Automatic Wake and Deep-Sleep Stage Classification Based on Wigner-Ville Distribution Using a Single Electroencephalogram Signal.

This research paper outlines a method for automatically classifying wakefulness and deep sleep stage (N3) based on the American Academy of Sleep Medicine (AASM) standards. The study employed a single-channel EEG signal, leveraging the Wigner-Ville Distribution (WVD) for time-frequency analysis to determine EEG energy per second in specific frequency bands (δ, θ, α, and entire band). Particle Swarm Optimization (PSO) was used to optimize thresholds for distinguishing between wakefulness and stage N3. This process aims to mimic a sleep technician's visual scoring but in an automated fashion, with features and thresholds extracted to classify epochs into correct sleep stages. The study's methodology was validated using overnight PSG recordings from 20 subjects, which were evaluated by a technician. The PSG setup followed the 10-20 standard system with varying sampling rates from different hospitals. Two baselines, T1 for the wake stage and T2 for the N3 stage, were calculated using PSO to ascertain the best thresholds, which were then used to classify EEG epochs. The results showed high sensitivity, accuracy, and kappa coefficient, indicating the effectiveness of the classification algorithm. They suggest that the proposed method can reliably determine sleep stages, being aligned closely with the AASM standards and offering an intuitive approach. The paper highlights the strengths of the proposed method over traditional classifiers and expresses the intentions to extend the algorithm to classify all sleep stages in the future.

Association between obstructive sleep apnea and optic neuropathy: a Taiwanese population-based cohort study.

PURPOSE: Obstructive sleep apnea (OSA) is associated with many systemic diseases including diabetes, hypertension, stroke, and cardiovascular disease. The aim of our study was to investigate the association between OSA and optic neuropathy (ON), and to evaluate the efficacy of treatment for OSA on the risk of ON. METHODS: We used the data from the Longitudinal Health Insurance Database, which involved one million insurants from Taiwan National Health Insurance program (Taiwan NHI). RESULTS: OSA patients had a 1.95-fold higher risk of ON compared with non-OSA patients in all age group. The risk was significantly higher (adjusted hazard ratio: 4.21) in the group aged <45 years and male individuals (adjusted hazard ratio: 1.93). Meanwhile, sleep apnea was associated with ON regardless of the existence of comorbidity or not. OSA patients treated with continuous positive airway pressure (CPAP) had an adjusted 2.31-fold higher hazard of developing ON compared to controls, and those without any treatment had an adjusted 1.82-fold higher hazard of developing ON compared to controls. Moreover, ON patients had a 1.45-fold higher risk of OSA, and those aged between 45 and 64 years (hazard ratio: 1.76) and male individuals (hazard ratio: 1.55) had highest risk. CONCLUSIONS: Our study showed that OSA increased the risk of developing ON after controlling the comorbidities; however, treatment with CPAP did not reduce the risk of ON. Further large population study accessing to medical records about the severity of OSA and treatment for OSA is needed to clarify the efficacy of treatment for OSA in reducing the risk of ON.

Correction to: Total analysis of clinical factors for surgical success of adenotonsillectomy in pediatric OSAS.

The authors would like to publish this erratum to indicate Dr Rayleigh Ping-Ying Chiang as the corresponding author of this article.

Total analysis of clinical factors for surgical success of adenotonsillectomy in pediatric OSAS.

