Changes in neuronal metabolites in brain following subarachnoid haemorrhage evaluated by proton MR spectroscopy.

Abstract

Recently, several advances in operative techniques and management of chronic cerebral vasospasm for patients with aneurysmal subarachnoid haemorrhage (SAH) have improved morbidity and mortality rates. However, even when the surviving SAH patients show no grossly evident neurological deficits, they frequently have subtle neurobehavioral problems [5, 9]. These problems have been suggested to result from widespread damage of neuronal cells from SAH [8], whereas ischaemic lesions observed by imaging study are not involved in such problems [9]. Though the details of the pathogenesis of this pathological condition is not obvious, possible causative mechanisms have been considered to explain: impairment of cerebral microcirculation at the onset of SAH and/or during chronic cerebral vasospasm [3], and secondary neuronal cell damage elicited by subarachnoid clot [6].