EEG Delta Power Research Articles

High cortical delta power correlates with aggravated allodynia by activating anterior cingulate cortex GABAergic neurons in neuropathic pain mice.

Patients with chronic pain often report being sensitive to pain at night before falling asleep, a time when the synchronization of cortical activity is initiated. However, how cortical activity relates to pain sensitivity is still unclear. Because sleep is characterized by enhanced cortical delta power, we hypothesized that enhanced cortical delta power may be an indicator of intensified pain. To test this hypothesis, we used pain thresholds tests, EEG/electromyogram recordings, c-Fos staining, and chemogenetic and pharmacological techniques in mice. We found that sleep deprivation or pharmacologic enhancement of EEG delta power by reserpine and scopolamine dramatically decreased mechanical pain thresholds, but not thermal withdrawal latency, in a partial sciatic nerve ligation model of neuropathic pain mice. On the contrary, suppression of EEG delta power using a wake-promoting agent modafinil significantly attenuated mechanical allodynia. Moreover, when EEG delta power was enhanced, c-Fos expression decreased in most regions of the cortex, except the anterior cingulate cortex (ACC), where c-Fos was increased in the somatostatin- and parvalbumin-positive GABAergic neurons. Chemogenetic activation of GABAergic neurons in ACC enhanced EEG delta power and lowered mechanical pain thresholds simultaneously in naive mice. However, chemogenetic inhibition of ACC GABAergic neurons could not block mechanical allodynia. These results provided compelling evidence that elevated EEG delta power is accompanied with aggravated neuropathic pain, whereas decreased delta power attenuated it, suggesting that enhanced delta power can be a specific marker of rising chronic neuropathic pain and that wake-promoting compounds could be used as analgesics in the clinic.

Ketamine effects on default mode network activity and vigilance: A randomized, placebo-controlled crossover simultaneous fMRI/EEG study.

In resting‐state functional connectivity experiments, a steady state (of consciousness) is commonly supposed. However, recent research has shown that the resting state is a rather dynamic than a steady state. In particular, changes of vigilance appear to play a prominent role. Accordingly, it is critical to assess the state of vigilance when conducting pharmacodynamic studies with resting‐state functional magnetic resonance imaging (fMRI) using drugs that are known to affect vigilance such as (subanesthetic) ketamine. In this study, we sought to clarify whether the previously described ketamine‐induced prefrontal decrease of functional connectivity is related to diminished vigilance as assessed by electroencephalography (EEG). We conducted a randomized, double‐blind, placebo‐controlled crossover study with subanesthetic S‐Ketamine in N = 24 healthy, young subjects by simultaneous acquisition of resting‐state fMRI and EEG data. We conducted seed‐based default mode network functional connectivity and EEG power spectrum analyses. After ketamine administration, decreased functional connectivity was found in medial prefrontal cortex whereas increased connectivities were observed in intraparietal cortices. In EEG, a shift of energy to slow (delta, theta) and fast (gamma) wave frequencies was seen in the ketamine condition. Frontal connectivity is negatively related to EEG gamma and theta activity while a positive relationship is found for parietal connectivity and EEG delta power. Our results suggest a direct relationship between ketamine‐induced functional connectivity changes and the concomitant decrease of vigilance in EEG. The observed functional changes after ketamine administration may serve as surrogate end points and provide a neurophysiological framework, for example, for the antidepressant action of ketamine (trial name: 29JN1556, EudraCT Number: 2009‐012399‐28).

Warm Steam Inhalation before Bedtime Improved Sleep Quality in Adult Men.

In humans, the inhalation of warm steam has been reported to decrease the respiratory rate. However, the effects of warm steam inhalation on sleep have not been studied closely. This study aimed to examine the effects of warm steam inhalation before bedtime on subsequent sleep quality. The participants included 17 adult men with mild sleep difficulties and anxiety. All experiments were conducted in the participants' homes. The participants were instructed to wear a warm steam-generating mask or sham mask over the nose and mouth for 15 minutes immediately before habitual bedtime and were then allowed to sleep until their habitual waking time. The functional mask provided approximately 600 mg of steam for 10 minutes and maintained an interior temperature of 38–40°C for 15 minutes. We evaluated the participants' electrocardiograms and subjective moods while wearing the mask. During sleep, electroencephalograms (EEGs) were recorded using a single-channel portable device. In the morning, each participant was instructed to report their sleep details subjectively using a visual analog scale. At bedtime, the subjects' subjective apprehension of the next day was reduced significantly under steam inhalation, compared with the sham condition. Compared to the sham condition, steam inhalation before bedtime was associated with a higher EEG delta power density during the first third of sleep episodes and better subjective sleep quality in the morning. These results suggest that safe and easy inhalation of warm steam via a steam-generating mask improves psychological relaxation and sleep.

