Contributions
Abstract: P531
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Imaging
Background: Diffusion basis spectrum imaging (DBSI) is a microstructural imaging method in which anisotropic and isotropic diffusion components are modeled to assess the different pathologies within MS lesion. Myelinated and unmyelinated axons are modeled as anisotropic diffusion tensors. Cells, edema, and increased extracellular space are modeled as isotropic diffusion tensors. By accounting for the proportion of inflammatory components within an imaging voxel, the anisotropic DBSI “fiber” fraction can be used to estimate the density of axons within that voxel. Reduction of DBSI axial diffusivity (AD) provides a surrogate of axon injury, whereas increased DBSI radial diffusivity (RD) suggests loss of myelin integrity. This ongoing study leverages our expertise in optic nerve diffusion MRI (dMRI) and clinical research setting of optic neuritis (ON) to translate the DBSI method to human.
Methods: Participants included those with acute ON (within 30 days of onset), chronic optic neuropathy due to remote ON (last episode > 1 year prior), and healthy controls (HC). Axial optic nerve data were collected using an inner-volume-imaging diffusion sequence at 1.3 mm isotropic resolution (10 slices) with four averages of 25 unique diffusion encoding directions at linearly spaced b-values (40-1000 s/mm2) plus two b0s. The optic nerve dMRI data were first pre-processed with a non-linear registration method and then underwent DBSI analysis. Region of interest (ROI) analysis were performed in each optic nerve.
Results: DBSI data from 6 patients with remote ON, and 3 with acute ON were compared to 6 HCs. Patients with remote ON had significantly decreased DBSI fractional anisotropy - FA (0.76±0.14 vs. 0.83±0.08, p< 0.05), decreased DBSI fiber fraction (0.42±0.16 vs. 0.62±0.15), and increased hindered isotropic diffusion tensor fraction (edema/extracellular fluid) (0.34±0.19 vs. 0.22±0.09). Patients with acute ON had similar changes with reduced DBSI FA and DBSI fiber fraction, and increased DBSI RD and hindered isotropic diffusion. In addition, optic nerves with acute ON showed reduced DBSI AD (injured axons) (1.62±0.51 vs. 1.93±0.25 mcm2/ms) and mildly increased restricted isotropic diffusion tensor fraction thought to represent cellularity (0.10±0.04 vs. 0.07±0.04).
Conclusion: DBSI has potential to determine the underlying pathology in ON by measuring axon injury and loss while accounting for cellularity, edema and increased extracellular space.
Disclosure:
RT Naismith has received fees for consulting from: Alkermes, Acorda, Bayer, Biogen, EMD Serono, Genentech, Genzyme, Mallinckrodt, EMD Serono, Novartis, Pfizer, Teva
J Xu has no disclosures.
C Dula has no disclosures.
S Peng has no disclosures.
JW Kim has no disclosures.
S Lancia has no disclosures.
AH Cross has received fees for consulting from: AbbVie, Biogen, EMD Serono, Genentech/Roche, Genzyme/Sanofi, Mallinckrodt, Novartis, Teva.
SK Song has no disclosures.
Funding: NIH R21NS090910 (RTN/SKS), C06RR014513 (JSP)
Abstract: P531
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Imaging
Background: Diffusion basis spectrum imaging (DBSI) is a microstructural imaging method in which anisotropic and isotropic diffusion components are modeled to assess the different pathologies within MS lesion. Myelinated and unmyelinated axons are modeled as anisotropic diffusion tensors. Cells, edema, and increased extracellular space are modeled as isotropic diffusion tensors. By accounting for the proportion of inflammatory components within an imaging voxel, the anisotropic DBSI “fiber” fraction can be used to estimate the density of axons within that voxel. Reduction of DBSI axial diffusivity (AD) provides a surrogate of axon injury, whereas increased DBSI radial diffusivity (RD) suggests loss of myelin integrity. This ongoing study leverages our expertise in optic nerve diffusion MRI (dMRI) and clinical research setting of optic neuritis (ON) to translate the DBSI method to human.
Methods: Participants included those with acute ON (within 30 days of onset), chronic optic neuropathy due to remote ON (last episode > 1 year prior), and healthy controls (HC). Axial optic nerve data were collected using an inner-volume-imaging diffusion sequence at 1.3 mm isotropic resolution (10 slices) with four averages of 25 unique diffusion encoding directions at linearly spaced b-values (40-1000 s/mm2) plus two b0s. The optic nerve dMRI data were first pre-processed with a non-linear registration method and then underwent DBSI analysis. Region of interest (ROI) analysis were performed in each optic nerve.
Results: DBSI data from 6 patients with remote ON, and 3 with acute ON were compared to 6 HCs. Patients with remote ON had significantly decreased DBSI fractional anisotropy - FA (0.76±0.14 vs. 0.83±0.08, p< 0.05), decreased DBSI fiber fraction (0.42±0.16 vs. 0.62±0.15), and increased hindered isotropic diffusion tensor fraction (edema/extracellular fluid) (0.34±0.19 vs. 0.22±0.09). Patients with acute ON had similar changes with reduced DBSI FA and DBSI fiber fraction, and increased DBSI RD and hindered isotropic diffusion. In addition, optic nerves with acute ON showed reduced DBSI AD (injured axons) (1.62±0.51 vs. 1.93±0.25 mcm2/ms) and mildly increased restricted isotropic diffusion tensor fraction thought to represent cellularity (0.10±0.04 vs. 0.07±0.04).
Conclusion: DBSI has potential to determine the underlying pathology in ON by measuring axon injury and loss while accounting for cellularity, edema and increased extracellular space.
Disclosure:
RT Naismith has received fees for consulting from: Alkermes, Acorda, Bayer, Biogen, EMD Serono, Genentech, Genzyme, Mallinckrodt, EMD Serono, Novartis, Pfizer, Teva
J Xu has no disclosures.
C Dula has no disclosures.
S Peng has no disclosures.
JW Kim has no disclosures.
S Lancia has no disclosures.
AH Cross has received fees for consulting from: AbbVie, Biogen, EMD Serono, Genentech/Roche, Genzyme/Sanofi, Mallinckrodt, Novartis, Teva.
SK Song has no disclosures.
Funding: NIH R21NS090910 (RTN/SKS), C06RR014513 (JSP)