Chronic metabolic sequelae of traumatic brain injury: prolonged suppression of somatosensory activation

Injuries to the brain acutely disrupt normal metabolic function and may dea ctivate functional circuits. It is unknown whether these metabolic abnormal ities improve over time. We used 2-deoxyglucose (2-DG) autoradiographic ima ge-averaging to assess local cerebral glucose utilization (1CMR(Glc)) of th e rat brain 2 mo after moderate (1.7-2.1 atm) fluid-percussion traumatic br ain injury (FPI). Four animal groups (n = 5 each) were studied: sham-injure d rats with and without stimulation of the vibrissae-barrel field ipsilater al to injury; and animals with prior FPI, with or without this stimulation. In sham-injured rats, resting 1CMR(Glc) was normal, and vibrissae stimulat ion produced right-sided metabolic activation of the ventrolateral thalamic and somatosensory-cortical projection areas. In rats with prior injury, 1C MR(Glc) contralateral to injury was normal, but 1CMR(Glc) of the ipsilatera l forebrain was depressed by similar to 38-45% compared with shams. Whisker stimulation in rats with prior trauma failed to induce metabolic activatio n of either cortex or thalamus. Image-mapping of histological material obta ined in the same injury model was undertaken to assess the possible influen ce of injury-induced regional brain atrophy on computed 1CMR(Glc); an effec t was found only in the lateral cortex at the trauma epicenter. Our results show that, 2 mo after trauma, resting cerebral metabolic perturbations per sist, and the whisker-barrel somatosensory circuit shows no signs of functi onal recovery.