Exploring the Brain Responses to Driving Fatigue Through Simultaneous EEG and fNIRS Measurements.

Fatigue is one problem with driving as it can lead to difficulties with sustaining attention, behavioral lapses, and a tendency to ignore vital information or operations. In this research, we explore multimodal physiological phenomena in response to driving fatigue through simultaneous functional near-infrared spectroscopy (fNIRS) and electroencephalography (EEG) recordings with the aim of investigating the relationships between hemodynamic and electrical features and driving performance. Sixteen subjects participated in an event-related lane-deviation driving task while measuring their brain dynamics through fNIRS and EEGs. Three performance groups, classified as Optimal, Suboptimal, and Poor, were defined for comparison. From our analysis, we find that tonic variations occur before a deviation, and phasic variations occur afterward. The tonic results show an increased concentration of oxygenated hemoglobin (HbO2) and power changes in the EEG theta, alpha, and beta bands. Both dynamics are significantly correlated with deteriorated driving performance. The phasic EEG results demonstrate event-related desynchronization associated with the onset of steering vehicle in all power bands. The concentration of phasic HbO2 decreased as performance worsened. Further, the negative correlations between tonic EEG delta and alpha power and HbO2 oscillations suggest that activations in HbO2 are related to mental fatigue. In summary, combined hemodynamic and electrodynamic activities can provide complete knowledge of the brain's responses as evidence of state changes during fatigue driving.

Nigrostriatal and mesolimbic control of sleep-wake behavior in rat.

The midbrain dopamine system via the dorsal and ventral striatum regulates a wide range of behaviors. To dissect the role of dopaminergic projections to the dorsal striatum (nigrostriatal projection) and ventral striatum (mesolimbic projection) in sleep-wake behavior, we selectively chemogenetically stimulated nigrostriatal or mesolimbic projections and examined the resulting effects on sleep in rats. Stimulation of nigrostriatal pathways increased sleep and EEG delta power, while stimulation of mesolimbic pathways decreased sleep and reduced cortical EEG power. These results indicate that midbrain dopamine signaling in the dorsal or ventral striatum promotes sleep or wake, respectively.

Electroencephalographic Slow-Wave Activity During Sleep in Different Phases of Blood Pressure and Respiration Oscillations.

Sleep is characterized by dynamic coupling between central (CNS) and peripheral autonomic (ANS) nervous systems. However, further research is needed to better understand the multiple interactions occurring among electroencephalographic (EEG) features and respiratory and cardiovascular (CV) outputs modulated by the ANS during sleep. Here, we developed new methods to study EEG slow-wave activity (SWA) during non-rapid eye movement (NREM) sleep with respect to the phases of peripheral oscillations. EEG, respiration, and continuous blood pressure signals recorded from 20 participants were analyzed. Digital filters, designed to decompose the signals into different frequency bands, and the Hilbert transform were applied to estimate the instantaneous phases and frequencies of the peripheral oscillations. The peripheral oscillations were categorized into four phases representing up and down states. EEG delta power (synchronized SWA) was computed and compared across these phases during NREM sleep. Results show that EEG delta power is higher during down phases of slow and respiratory frequency components of blood pressure and during up phases of respiration, suggestive of CNS-ANS coupling during NREM sleep. The developed techniques provide the preliminary framework to further analyze and interpret complex interactions between cortical and cardiac oscillations and their synchrony.

Quantitative electroencephalography measures in rapid eye movement and nonrapid eye movement sleep are associated with apnea-hypopnea index and nocturnal hypoxemia in men.

