Cognitive Function Decline in the Third Trimester of Pregnancy Is Associated with Sleep Fragmentation.

During late pregnancy, sleep deterioration is regularly observed. In concert with these observations, in previous studies by other researchers, a slight objective cognitive decline in pregnant women has been found. Sleep is essential for memory consolidation. The hypothesis of the study was that cognitive impairment could be related to sleep deterioration during pregnancy. The study included 19 pregnant women in their third trimester of pregnancy (28−40 weeks, median 33 weeks (IQR 32−37)) recruited at the Department of Gynecology and Obstetrics, Medical University of Warsaw, and 20 non-pregnant women as controls. The assessment was performed using the vocabulary subtest from the Wechsler Adult Intelligence Scale (WAIS), D2 Test of Attention, OSPAN task (Operational Span Task) to assess cognitive performance, actigraphy to examine sleep parameters, and a set of self-report instruments: Athens Insomnia Scale (AIS), Beck Depression Inventory (BDI), Ford Insomnia Response to Stress (FIRST), Regenstein Hyperarousal Scale (HS), and Epworth Sleepiness Scale (ESS). Although there were no differences between the groups in WAIS (p = 0.18), pregnant women had worse scores in working memory capacity (overall number of remembered letters: p = 0.012, WM span index: p = 0.004) and a significantly lower score in attention (p = 0.03). Pregnant women also had lower sleep efficiency (p = 0.001), more awakenings from sleep (p = 0.001), longer average awakenings (p < 0.0001), longer wake after sleep onset (WASO, p < 0.0001), and longer total time in bed (p < 0.0001). In psychological assessment, pregnant women had only a higher FIRST score (p = 0.02). Using mediation analysis, we found that frequent awakening might be the major factor contributing to deterioration in working memory performance, explaining almost 40% of the total effect. In conclusion, sleep fragmentation in the third trimester of pregnancy may impair working memory consolidation. Pregnant women often complain about poor daily performance as well as non-restorative sleep. In this study, we showed that there is a relationship between lower sleep quality in pregnancy and worse cognitive functioning. We can expect a cognitive decline in women with sleep disturbances in pregnancy. Therefore, we should pay more attention to the treatment of sleep disorders in pregnancy.

Emotional Dysregulation, Anxiety Symptoms and Insomnia in Individuals with Alcohol Use Disorder.

Alcohol craving is associated with insomnia symptoms, and insomnia is often reported as a reason for alcohol relapse. The current study examined associations between emotional regulation, anxiety, and insomnia among a group of 338 patients with alcohol use disorder (AUD). Because insomnia most often develops after stressful experiences, it was expected that anxiety symptoms would mediate the association between emotional dysregulation and insomnia severity. It was also expected that an insomnia diagnosis would moderate the association between emotional dysregulation and anxiety symptoms, namely that higher anxiety levels would be found in individuals with insomnia than in those without insomnia. Insomnia severity was assessed with a total score based on the Athens Insomnia Scale (AIS). Additionally, an eight-point cut-off score on the AIS was used to classify participants as with (n = 107) or without (n = 231) an insomnia diagnosis. Moreover, participants completed the Emotion Regulation Scale (DERS; total score) and the Brief Symptoms Inventory (BSI; anxiety). Individuals with insomnia did not differ from those without insomnia in age (p = 0.86), duration of problematic alcohol use (p < 0.34), mean days of abstinence (p = 0.17), nor years of education (p = 0.41). Yet, individuals with insomnia endorsed higher anxiety (p < 0.001) and higher emotional dysregulation (p < 0.001). Anxiety symptoms fully mediated the association between emotional dysregulation and insomnia severity (p < 0.001). Furthermore, insomnia diagnosis positively moderated the association between emotional dysregulation and anxiety (p < 0.001). Our results suggest that emotional dysregulation can lead to insomnia via anxiety symptoms. Treating anxiety symptoms and emotional dysregulation could help to prevent or alleviate symptoms of insomnia in people with AUD. Moreover, treating insomnia in people with AUD may also have a positive effect on anxiety symptoms.

