The Sleep Position ‘Aid and Toll’ in Obstructive Sleep Apnea: A Lung-Brain Axis Perspective

Research Article

Austin J Sleep Disord. 2016; 3(1): 1024.

The Sleep Position ‘Aid and Toll’ in Obstructive Sleep Apnea: A Lung-Brain Axis Perspective

Torabi-Nami M1,2,3*, Samrad Mehrabi2,4, Hadi Aligholi¹, Bijan Zare5 and Sabri Derman6

¹Department of Neuroscience, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Iran

²Sleep Disorders Laboratory, Namazi Hospital, Shiraz University of Medical Sciences, Iran

³Shiraz Neuroscience Research Center, Shiraz University of Medical Sciences, Iran

4Division of Pulmonology, Department of Internal Medicine, Shiraz University of Medical Sciences, Iran

5Department of Medical Biotechnology, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Iran

6Sleep Disorders Unit, American Hospital, Koç Foundation, Istanbul, Turkey

*Corresponding author: Mohammad Torabi Nami, Department of Neuroscience, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran

Received: December 03, 2015; Accepted: February 17, 2016; Published: February 19, 2016

Abstract

Background: Supine sleep position has been shown to induce or aggravate sleep-breathing disorders, namely obstructive sleep apnea. In patients suffering from moderate-to-severe Obstructive Sleep Apnea-Hypopnea Syndrome (OSAHS), sleeping supine may significantly rise the Apnea-Hypopnea Index (AHI) scores, often causing profound oxygen desaturation. As such, OSAHSrelated complications would emerge secondary to chronic hypoxemia. In a fraction of cases where the condition is even more-strongly dependent to sleeping position, the term positional-OSAHS would apply. In this study, we examined the sleep position and other polysomnographic bioparameters in sleep apnea patients, in relation to their AHI and the incidence of concurrent medical conditions. This report also discussed the emerging evidence regarding the potential effects of sleep position and OSAHS on the brain.

Materials and Methods: A retrospective analysis was done on 78 patients (mean age of 43.6 years), demonstrating increased AHI in supine compared to other positions, which referred to our sleep disorders unit and underwent polysomnography during 2013-2015. They were divided into mild (n=31) and moderate-to-severe (n=47) groups depending on their AHI scores (5=AHI=15 and AHI>15, respectively).

Results: There found to be a significantly higher prevalence of hypertension, coronary artery disease and cerebrovascular disease in moderate-to-severe OSAHS patients. Likewise, Epworth Sleepiness Score (ESS) was notably higher and the mean oxygen saturation was lower in moderate-to-severe compared to mild OSAHS patients. Moderate-to-severe OSAHS cases were spending more time in supine rather than non-supine positions during sleep. AHIs and arousal index were found to be higher in supine position.

Conclusion: Sleeping supine seems to worsen OSAHS and increase AHI, subsequently contributing to medical comorbidities. In case of positional- OSAHS, treatments should be individualized to prevent position-dependent airway collapse during sleep. Patients’ awareness on the significance of sleep position in preventing OSAHS-related complications needs to be improved, and medically-proven interventions to maintain non-supine position during sleep should be advised in such patients.

Keywords: Obstructive sleep apnea; Sleep position; AHI; Polysomnography; Lung-brain axis

Introduction

Sleep-Disordered Breathing (SDB) and Obstructive Sleep Apnea-Hypopnea Syndrome (OSAHS) in particular, are among the frequently encountered disorders in the practice of sleep medicine with their prevalence reaching up to 5% in men and 2% in women aging 20 years and beyond [1]. OSAHS encompasses breathing pauses and significant airflow limitations, referred to as apneas and hypopneas, respectively. Both event types follow a common pathophysiology and tend to leave patients with medical and neurocognitive consequences in long run. The severity of OSAHS can be quantified through various approaches such as measuring the number of apnea and hypopnea events per hour of sleep, number and depth of the oxygen desaturation during sleep or the presence and severity of diurnal symptoms, namely Excessive Daytime Sleepiness (EDS) [2].

Some baseline demographic particulars such as advanced age, male gender, high Body-Mass Index (BMI), short neck, use of drugs, genetic factors, upper airway anatomy and hyper-reactivity, and the habitual dominant sleep position are regarded as contributing factors to the development of OSAHS. Regardless of the cause, the outcome is partial or complete upper-airway collapse and consequent O2 desaturation during sleep. Oropharynx is perhaps the most common site where obstruction develops [3,4].

Sleep position and the role of gravity are among mechanical contributors to the development of upper-airway collapse during sleep. Across SDB and healthy subjects, the caliber of upper-airway is subject to decrease in supine sleep position and this phenomenon becomes critical in OSAHS [5]. The supine position leads to the back shift of the tongue and narrowing of the soft palate-pharyngeal air passage [3,4].

The term ‘position-dependent-or positional-OSAHS’ would apply when the supine AHI scores are twice higher than the AHI in non-supine positions [6,7]. As inferred from the terminology, the severity of the disease is markedly increased in the supine position.

