Contributions
Abstract: P1887
Type: Poster
Abstract Category: Late breaking news
Background: While axonal damage in the corpus callosum (CC) is a prominent feature of multiple sclerosis (MS), less is known about CC integrity in neuromyelitis optica spectrum disorder (NMOSD). Here we examined outcome measures with an advanced MRI technique: multicomponent Driven Equilibrium Single Pulse Observation of T1 and T2 (mcDESPOT). mcDESPOT is often used to study the myelin water fraction (MWF), which quantifies the amount of signal from water between the myelin bilayers, and is thus related to myelin content. We also examined the mcDESPOT-derived myelin water residence time (Tm), which estimates the time taken for water between the myelin bilayers to exchange with intra/extracellular water, and is therefore expected to reflect myelin thickness.
Goals:
1) To determine whether differences in myelin content and thickness within the CC previously described in histological studies can be detected with MWF and Tm.
2) To investigate differences in markers for myelin content and thickness between NMOSD and healthy control (HC) CC.
Methods: 13 patients (mean age: 43y (range: 24-59), 9 female) and 13 HC (40y (26-56), 9 female) were included. CC segmentation was performed using an atlas based approach to obtain regions of interest (ROI) for the genu, body and splenium. Mean Tm and MWF were extracted from each ROI. One-way repeated measures analysis of variance (ANOVA) was used to investigate within-group differences. The Mann-Whitney U test was employed to explore between-group differences.
Results:
HC Within HC, significant differences in both MWF and Tm were observed between the ROIs of the CC. MWF: genu 0.195 (0.017), body 0.196 (0.014), splenium 0.215 (0.009); p=0.005. Tm: genu 66.2ms (9.3), body 82.9 (10.9), splenium 76.1 (11.0); p=0.006.
NMOSD Within NMOSD, differences between CC ROIs were not as apparent as for HC, but significant for Tm. MWF: genu 0.186 (0.016), body 0.182 (0.019), splenium 0.192 (0.030); p=0.3. Tm: genu 64.3 (9.0), body 79.1 (10.3), splenium 77.0 (6.4); p=0.001.
NMOSD vs HC Only MWF in the body (p=0.04) and splenium (p=0.003) were significantly reduced in NMOSD compared to HC.
Conclusion:
1) MWF and Tm reflected expected variations in HC CC myelin, validating the measurements and establishing sensitivity.
2) Tm was not significantly reduced in NMOSD, implying preserved myelin thickness. MWF was significantly reduced in NMOSD CC body and splenium but not genu. This may relate to the greater likelihood of lesions in those regions.
Disclosure:
Shawna Abel: nothing to disclose.
Dr. Irene Vavasour: nothing to disclose.
Lisa Lee: nothing to disclose.
Dr. Robert Carruthers: is a site principal investigator for studies funded by MedImmune, Teva, and Guthy Jackson. He has received speaking fees for unbranded lectures from Biogen, Genzyme, and Teva. He has received consulting fees for Novartis, EMD Serono, and Genzyme.
Dr. Anthony Traboulsee: has received grant funding from the MS Society of Canada, Canadian Institute for Health Research, Roche, and Genzyme; received honoraria or travel grants from Teva Canada Innovation, Roche, Merck/EMD Serono, Genzyme, Chugai Pharmaceuticals.
Dr. Shannon Kolind: has received research support from Roche, MS Society of Canada; consulting for Acorda, Genzyme.
Anna Combes: nothing to disclose
Abstract: P1887
Type: Poster
Abstract Category: Late breaking news
Background: While axonal damage in the corpus callosum (CC) is a prominent feature of multiple sclerosis (MS), less is known about CC integrity in neuromyelitis optica spectrum disorder (NMOSD). Here we examined outcome measures with an advanced MRI technique: multicomponent Driven Equilibrium Single Pulse Observation of T1 and T2 (mcDESPOT). mcDESPOT is often used to study the myelin water fraction (MWF), which quantifies the amount of signal from water between the myelin bilayers, and is thus related to myelin content. We also examined the mcDESPOT-derived myelin water residence time (Tm), which estimates the time taken for water between the myelin bilayers to exchange with intra/extracellular water, and is therefore expected to reflect myelin thickness.
Goals:
1) To determine whether differences in myelin content and thickness within the CC previously described in histological studies can be detected with MWF and Tm.
2) To investigate differences in markers for myelin content and thickness between NMOSD and healthy control (HC) CC.
Methods: 13 patients (mean age: 43y (range: 24-59), 9 female) and 13 HC (40y (26-56), 9 female) were included. CC segmentation was performed using an atlas based approach to obtain regions of interest (ROI) for the genu, body and splenium. Mean Tm and MWF were extracted from each ROI. One-way repeated measures analysis of variance (ANOVA) was used to investigate within-group differences. The Mann-Whitney U test was employed to explore between-group differences.
Results:
HC Within HC, significant differences in both MWF and Tm were observed between the ROIs of the CC. MWF: genu 0.195 (0.017), body 0.196 (0.014), splenium 0.215 (0.009); p=0.005. Tm: genu 66.2ms (9.3), body 82.9 (10.9), splenium 76.1 (11.0); p=0.006.
NMOSD Within NMOSD, differences between CC ROIs were not as apparent as for HC, but significant for Tm. MWF: genu 0.186 (0.016), body 0.182 (0.019), splenium 0.192 (0.030); p=0.3. Tm: genu 64.3 (9.0), body 79.1 (10.3), splenium 77.0 (6.4); p=0.001.
NMOSD vs HC Only MWF in the body (p=0.04) and splenium (p=0.003) were significantly reduced in NMOSD compared to HC.
Conclusion:
1) MWF and Tm reflected expected variations in HC CC myelin, validating the measurements and establishing sensitivity.
2) Tm was not significantly reduced in NMOSD, implying preserved myelin thickness. MWF was significantly reduced in NMOSD CC body and splenium but not genu. This may relate to the greater likelihood of lesions in those regions.
Disclosure:
Shawna Abel: nothing to disclose.
Dr. Irene Vavasour: nothing to disclose.
Lisa Lee: nothing to disclose.
Dr. Robert Carruthers: is a site principal investigator for studies funded by MedImmune, Teva, and Guthy Jackson. He has received speaking fees for unbranded lectures from Biogen, Genzyme, and Teva. He has received consulting fees for Novartis, EMD Serono, and Genzyme.
Dr. Anthony Traboulsee: has received grant funding from the MS Society of Canada, Canadian Institute for Health Research, Roche, and Genzyme; received honoraria or travel grants from Teva Canada Innovation, Roche, Merck/EMD Serono, Genzyme, Chugai Pharmaceuticals.
Dr. Shannon Kolind: has received research support from Roche, MS Society of Canada; consulting for Acorda, Genzyme.
Anna Combes: nothing to disclose