Decreased Delta Activity Research Articles

Effects of head alignment devices on working memory and postural support during computer work.

The most common risk factor of computer workers is poor head and neck posture. Therefore, upright seated posture has been recommended repeatedly. However, maintaining an upright seated posture is challenging during computer work and induces various complaints, such as fatigue and discomfort, which can interfere working performance. Therefore, it is necessary to maintain an upright posture without complaints or intentional efforts during long-term computer work. Alignment devices are an appropriate maneuver to support postural control for maintaining head-neck orientation and reduce head weight. This study aimed to demonstrate the effects of workstations combined with alignment device on head-neck alignment, muscle properties, comfort and working memory ability in computer workers. Computer workers (n = 37) participated in a total of three sessions (upright computer (CPT_U), upright support computer (CPT_US), traction computer (CPT_T) workstations). The craniovertebral angle, muscles tone and stiffness, visual analog discomfort scale score, 2-back working memory performance, and electroencephalogram signals were measured. All three workstations had a substantial effect on maintaining head-neck alignment (p< 0.001), but only CPT_US showed significant improvement on psychological comfort (p = 0.04) and working memory performance (p = 0.024), which is consistent with an increase in delta power. CPT_U showed the increased beta 2 activity, discomfort, and false rates compared to CPT_US. CPT_T showed increased alpha and beta 2 activity and decreased delta activity, which are not conductive to working memory performance. In conclusion, CPT_US can effectively induce efficient neural oscillations without causing any discomfort by increasing delta and decreasing beta 2 activity for working memory tasks.

Neurophysiological correlates of suicidal ideation in major depressive disorder: Hyperarousal during sleep

BackgroundSuicide is a major public health concern, and a barrier to reducing the suicide rate is the lack of objective predictors of risk. The present study considers whether quantitative sleep electroencephalography (EEG) may be a neurobiological correlate of suicidal ideation. MethodsParticipants included 84 (45 female, mean age=26.6) adults diagnosed with major depressive disorder (MDD). The item that measures thoughts of death or suicide on the Quick Inventory of Depressive Symptomatology (QIDS) was used to classify 47 participants as low suicidal ideation (24 females, mean age=26.1) and 37 as high suicidal ideation (21 females, mean age=27.3). Data were obtained from archival samples collected at the University of Michigan and University of Texas Southwestern Medical Center between 2004 and 2012. Sleep EEG was quantified using power spectral analysis, and focused on alpha, beta, and delta frequencies. ResultsResults indicated that participants with high compared to low suicidal ideation experienced 1) increased fast frequency activity, 2) decreased delta activity, and 3) increased alpha-delta sleep after adjusting for age, sex, depression, and insomnia symptoms. LimitationsLimitations include the exclusion of imminent suicidal intent, a single suicidal ideation item, and cross-sectional archival data. ConclusionsThis is one of the first studies to provide preliminary support that electrophysiological brain activity during sleep is associated with increased suicidal ideation in MDD, and may point toward central nervous system (CNS) hyperarousal during sleep as a neurobiological correlate of suicidal ideation.

SY08-2 * NEUROPHYSIOLOGICAL AND NEUROIMAGING ASPECTS BETWEEN INTERNET GAMING DISORDER AND ALCOHOL USE DISORDER

Introduction. Internet Gaming Disorder (IGD) causes significant public mental health problems worldwide, especially in Korea. It is important to compare characteristics of IGD with those of substance addiction in order to elucidate the pathophysiology of IGD. In this study, we explored the neurophysiological and neuroimaging features among patients with IGD and those with Alcohol Use Disorder (AUD). Method. First, we performed resting-state EEG in male patients with IGD (N = 20) and compared the results with those of male patients with AUD (N = 20) and healthy controls (N = 20). All patients were seeking treatment at our clinics due to their excessive Internet game use or alcohol drinking. Second, we performed resting-state functional MRI study in same subjects. However, some subjects were excluded in the analysis due to their motion artifacts. Sixteen male patients with IGD, 14 male patients with AUD, and 15 healthy male controls were included in the final analysis. Result. Patients with IGD showed decreased beta activity compared with those with healthy controls, whereas patients with AUD showed increased beta activity compared with those with healthy controls. In addition, both clinical groups showed decreased delta activity compared with those with healthy controls. In the resting-state fMRI, IGD group showed a significant regional homogeneity (ReHo) decrease in the right superior temporal gyrus (STG) and increase in the posterior cingulate cortex (PCC) compared with healthy controls. AUD group showed significant decrease in the anterior cingulate cortex (ACC) and increase in the PCC compared with healthy controls. Conclusion. These results showed neurobiological similarity and disparity of resting-state EEG and fMRI features among IGD, AUD and healthy controls. These findings may contribute to elucidate the pathogenesis and neurobiological underpinning of IGD.

