Emotion dysregulation in multiple sclerosis: Impact on symptoms of depression and anxiety.

BACKGROUND: There is consistent evidence for higher prevalence of affective disorders, specifically mood and anxiety disorders, in people with MS (PwMS). PURPOSE: The goal of this study was to examine the role of emotion dysregulation in explaining symptoms of depression and anxiety in PwMS. METHODS: Data from 100 PwMS and 98 community controls (CC) were analyzed. Participants completed survey measures assessing symptoms of depression and anxiety, difficulties in emotion regulation, general and health-related quality of life, and use of emotion regulation strategies during emotionally evocative situations in the previous two weeks. RESULTS: PwMS had higher scores on depression, endorsed greater difficulty regulating emotions, and reported lower health-related quality of life compared with CC. Higher scores on both measures of depression and anxiety were associated with difficulties in emotion regulation and greater use of maladaptive emotion regulation strategies. Additionally, emotion dysregulation - quantified via use of maladaptive strategies and difficulties in regulating emotions - mediated the effect of MS on symptoms of depression. CONCLUSIONS: Emotion dysregulation is associated with symptoms of depression and anxiety in PwMS. Given the malleability of this construct, this study underscores the importance of further investigating emotion dysregulation, and possibly adopting it as a surrogate endpoint in interventions targeting affective disorders in PwMS.

Basal Ganglia Iron in Patients with Multiple Sclerosis Measured with 7T Quantitative Susceptibility Mapping Correlates with Inhibitory Control.

BACKGROUND AND PURPOSE: T2 hypointensity in the basal ganglia of patients with MS has been associated with clinical progression and cognitive decline. Our objectives were the following: 1) to compare signal in T2WI, R2 (ie, 1/T2), and R2* (ie, 1/T2*) relaxation rates and quantitative susceptibility mapping; and 2) to investigate the associations among MR imaging, clinical scores, and cognitive measures of inhibitory control linked to basal ganglia functioning. MATERIALS AND METHODS: Twenty-nine patients with MS underwent a battery of neuropsychological tests including the Flanker and Stroop tasks. 7T MR imaging included 3D gradient-echo and single-echo multishot spin-echo EPI. Quantitative susceptibility mapping images were calculated by using a Wiener filter deconvolution algorithm. T2WI signal was normalized to CSF. R2 and R2* were calculated by log-linear regression. Average MR imaging metrics for the globus pallidus, putamen, and caudate were computed from manually traced ROIs including the largest central part of each structure. RESULTS: Marked spatial variation was consistently visualized on quantitative susceptibility mapping and T2/T2*WI within each basal ganglia structure. MR imaging metrics correlated with each other for each basal ganglia structure individually. Notably, caudate and putamen quantitative susceptibility mapping metrics were similar, but the putamen R2 was larger than the caudate R2. This finding suggests that tissue features contribute differently to R2 and quantitative susceptibility mapping. Caudate and anterior putamen quantitative susceptibility mapping correlated with the Flanker but not Stroop measures; R2 did not correlate with inhibitory control measures. Putamen quantitative susceptibility mapping and caudate and putamen R2 correlated with the Expanded Disability Status Scale. CONCLUSIONS: Our study showed that quantitative susceptibility mapping and R2 may be complementary indicators for basal ganglia tissue changes in MS. Our findings are consistent with the hypothesis that decreased performance of basal ganglia-reliant tasks involving inhibitory control is associated with increased quantitative susceptibility mapping.

Cognitive impairments in relapsing-remitting multiple sclerosis: a meta-analysis.

There is debate in the literature regarding the magnitude, nature, and influence of cognitive impairment in individuals with relapsing-remitting multiple sclerosis (RRMS). Therefore, we conducted a meta-analysis that quantified the overall magnitude of cognitive impairment in individuals with RRMS and identified the domains of cognition and clinical/demographic variables that were moderators of the overall effect. We included 57 studies with 3891 participants that yielded a total of 755 effect sizes. Overall, there was a moderate decline in cognitive functioning in individuals with RRMS compared with healthy controls. Larger effects were observed in cognitive domains of motor functioning, mood status and memory and learning. Regarding demographic and clinical variables, age and gender were moderators of cognitive impairment in all cognitive domains, whereas neurological disability and disease duration primarily moderated performance on tasks assessing memory and learning.