Quantitative electroencephalography (EEG) measures of sleep may identify vulnerability to obstructive sleep apnea (OSA) sequelae, however, small clinical studies of sleep microarchitecture in OSA show inconsistent alterations. We examined relationships between quantitative EEG measures during rapid eye movement (REM) and non-REM (NREM) sleep and OSA severity among a large population-based sample of men while accounting for insomnia. All-night EEG (F4-M1) recordings from full in-home polysomnography (Embletta X100) in 664 men with no prior OSA diagnosis (age ≥ 40) were processed following exclusion of artifacts. Power spectral analysis included non-REM and REM sleep computed absolute EEG power for delta, theta, alpha, sigma, and beta frequency ranges, total power (0.5-32 Hz) and EEG slowing ratio. Apnea-hypopnea index (AHI) ≥10/h was present in 51.2% (severe OSA [AHI ≥ 30/h] 11.6%). In mixed effects regressions, AHI was positively associated with EEG slowing ratio and EEG power across all frequency bands in REM sleep (all p < 0.05); and with beta power during NREM sleep (p = 0.06). Similar associations were observed with oxygen desaturation index (3%). Percentage total sleep time with oxygen saturation <90% was only significantly associated with increased delta, theta, and alpha EEG power in REM sleep. No associations with subjective sleepiness were observed. In a large sample of community-dwelling men, OSA was significantly associated with increased EEG power and EEG slowing predominantly in REM sleep, independent of insomnia. Further study is required to assess if REM EEG slowing related to nocturnal hypoxemia is more sensitive than standard PSG indices or sleepiness in predicting cognitive decline.

Increased glymphatic influx is correlated with high EEG delta power and low heart rate in mice under anesthesia.

The glymphatic system is responsible for brain-wide delivery of nutrients and clearance of waste via influx of cerebrospinal fluid (CSF) alongside perivascular spaces and through the brain. Glymphatic system activity increases during sleep or ketamine/xylazine (K/X) anesthesia, yet the mechanism(s) facilitating CSF influx are poorly understood. Here, we correlated influx of a CSF tracer into the brain with electroencephalogram (EEG) power, heart rate, blood pressure, and respiratory rate in wild-type mice under six different anesthesia regimens. We found that glymphatic CSF tracer influx was highest under K/X followed by isoflurane (ISO) supplemented with dexmedetomidine and pentobarbital. Mice anesthetized with α-chloralose, Avertin, or ISO exhibited low CSF tracer influx. This is the first study to show that glymphatic influx correlates positively with cortical delta power in EEG recordings and negatively with beta power and heart rate.

Direct activation of G-protein-gated inward rectifying K+ channels promotes nonrapid eye movement sleep.

A major challenge in treating insomnia is to find effective medicines with fewer side effects. Activation of G-protein-gated inward rectifying K+ channels (GIRKs) by GABAB agonists baclofen or γ-hydroxybutyric acid (GHB) promotes nonrapid eye movement (NREM) sleep and consolidates sleep. However, baclofen has poor brain penetration, GHB possesses abuse liability, and in rodents both drugs cause spike-wave discharges (SWDs), an absence seizure activity. We tested the hypothesis that direct GIRK activation promotes sleep without inducing SWD using ML297, a potent and selective GIRK activator. Whole-cell patch-clamp recordings from hypocretin/orexin or hippocampal neurons in mouse brain slices were made to study neuronal excitability and synaptic activity; spontaneous activity, locomotion, contextual and tone-conditioned memory, and novel object recognition were assessed. Electroencephalogram/electromyogram (EEG/EMG) recordings were used to study GIRK modulation of sleep. ML297, like baclofen, caused membrane hyperpolarization, decreased input resistance, and blockade of spontaneous action potentials. Unlike baclofen, ML297 (5-10 µM) did not cause significant depression of postsynaptic excitatory and inhibitory currents (EPSCs-IPSCs), indicating preferential postsynaptic inhibition. ML297 (30 mg/kg, i.p.) inhibited wake activity and locomotion, and preferentially increased NREM sleep without altering EEG delta power, REM sleep, inducing SWDs, or impairing conditioned memory and novel object recognition. This study finds that direct activation of neuronal GIRK channels modulates postsynaptic membrane excitability and prolongs NREM sleep without changing sleep intensity, inducing SWDs, or impairing memory in rodents. These results suggest that direct GIRK activation with a selective compound may present an innovative approach for the treatment of chronic insomnia.

