title: In vivo proton magnetic resonance spectroscopy for metabolic changes in brain during chronic cerebral vasospasm in primates.
abstract: OBJECTIVE
  To study how neuronal cells are affected by development of chronic cerebral vasospasm after subarachnoid hemorrhage (SAH), the changes in neuronal metabolites during development of vasospasm were evaluated by in vivo localized proton magnetic resonance spectroscopy (MRS) in primates.
  
  
  METHODS
  SAH was produced by introduction of a blood clot around the right middle cerebral artery and the right side of the circle of Willis. MRS experiments were performed before SAH and on Days 7 and 14 after SAH. Multislice magnetic resonance images were obtained to locate the volume of interest (1.0 cm3) in the bilateral parietal regions. The peak areas for choline compounds, the sum of creatine and phosphocreatine, and N-acetyl-aspartate were calculated.
  
  
  RESULTS
  Angiograms revealed approximately 50% reduction of vessel caliber for the right main cerebral arteries on Day 7. Magnetic resonance imaging revealed no apparent cerebral infarction, even in the spasm-side hemisphere. MRS revealed a significant (P < 0.05) reduction of the N-acetyl-aspartate/creatine and phosphocreatine ratio on Days 7 and 14 and a significant increase in the choline/creatine and phosphocreatine ratio on Day 7, in the spasm-side parietal region. In the sham-operated animals, there were no significant changes in these ratios in the bilateral parietal region on Days 7 and 14 after the operation.
  
  
  CONCLUSIONS
  The results suggested that the development of cerebral vasospasm after SAH caused ischemic injury in a subpopulation of neuronal cells, even when no apparent cerebral infarction was shown. Proton MRS may be useful to evaluate how neuronal cells are affected by the ischemic insult during development of vasospasm in clinical situations.
authors.affiliation: Department of Neurosurgery, Fukui Medical School, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Handa
authors.forename: M
authors.initials: M
authors.lastname: Kaneko
authors.forename: T
authors.initials: T
authors.lastname: Matuda
authors.forename: H
authors.initials: H
authors.lastname: Kobayashi
authors.forename: T
authors.initials: T
authors.lastname: Kubota
mesh_terms: D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000032:analysis; D001921:Brain / Q000000981:diagnostic imaging / Q000378:metabolism*; D002545:Brain Ischemia / Q000000981:diagnostic imaging / Q000209:etiology / Q000378:metabolism; D002533:Cerebral Angiography; D002560:Cerebrovascular Circulation; D002794:Choline / Q000032:analysis; D002908:Chronic Disease; D003072:Cognition Disorders / Q000209:etiology; D003404:Creatinine / Q000032:analysis; D004734:Energy Metabolism; D005260:Female; D002546:Ischemic Attack, Transient / Q000000981:diagnostic imaging / Q000209:etiology / Q000378:metabolism*; D008252:Macaca fascicularis; D008279:Magnetic Resonance Imaging / Q000379:methods*; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D010725:Phosphocreatine / Q000032:analysis; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000378:metabolism
chemical_list: D010725:Phosphocreatine; D001224:Aspartic Acid; C000179:N-acetylaspartate; D003404:Creatinine; D002794:Choline