Pathophysiology of Delayed Ischaemic Dysfunction After Subarachnoid Haemorrhage: Experimental and Clinical Data

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Abstract
Cerebral arterial spasm from subarachnoid haemorrhage (SAH) may be associated with the clinical syndrome of delayed cerebral ischaemic dysfunction, but the two conditions are by no means synonymous. Patients in good clinical condition may be seen with severe vasospasm and vice versa. A variety of mechanisms may be responsible for the neurological dysfunction: current evidence indicates that most of these mechanisms produce a reduction in cerebral blood flow (CBF). In the early stages after SAH, there is a loss of autoregulation so that reduction in cerebral perfusion pressure (CPP) may produce ischaemia. This fall in CPP may be due to elevated intracranial pressure (ICP) or reduced mean arterial blood pressure (MABP). Delayed cerebral ischaemic dysfunction following SAH is a clinical syndrome which may also be caused by re-bleeding, hydrocephalus, dehydration, reduced cardiac output and/or blood pressure, hyperglycemia or epilepsy. The physical properties of the haemorrhage result in increased local tissue pressure around the lesion. This produces squeezing of the microcirculation and focal ischaemia. Vasoconstrictor elements in blood produce spasm which may further reduce CBF, sometimes even remotely from the lesion.