Background: Sleep-disordered breathing (SDB) is highly prevalent after stroke and is considered to be a risk factor for poor post-stroke outcomes. The aim of this observational study was to evaluate the effect of nocturnal respiratory-related indices based on nocturnal respiratory polygraphy on clinical outcomes (including mortality and non-fatal events) in patients with ischemic stroke. Methods: A total of 328 consecutive patients (181 (55%) males, mean age 65.8 ± 11.2 years old) with confirmed ischemic stroke admitted to a stroke unit within 24 h after stroke onset were included in the analysis. All patients underwent standard diagnostic and treatment procedures, and sleep polygraphy was performed within the clinical routine in the first 72 h after admission. The long-term outcomes were assessed by cumulative endpoint (death of any cause, new non-fatal myocardial infarction, new non-fatal stroke/transient ischemic attack, emergency revascularization, emergency hospitalization due to the worsening of cardiovascular disease). A Cox-regression analysis was applied to evaluate the effects of nocturnal respiratory indices on survival. Results: The mean follow-up period comprised 12 months (maximal—48 months). Patients with unfavourable outcomes demonstrated a higher obstructive apnea-hypopnea index, a higher hypoxemia burden assessed as a percent of the time with SpO₂ < 90%, a higher average desaturation drop, and a higher respiratory rate at night. Survival time was significantly lower (30.6 (26.5; 34.7) versus 37.9 (34.2; 41.6) months (Log Rank 6.857, p = 0.009)) in patients with higher hypoxemia burden (SpO₂ < 90% during ≥2.1% versus <2.1% of total analyzed time). However, survival time did not differ depending on the SDB presence assessed by AHI thresholds (either ≥5 or ≥15/h). The multivariable Cox proportional hazards regression (backward stepwise analysis) model demonstrated that the parameters of hypoxemia burden were significantly associated with survival time, independent of age, stroke severity, stroke-related medical interventions, comorbidities, and laboratory tests. Conclusion: Our study demonstrates that the indices of hypoxemia burden have additional independent predictive value for long-term outcomes (mortality and non-fatal cardiovascular events) after ischemic stroke.

Objective. To identify objective measures of sleep and molecular markers of sleep reactivity to stress to determine its role for insomnia prevention and management. Design and methods. The sample included 42 subjects with sleep disturbances and 23 subjects without sleep-related complaints (control group) aged 18 to 72 years. Altogether there are 19 men and 55 women. Nine participants were excluded from the study. Sleep reactivity to stress was assessed using the Ford Insomnia Response to Stress Test (FIRST) questionnaire. The Integrative Anxiety Test was used to screen for anxiety. Sleep indices were assessed by polysomnography (PSG). Blood plasma samples were collected in the morning after PSG to determine brain-derived neurotrophic factor (BDNF), and 24-hour urine was collected one week after PSG to assess metanephrine levels. Results. There were 64 % healthy subjects with low sleep reactivity to stress and low anxiety and 79 % subjects showed insomnia among persons with high sleep reactivity and anxiety. Significant differences in PSG measures were found in groups with low and high sleep reactivity: the efficiency of sleep and the percentage of the second stage of NREM sleep were higher in group with low reactivity, also sleep latency and wake time after sleep onset were lower in group with high reactivity. In addition, serum BDNF level was significantly higher in group with low reactivity, and it correlates positively with daily urinary metanephrine excretion and the absolute duration of stage N3 and negatively with sleep latency. Conclusions. Subjects with high reactivity to stress have lower sleep quality and depth that corresponds to other studies. The level of BDNF is a possible marker of sleep reactivity to stress and it can indicate the potential adaptation to stress.