Delirium detection using relative delta power based on 1-minute single-channel EEG: a multicentre study

BackgroundDelirium is frequently unrecognised. EEG shows slower frequencies (i.e. below 4 Hz) during delirium, which might be useful in improving delirium recognition. We studied the discriminative performance of a brief single-channel EEG recording for delirium detection in an independent cohort of patients. MethodsIn this prospective, multicentre study, postoperative patients aged ≥60 yr were included (n=159). Before operation and during the first 3 postoperative days, patients underwent a 5-min EEG recording, followed by a video-recorded standardised cognitive assessment. Two or, in case of disagreement, three delirium experts classified each postoperative day based on the video and chart review. Relative delta power (1–4 Hz) was based on 1-min artifact-free EEG. The diagnostic value of the relative delta power was evaluated by the area under the receiver operating characteristic curve (AUROC), using the expert classification as the gold standard. ResultsExperts classified 84 (23.3%) postoperative days as either delirium or possible delirium, and 276 (76.7%) non-delirium days. The AUROC of the relative EEG delta power was 0.75 [95% confidence interval (CI) 0.69–0.82]. Exploratory analysis showed that relative power from 1 to 6 Hz had significantly higher AUROC (0.78, 95% CI 0.72–0.84, P=0.014). ConclusionsDelirium/possible delirium can be detected in older postoperative patients based on a single-channel EEG recording that can be automatically analysed. This objective detection method with a continuous scale instead of a dichotomised outcome is a promising approach for routine detection of delirium. Clinical trial registrationNCT02404181.

Hard to wake up? The cerebral correlates of sleep inertia assessed using combined behavioral, EEG and fMRI measures

The first minutes following awakening from sleep are typically marked by reduced vigilance, increased sleepiness and impaired performance, a state referred to as sleep inertia. Although the behavioral aspects of sleep inertia are well documented, its cerebral correlates remain poorly understood. The present study aimed at filling this gap by measuring in 34 participants the changes in behavioral performance (descending subtraction task, DST), EEG spectral power, and resting-state fMRI functional connectivity across three time points: before an early-afternoon 45-min nap, 5 min after awakening from the nap and 25 min after awakening. Our results showed impaired performance at the DST at awakening and an intrusion of sleep-specific features (spectral power and functional connectivity) into wakefulness brain activity, the intensity of which was dependent on the prior sleep duration and depth for the functional connectivity (14 participants awakened from N2 sleep, 20 from N3 sleep). Awakening in N3 (deep) sleep induced the most robust changes and was characterized by a global loss of brain functional segregation between task-positive (dorsal attention, salience, sensorimotor) and task-negative (default mode) networks. Significant correlations were observed notably between the EEG delta power and the functional connectivity between the default and dorsal attention networks, as well as between the percentage of mistake at the DST and the default network functional connectivity. These results highlight (1) significant correlations between EEG and fMRI functional connectivity measures, (2) significant correlations between the behavioral aspect of sleep inertia and measures of the cerebral functioning at awakening (both EEG and fMRI), and (3) the important difference in the cerebral underpinnings of sleep inertia at awakening from N2 and N3 sleep.

Immature sleep pattern in newborn rats when dams encountered sleep restriction during pregnancy

There is a growing realization that proper sleep during pregnancy is essential for the health of the mother and the offspring. However, there are no reports on the effects of maternal sleep restriction on the sleep-wake profiles of newborns. So, this study was conducted to evaluate the effects of sleep restriction during the third term of pregnancy on the sleep-wake profiles of neonates born to them. The female pregnant Wistar rats were sleep restricted for 5 h/day on gestational days 15–20 by gentle handling. Sleep-wake profiles of the pups born to them and to the control rats were recorded on postnatal days 1–21. Pups of sleep restricted dams had higher active sleep (AS) and lower quiet sleep (QS) as well as wakefulness. Higher ratio of AS to QS, longer duration of sleep cycles, lesser bout frequency and reduced EEG delta power were also observed in these pups, all of which indicated brain immaturity. All these signs of delayed maturation, usually found in premature babies, were observed in the pups of sleep restricted mothers, who had longer gestation period. This report not only shows the importance of sleep during pregnancy, but it also suggests that neonatal sleep monitoring can be used as a tool for early assessment of retarded brain development.

