Stroke

Synonyms :  Apoplexy; Cerebral Infarction; Cerebral Vascular Accident, Cerebrovascular accident

Clinical features, Diagnosis, Management, Prognosis, Nutrition, Herbs,

Cerebrovascular accident (stroke) refers to damage to brain tissue due either to cerebral infarction (80-85%) or cerebral haemorrhage (15-20%). Stroke is uncommon below the age of 50 and affects males more often than females. It is one of the commonest causes of death in developed countries and also a prominent cause of disability, particularly in the elderly. The most common vascular disorder underlying stroke is atherosclerosis affecting intracranial and extracranial arteries, less common causes are embolism and aneurysms (pouch-like dilations) of major arteries. 

The major risk factors for stroke:

       hypertension

       cigarette smoking

       diabetes mellitus

       hyperlipidaemia (hypercholesterolaemia)

       cardiac arrhythmias, history of myocardial infarctions (risk for intracardial thrombosis)

       positive family history 

Mechanisms of stroke:

       Cerebral infraction (ischaemic stroke). Thrombosis at the site of atheromatous degeneration in a major cerebral vessel is probably the commonest mechanism, but embolism of thrombotic or atheromatous material from the heart or an extracranial artery is also frequent. Cardiac emboli (arising from mural thrombus after myocardial infarction, or associated with atrial fibrillation) tend to be large and cause usually major strokes. By contrast, emboli arising from the carotid artery are more often smaller, and cause minor strokes or transient cerebral or ocular symptoms (transient ischaemic attacks). Once completely deprived of blood supply cerebral tissue undergoes infarction within a few minutes, the resultant cerebral oedema causes more damage by compressing blood vessels and further impairing cerebral blood flow.

       Cerebral haemorrhage. The primary cause of cerebral haemorrhage is hypertension. About half the strokes caused by cerebral haemorrhage are due to subarachnoid bleeding, and the other half due to intracerebral bleeding into the brain tissue. Intracerebral bleeding is usually caused by rupture of small intracerebral arteries or arterioles weakened by hypertension and/or atheromatous degeneration. This type of stroke is more likely to occur during physical exertion or emotional stress when blood pressure is increased. On the other hand spontaneous (non-traumatic) subarachnoid haemorrhage usually results from a ruptured aneurysm of one of the major cerebral arteries or their branches, or inborn arteriovenous malformation (a mass of tangled, dilated blood vessels in which small arterioles flow directly into venules without a capillary network in-between). Aneurysms can be saccular (berry) which are thought to arise as a result of congenital defects in the media (muscle layer) of arteries at branch points and fusiform (spindle-shaped) which are a result of atherosclerotic weakening of blood vessel walls. The saccular aneurysms can be found in approximately 1% of the general population when they cause no problems until they burst, when no obvious precipitating factor is usually apparent. Haemorrhage from ruptured fusiform aneurysms often occurs during exertion (e.g., physical activity, sexual intercourse) when blood pressure is increased.

Clinical features:  < BACK TO TOP >

       Strokes usually evolve rapidly over a few minutes, and reach maximum disability within an hour or two.

       The precise features of a stroke depend on the vascular territory involved and mechanism of stroke.

       The majority of patients with ischaemic stroke exhibit greater or lesser degrees of hemiplegia (paralysis of the limbs and trunk on the contralateral side of the body), dysphasia (impaired coordination of speech - if the left hemisphere is involved), with hemianaesthesia (loss of sensation on the contralateral side of the body) and homonymous hemianopia (loss of vision in either the whole left or the whole right half of the visual field) in some.

       Initially the paralysed limbs may be flaccid and reflexes can be decreased, but after a few days, tone usually increases and reflexes become hyperactive on the affected side (the signs of upper motor neuron damage).

       Headache is a common feature and it is due to secondary brain oedema and increase of intracranial pressure.

       Epileptic seizures, vomiting and depressed consciousness may also occur, the latter usually indicating a severe lesion and marked increase of intracranial pressure.

       The brain stem lesions may also show dysphagia (difficulty in swallowing), facial numbness/weakness on the same side as the lesion, and often loss of consciousness because of damage to the reticular activating system.

       In some patients the symptoms worsen gradually or in a step-wise fashion over a matter of hours or days (‘evolving stroke?/i>).

       In most patients with brain infarction consciousness is preserved in contrast to haemorrhage in the brain when the patients suddenly develop signs of increased intracranial pressure, including severe headache (with neck pain and stiffness in subarachnoid haemorrhage), nausea and vomiting, and rapid loss of consciousness.

       Localising neurological signs in cerebral haemorrhage may be present but are often difficult to detect in the setting of a massive elevation in intracranial pressure and coma.

       Progression of the condition is associated with evidence of brain stem compression, including deep coma; irregular, intermittent respirations (Cheyne-Stokes respiration); bradycardia and hypertension; dilated, unresponsive pupils; and spasticity of skeletal muscles.

       Transient ischaemic attack (TIA) is an episode of focal neurological dysfunction due to cerebral ischaemia in which symptoms last less than 1 hour, often only a few minutes. It is due to minor embolism from the extracerebral arteries (carotid and vertebral) and less commonly from mural thrombi that develop in heart chambers. Certain patients present with vertigo (dizziness), diplopia (seeing in duplicate) and ataxia (loss of motor coordination commonly presenting as unsteady gait); in others symptoms and signs are similar to completed stroke only milder and transient. TIAs are important because they may herald a completed stroke (approximately one third of patients with TIAs develop clinically significant strokes within 5 years).