Objective. To assess subjective and objective sleep characteristics and urinary metanephrine levels in patients with insomnia. Design and methods. We included patients with insomnia complaints and those without sleep– related complaints (control group) 18–75 years old. Subjective evaluation of the main sleep characteristics during the last month was assessed by the Pittsburgh Sleep Quality questionnaire, daytime sleepiness — by the Epworth Sleepiness Scale. For objective sleep evaluation we performed one-night polysomnography (PSG). Within 1 week after the PSG, daily urine was collected to determine the level of metaepinephrine. Results. The groups did not differ by age, mean sleep duration over the past month, number of night awakenings by the Pittsburgh Questionnaire, and level of daytime sleepiness. Sleep latency in insomnia group was 15 minutes longer than in the control group. PSG showed higher apnea-hypopnea and desaturation indices in the control group. There were no differences in daily urinary metanephrine excretion in the main and control groups. Correlation analysis showed no significant association between the metanephrine levels and the severity of somnolence and the index of periodic limb movements. Conclusions. Our analysis showed no significant differences in the daily urine metanephrine levels and the main PSG sleep characteristics among subjects with and without insomnia. Further work is required to clarify markers of insomnia and their negative health effects.

Background. Wake-up stroke (WUS) is often combined with sleep-disordered breathing and may potentially have a more unfavorable course.Objective — to evaluate the association between the time of stroke onset and the pattern of sleep-disordered breathing, as well as the effect of wake-up stroke on stroke recovery and stroke severity in patients with ischemic stroke.Design and methods. We included patients 18–85 years old with acute ischemic stroke admitted within 24 hours of symptom onset to the neurological resuscitation unit, and performed polygraphy within the first day of hospitalization to assess the parameters and severity of sleep-disordered breathing. In 2018–2023, 2122 patients were screened, polygraphy was performed in 639 patients, and data from 292 patients were included in the final analysis. Stroke severity was assessed using the NIHSS scale, stroke type was determined using the TOAST classification. WUS was considered when symptoms were detected upon awakening. Functional status was assessed by the Barthel index, and rehabilitation outcomes by the modified Rankin scale. The cumulative end point included death from any cause, new nonfatal myocardial infarction, new nonfatal stroke/transient ischemic attack, emergency revascularization, or emergency hospitalization due to exacerbation of cardiovascular disease.Results. WUS was detected in 101 patients (34,6 %). The WUS group had more frequent diabetes mellitus and higher NIHSS (p = 0,021) and Barthel index (p = 0,026) at discharge, less frequent thrombolytic therapy and emergency endovascular procedures (p = 0,007) which in most cases was associated with hospitalization in time beyond the therapeutic window (p < 0,001). Endpoints were reached in 21,6 % with a median follow-up of 209 days. No significant differences were found in the main indices of sleep-disordered breathing in groups of different severity and pathogenetic type of stroke. The most significant factors related to Barthel index were stroke severity at discharge (p < 0,001) and age (p < 0,001). Stroke severity at discharge was most influenced by thrombolytic therapy (p = 0,006) and stroke severity on admission (p < 0,001).Conclusions. Our study did not show the previously described higher incidence of sleep-disordered breathing in WUS. The best outcomes were in subjects who received reperfusion therapy. Patients with WUS should be hospitalized in a hospital where reperfusion therapy is available. Lower Barthel index values at discharge of patients with WUS may characterize their lower rehabilitation potential.

Background. The model of sleep reactivity to stress considers sleep reactivity to stress as a link in the pathogenesis of insomnia disorder – the degree to which stress disturbs sleep, which manifests as difficulty in initiating and maintaining sleep.The aim. To study clinical and psychological features as well as subjective and objective sleep indexes of subjects with high level of sleep reactivity to stress.Materials and methods. The psychological status, subjective indexes of sleep and sleep reactivity to stress according to Ford Insomnia Response to Stress Test were studied among 18–75 year-old subjects without significant sleep disturbances and patients with chronic insomnia. Polysomnography was performed for objective evaluation of sleep parameters.Results. It was found that individuals with high levels of sleep reactivity to stress were characterized by high levels of anxiety, restlessness, and neuroticism. According to results of Pittsburg questionnaire, a lower quality of sleep was revealed. These findings were correlated with objective indexes of sleep according to polysomnographic studies: less deep sleep and its lower efficiency due to sleep disturbances.Conclusions. Individuals with high sleep reactivity to stress are characterized by greater anxiety combined with subjective and objective sleep disturbance like insomnia type.