Can Dog-Assisted Intervention Decrease Anxiety Level and Autonomic Agitation in Patients with Anxiety Disorders?

Few studies have explored the influence of an Animal-Assisted Intervention on patients with mental disorders. We investigated it's impact on anxiety symptoms. We divided 51 patients with anxiety symptoms into two groups-treatment group, that went for a short 15-20 min' walk with a dog, his handler and a researcher and control group, that went for a walk only with a researcher. We used State-Trait Anxiety Inventory (STAI), Visual Analogue Scale (VAS) of fear, Beck Depression Inventory (BDI), Ford Insomnia Response to Stress (FIRST), Brief symptom Inventory (BSI) and VAS of satisfaction after trial to assess. We also checked the resting blood pressure and resting heart rate before and after performing psychological tests while sitting. We have obtained full data of 21 people from the research group and 26 people from the control group. After the intervention, the treatment group reported lower anxiety levels as a state (Mean (M) = 34.35; Standard Deviation (SD) = 6.9 vs. M = 40.94; SD = 8.6) and fear (M = 1.05; SD = 1.0 vs. M = 2.04; SD = 2.2) than the control group. After a walk with a dog, trait anxiety (M = 34.35; SD = 6.9 vs. M = 46.3; SD = 9.6), state anxiety (M = 48.9; SD = 7.2 vs. M = 53.9; SD = 7.8), fear (M = 1.05; SD= 1.0 vs. M = 2.57; SD = 2.3) and resting heart rate (M = 71.05; SD = 12.3 vs. M = 73.67; SD = 13.1) decreased significantly, while walking without a dog only reduced state anxiety (M = 47.24; SD = 11.0 vs. M = 40.94; SD = 8.6). Multivariate analysis of variance showed that after the walk, state anxiety was significantly lower in the treatment group than in the control group, F(1.35) = 6.706, p <0.05, η2 = 0.161. Among those who walked with a dog, the intervention also led to significant decreases in fear and resting heart rate, F(1.44) = 11.694, p < 0.01, η2 = 0.210 and F(1.45) = 8.503; p < 0.01; η2 = 0.159, respectively. For anxious patients, a short walk with a dog is more beneficial than a walk without one. We found significant positive effects of a dog's company on vegetative arousal and mental comfort. This is another study confirming the possible therapeutic effect of the animal on anxiety symptoms. Further research is required, especially in the large groups of patients, as recommendations on the use of Animal Assisted Interventions (AAI) are needed.

Delta resting-state functional connectivity in the cognitive control network as a prognostic factor for maintaining abstinence: An eLORETA preliminary study.

BACKGROUND: Cortical regions that support cognitive control are increasingly well recognized, but the functional mechanisms that promote such control over emotional and behavioral hyperreactivity to alcohol in recently abstinent alcohol-dependent patients are still insufficiently understood. This study aimed to identify neurophysiological biomarkers of maintaining abstinence in alcohol-dependent individuals after alcohol treatment by investigating the resting-state EEG-based functional connectivity in the cognitive control network (CCN). METHODS: Lagged phase synchronization between CCN areas by means of eLORETA as well as the Barratt Impulsiveness Scale (BIS-11) and Beck Depression Inventory (BDI) were assessed in abstinent alcohol-dependent patients recruited from treatment centers. A preliminary prospective study design was used to classify participants into those who did and did not maintain abstinence during a follow-up period (median 12 months) after discharge from residential treatment. RESULTS: Alcohol-dependent individuals, who maintained abstinence (N = 18), showed significantly increased lagged phase synchronization between the left dorsolateral prefrontal cortex (DLPFC) and the left posterior parietal cortex (IPL) as well as between the right anterior insula cortex/frontal operculum (IA/FO) and the right inferior frontal junction (IFJ) in the delta band compared to those who later relapsed (N = 16). Regression analysis showed that the increased left frontoparietal delta connectivity in the early period of abstinence significantly predicted maintaining abstinence over the ensuing 12 months. Furthermore, right frontoinsular delta connectivity correlated negatively with impulsivity and depression measures. CONCLUSIONS: These results suggest that the increased delta resting-state functional connectivity in the CCN may be a promising neurophysiological predictor of maintaining abstinence in individuals with alcohol dependence.

