurrence. Anti-coagulants are indicated in certain conditions such as atrial fibrillation and valvular heart disease, but only after approximately 2 weeks and when blood pressure is controlled, to reduce the risk of haemorrhage into infarcted tissue.


Internal carotid endarterectomy is not justified unless there have been unequivocal transient ischaemic attacks or stroke within 6 months with good recovery and significant ipsilateral carotid artery stenosis (>70%). There is a 1–5% risk of stroke or death due to the surgery. The artery is clamped with cerebral blood flow maintained by collateral supply or by a shunt. The stenosing plaque is shelled out and the artery repaired by suture or a patch. The procedure is increasingly being done under local anaesthesia or by endovascular stenting.




Overall, 40% of patients die as the result of their stroke (mainly in the first month), 40% are left significantly disabled and 30% have reasonable recovery.

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