Cortical activity in tinnitus patients and its modification by phonostimulation

OBJECTIVE:The goal of this study was to observe spontaneous cortical activity and cortical activity modulated by tinnitus-matched sound in tinnitus patients and healthy subjects with no otoneurologic symptoms.METHOD:Data were prospectively collected from 50 tinnitus patients and 25 healthy subjects. Cortical activity was recorded in all subjects with eyes closed and open and during photostimulation, hyperventilation and acoustic stimulation using 19-channel quantitative electroencephalography. The sound applied in the tinnitus patients was individually matched with the ability to mask or equal the tinnitus. The maximal and mean amplitude of the delta, theta, alpha and beta waves and the type and amount of the pathologic EEG patterns were noted during each recording. Differences in cortical localization and the influence of sound stimuli on spontaneous cortical activity were evaluated between the groups.RESULTS:The tinnitus group exhibited decreased delta activity and increased alpha and beta activity. Hyperventilation increased the intensity of the differences. The tinnitus patients had more sharp-slow waves and increased slow wave amplitude. Sound stimuli modified the EEG recordings; the delta and beta wave amplitudes were increased, whereas the alpha-1 wave amplitude was decreased. Acoustic stimulation only slightly affected the temporal region.CONCLUSION:Cortical activity in the tinnitus patients clearly differed from that in healthy subjects, i.e., tinnitus is not a “phantom” sign. The changes in cortical activity included decreased delta wave amplitudes, increased alpha-1, beta-1 and beta-h wave amplitudes and pathologic patterns. Cortical activity modifications occurred predominantly in the temporal region. Acoustic stimulation affected spontaneous cortical activity only in tinnitus patients, and although the applied sound was individually matched, the pathologic changes were only slightly improved.

Characterisation of the effects of caffeine on sleep in the rat: a potential model of sleep disruption

Caffeine is known to disrupt sleep and its administration to human subjects has been used to model sleep disruption. We previously showed that its effects on sleep onset latency are comparable between rats and humans. This study evaluated the potential use of caffeine as a model of sleep disruption in the rat, by assessing its effects on sleep architecture and electroencephalogram (EEG) frequency spectrum, and using sleep-promoting drugs to reverse these effects. Rats were implanted with radiotelemetry devices for body temperature, EEG, electromyogram and locomotor activity. Following recovery, animals were dosed with caffeine (10 mg/kg) alone or in combination with zolpidem (10 mg/kg) or trazodone (20 mg/kg). Sleep was scored for the subsequent 12 h using automated analysis software. Caffeine dose-dependently disrupted sleep: it increased WAKE time, decreased NREM (non-REM) sleep time and NREM bout duration (but not bout number), and decreased delta activity in NREM sleep. It also dose-dependently increased locomotor activity and body temperature. When given alone, zolpidem suppressed REM whilst trazodone increased NREM sleep time at the expense of WAKE, increased NREM bout duration, increased delta activity in NREM sleep and reduced body temperature. In combination, zolpidem attenuated caffeine's effects on WAKE, whilst trazodone attenuated its effects on NREM sleep, NREM bout duration, delta activity, body temperature and locomotor activity. Caffeine administration produced many of the signs of insomnia that were improved by two of its most successful current treatments. This model may therefore be useful in the study of new drugs for the treatment of sleep disturbance.

P31.11 Intracranial current density distribution (LORETA) of decreased delta activity in depressed and non-depressed alcoholic patients

P31.11 Intracranial current density distribution (LORETA) of decreased delta activity in depressed and non-depressed alcoholic patients

Effects of hypnotics on the sleep EEG of healthy young adults: new data and psychopharmacologic implications

Benzodiazepine hypnotics increase NREM sleep and alter its EEG by reducing delta (0.3–3 Hz) and increasing sigma (12–15 Hz) and beta (15–23 Hz) activity. We tested whether the nonbenzodiazepine hypnotic, zolpidem (10 mg), produced the same pattern of sleep and EEG changes as two “classical” benzodiazepines, triazolam (0.25 mg) and temazepam (30 mg). Sleep EEG of 16 subjects was analyzed with period amplitude analysis for 3 nights during drug administration or placebo. The effects of zolpidem were in the same direction but generally of smaller magnitude than those of the classical benzodiazepines. These differences are more likely the result of non-equivalent dosages than different pharmacologic actions. Period amplitude analysis showed that the decreased delta activity resulted mainly from a decrease in wave amplitude. In contrast, the increased sigma and beta activity were produced by increased wave incidence. Delta suppression increased with repeated drug administration but sigma and beta stimulation did not. While these findings have little relevance for the clinical choice of hypnotics they may hold important implications for the brain mechanisms involved in hypnotic tolerance and withdrawal delirium.