Contributions
Abstract: P496
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - MRI and PET
Introduction: Brain tissue loss, particularly in grey matter, has been recognized as the primary cause of irreversible neurological disability in multiple sclerosis (MS). While cortical inflammatory demyelinating lesions are common, damage in connected white matter tracts and/or other mechanisms may contribute to grey matter atrophy. The visual pathway is frequently affected by MS and constitutes an ideal model for probing these patho-mechanisms, primarily due to retinotopic organization and advances in magnetic resonance imaging (MRI) that facilitate the simultaneous assessment of optic radiation (OR) and primary visual cortex (V1) damage.
Objective: To elucidate the relationship between OR and V1 structural integrity in RRMS patients.
Methods: diffusion MRI, 3D T1, and FLAIR sequences were acquired on a 3T GE MRI scanner from patients with relapsing MS, recruited at a single centre. The OR was constructed individually using probabilistic tractography. OR diffusion metrics (AD, RD, MD, FA) and OR lesion volume were assessed. V1 structure was parcellated using FREESURFER; and both cortical thickness and MD assessed. Asymmetry analysis was conducted between left and right hemisphere to minimise inter-subject variation. Patients without OR gadolinium-enhancing lesions and with OR lesion length differences > 1mm were included in the analysis. Pearson's correlation was used to assess the relationships between the imaging metrics.
Results: Twenty relapsing MS patients with asymmetrical OR T2 lesions were included in the study; 75% female; mean age 37.3(10.5) years; mean disease duration 4.8(5.2) years and mean EDSS 2.0 (1.5) were evaluated. OR lesion volume was associated with V1-ΔMD (r=.60, p=.005), but not with V1-ΔFA (r=-.26, p=.27) nor V1-Δthickness (r=.09, p=.7). OR-ΔMD/ΔAD/ΔRD were also correlated with V1-ΔMD, however, the relationships were no longer significant after correction for OR lesion volume.
Conclusion: By asymmetry analysis, a higher visual cortex MD was identified in the hemisphere with the higher OR lesion volume. This relationship may reflect the consequences of both Wallerian degeneration along the OR and subsequent trans-synaptic degeneration within the V1. The absence of correlation between OR lesion volume and V1 thickness suggests that MD may be a sensitive biomarker for early stage cortical tissue loss, indicative of microstructural injury that occurs prior to overt tissue collapse and measurable cortical thinning.
Disclosure: Chenyu Wang declared no conflict of interest.
Alexander Klistorner declared no conflict of interest.
Joshua Barton declared no conflict of interest.
Heidi N Beadnall has received compensation for education travel, speaker honoraria and consultant fees from Biogen, Novartis, Merck and Sanofi-Genzyme.
Linda Ly declared no conflict of interest.
Sidong Liu declared no conflict of interest.
Justin Garber declared no conflict of interest.
Stephen Reddel has received payments for grant support from Biogen, CSL, Novartis and Sanofi-Genzyme, travel support from Merck, Sanofi-Genzyme and Teva, membership on advisory councils from Biogen, Merck, Sanofi-Genzyme and Teva, speaker's bureau from Biogen, Novartis, and Sanofi-Genzyme, and is a shareholder in Medical Safety Systems P/L Australia.
Michael Barnett has received institutional support for research, speaking and/or participation in advisory boards for Biogen, Merck, Novartis, Roche and Sanofi Genzyme. Dr Barnett is a research consultant at Medical Safety Systems and research director for the Sydney Neuroimaging Analysis Centre.
Abstract: P496
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - MRI and PET
Introduction: Brain tissue loss, particularly in grey matter, has been recognized as the primary cause of irreversible neurological disability in multiple sclerosis (MS). While cortical inflammatory demyelinating lesions are common, damage in connected white matter tracts and/or other mechanisms may contribute to grey matter atrophy. The visual pathway is frequently affected by MS and constitutes an ideal model for probing these patho-mechanisms, primarily due to retinotopic organization and advances in magnetic resonance imaging (MRI) that facilitate the simultaneous assessment of optic radiation (OR) and primary visual cortex (V1) damage.
Objective: To elucidate the relationship between OR and V1 structural integrity in RRMS patients.
Methods: diffusion MRI, 3D T1, and FLAIR sequences were acquired on a 3T GE MRI scanner from patients with relapsing MS, recruited at a single centre. The OR was constructed individually using probabilistic tractography. OR diffusion metrics (AD, RD, MD, FA) and OR lesion volume were assessed. V1 structure was parcellated using FREESURFER; and both cortical thickness and MD assessed. Asymmetry analysis was conducted between left and right hemisphere to minimise inter-subject variation. Patients without OR gadolinium-enhancing lesions and with OR lesion length differences > 1mm were included in the analysis. Pearson's correlation was used to assess the relationships between the imaging metrics.
Results: Twenty relapsing MS patients with asymmetrical OR T2 lesions were included in the study; 75% female; mean age 37.3(10.5) years; mean disease duration 4.8(5.2) years and mean EDSS 2.0 (1.5) were evaluated. OR lesion volume was associated with V1-ΔMD (r=.60, p=.005), but not with V1-ΔFA (r=-.26, p=.27) nor V1-Δthickness (r=.09, p=.7). OR-ΔMD/ΔAD/ΔRD were also correlated with V1-ΔMD, however, the relationships were no longer significant after correction for OR lesion volume.
Conclusion: By asymmetry analysis, a higher visual cortex MD was identified in the hemisphere with the higher OR lesion volume. This relationship may reflect the consequences of both Wallerian degeneration along the OR and subsequent trans-synaptic degeneration within the V1. The absence of correlation between OR lesion volume and V1 thickness suggests that MD may be a sensitive biomarker for early stage cortical tissue loss, indicative of microstructural injury that occurs prior to overt tissue collapse and measurable cortical thinning.
Disclosure: Chenyu Wang declared no conflict of interest.
Alexander Klistorner declared no conflict of interest.
Joshua Barton declared no conflict of interest.
Heidi N Beadnall has received compensation for education travel, speaker honoraria and consultant fees from Biogen, Novartis, Merck and Sanofi-Genzyme.
Linda Ly declared no conflict of interest.
Sidong Liu declared no conflict of interest.
Justin Garber declared no conflict of interest.
Stephen Reddel has received payments for grant support from Biogen, CSL, Novartis and Sanofi-Genzyme, travel support from Merck, Sanofi-Genzyme and Teva, membership on advisory councils from Biogen, Merck, Sanofi-Genzyme and Teva, speaker's bureau from Biogen, Novartis, and Sanofi-Genzyme, and is a shareholder in Medical Safety Systems P/L Australia.
Michael Barnett has received institutional support for research, speaking and/or participation in advisory boards for Biogen, Merck, Novartis, Roche and Sanofi Genzyme. Dr Barnett is a research consultant at Medical Safety Systems and research director for the Sydney Neuroimaging Analysis Centre.