Altered glucose metabolism of the olfactory-related cortices in anosmia patients with traumatic brain injury.

Abstract

Impaired brain cortices contribute significantly to the pathophysiological mechanisms of post-traumatic olfactory dysfunction (PTOD). This study aimed to use 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) to measure cerebral cortices' metabolism activity and then to explore their associations with olfaction in patients with PTOD. Ethics committee-approved prospective studies included 15 patients with post-traumatic anosmia and 11 healthy volunteers. Olfactory function was assessed using the Sniffin' Sticks. Participants underwent 18F-FDG PET/CT scan and the image data were collected for the voxel-based whole brain analysis. Furthermore, the standardized uptake value ratio (SUVR) of the whole brain regions was measured and correlated with olfactory function. Patients with post-traumatic anosmia showed significantly reduced glucose metabolism in bilateral rectus, bilateral superior and medial orbitofrontal cortex (OFC), bilateral thalamus, left hippocampus and parahippocampus and left superior temporal pole (all p < 0.001). In contrast, patients with post-traumatic anosmia had significantly increased glucose metabolism in the bilateral insula (all p < 0.001). SUVR values among a total of 17 cerebral cortices including frontal, limbic, and temporal regions were significantly and positively correlated with olfactory function. The cerebral cortices with the top three correlations were the right middle frontal OFC (r = 0.765, p = 0.001), right caudate (r = 0.652, p = 0.010) and right putamen (r = 0.623, p = 0.002). Patients with post-traumatic anosmia presented with distinct patterns of brain metabolism and key cortices that highly associated with the retained olfactory function were identified. The preliminary results further support the potential use of PET imaging for precisely assessing brain metabolism in patients with PTOD.