The use of alcohol is associated with the development and worsening of sleep disorder. Alcohol is generally known to have a sedative effect, but it has an arousal or sedative effect depending on the timing and drinking dose and directly affects REM sleep physiology. Alcohol acts on the central nervous system (CNS) to interfere with the sleep-wake cycle and to affect sleep-related hormone secretion. In addition, the ingestion of alcohol pre-sleep is associated with deterioration and development of sleep related breathing disorders (SBD). The increase in resistance of the upper respiratory tract and the decrease in sensitivity of the CNS respiratory center and the respiratory muscles are major mechanisms of alcohol-induced SBD, and result in snoring or apnea in healthy men or aggravating apnea in patients with OSA. Sleep-related restless leg syndrome and circadian rhythm disorders are common in alcohol use disorder patients. This review provides an assessment of scientific studies that investigated on the impact of alcohol ingestion on nocturnal sleep physiology and sleep disorders.
Sleep disorder in chronic obstructive pulmonary disease (COPD) is common and typically is associated with oxygen desaturation. The mechanisms of desaturation include hypoventilation and ventilation to perfusion mismatch. Despite the importance of sleep in patients with COPD, this topic is under-assessed in clinical practice. Impaired sleep quality is associated with more severe COPD and may contribute to worse clinical outcomes. Recent data have indicated that specific respiratory management of patients with COPD and sleep disordered breathing improves clinical outcomes. Clinicians managing patients with COPD should pay attention to and actively manage symptoms of comorbid sleep disorders. Management of sleep-related problems in COPD should particularly focus on minimizing sleep disturbance.
Journal of the korean academy of Pediatric Dentistry
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v.46
no.1
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pp.38-47
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2019
The most common cause of mouth breathing is obstacles caused by mechanical factors in upper airway. Mouth breathing could be consequently pathological cause of sleep-disordered breathing. Sleep-disordered breathing in children can cause growth disorders and behavioral disorders. The purpose of this study was to investigate relationship between upper airway and sleep-disordered breathing in children with mouth breathing. Twenty boys between 7 - 9 years old who reported to have mouth breathing in questionnaire were evaluated with clinical examination, questionnaires, lateral cephalometric radiographs, and portable sleep testing. This study assessed apnea-hypopnea index (AHI) and oxygen desaturation index (ODI) for the evaluation of sleep-disordered breathing and was done to investigate the correlation between these values and the upper airway width measured by lateral cephalometric radiographs. There was no significant correlation with the size of the tonsils (p = 0.921), but the adenoid hypertrophy was higher in the abnormal group than in the normal group (p = 0.008). In the classification according to AHI and ODI, retropalatal and retroglossal distance showed a statistically significant decrease in the abnormal group compared to the normal group (p = 0.002, p = 0.001). As AHI and ODI increased, upper airway width tended to be narrower. This indicates that mouth breathing could affect the upper airway, which is related to sleep quality.
Stroke is a leading cause of death in most developed countries and some developing countries including South Korea. It is well known that stroke has is related in some way with several sleep disorders. At first, the onset time of stroke varies according to circadian rhythm. Early morning is the most prevalent time and late evening the least. The changes of blood pressure, catecholamine level, plasminogen activity and aggregation of platelet during sleep have been suggested as possible mechanisms. Sleep apnea (SA), a representative disorder in the field of sleep medicine, is found in more than 70% of acute stroke patients compared to 2-5% of the general population. Various sleep related breathing disorders occur after stroke and snoring is a distinct risk factor for stroke. So the relationship between stroke and SA is obvious, but the cause and effect are still not clearly known. Also, stroke may cause many sleep related problems such as insomnia, hypersomnia, parasomnia and changes in sleep architecture. Patients, family members and even medical personnel often ignore stroke-related sleep problems, being concerned only about the stroke itself. The clinical impacts of sleep problems in stroke patients may be significant not only in terms of quality of life but also as a risk factor or prognostic factor for stroke. More attention should be paid to the sleep problems of stroke patients.
Alcohol has extensive effects on sleep and daytime sleepiness. Alcohol has a sleep inducing effect and the effect of increased non-REM sleep and suppressed REM sleep during the first half portion of night sleep, but alcohol induces the effect of decreased non-REM sleep and increased light sleep and frequent awakenings and REM rebound during the second half portion of night sleep. Alcohol provokes chronobiological change such as the changes of amplitude or the phase shifts of hormones or core body temperature. The sleep disruption resulting from alcohol drinking may lead to daytime fatigue and sleepiness. The elderly are at particular in the increased risk of alcohol-related sleep disorders because they achieve higher levels of alcohol in the blood and brain than do younger adults after consuming an equivalent dose. Bedtime alcohol consumption among older adults may lead to unsteadiness if walking is attempted during the night, with increased risk of falls and injuries. Continued alcohol use for sleep induction often induces aggravation of insomnia, alcoholism or sleep related breathing disorders such as obstructive sleep apnea. Alcohol should not be used as substitution of sleep pill because of the dependence and tolerance for sleep inducing effect, and the sleep disruption produced by alcohol withdrawal.
