Brain activity, regional gray matter loss, and decision-making in multiple sclerosis

• Published in: Multiple sclerosis 2018-08, Vol.24 (9), p.1163-1173
• Main Authors: Weygandt, Martin, Wakonig, Katharina, Behrens, Janina, Meyer-Arndt, Lil, Söder, Eveline, Brandt, Alexander U, Bellmann-Strobl, Judith, Ruprecht, Klemens, Gold, Stefan M, Haynes, John-Dylan, Paul, Friedemann
• Format: Article
• Language: English
• Subjects: Adult; Brain mapping; Cognition; Cognitive ability; Decision making; Decision Making - physiology; Feedback; Female; Functional magnetic resonance imaging; Gray Matter - diagnostic imaging; Gray Matter - pathology; Humans; Magnetic Resonance Imaging; Male; Middle Aged; Morphometry; Multiple sclerosis; Multiple Sclerosis - complications; Multiple Sclerosis - diagnostic imaging; Multiple Sclerosis - pathology; Neuroimaging; Reinforcement; Substantia grisea
• ISSN: 1352-4585; 1477-0970
• DOI: 10.1177/1352458517717089

Background: Decision-making (DM) abilities deteriorate with multiple sclerosis (MS) disease progression which impairs everyday life and is thus clinically important. Objective: To investigate the underlying neurocognitive processes and their relation to regional gray matter (GM) loss induced by MS. Methods: We used a functional magnetic resonance imaging (fMRI) Iowa Gambling Task to measure DM-related brain activity in 36 MS patients and 21 healthy controls (HC). From this activity, we determined neural parameters of two cognitive stages, a deliberation (“choice”) period preceding a choice and a post-choice (“feedback”) stage reporting decision outcomes. These measures were related to DM separately in intact and damaged GM areas as determined by a voxel-based morphometry analysis. Results: Severely affected patients (with high lesion burden) showed worse DM-learning than HC (t = −1.75, p = 0.045), moderately affected (low lesion burden) did not. Activity in the choice stage in intact insular (t = 4.60, pFamily-Wise Error [FWE] corrected = 0.034), anterior cingulate (t = 4.50, pFWE = 0.044), and dorsolateral prefrontal areas (t = 4.43, pFWE = 0.049) and in insular areas with GM loss (t = 3.78, pFWE = 0.011) was positively linked to DM performance across patients with severe tissue damage and HC. Furthermore, activity in intact orbitofrontal areas was positively linked to DM-learning during the feedback stage across these participants (t = 4.49, pFWE = 0.032). During none of the stages, moderately affected patients showed higher activity than HC, which might have indicated preserved DM due to compensatory activity. Conclusion: We identified dysregulated activity linked to impairment in specific cognitive stages of reward-related DM. The link of brain activity and impaired DM in areas with MS-induced GM loss suggests that this deficit might be tightly coupled to MS neuropathology.