Purpose: To examine the optical coherence tomography (OCT) features of the retina in patients with chronic relapsing inflammatory optic neuropathy (CRION) and compare them with those of neuromyelitis optica spectrum disorder (NMOSD), relapsing-remitting multiple sclerosis (RRMS) with and without optic neuritis (ON), and healthy controls (HC). Methods: In this retrospective cross-sectional study, we used spectral domain OCT to evaluate the retinal structure of 14 participants with CRION, 22 with NMOSD, 40 with RRMS with unilateral ON, and 20 HC. The peripapillary retinal nerve fiber layer (pRNFL), total macular volume (TMV), and papillomacular bundle (PMB) were measured, and intra-retinal segmentation was performed to obtain the retinal nerve fiber (RNFL), ganglion cell (GCL), inner plexiform (IPL), inner nuclear (INL), outer plexiform (OPL) and outer nuclear (ONL) layer volumes. Results: The global pRNFL [39.33(±1.8) µm] and all its quadrants are significantly thinner in CRION compared with all other groups (p < 0.05). CRION patients have decreased volumes of TMV, RNFL, GCL, and IPL compared with all other groups (p < 0.05). Conclusion: Severe thinning in pRNFL and thinning in intra-retinal segments of IPL, GCL, RNFL, and TMV could be helpful in differentiating CRION from NMOSD and RRMS.

Few cross-sectional studies have investigated the correlation between neurochemical changes and multiple sclerosis (MS) fatigue, but little is known on the fatigue-related white matter differences between time points. We aim to investigate the longitudinal neurometabolite profile of white matter in MS fatigue. Forty-eight relapsing remitting multiple sclerosis (RRMS) patients with an expanded disability status scale (EDSS) ≤ 4 underwent high field ¹H-multivoxel magnetic resonance spectroscopy (MRS) at baseline and year 1. Fatigue severity was evaluated by the fatigue severity scale (FSS). Patients were divided into low (LF, FSS ≤ 3), moderate (MF, FSS = 3.1–5), and high fatigue (HF, FSS ≥ 5.1) groups. In a two-way analysis of variance (ANOVA), we observed a decline in the ratio of the sum of N-acetylaspartate (NAA) and N-acetylaspartylglutamate (NAAG) to the sum of creatine (Cr) and phosphocreatine (PCr) in the right anterior quadrant (RAQ) and left anterior quadrant (LAQ) of the MRS grid in the HF group at baseline and year 1. This decline was significant when compared with the LF group (p = 0.018 and 0.020). In a one-way ANOVA, the fatigue group effect was significant and the ratio difference in the right posterior quadrant (RPQ) and left posterior quadrant (LPQ) of the HF group was also significant (p = 0.012 and 0.04). Neurochemical changes in the bilateral frontal white matter and possibly parietooccipital areas were noted in the HF group at two different time points. Our findings may shed some light on the pathology of MS fatigue.

PURPOSE: MammaPrint (MP), a 70-gene expression profile assay, informs treatment decisions in early-stage breast cancer by classifying patients into high or low risk of recurrence categories. However, racial disparities in breast cancer outcomes necessitate an evaluation of MP's prognostic utility across diverse populations. This study explores differences in MP scores and associated outcomes among women of various racial backgrounds. MATERIALS AND METHODS: We retrospectively analyzed women with early-stage breast cancer who underwent MP testing (2013-2023) at University Hospitals Seidman Cancer Center. Patients were stratified by self-reported race and MP scores (high v low risk). Clinical outcomes, including recurrence-free survival (RFS) and overall survival (OS), were compared using Kaplan-Meier and Cox proportional hazards models. RESULTS: Among 1,349 women, 15.7% were African American (AA), 83.4% White, 0.6% Asian, and 0.3% from other racial groups. Overall, 64.7% had low-risk and 35.3% had high-risk scores. AA women had a significantly higher proportion of high-risk MP scores compared with White women (49.1% v 32.7%). Although the 5-year RFS rates were comparable between AA and White women (76.5% v 77.2%), the 5-year OS rates were slightly lower for AA women compared with White women (77.8% v 78.2%). MP remained prognostic for RFS at 3, 5, and 10 years regardless of race. Multivariable analysis revealed no significant differences in OS (hazard ratio [HR], 0.94 [95% CI, 0.47 to 1.89]; P = .866) or RFS (HR, 0.83 [95% CI, 0.43 to 1.59]; P = .572) between AA and White women after adjusting for MP risk groups and other clinical factors. High-risk MP scores were associated with worse OS (HR, 3.06 [95% CI, 1.64 to 5.70]; P < .001) and RFS (HR, 2.68 [95% CI, 1.55 to 4.62]; P < .001) compared with low-risk scores. Other factors associated with worse RFS and OS were tumor size, nodal involvement, and age. Interaction models indicated no difference is OS or RFS in AA women and White women with either low-risk or high-risk MP, respectively. CONCLUSION: Despite AA women exhibiting a higher proportion of high-risk MP scores, survival outcomes were comparable with those of White women. These findings underscore MP's consistent prognostic performance across racial groups but further highlight the need to address additional clinical and social determinants influencing breast cancer outcomes beyond genomic risk alone.