title: Traumatic brain injury and subarachnoid hemorrhage: in vivo occult pathology demonstrated by magnetic resonance spectroscopy may not be "ischaemic". A primary study and review of the literature.
abstract: OBJECTIVE
  To look for evidence of early ischaemic neurochemical changes in patients suffering severe traumatic brain injury (TBI) and severe subarachnoid haemorrhage (SAH). Proton metabolite concentrations were measured in normal and abnormal areas of brain on T2 MR imaging, in regions considered particularly vulnerable to ischaemic injury.
  
  
  METHODS
  Intensive care patients underwent T2 weighted imaging in a 1.5 Tesla MR scanner and proton magnetic resonance spectroscopy (single voxel or chemical shift imaging). Metabolite values in areas that appeared 'normal' and 'abnormal' on T2 MR imaging were compared with those obtained from normal controls.
  
  
  RESULTS
  18 TBI and 6 SAH patients were imaged at 1 to 26 days. N-acetyl aspartate (NAA) was lower in TBI and SAH patients compared to controls in both T2 normal and T2 abnormal areas (p<0.0005). SAH, but not TBI patients also had increased choline and creatine compared to controls in the T2 normal (p<0.02, p<0.02 respectively) and T2 abnormal (p=0.0003, p=0.003) areas. No lactate was found in TBI or SAH patients.
  
  
  CONCLUSIONS
  Significant loss of normal functioning neurones was present in TBI and SAH, but no evidence of anaerobic metabolism using lactate as a surrogate marker, questioning the role of 'ischemia' as a major mechanism of damage. Increased choline and creatine were found in SAH patients suggestive of increased cell-wall turnover. Current theories of brain injury after TBI or SAH do not explain these observed neurochemical changes and further research is required.
authors.affiliation: Department of Clinical Neurosciences, University of Edinburgh, Western General Hospital, Edinburgh, UK.
authors.forename: C S A
authors.initials: CS
authors.lastname: Macmillan
authors.forename: J M
authors.initials: JM
authors.lastname: Wild
authors.forename: J M
authors.initials: JM
authors.lastname: Wardlaw
authors.forename: P J D
authors.initials: PJ
authors.lastname: Andrews
authors.forename: I
authors.initials: I
authors.lastname: Marshall
authors.forename: V J
authors.initials: VJ
authors.lastname: Easton
mesh_terms: D000293:Adolescent; D000328:Adult; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000378:metabolism; D001921:Brain / Q000473:pathology; D001930:Brain Injuries / Q000473:pathology* / Q000601:surgery; D002545:Brain Ischemia / Q000473:pathology* / Q000601:surgery; D002648:Child; D002794:Choline / Q000378:metabolism; D003401:Creatine / Q000378:metabolism; D003422:Critical Care / Q000379:methods; D020833:Diffuse Axonal Injury / Q000473:pathology / Q000601:surgery; D004734:Energy Metabolism / Q000502:physiology*; D005260:Female; D005500:Follow-Up Studies; D015600:Glasgow Coma Scale; D006801:Humans; D019344:Lactic Acid / Q000378:metabolism; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D009474:Neurons / Q000473:pathology; D013345:Subarachnoid Hemorrhage / Q000473:pathology* / Q000601:surgery; D014057:Tomography, X-Ray Computed
chemical_list: D001224:Aspartic Acid; D019344:Lactic Acid; C000179:N-acetylaspartate; D003401:Creatine; D002794:Choline