• M J Passineau, W Zhao, R Busto, W D Dietrich, O Alonso, J Y Loor, H M Bramlett, and M D Ginsberg.
• Neurotrauma Research Center, University of Miami School of Medicine, Miami, Florida 33101, USA.
• Am. J. Physiol. Heart Circ. Physiol. 2000 Sep 1; 279 (3): H924-31.

AbstractInjuries 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.

23 keywords...

hide…