BACKGROUND: No general recommendations are yet available for the application of robot-assisted treadmill therapy for children with cerebral palsy regarding the length and intensity of the intervention. OBJECTIVE: The aim of the study was to evaluate patient-specific determinants of responsiveness to robot-assisted gait training (RAGT) in patients with bilateral spastic cerebral palsy. METHOD: During 12 months, the patients underwent 1–4 blocks of RAGT, representing 16–82 TUs. The following parameters were evaluated before (V0) and after each therapeutic block (V1–V4): dimension A (lying and rolling), B (sitting), C (crawling and kneeling), D (standing), E (walking, running and jumping) of the Gross Motor Function Measure (GMFM-88). We evaluated the change in motor functions in relation to the severity of disability, age, gender and number of therapeutic units. RESULTS: Ninety-seven patients aged between 3.7 and 27 years (mean age 10.02 years (SD±5.29); Gross Motor Function Classification System level I [n = 5], II [n = 25], III [n = 48], IV [n = 19]) underwent 16–82 TUs (overall average number 34.06 TUs, SD±16.41) of RAGT. In the patient group, we recorded clinically meaningful improvement and statistically significant improvement (p < 0.001) in gross motor functions with gradual increase in the effect size after each therapeutic block. Using correlation and regression analysis, we found a statistically significant associations between the number of therapeutic units, severity of disability, and improvement in motor functions after RAGT. CONCLUSION: We have identified two determinants –the severity of disability and the number of therapeutic units –which could have a decisive and predictive character in setting rehabilitation/designing programmes. The duration of the applied RAGT period, frequency and intensity could be a crucial factor for the potential of improvement in children with BS-CP.

Background: Obstructive sleep apnea (OSA) activates several pathophysiological mechanisms which can lead to the development of vascular diseases. Endothelial dysfunction (ED) is an initial step in the development of atherosclerosis. The association between ED and OSA has been described in several studies, even in previously healthy subjects. High-density lipoproteins (HDL) were generally considered to be atheroprotective, and low-density lipoprotein (LDL) to be an atherogenic component of lipoproteins. However, recent findings suggest a pro-atherogenic role of small HDL subfractions (8–10) and LDL subfractions (3–7). This study aimed to evaluate the relationship between endothelial function and lipid subfractions in previously healthy OSA subjects. Material and Methods: We prospectively enrolled 205 subjects with sleep monitoring. Plasma levels of triacylglycerols, total cholesterol, LDL, HDL, and their subfractions were assessed. Endothelial function was determined using peripheral arterial tonometry, and reperfusion hyperemia index (RHI) was assessed. Results: Plasma levels of small and intermediate HDL subfractions have statistically significant pro-atherogenic correlations with endothelial function (p = 0.015 and p = 0.019). In other lipoprotein levels, no other significant correlation was found with RHI. In stepwise multiple linear regression analysis, small HDL (beta = −0.507, p = 0.032) was the only significant contributor in the model predicting RHI. Conclusions: In our studied sample, a pro-atherogenic role of small HDL subfractions in previously healthy subjects with moderate-to-severe OSA was proven.

Mitochondrial dysfunction is implicated in the pathophysiology of multiple sclerosis (MS) and may contribute to its fatigue and muscle weakness. Whether skeletal muscle metabolic changes are present at disease onset is unclear. In this observational matched case-control study we investigated muscle metabolism and its relation to systemic metabolic measures in newly diagnosed, treatment-naïve patients with MS (PwMS) and matched healthy controls. Gastrocnemius metabolism was assessed using static and dynamic 7 T ¹ H/ ³¹ P magnetic resonance spectroscopy (MRS), measuring energy metabolites, membrane-related compounds, and post-exercise phosphocreatine (PCr) recovery. Systemic metabolism was assessed by oral glucose tolerance test (OGTT) measuring glucose, insulin, and GLP-1. Static MRS revealed lower carnosine ( p = 0.044) and a trend toward lower acetylcarnitine in PwMS. Dynamic ³¹P-MRS showed elevated pre-exercise inorganic phosphate (Pi; p = 0.012), trend toward reduced PCr/Pi ratio, and prolonged PCr recovery ( p = 0.031) in PwMS. PwMS also had reduced GLP-1 response during OGTT ( p = 0.032) despite preserved insulin sensitivity. Higher PCr levels were associated with greater GLP-1 response in PwMS only; longer PCr recovery was associated with insulin resistance parameters in controls only. Newly diagnosed MS is associated with skeletal muscle mitochondrial impairment during energetic stress, despite largely preserved systemic metabolic status. Altered metabolites, delayed recovery, and association with reduced GLP-1 response suggest impaired muscle bioenergetics and altered systemic metabolic regulation present at disease onset. Targeting mitochondrial and metabolic pathways offers therapeutic potential in early MS. Trial registration number: ClinicalTrials.gov: NCT03052595, date of registration: 14th Feb 2017.

Background: Wake-up stroke (WUS) is a certain type of ischemic stroke in which a patient wakes up with a new neurological deficit due to cerebral ischemia. Sleep-disordered breathing is an independent risk factor for stroke, but the role of nocturnal oxygen desaturation in the pathophysiology of WUS is still insufficiently explored. According to several studies, patients with WUS have a significantly more severe sleep apnea syndrome and lower mean blood oxygen saturation. This study aimed to assess the severity of nocturnal desaturations in acute WUS and non-WUS patients using nocturnal pulse oximetry. Material and Methods: The cohort of 225 consecutive patients with neuroimaging-verified acute cerebral ischemia was prospectively enrolled. For further analyses, 213 subjects with known WUS/non-WUS status were selected (111 males and 102 females, average age 70.4 ±12.9, median baseline NIHSS = 5, median baseline mRS = 3). Patients were divided into the WUS group (n = 45) and the non-WUS group (n = 168). Overnight pulse oximetry was performed within 7 days of the stroke onset and data of both of the studied groups were compared. Results: We found oxygen desaturation index (ODI) in the WUS group was 14.5 vs. 16.6 (p = 0.728) in the non-WUS group, basal O2 saturation was 92.2% vs. 92.5% (p = 0.475), average low O2 saturation was 90.3% vs. 89.6% (p = 0.375), minimal O2 saturation was 79.5% vs. 80.6% (p = 0.563), and time with O2 saturation <90% (T90) was 4.4% vs. 4.7% (p = 0.729). Conclusions: In the studied sample, monitored respiratory parameters including ODI, basal O2 saturation, average low O2 saturation, minimal O2 saturation, and T90 did not significantly differ between groups of WUS and non-WUS patients.