Analysis of generic coupling between EEG activity and PETCO2 in free breathing and breath-hold tasks using Maximal Information Coefficient (MIC)

Brain activations related to the control of breathing are not completely known. The respiratory system is a non-linear system. However, the relationship between neural and respiratory dynamics is usually estimated through linear correlation measures, completely neglecting possible underlying nonlinear interactions. This study evaluate the linear and nonlinear coupling between electroencephalographic (EEG) signal and variations in carbon dioxide (CO2) signal related to different breathing task. During a free breathing and a voluntary breath hold tasks, the coupling between EEG power in nine different brain regions in delta (1–3 Hz) and alpha (8–13 Hz) bands and end-tidal CO2 (PET CO2) was evaluated. Specifically, the generic associations (i.e. linear and nonlinear correlations) and a “pure” nonlinear correlations were evaluated using the maximum information coefficient (MIC) and MIC-ρ2 between the two signals, respectively (where ρ2 represents the Pearson’s correlation coefficient). Our results show that in delta band, MIC indexes discriminate the two tasks in several regions, while in alpha band the same behaviour is observed for MIC-ρ2, suggesting a generic coupling between delta EEG power and PETCO2 and a pure nonlinear interaction between alpha EEG power and PETCO2. Moreover, higher indexes values were found for breath hold task respect to free breathing.

Excitation of Cortical nNOS/NK1R Neurons by Hypocretin 1 is Independent of Sleep Homeostasis

We have proposed that cortical nNOS/NK1R interneurons have a role in sleep homeostasis. The hypocretins (orexins) are wake-promoting neuropeptides and hypocretin/orexin (Hcrt) neurons project to the cortex. Hcrt peptides affect deep layer cortical neurons, and Hcrt receptor 1 (Hcrtr1; Ox1r) mRNA is expressed in cortical nNOS/NK1R cells. Therefore, we investigated whether Hcrt neuron stimulation affects cingulate cortex nNOS/NK1R neurons. Bath application of HCRT1/orexin-A evoked an inward current and membrane depolarization in most nNOS/NK1R cells which persisted in tetrodotoxin; optogenetic stimulation of Hcrt terminals expressing channelrhodopsin-2 confirmed these results, and pharmacological studies determined that HCRTR1 mediated these responses. Single-cell RT-PCR found Hcrtr1 mRNA in 31% of nNOS/NK1R cells without any Hcrtr2 mRNA expression; immunohistochemical studies of Hcrtr1-EGFP mice confirmed that a minority of nNOS/NK1R cells express HCRTR1. When Hcrt neurons degenerated in orexin-tTA;TetO DTA mice, the increased EEG delta power during NREM sleep produced in response to 4 h sleep deprivation and c-FOS expression in cortical nNOS/NK1R cells during recovery sleep were indistinguishable from that of controls. We conclude that Hcrt excitatory input to these deep layer cells is mediated through HCRTR1 but is unlikely to be involved in the putative role of cortical nNOS/NK1R neurons in sleep homeostasis.

Voice Navigation Effects on Real-World Lane Change Driving Analysis Using an Electroencephalogram

Improving the degree of assistance given by in-car navigation systems is an important issue for the safety of both drivers and passengers. There is a vast body of research that assesses the usability and interfaces of the existing navigation systems but very few investigations study the impact on the brain activity based on navigation-based driving. In this paper, a real-world experiment is designed to acquire the electroencephalography (EEG) and in-car information to analyze the dynamic brain activity while the driver is performing the lane-changing task based on the auditory instructions from an in-car navigation system. The results show that auditory cues can influence the speed and increase the frontal EEG delta and beta power, which is related to motor preparation and decision making during a lane change. However, there were no significant results on the alpha power. A better lane-change assessment can be obtained using specific vehicle information (lateral acceleration and heading angle) with EEG features for future naturalized driving study.