The objective of this study is the total evaluation of most common clinical factors influencing the successful rate of adenotonsillectomy for pediatric obstructive sleep apnea syndrome (OSAS). Retrospectively, 63 pediatric patients ranged from 2 to 16 years old were included. Syndromics and patients who had received orthodontic treatment or orthognathic surgery were excluded. All patients received pre-operative and postoperative polysomnography and cephalometry. Each patient received adenotonsillectomy by single surgeon. Surgical success was defined as apneahypopnea index (AHI) decreased ≧50 % or post-operative AHI <5. Total evaluated clinical factors related to success of adenotonsillectomy for pediatric OSAS include age, gender, body mass index (BMI), tonsil size, adenoid/nasopharynx ratio (A/N Ratio), pre-operative data of polysomnography, including AHI, apnea index (AI), hypopnea index (HI), mean O2 saturation and nadir O2 saturation, and 18 cephalometry parameters. Mean age of the total 63 patients was 7.78 years old. Mean BMI of the patients was 19.02. The proportion of obese patients was 25.4% (16/63). Surgical success was achieved in 42 out of 63 patients (66.7%). The surgical success was not statistically significant related to all pre-operative cephalometric parameters, age, gender, BMI and adenoid size by multiple logistic regression model. However, the surgical success was significantly related to pre-operative AHI and tonsil size. In addition, all patients who received adenotonsillectomy showed improved polysomnography parameters, including AHI, AI, HI, mean O2 saturation and nadir O2 saturation which all reached statistically significant improvement. Although adenotonsillectomy cannot cure pediatric OSAS in our research, all patients showed significant improvement of polysomnography parameters after this procedure. Pre-operative cephalometry parameters, BMI and age did not show significant correlation with surgical success, however, pre-op AHI and tonsil size correlated with surgical success. Higher pre-op AHI value and higher tonsil grade showed higher rate of surgical success. Based on the total evaluation of clinical data, surgical success after adenotonsillectomy might be predicted by pre-op AHI severity and tonsil grade.

Serotnin as a possible biomarker in obstructive sleep apnea.

Obstructive sleep apnea (OSA) is a highly prevalent disease which carries substantial public health burden. Polysomnography is the standard procedure used to diagnose OSA. However cost, accessibility, technical requirements, and skilled interpretation needs constrain its widespread use and have a role in the under-diagnosis of sleep disordered breathing. There is a clinical need to develop expedient and widely accessible tools to detect this disorder., Several biochemical markers have recently been proposed as diagnostic tools in OSA. Numerous neurochemicals directly influence the activity of upper airway dilator motor neurons, which subsequently influence respiration during sleep. Serotonin (5-HT) is one such neurochemical that has a key role in ventilatory stimulation. Herein, we review the current evidence demonstrating relationships between multiple biomarkers and sleep disordered breathing and focus on relationships between OSA and 5-HT. We discuss the possibility of biomarker-driven detection technology in the future as a means of diagnosing and monitoring OSA. Finally, we explore the specific role 5-HT may have in the future in both the diagnosis and treatment of OSA.

The role of lateral pharyngoplasty in obstructive sleep apnea syndrome.

Recent studies have shown that lateral pharyngoplasty is an effective procedure to correct obstructive sleep apnea. The objective of the paper was to evaluate factors contributing to obstructive sleep apnea syndrome and identify the different severity categories of obstructive sleep apnea that could benefit from lateral pharyngoplasty. We included 60 patients undergoing uvulopalatopharyngoplasty with or without lateral pharyngoplasty from December 1, 2008 to May 31, 2012. Six who did not complete the post-operative survey were excluded. 54 participants were assigned alternatively to either uvulopalatopharyngoplasty alone (control group, n = 29) or to uvulopalatopharyngoplasty with lateral pharyngoplasty (intervention group, n = 25). The reduction of apnea-hypoxia index in the intervention group (49.3%) was higher than it was in the control group (30.4%), but the average value was not statistically significant (p = 0.088). Only patients with moderate obstructive sleep apnea in the intervention group achieved a significant reduction of apnea-hypoxia index (30.7 vs. 10.8%; p = 0.020). Factors such as body mass index, nadir/mean SpO2, snoring index, Epworth sleepiness scale and periodic limb movement index did not change significantly following lateral pharyngoplasty. To evaluate patients' upper airway anatomy, we employed cephalometry, and found that the retroglossal space played a critical role in severe obstructive sleep apnea. Our study showed that only patients in the moderate category can be benefited from adding lateral pharyngoplasty to uvulopalatopharyngoplasty; however, patients in the mild or severe category did not benefit from adding this procedure. This information is vital when considering surgery for patients with obstructive sleep apnea syndrome. Level of evidence Prospective cohort study, Level II.

Sleep deprivation aggravates median nerve injury-induced neuropathic pain and enhances microglial activation by suppressing melatonin secretion.