Insomnia in Pregnancy Is Associated With Depressive Symptoms and Eating at Night.

STUDY OBJECTIVES: Deterioration in sleep quality seems to be a natural consequence of physical changes during pregnancy. It is still unclear if insomnia in pregnancy is associated with the same factors as chronic insomnia in the general population. The aim of this study was to explore the determinants of insomnia during pregnancy. METHODS: The study included 266 women (mean age: 30.6 ± 5 years, weeks of pregnancy: 36 [interquartile range 32-38]) recruited at the Department of Gynecology and Obstetrics, Medical University of Warsaw. The assessment of variables was performed using the Athens Insomnia Scale (AIS), Beck Depression Inventory (BDI), Regestein Hyperarousal Scale (HS), Epworth Sleepiness Scale (ESS), General Practice Physical Activity Questionnaire, and a semi-structured interview about different sleep disorders. RESULTS: Almost 40% of the women in our study received a diagnosis of insomnia based on AIS cutoff scores. The between-group analyses indicated that HS score, BDI score, eating at night, legs tingling, nightmares, snoring, and myoclonus differentiated the groups of individuals with insomnia from those without insomnia. Other variables were not significantly different between the groups. We divided individuals with insomnia in terms of insomnia duration: 49% developed insomnia at least 1 year before the study onset and 39.6% during pregnancy. For further analyses we used only the women in whom insomnia developed during pregnancy. Logistic regression confirmed that depressive symptoms (BDI) and eating at night were significant predictors of insomnia in pregnancy. CONCLUSIONS: Depressive symptoms and night eating are key factors related to insomnia developed during pregnancy.

Narcolepsy type 1 and hypersomnia associated with a psychiatric disorder show different slow wave activity dynamics.

The aim of the study was to compare electrophysiological parameters of night sleep in narcolepsy type 1 and hypersomnia associated with a psychiatric disorder. Fortyfour patients: 15 with narcolepsy type 1, 14 with hypersomnia associated with a psychiatric disorder and 15 age- and sex-matched controls participated in the study. The study subjects filled in the Athens Insomnia Scale (AIS) and the Beck Depression Inventory (BDI). The severity of daytime sleepiness was quantified subjectively using the Epworth Sleepiness Scale (ESS) and the Stanford Sleepiness Scale (SSS), and objectively using the Multiple Sleep Latency Test (MSLT). All subjects underwent polysomnography (PSG) on the two consecutive nights. The data from the second night was analysed. The slow wave activity (SWA, 1-4 Hz) was calculated for the three consecutive sleep cycles, and topographic delta power maps were plotted. In contrast to narcoleptics, psychiatric hypersomniacs had undisturbed nocturnal sleep, high sleep efficiency, normal non-rapid eye movement (NREM) and rapid eye movement (REM) sleep proportions, normal REM latency and sleep latencies on MSLT and PSG. The subjective and objective sleepiness was significantly higher in narcolepsy group than in psychiatric hypersomnia group. In all the study groups SWA was the most prominent in frontal areas, while the greatest between-group differences were found in the central areas. There were significant differences between the groups in SWA in the second NREM episode. The highest SWA was observed in the hypersomnia group, while the lowest in the narcolepsy group. Psychiatric hypersomniacs and controls did not differ in the SWA exponential decline over consecutive NREM episodes, whereas narcoleptics exhibited a steeper dissipation of sleep pressure from the first to the second NREM episode. In conclusion, narcolepsy type1 and hypersomnia associated with psychiatric disorder differ in the SWA dynamics. Narcoleptics presented with the altered dynamics of sleep homeostasis, whereas psychiatric hypersomniacs showed normal nocturnal sleep and normal sleep homeostasis.

Frontal EEG alpha band asymmetry as a predictor of reasoning deficiency in depressed people.