From the neuroscience perspective, a perivascular pathway has been introduced by which interstitial solutes including amyloid β (Aβ) are removed from the brain parenchyma. In this so-called “glymphatic“ pathway, a large amount of subarachnoid cerebrospinal fluid (CSF) enters the parenchyma along the perivascular spaces, exchanges with the Interstitial Fluid (ISF), and exits via para-venous pathway [8].

Accumulating evidence have indicated that the function of glymphatic pathway is influenced by the arousal level. In the other words, natural sleep increases exchange of CSF with ISF compared with the awake state [9]. Such novel insights corroborate other study findings indicating the restorative function of sleep [10,11]. On the other hand, with reference to sleep position-related functions, a recent investigation has suggested the brain’s waste removal capacity in terms of brain glymphatic transport as well as amyloid beta (Aβ) clearance. Translational research in animal models have employed dynamic contrast-enhanced Magnetic Resonance Imaging (MRI) and kinetic modeling in anesthetized rodents, showing that most glymphatic transport occurs in the lateral-compared to supine position. In addition, optical imaging and radiotracer studies showed that Aβ clearance tend to be lower in supine sleep position compared to lateral [12].

Based on these findings, and considering the fact that most apnea/ hypopnea events occur in supine position, it might be speculated that lateral sleep position possibly acts as a protective factor for the brain by providing an optimal condition for removing waste materials from its parenchyma.

OSAHS patients are found to suffer from neurocognitive function decline in long-term [5,13,14]. The question of “in addition to respiratory events, to what extent neurocognitive consequences of OSAHS is related to patients’ sleep position and the impaired function of the brain glymphatic system?’ deserves systematic research endeavors.

Though a significant number of patients who refer to our sleep facility are found to have SDB, their awareness on the significance of sleeping position is scant. The emerging need to define our OSAHS patients’ sleeping position, its clinical impact, and potential remediative strategies prompted us to pursue with the present study.

The current investigation attempted to compare cases with mild and moderate-severe position-dependent OSAHS in relation with their medical comorbidities, and polysomnographic features. Further to this, the present report tried to review current remediative approaches and emphasize the significance of sleep position not only in the severity of OSAHS but also brain health.

Material and Methods

Subjects

We conducted a retrospective study on patients who underwent polysomnographic evaluation at our sleep disorders unit (Namazi Hospital, Shiraz University of Medical Sciences, Shiraz, Iran) during 2013-2015. Demographic data sleep questionnaires and polysomnographic study reports of a total number of 138 patients were reviewed. The AHI cut-off of 5 was used to isolate patient files with OSAHS. AHI score of all patients in non-supine and supine positions were evaluated. Positional-OSAHS was defined when supine-AHI was at least twice higher than non-supine AHI. Accordingly, we extracted the files of 78 patients who fulfilled our inclusion criteria. Based on the most recent American Academy of Sleep Medicine (AASM) task force criteria [15] and depending on the values of 5=AHI=15 and AHI>15, patients were categorized into mild (n=31) and moderate-to-severe (n=47) OSAHS, respectively. Patients diagnosed with Upper-Airway Resistance Syndrome (UARS), central- or mixed-type sleep apneas or Periodic Limb Movements during Sleep (PLMS) were excluded from the analysis.

Our polysomnography setup used a built-in position sensor (accelerometer) which enabled determining sleeping positions and positional transitions of the subjects during sleep. The Persian version of Epworth sleepiness scale (ESS) was used to assess Excessive Daytime Sleepiness (EDS) [16]. Informed consents were obtained from all patients during their polysomnographic assessment.

Polysomnography

Full-night polysomnography evaluations were done at our hospital-based sleep disorders laboratory using the SOMNO screen TM system and DOMINOTM analysis software. A technician was present during the entire recordings. Acquired data were documented to a special sleep recording computer and manually scored by a sleep specialist according to the latest AASM manual for sleep scoring and analysis. Electroencephalogram (F3-A2, F4- A1, C3-A2, C4-A1, O1-A2 and O1-A2), electro-occulogram (right and left), surface electromyogram (sub mental/right and left anterior tibialis), breathing effort (chest and abdomen), air intake (mouth/ nose air flow), snoring sounds, oxygen saturation, plethysmogram, electrocardiogram, heart rate and sleeping position were recorded during all polysomnography studies.

Apneas and hypopneas were scored by at least 10-second airflow cessation and the reduction in ventilation by at least 50% causing decreased arterial O2 saturation of 4% or more due to total or partial airway obstruction, respectively [17]. The sleep position data and other sleep-related biopapameters from all included patients were extracted to undergo comparative analyses.

Statistical analysis

All statistical analyses were done using the SPSS statistical software (version 19.0 for Windows). Statistical differences were considered significant at p<0.05 cut-off. Independent t test was used to determine the significance of differences between the groups. When the data lacked normal distribution, Mann-Whitney U test was applied. In addition, Chi-square (X2) and Fisher Exact Chi-square tests were employed to analyze the categorical data. Arithmetic Means And Standard Errors Of Mean (M±SEM) were calculated for all obtained values.

Results

A total of 78 cases with position-dependent OSAHS (63 male), with a mean age of 43.6±14 years, were enrolled in our analysis. Based on the total AHI scores, patients were classified into two groups, i.e. mild (n=31) and moderate-to-severe (n=47) OSAHS. The demographic and clinical data of patients are outlined in (Table 1).