ОСОБЕННОСТИ ДИНАМИКИ СПЕКТРА ЭЭГ ЧЕЛОВЕКА ПРИ ПОСТОЯННОМ УРОВНЕ ОСТРОГО ГИПОКСИЧЕСКОГО ВОЗДЕЙСТВИЯ, "Российский физиологический журнал им. И.М. Сеченова"

У 12 испытуемых с помощью Фурье-анализа исследованы изменения амплитудно-частотного спектра ЭЭГ при постоянном уровне нормобарического гипоксического воздействия (дыхание кислородо-азотной смесью с 8%-ным содержанием кислорода в течение 25 мин). При помощи кластерного анализа 16-канальных ЭЭГ были выделены две группы испытуемых, различающихся по средней за период гипоксического воздействия относительной спектральной мощности (СМ) дельта-диапазона ЭЭГ. У 6 испытуемых первой группы (п = 7), имеющих более высокую относительную СМ дельта-диапазона при гипоксии, после 6 мин гипоксии во всех последующих одноминутных отрезках и во всех отведениях отмечалось доминирование дельта-активности. У испытуемых второй группы (п = 5) в затылочных отведениях в целом за 25 мин гипоксии доминировала альфа-активность. В последовательных одноминутных отрезках записи доминирование альфа-активности у некоторых испытуемых данной группы перемежалось с доминированием активности дельта- и тета-диапазонов. Показано, что динамика амплитудно-частотного спектра ЭЭГ при постоянном уровне гипоксического воздействия не всегда соответствует последовательному «замедлению» ЭЭГ, описанному для нарастающего по силе гипоксического воздействия.

Effects of bedtime periocular and posterior cervical cutaneous warming on sleep status in adult male subjects: a preliminary study

Appropriate warming of the periocular or posterior cervical skin has been reported to induce autonomic or mental relaxation in humans. To clarify the effects of cutaneous warming on human sleep, eight male subjects with mild sleep difficulties were asked to try three experimental conditions at home, each lasting for 5 days, in a cross-over manner: warming of the periocular skin with a warming device for 10 min before habitual bedtime, warming of the posterior cervical skin with a warming device for 30 min before habitual bedtime, and no treatment as a control. The warming device had a heat- and steam-generating sheet that allowed warming of the skin to 40 °C through a chemical reaction with iron. Electroencephalograms (EEGs) were recorded during nocturnal sleep using an ambulatory EEG device and subjected to spectral analysis. All the participants reported their sleep status using a visual analog scale. We found that warming of the periocular or posterior cervical skin significantly improved subjective sleep status relative to the control. The EEG delta power density in the first 90 min of the sleep episode was significantly increased under both warming of the periocular or posterior cervical skin relative to the control. These results suggest that warming of appropriate skin regions may have favorable effects on subjective and objective sleep quality.

Performance of an automated algorithm to process artefacts for quantitative EEG analysis during a simultaneous driving simulator performance task

BackgroundArtefact removal from noisy EEG signals is cumbersome, and often requires manual intervention. We tested the performance of an automated method to detect and remove artefacts from EEG recorded during a driving simulation task. MethodsFive patients with obstructive sleep apnea (OSA) and five healthy controls were randomly selected from 17 participants undergoing a 40-h extended wakefulness study with 2-hourly 30-minute simulated driving tasks with simultaneous EEG. Two EEG recordings from each individual were studied. EEG data was first processed by independent component analysis (ICA). The accuracy of the automated algorithm (AA) to detect residual EEG artefact was evaluated against a reference-standard (RS) of visually identified artefact-contaminated epochs. EEG spectral power was calculated using 1) the RS method, 2) the AA, and 3) raw data without any artefact rejection (ICA only). ResultsThe algorithm showed good sensitivity (median: 83.9%), excellent specificity (91.1%), and high accuracy (87.0%) to detect noisy epochs. Cohen's κ indicated a substantial agreement between the two methods (0.72). EEG spectral power calculated using the RS and the AA did not differ significantly, while the power of the raw signal was significantly higher than those produced by any artefact rejection method. Increased EEG delta and theta power were significantly correlated with poorer driving performance. ConclusionsThese preliminary findings demonstrate an effective automated method to process EEG artefact recorded during driving simulation. This approach may facilitate the routine application of quantitative EEG analyses in future studies and identify new markers of impaired driving performance associated with sleep disorders.