Sleep-disordered breathing (SDB) is associated with increased cardiovascular and cerebrovascular morbidity. Epidemiological and clinic-based studies have shown that SDB is related to impaired glucose tolerance and increased insulin resistance, independent of obesity. Despite of a consistent association between SDB and impaired glucose-insulin metabolism, the mechanism underlying this relationship has not been fully elucidated. It is recognized that hypoxemia and hypercapnia that occur in SDB provoke sympathetic nervous activity and catecholamine, epinephrine and norepinephrine, and cortisol are released. Sympathetic hyperactivity and increased catecholamines can impair glucose homeostasis by increasing glycogenolysis and gluconeogenesis, which can result in increased circulating insulin levels and increased risk of insulin resistance. A prospective study is needed to investigate the causal relationship between SDB and impaired glucose-insulin metabolism in a healthy population without diabetes, hypertension and obesity as etiologic risk factors.
Journal of Physiology & Pathology in Korean Medicine
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v.31
no.2
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pp.83-93
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2017
This study covers pattern differentiation based on Korean medical references, research trend and modern clinical applications about Sleep-Wake disorders of Diagnostic and Statistical Manual of Mental Disorders(DSM-V) published by American Psychiatric Association. Insomnia disorder is mostly caused by yin deficiency of liver-kidney or liver qi depression and main patterns are heart-kidney non-interaction, deficiency-excess complex pattern containing phlegm-heat due to qi stagnation and blood stasis. Hypersomnolence disorder is more due to yang deficiency rather than yin deficiency and it's major pattern is spleen-kidney yang deficiency. Cataplexy is main feature in narcolepsy and corresponds to depressive psychosis or fainting in terms of Korean Medicine and narcolepsy is assumed to be relevant to liver wind. Breathing-related sleep disorders are related with phlegm-fluid retention brought on spleen deficiency with dampness encumbrance. Pattern of circadian rhythm sleep-wake disorders is combined with yin deficiency of liver-kidney or liver qi depression of insomnia disorder and spleen-kidney yang deficiency or dampness-phlegm of hypersomnolence disorder. Yin deficiency with effulgent fire brought on drugs or alcohol is one of main patterns of substance/medication-induced sleep disorder and combined patterns with yin deficiency of liver-kidney and blood stasis or dampness-phlegm-heat are mostly applied clinically. This study drew major and frequently applied patterns of sleep-wake disorders based on Koran medical literature and modern clinical applications. And that can be the groundwork for the task ahead like clinical practice guideline of sleep-wake disorders containing pattern differentiation, diagnosis and prescriptions.
It has been controversial whether upper airway resistance syndrome (UARS) is a distinct syndrome or not since it was reported in 1993. The International Classification of Sleep Disorders classified UARS under obstructive sleep apnea syndrome (OSAS) in 2005. UARS can be diagnosed when the apnea-hypopnea index (AHI) is fewer than 5 events per hour, the simultaneously calculated respiratory disturbance index (RDI) is more than 5 events per hour due to abnormal non-apneic non-hypopneic respiratory events accompanying respiratory effort related arousals (RERAs), and oxygen saturation is greater than 92% at termination of an abnormal breathing event. Although esophageal pressure measurement remains the gold standard for detecting subtle breathing abnormality other than hypopnea and apnea, nasal pressure transducer has been most commonly used. RERAs include phase A2 of cyclical alternating patterns (CAPs) associated with EEG changes. Symptoms of OSAS can overlap with UARS, but chronic insomnia tends to be more common in UARS than in OSAS and clinical symptoms similar with functional somatic syndrome are also more common in UARS. In this journal, diagnostic and clinical differences between UARS and OSAS are reviewed.