STUDY OBJECTIVES: Sleep deprivation is common in patients with neuropathic pain, but the effect of sleep deprivation on pathological pain remains uncertain. This study investigated whether sleep deprivation aggravates neuropathic symptoms and enhances microglial activation in the cuneate nucleus (CN) in a median nerve chronic constriction injury (CCI) model. Also, we assessed if melatonin supplements during the sleep deprived period attenuates these effects. DESIGN: Rats were subjected to sleep deprivation for 3 days by the disc-on-water method either before or after CCI. In the melatonin treatment group, CCI rats received melatonin supplements at doses of 37.5, 75, 150, or 300 mg/kg during sleep deprivation. Melatonin was administered at 23:00 once a day. PARTICIPANTS: Male Sprague-Dawley rats, weighing 180-250 g (n = 190), were used. MEASUREMENTS: Seven days after CCI, behavioral testing was conducted, and immunohistochemistry, immunoblotting, and enzyme-linked immunosorbent assay were used for qualitative and quantitative analyses of microglial activation and measurements of proinflammatory cytokines. RESULTS: In rats who underwent post-CCI sleep deprivation, microglia were more profoundly activated and neuropathic pain was worse than those receiving pre-CCI sleep deprivation. During the sleep deprived period, serum melatonin levels were low over the 24-h period. Administration of melatonin to CCI rats with sleep deprivation significantly attenuated activation of microglia and development of neuropathic pain, and markedly decreased concentrations of proinflammatory cytokines. CONCLUSIONS: Sleep deprivation makes rats more vulnerable to nerve injury-induced neuropathic pain, probably because of associated lower melatonin levels. Melatonin supplements to restore a circadian variation in melatonin concentrations during the sleep deprived period could alleviate nerve injury-induced behavioral hypersensitivity.

Can pillar suturing promote efficacy of adenotonsillectomy for pediatric OSAS? A prospective randomized controlled trial.

OBJECTIVES/HYPOTHESIS: Pediatric obstructive sleep apnea syndrome (OSAS) is a common disorder with serious clinical implications if left untreated. The recommended initial treatment for pediatric patients with obstructive sleep apnea syndrome (OSAS) is adenotonsillectomy. However, recent reports have shown variable surgical results with adenotonsillectomy in the treatment of pediatric OSAS. STUDY DESIGN: Prospective, controlled study. METHODS: From April 2007 to August 2010, 24 participants were assigned alternatively to either adenotonsillectomy with pillar suturing (intervention group) or adenotonsillectomy alone (control group). RESULT: The average improvement in apnea hypopnea index (AHI) was 42.6% in the control group and 79.9% in the intervention group (P=0.037). The success rate was 50% in the control group and 91.6% in the intervention group (P=0.034). Six patients (50%) in the intervention group achieved complete resolution of pediatric OSAS, as defined by an AHI <1/hour, compared to 2 patients (16.7%) in the control group (P=0.097). CONCLUSION: Adenotonsillectomy with pillar suturing showed significant improvement in treating pediatric patients with OSAS compared to adenotonsillectomy alone. The procedure is simple and safe. LEVEL OF EVIDENCE: 4.

Intratympanic dexamethasone on cochlear blood flow in Guinea pigs.

UNLABELLED: To determine the effect of intratympanically delivered dexamethasone on cochlear blood flow. 29 white Hartly guinea pigs were divided into 2 groups. By laser Doppler flowmeter, baseline data were recorded in the first 15-20 min, followed by 20 min' recording after applying dexamethasone or normal saline, with a record of flow every 5 min in 2 groups. Friedman Test was used to test the change of blood flow in these four timing. There were no significant changes of blood flow after injecting dexamethasone (p = .18 > .05) and normal saline (p = .93 > .05). The effects of dexamethasone on cochlear blood flow were variable and not significant. The following research would be designed under pathological conditions, such as cochlear ischemia, to show the possible mechanism of dexamethasone for specific inner ear disease. LEVEL OF EVIDENCE: 3a (SR of case-control studies).

Peripheral neuropathology of the upper airway in obstructive sleep apnea syndrome.

