Abstract
Brain plasticity is the basis for systems‐level functional reorganization that promotes recovery in multiple sclerosis (MS). As inflammation interferes with plasticity, its pharmacological modulation may restore plasticity by promoting desired patterns of functional reorganization. Here, we tested the hypothesis that brain plasticity probed by a visuomotor adaptation task is impaired with MS inflammation and that pharmacological reduction of inflammation facilitates its restoration. MS patients were assessed twice before (sessions 1 and 2) and once after (session 3) the beginning of Interferon beta (IFN beta), using behavioural and structural MRI measures. During each session, 2 functional MRI runs of a visuomotor task, separated by 25‐minutes of task practice, were performed. Within‐session between‐run change in task‐related functional signal was our imaging marker of plasticity. During session 1, patients were compared with healthy controls. Comparison of patients' sessions 2 and 3 tested the effect of reduced inflammation on our imaging marker of plasticity. The proportion of patients with gadolinium‐enhancing lesions reduced significantly during IFN beta. In session 1, patients demonstrated a greater between‐run difference in functional MRI activity of secondary visual areas and cerebellum than controls. This abnormally large practice‐induced signal change in visual areas, and in functionally connected posterior parietal and motor cortices, was reduced in patients in session 3 compared with 2. Our results suggest that MS inflammation alters short‐term plasticity underlying motor practice. Reduction of inflammation with IFN beta is associated with a restoration of this plasticity, suggesting that modulation of inflammation may enhance recovery‐oriented strategies that rely on patients' brain plasticity. Hum Brain Mapp 37:2431–2445, 2016. © 2016 The Authors Human Brain Mapping Published by Wiley Periodicals, Inc.
Highlights
The neural reorganization that mitigates the functional impact of damage [Enzinger and Fazekas, 2015] and promotes recovery in multiple sclerosis (MS) is based on brain plasticity [Tomassini et al, 2012a] that is the dynamic reorganization of brain function in response to experience [Doyon and Benali, 2005; Nudo 2013] or damage [Nudo, 2013]
At session 3, the number of Gdactive scans (3 out of 24) reduced by 72% compared to session 2, with a significant difference in the number of Gdpositive vs. Gd-negative scans (P 5 0.001)
Our results suggest that MS inflammation alters plasticity underlying short-term training of a simple motor task [Morgen et al, 2004], as reflected in abnormally greater practice-related functional MRI (fMRI) signal changes in the patients compared to healthy volunteers that were over and above structural differences in grey matter (GM) volume
Summary
The neural reorganization that mitigates the functional impact of damage [Enzinger and Fazekas, 2015] and promotes recovery in multiple sclerosis (MS) is based on brain plasticity [Tomassini et al, 2012a] that is the dynamic reorganization of brain function in response to experience (e.g., skill learning) [Doyon and Benali, 2005; Nudo 2013] or damage [Nudo, 2013]. Advanced neuroimaging shows that clinically meaningful functional changes occur during and after an active phase of MS [Lee et al, 2000; Mezzapesa et al, 2008; Pantano et al, 2002, 2005] With this functional compensation, damage-related altered patterns of functional reorganisation occur in MS, even early during the course of the disease [Pantano et al, 2002] or in the presence of preserved [Hulst et al, 2012] or fully recovered behaviour [Reddy et al, 2000]. The effects of inflammation and its modulation on brain plasticity, remain largely unexplored, hampering the development of Abbreviations
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