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.

Our results suggest a significant association of ESS with RLS, diabetes mellitus, and obesity in patients with acute ischemic stroke.

Study Objectives: 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). Methods: 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. Results: 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. I NTRO DUCTI O NA recent population-based study has shown that wake-up strokes (WUS) comprise 14% of all ischemic strokes. The same study concludes, that WUS do not differ from non-wake up strokes (NWUS) in clinical features, risk factors, or outcome.1 There is a diurnal variation in the onset of stroke. Sleep tends to promote ischemic stroke, and there is a higher frequency of strokes occurring in the morning.2,3 Sleep disordered breathing (SDB) is present in up to 72% of stroke patients and is one of the independent risk factors for stroke. 4,5 However, stroke may also aggravate premorbid SDB or even contribute to SDB onset. 6 Multiple mechanisms might link SDB with the onset of cerebral ischemia during the sleep, including coagulation changes, hemodynamic changes, blood pressure (BP) surges, inflammatory overactivity, increased arterial stiffness, increased sympathetic tone, paradoxical embolization, or the development of cardiac arrhythmias. 7-11Currently, WUS patients are excluded from revascularization therapy; therefore, a thorough search for predictors and risk factors of WUS is desirable. The aim of this study was to compare polysomnographic, clinical, and laboratory characteristics of WUS and NWUS with mild-to-moderate severity. SCIENTIFIC INVESTIGATIONS Association of Sleep M ETHO DSThe study population consists of patients hospitalized in the stroke unit of the 1 st Department of Neurology, Comenius University Bratislava from January 2011 to December 2014 with the BRIEF SUMMARY Current Knowledge/Study Rationale: Currently, wake-up stroke patients are excluded from revascularization therapy, so a precise search for predictors and risk factors of wake-up strokes is desirable. The aim of this study was to compare polysomnographic, clinical, and laboratory characteristics of wake-up strokes and non-wake-up strokes with mild-to-moderate severity. Study Impact: We emphasize the importance of significantly higher frequency of moderate-to-severe sleep apnea syndrome among the wake-up stroke population, as this population is indicated for positive...

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Background Obstructive sleep apnea (OSA) is a disorder with a significant risk for cardiovascular diseases. Dyslipidemia and redox imbalance belong to potential mechanisms linking OSA with the development of vascular diseases. The main aim of this study was the evaluation of the presence of lipid abnormalities in OSA patients, focusing on small dense low-density lipoprotein (LDL) and high-density lipoprotein (HDL) subfractions and determination of the redox imbalance by evaluating the marker of oxidative damage to plasma lipids - lipoperoxides. Methods The study included 15 male subjects with polysomnographically confirmed OSA and 16 male healthy controls. Plasma levels of total cholesterol, LDL and HDL and their subfractions, triacylglycerols and lipoperoxides were determined in all study individuals. Plasma LDL and HDL subfractions were separated by the Lipoprint system which is a polyacrylamide gel electrophoresis. Lipoperoxide levels were determined spectrophotometrically. Results OSA patients had significantly higher triacylglycerols, total cholesterol and LDL-cholesterol compared to healthy controls. HDL cholesterol was not significantly different. Of the LDL and HDL subfractions, OSA patients had significantly lower levels of atheroprotective LDL1 and large HDL subfractions and significantly higher levels of atherogenic small dense LDL3–7 and HDL8–10 subfractions. Lipoperoxide levels in patients with OSA were significantly elevated compared to healthy individuals. Conclusion The lipoprotein pro-atherogenic phenotype was found in individuals with OSA characterized by increased levels of atherogenic lipoprotein subfractions and reduced levels of atheroprotective subfractions. In addition, a plasma redox imbalance was found in patients with OSA compared to controls by detecting higher oxidative damage to lipids. Abnormalities in lipoprotein levels in patients with OSA, as well as the redox imbalance, could lead to an acceleration of the atherosclerotic process in predisposed individuals and thus represent a significant risk factor for vasular diseases.

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Hyperglycaemia-induced oxidative stress makes an important contribution to the aetiology of diabetic neuropathy. The aim of our study was to evaluate the effect of the antioxidant stobadine (STB) in comparison with a treatment by a high-dose of α-lipoic acid (ALA), on the neurological consequences of chronic hyperglycaemia in an animal model of diabetes in Wistar rats (16 weeks old), made diabetic by streptozotocin (STZ 3 × 20 mg i.v.). Neuropathy was evaluated electrophysiologically by measuring motor nerve conduction velocity (NCV) in the 4 th and 8 th week in vivo and motor NCV and resistance to ischaemic conduction failure (RICF) of the sciatic nerve in the 10 th week of the experiment in vitro. The therapy with ALA (100 mg/kg i.p., 5 times a week) and STB (25 mg/kg i.p., 5 times a week) had a significant effect on NCV in vivo in the 8 th week of the experiment and no effect in the 10 th week in vitro. The RICF elevated in diabetic animals was significantly modified by ALA. The effect of the antioxidant STB on NCV was comparable with that of ALA, while RICF was affected only by ALA. We conclude that treatment with appropriate antioxidants might partially prevent nerve dysfunction in diabetic rats.

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