Additional file 5: of Predictive value of early magnetic resonance imaging measures is differentially affected by the dose of interferon beta-1a given subcutaneously three times a week: an exploratory analysis of the PRISMS study

Figure S4. Proportion relapsed at each year by ≥2 versus 0–1 active T2 lesions at 6 months. (a) Placebo/delayed treatment group; (b) IFN β-1a 22 μg SC tiw group; (c) IFN β-1a 44 μg SC tiw group. (PDF 269 kb

Additional file 1: of Predictive value of early magnetic resonance imaging measures is differentially affected by the dose of interferon beta-1a given subcutaneously three times a week: an exploratory analysis of the PRISMS study

Figure S1. Proportion with EDSS progression at each year by ≥2 versus 0–1 active T2 lesions at 6 months. (a) Placebo/delayed treatment group; (b) IFN β-1a 22 μg SC tiw group; (c) IFN β-1a 44 μg SC tiw group. (PDF 258 kb

Additional file 3: of Predictive value of early magnetic resonance imaging measures is differentially affected by the dose of interferon beta-1a given subcutaneously three times a week: an exploratory analysis of the PRISMS study

Table S1. (a) Performance of T2 lesions on predicting EDSS progression at Year 2 and Year 4. (b) Performance of T2 lesions on predicting relapse at Year 2 and Year 4. (DOCX 15 kb

Additional file 2: of Predictive value of early magnetic resonance imaging measures is differentially affected by the dose of interferon beta-1a given subcutaneously three times a week: an exploratory analysis of the PRISMS study

Figure S2. Proportion with EDSS progression at each year in the placebo/delayed treatment and IFN β-1a 44 μg SC tiw groups by ≥4 versus 0 active T2 lesions at 6 months. (PDF 189 kb

Additional file 7: of Predictive value of early magnetic resonance imaging measures is differentially affected by the dose of interferon beta-1a given subcutaneously three times a week: an exploratory analysis of the PRISMS study

Figure S6. Proportion relapsed at each year by ≥2 versus 0–1 active T2 lesions at 12 months. (a) Placebo/delayed treatment group; (b) IFN β-1a 22 μg SC tiw group; (c) IFN β-1a 44 μg SC tiw group. (PDF 273 kb

Additional file 4: of Predictive value of early magnetic resonance imaging measures is differentially affected by the dose of interferon beta-1a given subcutaneously three times a week: an exploratory analysis of the PRISMS study

Figure S3. Time to sustained EDSS progression by ≥2 versus 0–1 active T2 lesions at 6 months. (a) Placebo/delayed treatment group; (b) IFN β-1a 22 μg SC tiw group; (c) IFN β-1a 44 μg SC tiw group. (PDF 229 kb

Imaging Surrogates of Disease Activity in Neuromyelitis Optica Allow Distinction from Multiple Sclerosis

<div><p>Inflammatory demyelinating lesions of the central nervous system are a common feature of both neuromyelitis optica and multiple sclerosis. Despite this similarity, it is evident clinically that the accumulation of disability in patients with neuromyelitis optica is relapse related and that a progressive phase is very uncommon. This poses the question whether there is any pathological evidence of disease activity or neurodegeneration in neuromyelitis optica between relapses. To investigate this we conducted a longitudinal advanced MRI study of the brain and spinal cord in neuromyelitis optica patients, comparing to patients with multiple sclerosis and controls. We found both cross-sectional and longitudinal evidence of diffusely distributed neurodegenerative surrogates in the multiple sclerosis group (including thalamic atrophy, cervical cord atrophy and progressive widespread diffusion and myelin water imaging abnormalities in the normal appearing white matter) but not in those with neuromyelitis optica, where localised abnormalities in the optic radiations of those with severe visual impairment were noted. In addition, between relapses, there were no new silent brain lesions in the neuromyelitis optica group. These findings indicate that global central nervous system neurodegeneration is not a feature of neuromyelitis optica. The work also questions the theory that neurodegeneration in multiple sclerosis is a chronic sequela to prior inflammatory and demyelinating pathology, as this has not been found to be the case in neuromyelitis optica where the lesions are often more destructive.</p></div

Cross-sectional fractional anisotropy of the normal appearing white matter.

<p>Voxelwise comparison of fractional anisotropy (FA) within white matter skeletons created with TBSS where significantly lower FA is shown in yellow for (A) neuromyelitis optica group versus control group, (B) multiple sclerosis group versus control group, and (C) multiple sclerosis group versus neuromyelitis optica group.</p

Cross-sectional myelin water fraction (MWF) of the normal appearing white matter.

<p>Voxelwise analysis of MWF in the white matter skeleton created with TBSS where significantly lower MWF is shown in red for (A) multiple sclerosis group versus control group, and (B) multiple sclerosis group MWF versus neuromyelitis optica group.</p

Longitudinal volumetric measures.

<p>(A) Percentage change in brain volume over one year in subject groups. (B) Voxelwise within-group analysis found a small significant area of atrophy in the region of the insula cortex within the multiple sclerosis group (shown) but not the neuromyelitis optica or control groups over the course of one year. (C) Change in thalamic volume over one year. NS = not significant, * = significant difference (corrected p< 0.05).</p