• W D Dietrich, O Alonso, R Busto, and M D Ginsberg.
• Department of Neurology, University of Miami School of Medicine, Florida, USA.
• J. Neurotrauma. 1994 Dec 1; 11 (6): 629-40.

AbstractThe effects of fluid percussion brain injury on the basal metabolic state and responsiveness of a somatosensory circuit to physiologic activation were investigated with [14C]2-deoxyglucose autoradiography. Under controlled physiologic conditions and normothermic brain temperature (37 degrees C), rats were injured with a moderate fluid percussion pulse ranging from 1.7 to 2.1 atm. At 4 or 24 h after traumatic brain injury (TBI), unilateral vibrissae stimulation was carried out, resulting in the metabolic activation of the whisker-barrel circuit. In sham-operated control animals, whisker stimulation resulted in the metabolic activation of the ipsilateral trigeminal medullary complex (177% of control), contralateral ventrobasal thalamus (143% control), and primary somatosensory cortex (153% control). At 4 h after injury, local cerebral metabolic rates of glucose (ICMRglu) were significantly depressed throughout the traumatized hemisphere. Although depressed ICMRglu was most pronounced in cortical regions adjacent to the evolving contusion (53% of control), significant decreases were also seen in more remote areas, including the frontal cortex (75% of control), hippocampus (79% control), and lateral thalamus (68% of control). At 24 h following TBI, ICMRglu remained significantly reduced at the impact site, within the ipsilateral somatosensory cortex and lateral thalamus. Stimulus-evoked increases in ICMRglu were depressed within all three relay stations of the vibrissae-barrel-field circuit at 4 and 24 h after TBI. These results demonstrate both focal and diffuse metabolic depression after moderate TBI. Although the most severe and longer lasting metabolic consequences occurred in cortical and thalamic regions destined to exhibit histopathologic damage, milder abnormalities, most prominent in the early posttraumatic period, were also seen in noninjured areas. The inability to activate the somatosensory circuit metabolically indicates that circuit dysfunction is an acute consequence of TBI. Widespread circuit or synaptic dysfunction would be expected to participate in the functional and behavioral consequences of TBI.

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