Pilot prospective study of post-surgery sleep and EEG predictors of post-operative delirium.

Delirium is a common post-operative complication associated with significant costs, morbidity, and mortality. We sought sleep/EEG predictors of delirium present prior to delirium symptoms to facilitate developing and targeting therapies. Continuous EEG data were obtained in 12 patients post-orthopedic surgery from the day of surgery until delirium assessment on post-operative day 2 (POD2). Diminished total sleep time (r=-0.68; p<0.05) and longer latency to sleep onset (r=0.67; p<0.05) on the first night in the hospital were associated with greater POD2 delirium severity. Patients experiencing delirium slept 2.4h less and took 2h longer to fall asleep. Greater waking EEG delta power (r=0.84; p<0.05) on POD1 and less non-REM sleep EEG delta power (r=-0.72; p<0.05) on night 2 also predicted POD2 delirium severity. Loss of sleep on night1 post-surgery is an early predictor of subsequent delirium. EEG Delta Power alterations in waking and sleep appear to be later indicators of impending delirium. Further work is needed to evaluate reproducibility/generalizability and assess whether sleep loss contributes to causing delirium. This first study to prospectively collect continuous EEG data for an extended period prior to delirium onset identified EEG-derived indices that predict subsequent delirium that could aid in developing and targeting therapies.

0514 SIX MONTHS OF CONTINUOUS POSITIVE AIRWAY PRESSURE TREATMENT IMPROVES NEUROBEHAVIORAL FUNCTION AND QUANTITATIVE SLEEP ELECTROENCEPHALOGRAM MEASURES IN OBSTRUCTIVE SLEEP APNEA

Untreated obstructive sleep apnea (OSA) is associated with neurobehavioral deficits and altered brain electrophysiology. We evaluated the effect of continuous positive airway pressure (CPAP) treatment on quantitative electroencephalogram (EEG) measures during sleep and cognitive function in OSA. We studied 162 OSA patients (age 50 ± 13, AHI 35.0 ± 26.8) before and after 6 months of CPAP treatment. Neurobehavioural tests were performed to assess working memory (2-back and 3-back accuracy), sustained attention (Psychomotor Vigilance Task, PVT), visual-spatial scanning (Letter Cancellation Task, LCT) and executive function (Stroop). All participants attended the sleep laboratory for overnight PSG at baseline and after CPAP. Power spectral analysis was performed on all-night EEG data (C3/M2) in a sub-set of 90 participants. Slow wave activity (SWA, absolute delta EEG power) and spindle frequency activity (SFA, sigma EEG power) in NREM sleep and a measure of EEG slowing in REM were calculated. Spindle density (events p/min) & characteristics (duration, amplitude, frequency) in stage N2 sleep were also derived using an automated spindle event detection algorithm. All outcomes analysed as change from baseline, and are mean [95%CI] or median [IQR]. Six months of CPAP improved neurobehavioural function across all cognitive domains: 2-back (accuracy: 4.5[24%], p<0.0001); 3-back (accuracy: 6[24%], p<0.0001); and PVT (mean slowest 10% RRT: 0.12[0.8], p=0.002) LCT (average hits: 3.8[8.5], p<0.0001) and Stroop colour (accuracy: 2.0[19.2%], p<0.0001). In our sub-set, CPAP increased SWA (105.3[61.7–148.8µV2], p<0.0001) and SFA (1.50[0.70–1.18], p=0.0003) in NREM. CPAP significantly increased sleep spindle density (p=0.003), spindle duration (p=0.019) and amplitude (p<0.0001). Associations between baseline sleep EEG and change in performance with CPAP were found with less SWA in NREM and improved sustained attention on the PVT(rho=0.24, p=0.03) and greater EEG slowing in REM and improved working memory(rho=0.25, p=0.01). Six months of CPAP improved performance and enhanced sleep EEG features. Reduced SWA in NREM and greater EEG slowing in REM at baseline showed the greatest improvement in some measures of performance with CPAP. Sleep EEG measures via PSG may provide information on which patients are most at risk of neurobehavioural dysfunction. Australian National Health and Medical Research Council Project Grant 57355.