Cerebral Infarction Management

Specific measures (contd.) Decreasing blood viscosity

Improving hydration and venesection lower the haematocrit and reduce blood viscosity, thereby increasing cerebral blood flow (to a greater extent than the oxygen carrying capacity is reduced). Preliminary studies of venesection have produced encouraging results. Plasma expanders, low molecular weight dextran and drugs that effect red blood cell deformity (pentoxifylline) lower blood viscosity but seem of less value.

Neuronal rescue

Experimental work indicates a pathological role for intracellular calcium influx in neuronal injury. Excitatory amino acids - glutamate and glycine - promote calcium influx by acting on receptor-mediated membrane channels. (N-methyl-D-aspartate-NMDA channels.) The NMDA channel has at least 6 sites which may be pharmacologically blocked. Agents such as MK801, Mg^ CGS-19755 and d-Methorphan have been evaluated in animal models and some await evaluation in human clinical trials. Voltage dependent calcium channel antagonists (Nimodipine, Diltiazem, Nifedipine and Verapamil) have been assessed, with, to date, disappointing results, in large multicentre studies of acute infarction.

Treatment of oedema

The degree of concomitant oedema relates to the magnitude of infarction. Oedema develops early and may cause ventricular displacement and transtentorial herniation with secondary brain stem damage. Controversy exists as to whether oedema is vasogenic or cytotoxic (as associated with metabolic encephalopathies), or a mixture of the two. Its effective treatment should lower morbidity and mortality but steroids and hyperosmolar agents (e.g. mannitol) have been used with little effect on outcome. The poor response probably reflects the 'mixed' nature of the oedema.

Prevention of further stroke

The recognition of risk factors and their correction to minimise the risk of further events forms a necessary and important step in long-term treatment.

- Control hypertension

- Emphasise the need to stop cigarette smoking

- Correct lipid abnormality

- Give platelet antiaggregation drugs (aspirin or in selected cases ticlopidine) to reduce the rate of reinfarction

- Remove or treat embolic source (long term anticoagulation in atrial fibrillation)

- Treat inflammatory or vascular inflammatory diseases

- Stop thrombogenic drugs, e.g. oral contraceptives.

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