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]. In vivo proton magnetic resonance spectroscopy (MRS) has been recognized as a valuable method for observation of the longitudinal changes in the biochemical status of the injured brain under various pathological conditions [1, 2, 4, 7] in which MRS could demonstrate remarkable changes in N-acetyl-aspartate (NAA) and/or choline compounds (Cho) concentrations [4, 7]. NAA, neuron specific amino acid, exists largely within the neurons and its decrease is an indication of neuronal cell loss. The changes in Cho concentration has been proposed to result from the destruction of the neuronal cell membrane or active membrane metabolism. When widespread neuronal cell damage presumably exists in the brain following SAH, it may be able to detect the changes in these neuronal metabolites by means of proton MRS. For confirmation of this hypothesis, we observed changes in the neuronal metabolites in the cerebral hemisphere by means of in vivo proton MRS to evaluate whether or how neuronal cells are affected by SAH and/or cerebral vasospasm.