ArticleAnnals of clinical and translational neurology2026
Lesion Location and Functional Connections Reveal Cognitive Impairment Networks in Multiple Sclerosis.
Article in Annals of clinical and translational neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Increased functional network connectivity following cognitive rehabilitation in progressive multiple sclerosis with moderate to severe disabilty: findings from the CogEx study.Journal of neurology · 2026Trial
- Dissociating Fatigue and Fatigability in Multiple Sclerosis: The Role of Cognitive Processing Speed.European journal of neurology · 2026Article
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Authors and funding
8 authors.
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Abstract
objectiveCognitive impairment, fatigue, and depression are common in multiple sclerosis (MS), potentially due to disruption of regional functional connectivity caused by white matter (WM) lesions. We explored whether WM lesions functionally connected to specific brain regions contribute to these MS-related manifestations.
methodsA total of 596 MS patients underwent 3T brain MRI acquisition, neurologic assessment, and neuropsychological evaluation (Brief Repeatable Battery, Modified Fatigue Impact Scale [MFIS], and Montgomery-Åsberg Depression Rating Scale [MADRS]). Voxel-wise lesion probability maps were compared between subgroups based on cognition, fatigue, or depression. Lesion distributions were linked to a brain functional connectivity atlas to map lesion network associations. Lesion network maps (LNMs) were then compared among subgroups (p < 0.05, FWE-corrected).
resultsOne hundred twenty-six (27.2%) MS patients were cognitively impaired and showed significantly more widespread WM lesions, more strongly functionally connected to bilateral hippocampi, thalami, cerebellum, and occipital cortices (corrected-p < 0.05) than cognitively preserved patients. Lesion networks were similar for impaired processing speed/attention. Verbal memory deficits were associated with WM lesions connected to parahippocampi, temporal pole, and cerebellum (corrected-p ≤ 0.05), while verbal fluency deficits involved connections to thalami, putamen, caudate nuclei, anterior cingulate cortex, and cerebellum (corrected-p ≤ 0.05). No significant lesion distribution or network connectivity differences were found in patients with visual memory deficits, fatigue (MFIS ≥ 38, 184/493 [37.3%]) or depression (MADRS > 9, 192/495 [38.8%]).
interpretationRegional WM lesions disrupting connections to the hippocampus, thalamus, cerebellum, and temporo-occipital cortices contribute to cognitive impairment, but not fatigue or depression. LNM may clarify mechanisms underlying cognitive deficits in MS.
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