LAUSR

An indication of 50 sessions of hyperbaric oxygen therapy (HBOT) over a period of 6 weeks was retained in a 31-yearold man presenting with a chronic fatigue syndrome (CFS) evolving for 15 months with asthenia, memory complaints, dizziness, and muscle/joint pains. This CFS followed an EBV (Epstein-Barr virus) infectious mononucleosis. Brain F-FDG PET/CT scans were performed before and after HBOT, using GE Discovery 710 camera, at resting state, after fasting of at least 4 h and checking of normal blood glucose, 30 min after intravenous injection of 110 MBq of F-FDG. Brain images are displayed using anatomical convention (the left hemisphere is on the left side), after metabolic normalization to the pons with a color scale ranged from 0 to 3 (3-fold the metabolism of the pons). Whole-brain voxel-based SPM analysis was used to compare the metabolism to 20 healthy subjects of the same age acquired locally in the same department with the same protocol (31.25 years ± 5.94, 21– 41 years; p-voxel < 0.001, k-cluster > 85; metabolic normalization to the pons; clinical trial registration: NCT00484523). Initial brain F-FDG PET/CT demonstrated widespread hypometabolism (A: axial slices; C: SPM 3D-rendered of brain hypometabolism), reversible after treatment (B: axial slices; D: SPM 3D-rendered of brain hypometabolism; E: axial slices of metabolic improvement of at least 5%), concomitant with an improvement of quality of life measured by SF36 scale (the physical and mental functioning scales of the SF36 were, respectively, of 70 and 69 after HBOT versus 57 and 48 initially), without hyperbaric complication. In more details, brain hypometabolisms initially involved bilateral cortex with a right-sided predominance, including the amygdala and hippocampus/parahippocampus regions, as well as the bilateral basal ganglia, thalamus, midbrain, and cerebellum, with persistence of the right opercular frontal and left cerebellar hypometabolisms after HBOT. This profile is mostly concordant with previous F-FDG reports in CFS patients identifying hypometabolisms in the frontal cortex [1, 2], and extensively in the posterior cortical regions (precuneus, parietal, temporal, and occipital), amygdala-hippocampal complexes, and cerebellum [3]. HBOT is suggested as a potential indication for several treatment-resistant functional brain disorders, such as CFS or fibromyalgia [4–6]. Increasing oxygen concentration and hyperbaric pressure is supposed to induce neuroplasticity, and consequently, to improve brain metabolism and glial function through also an anti-inflammatory effect [7]. This report exhibits brain PET hypometabolism as previously shown in CFS [1–3], and also in fibromyalgia [8], reversible after clinical improvement with possible positive impact of HBOT. F-FDG brain PET could be used as a metabolic biomarker to assess brain dysfunction in HBOT indications of functional disorders and evaluate therapeutic effects. This article is part of the Topical Collection on Neurology