Superficial white matter integrity in neuromyelitis optica spectrum disorder and multiple sclerosis
- PMID: 38269006
- PMCID: PMC10807332
- DOI: 10.1177/20552173231226107
Superficial white matter integrity in neuromyelitis optica spectrum disorder and multiple sclerosis
Abstract
Background: Superficial white matter (SWM) is a particularly vulnerable area of white matter adjacent to cerebral cortex that was shown to be a sensitive marker of disease severity in several neurological and psychiatric disorders, including multiple sclerosis (MS), but has not been studied in neuromyelitis optica spectrum disorder (NMOSD).
Objective: To compare the integrity of SWM between MS patients, NMOSD patients and healthy controls, and explore the correlation of SWM integrity with cognitive performance and overall disability.
Methods: Forty NMOSD patients, 48 MS patients and 52 healthy controls were included in the study. Mean diffusivity (MD) values obtained by diffusion tensor imaging were used as a measure of SWM integrity. Cognitive performance and overall disability were assessed with standardized tests.
Results: Superficial white matter MD was increased in MS patients compared to healthy controls. Higher MD was associated with poorer spatial memory (most prominently in right temporal and right limbic lobe) and poorer information processing speed in MS patients. After adjusting for age, no significant differences of SWM MD were observed between NMOSD patients and healthy controls.
Conclusion: Integrity of SWM is compromised in MS, but not in NMOSD, and can serve as a sensitive marker of disease severity.
Keywords: cognition; diffusion tensor imaging; disability; mean diffusivity; multiple sclerosis; neuromyelitis optica spectrum disorder; superficial white matter.
© The Author(s), 2024.
Conflict of interest statement
The author(s) declared the following potential conflicts of interest with respect to the research, authorship and/or publication of this article: D.K., O.R.P., S.H.J., and C.F. declare that there is no conflict of interest. C.C. has received research support from Novartis and Alexion and speaking and writing honoraria from Bayer Healthcare and the British Society for Immunology; and serves as a member of the Standing Committee on Science for the Canadian Institutes of Health Research (CIHR). T.S.-H. declares that there is no conflict of interest related to the content of this manuscript and reports the following financial disclosures: received research funding from Celgene/BMS, and speaker’s honoraria from Bayer. S.A. received speaker’s honoraria from Alexion, Bayer and Roche. F.P. provided research support to Neurosciences Clinical Research Center, German Ministry for Education and Research (BMBF), Deutsche Forschungsgemeinschaft (DFG), Einstein Foundation, Guthy Jackson Charitable Foundation, EU FP7 Framework Program, Biogen, Genzyme, Merck Serono, Novartis, Bayer, Roche, Parexel and Almirall, received honoraria for lectures, presentations, speakers from Guthy Jackson Foundation, Bayer, Biogen, Merck Serono, Sanofi Genzyme, Novartis, Viela Bio, Roche, UCB, Mitsubishi Tanabe and Celgene, in addition received compensation for serving on a scientific advisory board of Celgene, Roche, UCB and Merck, is an Academic Editor of PLos One and Associate Editor of Neurology® Neuroimmunology & Neuroinflammation, all unrelated to the presented work.
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