Cortical and white matter lesion topology influences focal corpus callosum atrophy in multiple sclerosis. Issue 3 (14th February 2022)

• Record Type: Journal Article
• Authors: Platten, Michael; Ouellette, Russell; Herranz, Elena; Barletta, Valeria; Treaba, Constantina A.; Mainero, Caterina; Granberg, Tobias
• Is Part Of: Journal of neuroimaging. Volume 32:Issue 3(2022)
• Page Start: 471
• Page End: 479
• Publication Date: 2022-02-14
• Subjects: atrophy -- corpus callosum -- magnetic resonance imaging -- multiple sclerosis; Diagnostic imaging -- Periodicals; Nervous system -- Diseases -- Diagnosis -- Periodicals; Imagerie pour le diagnostic -- Périodiques; Système nerveux -- Maladies -- Diagnostic -- Périodiques; Imagerie médicale; Neuroimagerie; Neurologie; Système nerveux; Périodique électronique (Descripteur de forme); Ressource Internet (Descripteur de forme); 616.804754
• DOI: 10.1111/jon.12977
• Languages: English
• ISSNs: 1051-2284

Abstract

Abstract: Background and Purpose: Corpus callosum (CC) atrophy is a strong predictor of multiple sclerosis (MS) disability but the contributing pathological mechanisms remain uncertain. We aimed to apply advanced MRI to explore what drives the often nonuniform callosal atrophy. Methods: Prospective brain 7 Tesla and 3 Tesla Human Connectom Scanner MRI were performed in 92 MS patients. White matter, leukocortical, and intracortical lesions were manually segmented. FreeSurfer was used to segment the CC and topographically classify lesions per lobe or as deep white matter lesions. Regression models were calculated to predict focal CC atrophy. Results: The frontal and parietal lobes contained the majority (≥80%) of all lesion classifications in both relapsing‐remitting and secondary progressive MS subtypes. The anterior subsection of the CC had the smallest proportional volume difference between subtypes (11%). Deep, temporal, and occipital white matter lesions, and occipital intracortical lesions were the strongest predictors of middle‐posterior callosal atrophy (adjusted R 2 = .54‐.39, P < .01). Conclusions: Both white matter and cortical lesions contribute to regional corpus callosal atrophy. The lobe‐specific lesion topology does not fully explain the inhomogeneous CC atrophy.