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      Relationship between the Spectral Power Density of Sleep Electroencephalography and Psychiatric Symptoms in Patients with Breathing-related Sleep Disorder

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          Abstract

          Objective

          Patients with breathing-related sleep disorder (BRSD) often complain of psychiatric symptoms such as depression in addition to snoring, excessive sleepiness, and disturbed sleep. However, the relationship between psychiatric symptoms and severity of sleep apnea in BRSD is controversial. We conducted this study to investigate the relationship between psychiatric symptoms and sleep electroencephalography (EEG) findings in BRSD patients using spectral analysis.

          Methods

          All participants underwent polysomnography and evaluation using Symptom Checklist-90-Revised (SCL-90-R) scale. We analyzed the absolute spectral power density values of standard EEG frequency bands in the participants (n = 169) with BRSD during the non-rapid eye movement (NREM) sleep period. We performed correlation analysis between the domain scores of SCL-90-R scale and the absolute values of the EEG frequency bands.

          Results

          Significant positive correlation was observed between the absolute spectral power density values in the slow oscillation band and the degree of paranoid ideation ( r = 0.226, p = 0.028) and depression ( r = 0.216, p = 0.044) in SCL-90-R. The multiple linear regression model showed that higher paranoid ideation domain score (B = 0.007, p = 0.020), younger age (B = −0.011, p < 0.001), and female sex (B = 0.213, p = 0.004) were associated with higher slow oscillation power during NREM sleep.

          Conclusion

          The results of the present study suggested a relationship between sleep EEG and psychiatric symptoms in patients with BRSD. This relationship needs to be validated with further studies.

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          Most cited references 61

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          Reduced sleep spindles and spindle coherence in schizophrenia: mechanisms of impaired memory consolidation?

          Sleep spindles are thought to induce synaptic changes and thereby contribute to memory consolidation during sleep. Patients with schizophrenia show dramatic reductions of both spindles and sleep-dependent memory consolidation, which may be causally related. To examine the relations of sleep spindle activity to sleep-dependent consolidation of motor procedural memory, 21 chronic, medicated schizophrenia outpatients and 17 healthy volunteers underwent polysomnography on two consecutive nights. On the second night, participants were trained on the finger-tapping motor sequence task (MST) at bedtime and tested the following morning. The number, density, frequency, duration, amplitude, spectral content, and coherence of stage 2 sleep spindles were compared between groups and examined in relation to overnight changes in MST performance. Patients failed to show overnight improvement on the MST and differed significantly from control participants who did improve. Patients also exhibited marked reductions in the density (reduced 38% relative to control participants), number (reduced 36%), and coherence (reduced 19%) of sleep spindles but showed no abnormalities in the morphology of individual spindles or of sleep architecture. In patients, reduced spindle number and density predicted less overnight improvement on the MST. In addition, reduced amplitude and sigma power of individual spindles correlated with greater severity of positive symptoms. The observed sleep spindle abnormalities implicate thalamocortical network dysfunction in schizophrenia. In addition, the findings suggest that abnormal spindle generation impairs sleep-dependent memory consolidation in schizophrenia, contributes to positive symptoms, and is a promising novel target for the treatment of cognitive deficits in schizophrenia. Copyright © 2012 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
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            Sleep homeostasis and cortical synchronization: I. Modeling the effects of synaptic strength on sleep slow waves.

            Sleep slow-wave activity (SWA, electroencephalogram [EEG] power between 0.5 and 4.0 Hz) is homeostatically regulated, increasing with wakefulness and declining with sleep. Sleep SWA is thought to reflect sleep need, but the mechanisms of its homeostatic regulation remain unknown. Based on a recent hypothesis, we sought to determine whether a decrease in cortical synaptic strength can account for changes in sleep SWA. A large-scale computer model of the sleeping thalamocortical system was used to reproduce in detail the cortical slow oscillations underlying EEG slow waves. N/A. N/A. Simulated reductions in the strength of corticocortical synapses. Decreased synaptic strength led to (1) decreased single cell membrane potential oscillations and reduced network synchronization, (2) decreased rate of neural recruitment and decruitment, and (3) emergence of local clusters of synchronized activity. These changes were reflected in the local EEG as (1) decreased incidence of high-amplitude slow waves, (2) decreased wave slope, and (3) increased number of multipeak waves. Spectral analysis confirmed that these changes were associated with a decrease in SWA. A decrease in cortical synaptic strength is sufficient to account for changes in sleep SWA and is accompanied by characteristic changes in slow-wave parameters. Experimental results from rat cortical depth recordings and human high-density EEG show similar changes in slow-wave parameters with decreasing SWA, suggesting that the underlying mechanism may indeed be a net decrease in synaptic strength.
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              The effects of normal aging on sleep spindle and K-complex production.

               K. Crowley (2002)
              Despite a relatively large body of literature describing the characteristics of sleep spindles and K-complexes in young adults, relatively little research has been conducted in older individuals. The general consensus from the few studies that have addressed this issue is that there is a progressive decrease in the number of spindles and K-complexes with age, although there is large intra-individual variation. Whether or not these changes are an inevitable consequence of the aging process can be addressed by studying healthy older adults who provide an example of the effects of age independently from those of disease. Fourteen young adults (mean age=21.4+/-2.5 years) and 20 older adults (mean age=75.5+/-6.3 years) participated in the study. All subjects were neurologically and medically healthy and were not taking any medications with a known effect on the central nervous system or sleep. For each subject, a number of characteristics were determined including the number, density (SS/min), amplitude and frequency of all spindles as well as the number and density of K-complexes (KC/min). Spindle number, density and duration as well as K-complex number and density were all significantly lower in the elderly compared to the young adults. The EEG frequency within the spindles was significantly higher in the elderly, although the absolute difference was less than 0.5 Hz. Multiple regression analysis indicated that spindle duration and K-complex density were able to predict over 90% of the variance in age. The age-related decrease in sleep spindle and K-complex density is consistent with previous reports and may be interpreted as an age-related alteration of thalamocortical regulatory mechanisms.
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                Author and article information

                Journal
                Clin Psychopharmacol Neurosci
                Clin Psychopharmacol Neurosci
                Clinical Psychopharmacology and Neuroscience
                Korean College of Neuropsychopharmacology
                1738-1088
                2093-4327
                31 August 2021
                31 August 2021
                31 August 2021
                : 19
                : 3
                : 521-529
                Affiliations
                [1 ]Department of Psychiatry, Gachon University Gil Medical Center, Gachon University College of Medicine, Incheon, Korea
                [2 ]Gachon Sleep Medicine Center, Gachon University Gil Medical Center, Incheon, Korea
                [3 ]Department of Neurology
                [4 ]Department of Otolaryngology, Gachon University Gil Medical Center, Gachon University College of Medicine, Incheon, Korea
                Author notes
                Address for correspondence: Seung-Gul Kang Department of Psychiatry, Gachon University Gil Medical Center, Gachon University College of Medicine, 21 Namdong-daero 774beon-gil, Namdong-gu, Incheon 21565, Korea, E-mail: kangsg@ 123456gachon.ac.kr , ORCID: https://orcid.org/0000-0003-4933-0433
                Article
                cpn-19-3-521
                10.9758/cpn.2021.19.3.521
                8316670
                34294621
                4e24c23f-8aad-4357-8e07-e444ecf114dd
                Copyright© 2021, Korean College of Neuropsychopharmacology

                This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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