Cognitive deficits in depression are mostly apparent in executive functions, especially when integration of information and reasoning is required. In parallel, there are also numerous studies pointing to the frontal alpha band asymmetry as a psychophysiological marker of depression. In this study, we explored the role of frontal alpha asymmetry as a potential factor explaining the cognitive problems accompanying depression. Twenty-six depressed and 26 control participants completed a reasoning task and underwent 5 minutes of electroencephalography recording. In line with the previous studies, depressed people showed difficulties with reasoning but we did not observe the relationship between frontal asymmetry in the alpha band and depression. However, we found that in the depressed group the frontal alpha asymmetry index was characterised by larger variance than in the control group, and it was also a strong predictor of cognitive functioning exclusively in the depressed group. Our results point to the disruption of a psychophysiological balance, reflected in changed frontal alpha asymmetry (into more left-sided frontal asymmetry in the alpha band, reflecting more right-sided cortical activity) as a possible brain correlate of cognitive disturbances present in depressive disorders.

EEG source activity during processing of neutral stimuli in subjects with anxiety disorders.

Anxiety disorders are a social problem due to their prevalence and consequences. It is crucial to explore the influence of anxiety on cognitive processes. In this study we recorded EEG activity from 73 subjects (35 patients, 38 controls, matched for age and education) during performance of the Continuous Attention Task. We used low resolution electromagnetic tomography (LORETA) for evaluation of mechanisms of impaired cognitive performance in anxiety disorders. Analysis showed that patients with anxiety disorders committed more errors than the controls, had a short latency of P300 and higher amplitude of ERPs at all steps of stimulus processing. Furthermore, we showed that there was a relationship between the scores of Hamilton Anxiety Scale and Beck Depression Inventory, and amplitudes and latencies of ERPs. The results of LORETA analysis showed that enhanced neural responses were found within circuits mediating visual information processing, sustained attention and anxiety. Also, we found higher current density within areas playing an important role in the brain fear network - anterior cingulate and anterior part of insula. Electrophysiological neuroimaging showed greater recruitment of cognitive resources in anxiety disorders, evidenced by higher current density and activation of greater number of brain areas. Despite the strategy employed to compensate for cognitive problems, the anxiety patients did not achieve the same performance as controls. Present study demonstrates that anxiety disorders influence processing of neutral stimuli and this influence is observable at both behavioral and electrophysiological level. The data suggests instability of neural systems responsible for information selection, working memory, engagement and focusing of attention.

Sleepwalking episodes are preceded by arousal-related activation in the cingulate motor area: EEG current density imaging.

OBJECTIVE: To investigate local arousal fluctuations in adults who received ICSD-2 diagnosis of somnambulism. METHODS: EEG neuroimaging (eLORETA) was utilized to compare current density distribution for 4s epochs immediately preceding sleepwalking episode (from -4.0 s to 0 s) to the distribution during earlier 4s epochs (from -8.0 s to -4.0 s) in 20 EEG segments from 15 patients. RESULTS: Comparisons between eLORETA images revealed significant (t>4.52; p<0.05) brain activations before onset of sleepwalking, with greater current density within beta 3 frequency range (24-30 Hz) in Brodmann areas 33 and 24. CONCLUSIONS: Sleepwalking motor events are associated with arousal-related activation of cingulate motor area. SIGNIFICANCE: These results support the notion of blurred boundaries between wakefulness and NREM sleep in sleepwalking.

Association between FKBP5 Functional Polymorphisms and Completed Suicide.

OBJECTIVES: Dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis leads to impaired stress response. FK506-binding protein 51 (FKBP5), which influences HPA axis activity via glucocorticoid receptors, is supposed to play an important role in the regulation of negative feedback and glucocorticoid resistance. Since ineffective stress response mechanisms are considered as a biological background of suicide behavior, we aimed to analyze a possible association between FKBP5 functional polymorphisms and completed suicide. METHODS: The selected FKBP5 polymorphisms rs1360780 and rs3800373 were genotyped in a sample of 563 suicide victims and 475 controls. RESULTS: A significant association between the high-induction rs3800373 C allele and completed suicide was detected (OR = 1.36, p = 0.007). In this polymorphism, genotype distribution supported a codominant model of inheritance. The analyzed SNPs were in strong linkage disequilibrium (D' = 0.916 and r2 = 0.826) with the rs1360780 (T)-rs3800373 (C) haplotype apparently responsible for the observed association (OR = 1.34, p = 0.010). CONCLUSION: The results of the present study indicate that genetic alterations in FKBP5 may influence vulnerability to suicide.