Objectives : Upper airway resistance syndrome(UARS) is a sleep-related breathing disorder characterized by abnormal negative intrathoracic pressure during sleep. Abnormally increased negative intrathoracic pressure results in microarousal and sleep fragmentation which underlay UARS-associated complaints of daytime fatigue and sleepiness. Although daytime dysfunction in patients with UARS is comparable to that of sleep apnea syndrome, UARS has been relatively unnoticed in clinical setting. That is why UARS is apt to be excluded in diagnosing of sleep-related breathing disorders since its respiratory disturbance index and arterial oxygen saturation are within normal limits. The current study presents a summary of clinical and polysomnographic characteristics found in patients with UARS. The present study aims (1) to explore characteristics of patients diagnosed with UARS, (2) to characterize the polysomnographic findings of UARS patients, and (3) to enhance the understanding of UARS through those clinical and laboratory characteristics. Methods : This was a retrospective study of 20 UARS patients (male 15, female 5) and 30 obstructive sleep apnea (OSA) patients (male 21, female 9) at the Stanford Sleep Disorders Clinic. We diagnosed patients as having UARS when they met critenia, RDI < 5 characteristic findings of an elevated esophageal pressure($<-10\;cmH_2O$), frequent arousals secondary to an elevated esophageal pressure, and symptoms of daytime fatigue and sleepiness. We used polysomnographic value, which is standardized by Williams et al(1974), as normal control. Statiotical test were done with student t-tests. Results : (1) Mean age of UARS was $41.0\;{\pm}\;14.8$ years and OSA was $50.9\;{\pm}\;12.0$ years. UARS subject was significantly younger than OSA subject (p<0.05). (2) The total score of Epworth Sleepiness Scale (ESS) was UARS $9.7\;{\pm}\;6.3$ and OSAS $11.2\;{\pm}\;6.3$. There was no significant difference between two groups. (3) The mean body mass index was UARS $28.1\;{\pm}\;5.7\;kg/m^2$ and OSAS $32.9\;{\pm}\;7.0\;kg/m^2$. UARS had significantly lower meen body man index than OSAS subjects (p<0.05). (4) The polysomnographic parameters of UARS were not significantly different from those of OSA except RDI(p<0.001), $SaO_2$ (p<0.001) and slow wave sleep latency (p<0.05). (5) Compared with normal control, Total sleep time in UARS subjects was significantly shorter (p<0.001), sleep efficiency index was significantly lower (p<0.001), total awakening percentage was significantly higher (p<0.001), and sleep stage 1 (p<0.001) were significantly higher. (6) OSA patients showed poor sleep quality and distinct abnormal sleep architectures compared with normal control. Conclusions : Conclusions from the above results are as follows : (1) UARS patients were younger and had lower body mass index when umpared with OSA patients. (2) The quality of sleep and sleep architectures of the UARS and OSA patients are significantly different from those of normal control. (3) ESS scores and awakening frequencies of UARS are similar with those of OSA, suggesting that daytime dysfunction of UARS patients may be comparable to those of OSA patients. (4) The RDI and the $SaO_2$ which are important indicators in diagnosing sleep-related breathing disorders, of UARS subjects are close to normal value. (5) According to the the above results, we unclude that despite the absence of $SaO_2$ drops and the absence of an elevated number of apnea and hypopnea, subjects developed clinical complaints which were associated with laborious breathing, elevated Pes nadir, and frequently snoring. (6) Accordingly, we suggest including LIARS in the differential diagnosis list when sleep related breathing disorder is suspected clinically and overnight polysomnographic findings except snoring and frequent microarousal are within normal limits.
Background: Sleep-related breathing disorders(SRBD) and periodic leg movements disorder(PLMD) are both common, and are considered as separate sleep disorders. However, both disorders show high comorbidity. SRBD and PLMD can result in excessive daytime sleepiness and insomnia due to frequent sleep fragmentation. So, it is very important to consider the presence of PLMD, when we are dealing with the diagnosis and management of SRBD. The objectives of this study were to determine the incidence of PLMD in patients with SRBD, and to describe any differences between patients with and without PLMD. Method: The authors reviewed the sleep recordings of 106 patients with a final diagnosis of SRBD(obstructive sleep apnea or upper airway resistance syndrome), who underwent full nocturnal polysomnography, including the monitoring of the anterior tibialis electromyogram. All sleep records were recorded and scored using the standard criteria. The data was analyzed by the student t-test. Result: 106 patients(M=76, F=30) were included in the analysis. Data revealed a mean age of $49.5{\pm}13.6$ years, a respiratory disturbance index(RDI) of $22.3{\pm}25.4$/hour sleep, a lowest oxygen saturation of $84.9{\pm}11.3%$, a maximal esophageal pressure of $-41.0{\pm}19.1cmH_2O$, and PLM index(PLMI) of $13.1{\pm}22.4$movements/hour sleep. Forty four percent(47 of 106 patients) had a PLMI of greater than 5 on this study. The mean age of the patients with PLMD was significantly higher than that of the patients without PLMD(p<0.005). Female patients with SRBD accompanied more PLMD(p<0.05). The apnea index of the patients with PLMD was significantly lower than that of the patients without PLMD(p<0.01). The percentage of stage 1 sleep in the patients with PLMD was significantly lower than that of the patients without PLMD(p<0.05). Conclusion: The prevalence of PLMD in the patients with SRBD was high at 44.3%. The patients with PLMD were older and had more high RDI in comparison to the patients without PLMD, which was consistent with previous findings. The authors recommend that more careful consideration of PLMD is required when diagnosing and treating SRBD.
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