Contributions
Abstract: P486
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Imaging
Introduction: Fatigue affects between 50% and 80% of patients with multiple sclerosis (MS). Despite its clinical significance, the pathophysiology of fatigue is still not completely understood.
Objectives: To explore the underlying neural basis of fatigue in patients with MS.
Methods: We enrolled 60 consecutive MS patients and 60 healthy controls (HC) matched on age, gender, and education. Fatigue was assessed using the Portuguese version of Modified Fatigue Impact Scale (MFIS). All participants underwent 3Tesla brain MRI including conventional and diffusion tensor imaging (DTI) sequences. White matter (WM) focal lesions were identified and T1 and T2 lesion volume were computed. Tract-based spatial statistics (TBSS) were applied for voxel-wise analysis of DTI metrics fractional anisotropy (FA) and mean diffusivity (MD) on normal-appearing WM (NAWM). Using Freesurfer software, total and regional volumes of cortical and subcortical gray matter (GM) were calculated.
Results: Compared to HC, patients with MS scored significantly higher on MFIS (33.8±19.7 vs. 16.5±15.1, p< 0.001). Patients with MS presented a multifocal pattern of GM atrophy and an extensive NAWM damage. The total T1 lesion and the T2 lesion volumes were 12.9±5.3 ml and 16.8±15.8 ml, respectively.
MFIS scores were not significantly correlated with T1/T2 lesion volumes, total GM volume, or with any regional volume of cortical and subcortical GM. Regarding TBSS analysis, significant correlations (p< 0.05 corrected for multiple testing by family-wise error rates) were found between global scores of MFIS and DTI-derived measures (FA decrease and/or MD increase) of the NAWM skeleton, including: corona radiata, internal capsule, external capsule, corticospinal tract, cingulum, corpus callosum, fornix, superior longitudinal fasciculus, superior fronto-occipital fasciculus, sagittal stratum, posterior thalamic radiation, cerebral peduncle and uncinate fasciculus.
Conclusions: Fatigue was associated with a widespread NAWM damage but not with lesion load or GM atrophy. This finding supports the theory that functional disconnection, caused by diffuse microstructural WM damage, might be the main neural basis of fatigue in MS.
Disclosure: This research was supported by a grant from Biogen. The sponsor did not participate in any aspect of the design or performance of the study, including the data collection, management, analysis, and interpretation or preparation of the work.
S. Batista has received honoraria for serving on scientific advisory boards of Biogen and Novartis Pharma, and for speaking in scientific meetings of Teva, Merck Serono, Biogen, and Novartis Pharma.
C. Macário and L. Sousa have received honoraria for serving on scientific advisory boards or speaking in scientific meetings of Teva, Merck Serono, Bayer, Genzyme, Biogen, and Novartis Pharma.
AM Novo, C. Alves, O. C. d"Almeida, II.B. Marques, M. Castelo-Branco, I. Santana and L. Cunha have nothing to disclose.
Abstract: P486
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Imaging
Introduction: Fatigue affects between 50% and 80% of patients with multiple sclerosis (MS). Despite its clinical significance, the pathophysiology of fatigue is still not completely understood.
Objectives: To explore the underlying neural basis of fatigue in patients with MS.
Methods: We enrolled 60 consecutive MS patients and 60 healthy controls (HC) matched on age, gender, and education. Fatigue was assessed using the Portuguese version of Modified Fatigue Impact Scale (MFIS). All participants underwent 3Tesla brain MRI including conventional and diffusion tensor imaging (DTI) sequences. White matter (WM) focal lesions were identified and T1 and T2 lesion volume were computed. Tract-based spatial statistics (TBSS) were applied for voxel-wise analysis of DTI metrics fractional anisotropy (FA) and mean diffusivity (MD) on normal-appearing WM (NAWM). Using Freesurfer software, total and regional volumes of cortical and subcortical gray matter (GM) were calculated.
Results: Compared to HC, patients with MS scored significantly higher on MFIS (33.8±19.7 vs. 16.5±15.1, p< 0.001). Patients with MS presented a multifocal pattern of GM atrophy and an extensive NAWM damage. The total T1 lesion and the T2 lesion volumes were 12.9±5.3 ml and 16.8±15.8 ml, respectively.
MFIS scores were not significantly correlated with T1/T2 lesion volumes, total GM volume, or with any regional volume of cortical and subcortical GM. Regarding TBSS analysis, significant correlations (p< 0.05 corrected for multiple testing by family-wise error rates) were found between global scores of MFIS and DTI-derived measures (FA decrease and/or MD increase) of the NAWM skeleton, including: corona radiata, internal capsule, external capsule, corticospinal tract, cingulum, corpus callosum, fornix, superior longitudinal fasciculus, superior fronto-occipital fasciculus, sagittal stratum, posterior thalamic radiation, cerebral peduncle and uncinate fasciculus.
Conclusions: Fatigue was associated with a widespread NAWM damage but not with lesion load or GM atrophy. This finding supports the theory that functional disconnection, caused by diffuse microstructural WM damage, might be the main neural basis of fatigue in MS.
Disclosure: This research was supported by a grant from Biogen. The sponsor did not participate in any aspect of the design or performance of the study, including the data collection, management, analysis, and interpretation or preparation of the work.
S. Batista has received honoraria for serving on scientific advisory boards of Biogen and Novartis Pharma, and for speaking in scientific meetings of Teva, Merck Serono, Biogen, and Novartis Pharma.
C. Macário and L. Sousa have received honoraria for serving on scientific advisory boards or speaking in scientific meetings of Teva, Merck Serono, Bayer, Genzyme, Biogen, and Novartis Pharma.
AM Novo, C. Alves, O. C. d"Almeida, II.B. Marques, M. Castelo-Branco, I. Santana and L. Cunha have nothing to disclose.