Obstructive sleep apnea syndrome (OSAS) is a common sleep disorder that leads to significant morbidity and mortality without adequate treatment. Though much emphasis on the pathogenesis of OSAS has been placed on a narrow upper airway space and associated muscular factors, possible neuropathy of the upper airway has not been fully elucidated. Increasing peer reviewed evidence suggests involvement of neurologic lesions of the upper airway in OSAS patients. In this article, we review the etiology and pathophysiology of OSAS, the evidence and possible mechanisms leading to upper airway neuropathy, and the relationship between upper airway neuropathy and OSAS. Further studies should focus on the long term effects of the upper airway neuropathy as related to the duration and severity of snoring and or apnea, and also on the potential methods of prevention and management of the neuropathy in sleep disordered breathing.

Melatonin reduces median nerve injury-induced mechanical hypersensitivity via inhibition of microglial p38 mitogen-activated protein kinase activation in rat cuneate nucleus.

In this study, we examined the relationships between p38 mitogen-activated protein kinase (MAPK) activation in the cuneate nucleus (CN) and behavioral hypersensitivity after chronic constriction injury (CCI) of the median nerve. We further investigated effects of melatonin administration and pinealectomy on p38 MAPK activation and development of hypersensitivity. Using immunohistochemistry and immunoblotting, low levels of phosphorylated p38 (p-p38) MAPK were detected in CN of normal rats. As early as 1 day after CCI, p-p38 MAPK levels in the ipsilateral CN were significantly increased (1.4 ± 0.2-fold, P < 0.05), which reached a maximum at 7 days (5.1 ± 0.4-fold, P < 0.001). Double immunofluorescence labeling with cell-specific markers showed that p-p38 MAPK immunoreactive cells co-expressed OX-42, a microglia activation maker, suggesting the expression of p-p38 MAPK in microglia. Microinjection of SB203580, a p38 MAPK inhibitor, into the CN 1 day after CCI attenuated injury-induced behavioral hypersensitivity in a dose-dependent manner. Furthermore, animals received melatonin treatment at daily doses of 37.5, 75, 150, or 300 mg/kg from 30 min before until 3 days after CCI. Melatonin treatment dose-dependently attenuated p-p38 MAPK levels, release of pro-inflammatory cytokines, and behavioral hypersensitivity following CCI; conversely, pinealectomy that resulted in a reduction in endogenous melatonin levels exacerbated these effects. In conclusion, median nerve injury-induced microglial p38 MAPK activation in the CN modulated development of behavioral hypersensitivity. Melatonin supplementation eased neuropathic pain via inhibition of p38 MAPK signaling pathway; contrarily, reducing endogenous blood melatonin levels by pinealectomy promoted phosphorylation of p38 MAPK and made rats more vulnerable to nerve injury-induced neuropathic pain.

Development of the Insomnia Screening Scale based on ICSD-II.

OBJECTIVE: Although various instruments have been developed to evaluate insomniac symptoms in individuals, none of them are based on the International Classification of Sleep Disorder, 2nd (ICSD-II). The purpose of this study is to develop a new scaling system, the Insomnia Screening Scale (ISS) to fit the new diagnostic criteria. METHODS: Study 1 was conducted to formulate the new items of the insomnia screening scale (ISS), which were divided into four major subscales, and establish the reliability and validity of the ISS in clinical insomniac subjects. Study 2 tested the external validity of the ISS, which was used in a community survey, and investigated the relationship between ISS and daytime function, especially working memory. RESULTS: The final version of the ISS has good internal consistency (α = 0.87-0.98), and explains 64% of the variance. The insomnia group had poor working memory performance on the cognitive tasks. CONCLUSIONS: The ICSD-II based ISS is a reliable and valid instrument for evaluating an individual's insomniac symptoms. The major difference between the ISS and the previous instruments is that the ISS not only assess the subjective insomniac and daytime symptoms but also examines the sleep environment and sleep opportunities of the participants.

A Lemierre syndrome variant caused by Klebsiella pneumoniae.

