title: Metabolic changes in the vicinity of brain contusions: a proton magnetic resonance spectroscopy and histology study.
abstract: Proton MR spectroscopy (1H-MRS) has been previously used to monitor metabolic changes in areas of diffuse brain injury. We studied metabolism in the close vicinity of experimental traumatic brain contusions and remote on the contralateral side from 1h to 28d post-injury. Changes of creatine and phosphocreatine (Cr&PCr), N-acetylaspartate (NAA), choline (Cho), inositol (Ino), taurine (Tau), glutamate (Glu), and lactate (Lac) were assessed and compared to neuronal, glial and inflammatory changes in histology. In the pericontusional zone Cr&PCr, NAA, and Glu decreased immediately after trauma by -35%, -60%, and -37%, respectively, related to primary cell disintegration and secondary perturbations as reflected in histology. These metabolites partially recovered at 7d (-15%, -37%, and -21% respectively), in parallel to indicators of repair in immunhistochemistry. Control levels were not regained at 28d, in correlation to a decrease of viable neurons. Cho and Ino, initially lowered by -26% and -31% respectively, increased at 7d by +74% and 31%, reflecting glial activation and proliferation. The signal including the lactate resonance increased by >1000% with a maximum at 7d, possibly related to energy failure, inflammation and glial activation. A partial contribution of lipids to this signal cannot be fully excluded. The contralateral side showed mild astroglial activation in histology, but no changes in 1H-MRS. The study demonstrates the feasibility of volume selective 1H-MRS using the LCModel (Linear Combination of Model in vitro spectra of metabolites solutions) to monitor metabolic changes close to focal traumatic lesions and suggests how metabolic alterations can be differentiated in cause.
authors.affiliation: Department of Pediatric Neurosurgery, Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, Michigan, USA. mschuh@gmx.de
authors.forename: Martin Ulrich
authors.initials: MU
authors.lastname: Schuhmann
authors.forename: Detlef
authors.initials: D
authors.lastname: Stiller
authors.forename: Marco
authors.initials: M
authors.lastname: Skardelly
authors.forename: Johannes
authors.initials: J
authors.lastname: Bernarding
authors.forename: Petra Margarete
authors.initials: PM
authors.lastname: Klinge
authors.forename: Amir
authors.initials: A
authors.lastname: Samii
authors.forename: Madjid
authors.initials: M
authors.lastname: Samii
authors.forename: Thomas
authors.initials: T
authors.lastname: Brinker
mesh_terms: D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000032:analysis; D015415:Biomarkers / Q000032:analysis; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology*; D002794:Choline / Q000032:analysis; D003401:Creatine / Q000032:analysis; D007839:Functional Laterality; D018698:Glutamic Acid / Q000032:analysis; D007150:Immunohistochemistry; D007294:Inositol / Q000032:analysis; D019344:Lactic Acid / Q000032:analysis; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D010725:Phosphocreatine / Q000032:analysis; D011522:Protons; D051381:Rats; D017207:Rats, Sprague-Dawley; D013654:Taurine / Q000032:analysis; D013997:Time Factors
chemical_list: D015415:Biomarkers; D011522:Protons; D010725:Phosphocreatine; D013654:Taurine; D001224:Aspartic Acid; D019344:Lactic Acid; D018698:Glutamic Acid; D007294:Inositol; C000179:N-acetylaspartate; D003401:Creatine; D002794:Choline