Abstract

ObjectiveTo assess the change in cerebral lesions and atrophy associated with pregnancy in patients with multiple sclerosis (MS). BackgroundMultiple sclerosis often affects women of reproductive age. Disease stabilization typically occurs during pregnancy, with transient recrudescence post-partum. Previous studies showed increased MRI-defined inflammatory Gadolinium enhancing disease activity and T2 lesion load in the 6 months' post-partum. The effect of pregnancy on T1 lesion load and brain atrophy in MS is not well understood. MethodsWe retrospectively identified 16 patients with relapsing-2remitting MS (RRMS) with pre-pregnancy and post-partum 1.5 T brain MRI separated by (mean ± SD) 15.4 ± 3.2 months. The time between delivery and post-partum MRI was 2.2 ± 1.5 months. Baseline characteristics were age 33.0 ± 4.1 years, disease duration 7.2 ± 4.8 years, and Expanded Disability Status Score (EDSS) 1.0 ± 1.0. T2 hyperintense (T2LV) and T1 hypointense (T1LV) lesion volumes were quantified and the number of Gd + lesions was assessed. An SPM12 pipeline estimated global atrophy using brain parenchymal fraction (BPF) and global cortical gray matter (GM) atrophy using the cortical GM fraction (cGMF). Paired t-tests assessed within subject changes. Spearman's correlation coefficients assessed MRI-clinical associations. ResultsPost-partum, there was an increase in both T1LV (p = .048, p = .023 with cube root transformation (CRT) and T2LV (p = .022, CRT p = .065). There were no changes in Gd + lesions, BPF, or cGMF (all p > .05). ConclusionsPregnancy is associated with increased in T2 and T1 cerebral lesion load in MS. However, a de-coupling is apparent, with no whole brain or cortical atrophy developing despite the increase in destructive lesions and despite the expected pregnancy-related decline in brain volume. While in the short term, pregnancy may be protective against the brain volume loss expected with increased lesion load, longer duration of follow-up is needed to verify these findings.

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