Lemierre syndrome is an extremely rare disease characterized by oropharyngeal infection, septicemia, internal jugular vein thrombosis, and skip lesions. The most common causative pathogen is Fusobacterium necrophorum. We reported a 45-year-old woman who presented with left neck painful swelling and septicemia. Magnetic resonance imaging of the head and neck demonstrated venous thrombosis extending from the left internal jugular vein to the sigmoid sinus. During admission we discovered that the patient had uncontrolled diabetes mellitus. We also found a metastatic lesion through chest radiography. Klebsiella pneumoniae was cultivated from both blood samples and pus from deep neck spaces. Surgical drainage, early and adequate antibiotic treatment, anticoagulation, and strict control of blood glucose led to the patient's complete recovery. Because Lemierre syndrome is a forgotten disease in the era of antibiotics, awareness of the signs and symptoms of this disease is important because of its associated high mortality rate. This case illustrated that the presence of K pneumoniae can lead to Lemierre syndrome.

Effects of pre-emptive drug treatment on astrocyte activation in the cuneate nucleus following rat median nerve injury.

In this study, we examined the relationship between astrocyte activation in the cuneate nucleus (CN) and behavioral hypersensitivity after chronic constriction injury (CCI) of the median nerve. In addition, we also examined the effects of pre-emptive treatment with a number of drugs on astrocyte activation and hypersensitivity development in this model. Using immunohistochemistry and immunoblotting, little glial fibrillary acidic protein (GFAP; an astrocyte marker) immunoreactivity was detected in the CN of the normal rats. As early as 3 days after CCI, there was a significant increase in GFAP immunoreactivity in the lesion side of CN, and this reached a maximum at 7 days, and was followed by a decline. Counting of GFAP-immunoreactive astrocytes revealed that astrocytic hypertrophy, but not proliferation, contributes to increased GFAP immunoreactivity. Furthermore, microinjection of the glial activation inhibitor, fluorocitrate, into the CN at 3 days after CCI attenuated injury-induced behavioral hypersensitivity in a dose-dependent manner. These results suggest that median nerve injury-induced astrocytic activation in the CN modulated the development of behavioral hypersensitivity. Animals received MK-801 (glutamate N-methyl-d-aspartate (NMDA) receptor antagonist), clonidine (alpha(2)-adrenoreceptor agonist), tetrodotoxin (TTX, sodium channel blocker) or lidocaine (local anesthetic) 30 min prior to median nerve CCI. Pre-treatment with MK-801, TTX, and 2% lidocaine, but not clonidine, attenuated GFAP immunoreactivity and behavioral hypersensitivity following median nerve injury. In conclusion, suppressing reactions to injury, such as the generation of ectopic discharges and activation of NMDA receptors, can decrease astrocyte activation in the CN and attenuate neuropathic pain sensations.

Sleepy driver near-misses may predict accident risks.

STUDY OBJECTIVES: To quantify the prevalence of self-reported near-miss sleepy driving accidents and their association with self-reported actual driving accidents. DESIGN: A prospective cross-sectional internet-linked survey on driving behaviors. SETTING: Dateline NBC News website. RESULTS: Results are given on 35,217 (88% of sample) individuals with a mean age of 37.2 +/- 13 years, 54.8% women, and 87% white. The risk of at least one accident increased monotonically from 23.2% if there were no near-miss sleepy accidents to 44.5% if there were > or = 4 near-miss sleepy accidents (P < 0.0001). After covariate adjustments, subjects who reported at least one near-miss sleepy accident were 1.13 (95% CI, 1.10 to 1.16) times as likely to have reported at least one actual accident as subjects reporting no near-miss sleepy accidents (P < 0.0001). The odds of reporting at least one actual accident in those reporting > or = 4 near-miss sleepy accidents as compared to those reporting no near-miss sleepy accidents was 1.87 (95% CI, 1.64 to 2.14). Furthermore, after adjustments, the summary Epworth Sleepiness Scale (ESS) score had an independent association with having a near-miss or actual accident. An increase of 1 unit of ESS was associated with a covariate adjusted 4.4% increase of having at least one accident (P < 0.0001). CONCLUSION: A statistically significant dose-response was seen between the numbers of self-reported sleepy near-miss accidents and an actual accident. These findings suggest that sleepy near-misses may be dangerous precursors to an actual accident.