Analysis of Cortical Metabolism in Multiple Sclerosis: A 3T 18F-FDG PET/MRI Study (P4.166)

Background. Irreversible cortical atrophy is a major feature of multiple sclerosis (MS) pathology and can be demonstrated in very early disease phases. Whether cortical atrophy is preceded by a metabolic dysfunction has not been investigated yet. Objectives. To analyse cortical metabolism in MS patients at clinical onset and in patients with long disease duration and clinical evidence of cortical dysfunction, and to investigate its possible association with cortical thickness (Cth) by means of a fully integrated 3T-Positron Emission Tomography/Magnetic Resonance Imaging (PET/MRI) system. Methods. 28 patients were studied: 13 clinically isolated syndromes/early Relapsing Remitting MS (CIS/eRRMS) with very short disease duration and no sign of cognitive impairment, and 15 RRMS patients with a long disease duration and clinical evidence of cognitive dysfunction. 3T18F-FDG-PET/MRI (Siemens Biograph mMR) images were obtained from all patients. The absolute cortical metabolic rate of glucose (aMRglu) was obtained with a new methodology using PMOD 3.6 software according to Desikan-Killiany atlas (66 cortical areas). Regional Cth was obtained from data sets of anatomical 3D-T1 by Freesurfer suite in the same areas. Results. As expected, Cth was significantly lower in RRMS compared to CIS/eRRMS patients in 21/66 cortical areas (p<0.05). Surprisingly, no significant difference in cortical aMRglu was found between RRMS and CIS/eRRMS groups except for the right paracentral area and the left parietal lobe. Only in RRMS group significant positive correlations were found in some cortical areas between Cth and aMRglu, whereas no correlation was found in CIS/eRRMS group. Conclusions. This study shows that CIS/eRRMS and RRMS have similar values of cortical metabolism despite they significantly differ in cortical thickness. This suggests that a metabolic dysfunction probably precedes MRI detectable structural damage in the cortex of MS. The identification of hypometabolic areas in very early disease phases may have important pathological and clinical (therapeutic) consequences. Disclosure: Dr. Margoni has nothing to disclose. Dr. Favaretto has nothing to disclose. Dr. Cecchin has nothing to disclose. Dr. Poggiali has nothing to disclose. Dr. Lazzarotto has nothing to disclose. Dr. Pravato has nothing to disclose. Dr. Riccardi has received personal compensation for activities with Novartis, Biogen Idec, and Merck Serono. Dr. Bui has nothing to disclose. Dr. Paolo Gallo has received personal compensation for activities with Biogen Idec, Novartis, Merck Serono, Bayer Schering and Genzyme as a speaker and consultant.