title: Chronic metabolic sequelae of traumatic brain injury: prolonged suppression of somatosensory activation.
abstract: Injuries to the brain acutely disrupt normal metabolic function and may deactivate functional circuits. It is unknown whether these metabolic abnormalities improve over time. We used 2-deoxyglucose (2-DG) autoradiographic image-averaging to assess local cerebral glucose utilization (lCMR(Glc)) of the rat brain 2 mo after moderate (1.7-2.1 atm) fluid-percussion traumatic brain injury (FPI). Four animal groups (n = 5 each) were studied: sham-injured rats with and without stimulation of the vibrissae-barrel field ipsilateral to injury; and animals with prior FPI, with or without this stimulation. In sham-injured rats, resting lCMR(Glc) was normal, and vibrissae stimulation produced right-sided metabolic activation of the ventrolateral thalamic and somatosensory-cortical projection areas. In rats with prior injury, lCMR(Glc) contralateral to injury was normal, but lCMR(Glc) of the ipsilateral forebrain was depressed by approximately 38-45% compared with shams. Whisker stimulation in rats with prior trauma failed to induce metabolic activation of either cortex or thalamus. Image-mapping of histological material obtained in the same injury model was undertaken to assess the possible influence of injury-induced regional brain atrophy on computed lCMR(Glc); an effect was found only in the lateral cortex at the trauma epicenter. Our results show that, 2 mo after trauma, resting cerebral metabolic perturbations persist, and the whisker-barrel somatosensory circuit shows no signs of functional recovery.
authors.affiliation: Neurotrauma Research Center, University of Miami School of Medicine, Miami, Florida 33101, USA.
authors.forename: M J
authors.initials: MJ
authors.lastname: Passineau
authors.forename: W
authors.initials: W
authors.lastname: Zhao
authors.forename: R
authors.initials: R
authors.lastname: Busto
authors.forename: W D
authors.initials: WD
authors.lastname: Dietrich
authors.forename: O
authors.initials: O
authors.lastname: Alonso
authors.forename: J Y
authors.initials: JY
authors.lastname: Loor
authors.forename: H M
authors.initials: HM
authors.lastname: Bramlett
authors.forename: M D
authors.initials: MD
authors.lastname: Ginsberg
mesh_terms: D000818:Animals; D001345:Autoradiography; D001921:Brain / Q000378:metabolism; D001930:Brain Injuries / Q000378:metabolism*; D002908:Chronic Disease; D003847:Deoxyglucose / Q000493:pharmacokinetics; D004195:Disease Models, Animal; D005947:Glucose / Q000378:metabolism; D007091:Image Processing, Computer-Assisted; D008297:Male; D010296:Parietal Lobe / Q000293:injuries; D010812:Physical Stimulation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013003:Somatosensory Cortex / Q000378:metabolism*
chemical_list: D003847:Deoxyglucose; D005947:Glucose