Poor sleep is a frequent symptom in patients with multiple sclerosis (MS). The objective of the study was to assess the relationship between nocturnal polysomnographic (PSG) findings and quality of sleep, fatigue, and increased daytime sleepiness among patients with MS. Clinical characteristics were collected. Pittsburgh Sleep Quality Index (PSQI), Fatigue Severity Scale (FSS), Epworth Sleepiness Scale (ESS), and International Restless Legs Syndrome Rating Scale were used to assess quality of sleep, fatigue, excessive daytime sleepiness, and the presence of restless legs syndrome (RLS). All patients underwent nocturnal diagnostic PSG examination. Fifty patients with MS were enrolled into the study. Age was the only independent variable significantly determining apnea-hypopnea index and desaturation index (DI) (beta = 0.369, p = 0.010, beta 0.301, p = 0.040). PSQI and ESS score were significantly higher in a population with RLS (p = 0.004, p = 0.011). FSS significantly correlated with DI (r = 0.400, p = 0.048). Presence of RLS was the only independent variable significantly determining PSQI and ESS (p = 0.005, p = 0.025). DI and presence of RLS were independent variables determining FSS (p = 0.015, p = 0.024). Presence of RLS seems to be the main factor determining poor sleep, fatigue, and daytime somnolence. Sleep disordered breathing and its severity influences only fatigue in patients with MS.

Sleep disordered breathing (SDB) is a frequent comorbidity in stroke patients. SDB is one of the independent risk factors for ischemic stroke. Conversely, stroke may contribute to SDB onset or aggravate premorbid SDB. Multiple mechanisms underlying SDB might be responsible for the development of stroke. The aim of this study was to compare polysomnographic, clinical, and laboratory characteristics of wake-up (WUS) and non-wake-up acute ischemic strokes (NWUS). We prospectively enrolled 88 patients with acute ischemic stroke. Clinical characteristics of the population were recorded on admission, and blood samples were obtained in the fasting condition following morning. SDB was assessed using standard overnight polysomnography in the acute phase of the stroke. WUS were present in 16 patients (18.2%), and NWUS in 72 patients (81.8%). In WUS compared to NWUS, we observed significantly higher values of apnea-hypopnea index (24.8 vs. 7.6, p = 0.007), desaturation index ([DI] 26.9 vs. 8.8, p = 0.005), arousal index (22.6 vs. 13.1, p = 0.035), diastolic blood pressure (91.6 mm Hg vs. 85.2 mm Hg, p = 0.039), triglyceride levels ([TG] 1.9 mmol/L vs. 1.2 mmol/L, p = 0.049), and significantly lower levels of D-dimer (0.4 μg/L vs. 0.7 μg/L, p = 0.035). DI (CI: 1.003-1.054, p = 0.031) and TG (CI: 1.002-1.877, p = 0.049) were the only independent variables significantly associated with WUS in binary logistic regression model. Although the design of our study does not prove the causal relationship between SDB and WUS, higher severity of SDB parameters in WUS supports this hypothesis. A commentary on this article appears in this issue on page 467.

Introduction: Epidemiological studies have suggested an increased vascular risk in patients with multiple sclerosis (MS). There is increasing evidence of the beneficial effects of GLP-1 agonists (GLP-1a) in preventing vascular complications and slowing the progression of neurodegeneration. Our objective was to explore the changes in the endothelial function of MS patients after 12 months of GLP-1a therapy. We also explored the role of lipoprotein subfractions and the antioxidant capacity of plasma. Methods: MS patients were enrolled in a prospective, unicentric study. GLP-1a (dulaglutide) was administered to 13 patients. The control population consisted of 12 subjects. Endothelial function was determined by peripheral arterial tonometry and expressed as reperfusion hyperemia index (RHI). Trolox equivalent antioxidant capacity (TEAC) was used to assess the total antioxidant capacity of the plasma. The levels of lipoprotein subfractions were evaluated. Results: The GLP-1a group did not have a significant change in their RHIs after 12 months (2.1 ± 0.6 vs. 2.1 ± 0.7; p = 0.807). However, a significant increase in their TEACs was observed (4.1 ± 1.4 vs. 5.2 ± 0.5 mmol/L, p = 0.010). On the contrary, the subjects in the control group had a significant worsening of their RHIs (2.1 ± 0.5 vs. 1.8 ± 0.6; p = 0.030), without significant changes in their TEACs. Except for a significant decrease in very-low-density lipoprotein (VLDL) (30.8 ± 10.2 vs. 22.6 ± 8.3 mg/dL, p = 0.043), no other significant changes in the variables were observed in the control group. VLDL levels (beta = −0.637, p = 0.001), the use of GLP-1a therapy (beta = 0.560, p = 0.003), and small LDL (beta = 0.339, p = 0.043) were the only significant variables in the model that predicted the follow-up RHI. Conclusion: Our results suggest that the application of additional GLP-1a therapy may have atheroprotective and antioxidant effects in MS patients with high MS activity and thus may prospectively mitigate their vascular risk. However, the lipoprotein profile may also play an important role in the atherogenic risk of MS subjects.