Browsing by Subject "sleep"

Poor quality of sleep and the following health problems affecting daily life are in many cases caused by cognitive and physiological arousal resulted from a stressful event. Such stress detrimental to sleep may originate from psychosocial factors such as feelings of shame and social rejection. Our goal was to elucidate the impact of acute psychosocial stress occurring before bedtime on sleep macrostructure and the early night non-rapid eye movement sleep (NREMS). In addition, virtual reality solutions are emerging as options to simulate social threats in laboratory environments. We studied whether a virtual reality variation of a public speaking scenario was sufficient in producing a physiological stress response evident in heart rate variability (HRV) parameters. We compared two experimental groups of healthy young adults (n=34), which differed in the scenario completed within the virtual reality. The stress condition involved a public speaking simulation in front of an attentive virtual audience whereas the control condition involved listening to a neutral presentation in the same but empty virtual seminar room. The participants’ physiological responses were measured with a HRV monitor for 38 hours and the quality of sleep during the laboratory night following stress induction with electroencephalography (EEG). The examined early sleep period was divided into two separate cycles of NREMS, whose results were juxtaposed. For analysing frequency band activity during sleep, we processed the data from EEG with Fourier transformation to yield power spectral density values i.e. frequency activity values. Comparing the two conditions, we observed a distinct effect of stress both during the virtual public speaking scenario and in the subsequent early sleep in the participants from the stress group. We found a significant increase in heart rate and rising fluctuations in the LF/HF (HRV power spectrum high frequency/low frequency) ratio around the stress task period contrasting the results of the control condition, reflecting increased sympathetic tone in the stress group. In the following night, the percentage of stage N3 sleep significantly increased at the cost of N2 sleep during the first NREMS cycle in the stress condition, but this effect resolved in the second NREMS cycle where group differences were absent. As a key finding, the stress group exhibited higher beta frequency activity in proportion to delta activity throughout both cycles and sleep stages. This effect was significantly magnified in N3 sleep where the delta/beta activity ratio decreased in the stress group from cycle 1 to 2, indicating worsening quality of sleep as the night progressed. We reflected our results through a homeostatic point of view, where the increased high frequency beta activity at sleep onset and early sleep in the stress group might explain their increased N3 sleep duration in the first NREMS cycle. A stronger affinity for the important N3 sleep may be a sleep protective mechanism to counter the stress induced abnormally high frequency EEG activity at sleep onset and early sleep to ensure the restorative benefits of slow-wave activity.

Schizophrenia (SZ) is a neurodevelopmental psychiatric disorder with high heritability. Patients with SZ commonly suffer from sleep problems of different types, some of them with potential underlying abnormalities in sleep oscillations. These changes in sleep are usually accompanied by deficits in cognitive performance. However, the relationship between sleep, cognitive performance and genetic risk factors are not well known in SZ. In this study, patients were selected from a nation-wide SUPER -cohort. Sleep and circadian rhythm of patients with SZ (n = 26) and age-matched healthy controls (n = 11) were followed for a week with actigraphy and sleep diary, combined with word-pair -memory task and polysomnography at the end of the week. The results showed that patients spend more time in lighter sleep and awake during the night than controls. As expected, patients had impaired sleep spindle density compared to controls. Additionally, patient had worse overnight memory consolidation. However, sleep spindle density was not associated with memory performance. Lastly, polygenic risk score (PRS) for long sleep, but not PRS for SZ, predicted lower spindle density in patients, which could be indirect evidence for deviated neurophysiological processes of sleep behind the observed deviations in EEG oscillations among the patients. These results show that, as compared to controls, patients with SZ demonstrate abnormalities in their sleep, which can be seen both in macro- and microstructures of sleep. Further analyses of the interplay between sleep oscillations and genetic risk factors are likely needed to link sleep problems with overnight memory consolidation.