Figure 6.

Association between early metabolic derangements and tissue fate. Imaging obtained in a 17-year-old male with moderate TBI following a road traffic accident with initial GCS of 12, but who required sedation and ventilation for control of raised ICP. Co-registered CBF, CMRO₂, OEF, ¹⁸F-FDG kinetic parameters and CT imaging obtained on Day 8 following TBI. Plasma glucose during imaging was 5.4 mmol/l. The CT demonstrates left frontal and temporal haemorrhagic contusions and is shown with the T₁-weighted MRI obtained at 9 months post-injury; the MRI has been non-rigidly registered to the CT. Both structural images are displayed with the region of k₃ hotspot outlined in red, but both lesion core and penumbra have been excluded from the hotspot to ensure that only increases in k₃ outside of the lesion identified on CT imaging are shown. The volume of brain within the k₃ hotspot in this subject was 149 ml and, in comparison with brain that appeared structurally normal, had CBF 19.6 versus 19.6 ml/100 ml/min, CMRO₂ 55.2 versus 60.2 µmol/100 ml/min, OEF 37.8 versus 42.4%, K₁ 0.097 versus 0.087 ml/ml/min, K_i 0.018 versus 0.012 ml/ml/min and k₃ 0.058 versus 0.024/min, respectively. The T₁-weighted MRI demonstrates established lesions within the left frontal and temporal brain regions in close proximity with k₃ increases outside of lesion core and penumbra identified on the CT image.