BackgroundFatigue is a frequent disabling symptom in multiple sclerosis (MS), but its pathophysiology remains incompletely understood. This study aimed to explore the underlying neural basis of fatigue in patients with MS. MethodsWe enrolled 60 consecutive patients with MS and 60 healthy controls (HC) matched on age, sex, and education. Fatigue was assessed using the Portuguese version of the Modified Fatigue Impact Scale (MFIS). All participants underwent 3T brain MRI (conventional and diffusion tensor imaging [DTI] sequences). White matter (WM) focal lesions were identified and T1/T2 lesion volumes were computed. Tract-based spatial statistics were applied for voxel-wise analysis of DTI metrics fractional anisotropy and mean diffusivity (MD) on normal-appearing WM (NAWM). Using Freesurfer software, total and regional volumes of cortical and subcortical gray matter (GM) were calculated. ResultsCompared to HC, patients with MS scored significantly higher on MFIS (33.8 ± 19.7 vs 16.5 ± 15.1, p < 0.001). MFIS scores were not significantly correlated with T1/T2 lesion volumes, total GM volume, or any regional volume of cortical and subcortical GM. Significant correlations were found between global scores of MFIS and MD increase of the NAWM skeleton, including corona radiata, internal capsule, external capsule, corticospinal tract, cingulum, corpus callosum, fornix, superior longitudinal fasciculus, superior frontooccipital fasciculus, sagittal stratum, posterior thalamic radiation, cerebral peduncle, and uncinate fasciculus. ConclusionsIn this study, fatigue was associated with widespread NAWM damage but not with lesion load or GM atrophy. Functional disconnection, caused by diffuse microstructural WM damage, might be the main neural basis of fatigue in MS.
Apathy has been recognized as a frequent symptom in multiple sclerosis (MS) but uncertainty remains about its prevalence and clinical correlates. Therefore, the objective of this work was to assess the prevalence of apathy in patients with MS and to identify clinical and demographic correlates. A case-control study with 30 patients and 30 healthy controls matched for age, gender and education was performed. Apathy diagnosis was established using Robert et al.'s criteria. Additionally, apathy was assessed using the 10-item short version of the clinical-rated Apathy Evaluation Scale (AES-C-10). The Beck Depression Inventory (BDI), Modified Fatigue Impact Scale (MFIS), and Montreal Cognitive Assessment (MoCA) were used to evaluate depression, fatigue and cognitive impairment, respectively. Apathy prevalence in MS patients was 43.3%. Patients with MS had higher AES-C-10 scores than controls (13.9 vs. 12.0, p=0.015). Patients with apathy presented a higher proportion of males (53.8% vs. 11.8%, p=0.02), lower educational level (53.8% vs. 11.8% of patients with up to 9years of education), higher scores on cognitive dimension of MFIS (18.0 vs. 8.0, p=0.048) and BDI (13.0 vs. 7.0, p=0.035) and worse performance on MoCA (24.0 vs. 26.0, p=0.028). Gender was the only independent predictor of apathy, with men presenting a higher risk compared to women (OR: 9.62; 95%CI: 1.02-90.61; p=0.048). In conclusion, apathy is a common neuropsychiatric disorder in MS and it is probably underdiagnosed. Male patients seem to have an increased risk of apathy, and this finding may be related to the generally more unfavorable course of MS in men.
Introduction: Several questions about pregnancy in women with multiple sclerosis (MS) have been discussed, but clarification is still needed in some very practical issues. Portuguese data on this subject remain scattered and need to be analyzed in order to standardize clinical practice. Objective: This study aimed to describe and analyze the impact of MS on pregnancy and perinatal health of children born to Portuguese mothers with the disease. Material and methods: This is a multicenter, retrospective study of a cohort of Portuguese women with MS who were pregnant and who gave birth between 01/01/2011 and 31/12/2015. Demographic and clinical data related to maternal disease, pregnancy progression and events, childbirth and newborn health were collected. Results: Ninety-seven women were recruited and 90 live births were evaluated. The mean maternal age at conception was 32.5 years, and 63.9% had no relapses in the previous year (98.0% had a relapsing-remitting MS and the EDSS score was ≤ 3 in 92.8% of the cases). Only 50.5% of the women had a preconception specific evaluation and 60 children were exposed to immunomodulatory therapies during pregnancy. Nineteen women had relapses during pregnancy. Childbirth was induced in 22.7% of the cases, and the caesarean section rate was 34%. Children exposed to immunomodulatory drugs during pregnancy had a lower birth length (p = 0.014), and there was also a trend toward lower birth weight (p = 0.054) in these newborns. Pre-conception EDSS score negatively correlated with the duration of pregnancy (r = -0.22; p = 0.029), weight (r = -0.23; p = 0.031) and cephalic perimeter at birth (r = -0.24; p = 0.033). There was no relationship between the occurrence of relapses or progression in EDSS score during pregnancy with any variables related to the newborn. Conclusions: In our cohort, it has been confirmed that MS has no negative effect on pregnancy or on children's perinatal health. However, the use of immunomodulatory drugs may have some impact on newborns' somatometric features.
Since the discovery of the remarkable properties of adipose tissue as a metabolically active organ, several evidences on the possible link between obesity and the pathogenesis of multiple sclerosis (MS) have been gathered. Obesity in early life, mainly during adolescence, has been proposed as a relevant risk factor for late MS development. Moreover, once MS is initiated, obesity can contribute to increase disease severity by negatively influencing disease progress. Despite the fact that clinical data are not yet conclusive, many biochemical links have been recently disclosed. The "low-grade inflammation" that characterizes obesity can lead to neuroinflammation through different mechanisms, including choroid plexus and blood-brain barrier disruption. Furthermore, it is well known that resident immune cells of central nervous system and peripheral immune cells are involved in the pathogenesis of MS, and adipokines and neuropeptides such as neuropeptide Y may mediate the cross talk between them.
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