Waking EEG in primary insomnia.

Quantitative analysis of the waking EEG has been proposed as an objective method for measuring neurobehavioral impairment in primary insomnia. Thirty six patients with DSM-IV primary insomnia diagnosis (mean age 36 years) and 29 controls, matched for age and education, participated in the study. Waking EEG from 21 scalp electrodes was subjected to spectral analyses using a fast Fourier transform algorithm. Significantly lower values of power in the theta range and higher values of beta power were found in insomniacs as compared to control subjects. This theta power decrease in patients suffering from insomnia was not uniform throughout the brain, but it was pronounced in prefrontal derivations. Lower values of theta power correlated negatively and higher values of beta power correlated postively with Hyperarousal Scale score. Results of the research presented here support the notion of twenty-four hour hyperarousal in primary insomnia. Attenuated theta and enhanced beta power can be electrophysiological correlates of dysfunctional arousal in insomnia. Less waking theta power in insomniacs suggests a decrease in homeostatic sleep propensity.

[Validation of the Polish version of the Athens Insomnia Scale]. / Walidacja Atenskiej Skali Bezsennosci.

AIMS: To validate the Polish version of the Athens Insomnia Scale (AIS), the instrument designed for quantitative measurement of the severity of insomnia based on the ICD-10 criteria. METHOD: The AIS was administered to 356 subjects: 160 patients from the sleep clinic presenting with ICD-10 non-organic insomnia (90f; mean age: 44.9 +/- 15.7y) and 196 self-defined good sleepers (106f; mean age: 43.9 +/- 13.4y). To assess psychometric properties of the scale, principal component analysis, Cronbach's alpha, Pearson's correlation (test-retest reliability: two weeks interval; n = 48) and sensitivity-specificity analysis were computed. RESULTS: Using the factor analysis only one factor was extracted, which accounted for 60.2% of the variance. The internal consistency (Cronbach's alpha = 0.90) and the test-retest reliability (r2 = 0.92) of the AIS were found to be very satisfactory. These values remain practically unchanged when any of the items was removed from the analysis. As expected, subjects with insomnia scored significantly higher on the AIS than good sleepers (14.2 +/- 3.9 pts vs. 4.8 +/- 3 pts; t = 24.9; p < 0.001). Considering the balance between sensitivity and specificity, a score of 8 was indicated as the optimum cut-off, with 89% overall correct case identification--94% patients with insomnia and 84% healthy controls. CONCLUSIONS: Standardisation of the diagnostic process of insomnia is a highly important task in clinical practice, epidemiological considerations and treatment outcomes assessment. The AIS is a brief, self-reported measure of insomnia that may improve these assessments. The good psychometric properties of the Polish version of the AIS were confirmed in the present study.

[The brain and cytokines - the mutual origin of depression, obesity and cardiovascular diseases?]. / Mózg i cytokiny - wspólne podloze depresji, otylosci i chorób ukladu krazenia?

Accumulating evidence points to a pivotal role of the brain in the regulation of the circulatory system and energy balance. It has also been found that common civilization diseases such as depression, obesity, hypertension, myocardial infarction or heart failure are accompanied by an increase in concentration of inflammatory mediators in the blood, cerebrospinal fluid and various tissues. Recent studies have revealed that inflammatory mediators that are synthesized peripherally or in the brain may affect the nervous regulation of animal body systems. For example, it has been found that non-specific pro-inflammatory stimuli as well as treatment with several cytokines may cause depressive behavior, disturbances in energy balance and alterations in the circulatory system. On the other hand, knockout of genes for pro-inflammatory cytokines or administration of anti-inflammatory mediators may normalize the pathological changes. In the present manuscript we will review studies that imply the common neuroinflammatory pathogenesis of cardiovascular diseases, depression and energy balance disorders.