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Updated: Feb 7, 2026
Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
Published on: July 19, 2019
Quantitative MRI analysis of cerebral lesions and atrophy in post-partum patients with multiple sclerosis
Fariha Khalid1, Brian C Healy1, Sheena L Dupuy1
1Department of Neurology, , Brigham and Women's Hospital, Laboratory for Neuroimaging Research, Partners MS Center, Ann Romney Center for Neurologic Diseases, Harvard Medical School, Boston, MA, USA.
Objective:
To assess the change in cerebral lesions and atrophy associated with pregnancy in patients with multiple sclerosis (MS).
Background:
Multiple 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.
Methods:
We 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.
Results:
Post-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).
Conclusions:
Pregnancy 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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