A 56-year-old married white male with a past medical history of obesity, diabetes, and hypertension presented to an outpatient psychiatry clinic with depressed mood nearly every day for more than 6 weeks. The patient reported diminished interest in activities, significant weight gain in the last several years, sleep maintenance insomnia, fatigue and excessive daytime sleepiness, difficulty with memory, and poor concentration. The family noted his diminished activity. His patient health questionnaire-9 (PHQ-9) score was 23 (>10 indicative of depression) at his first visit. Upon physical examination, his body mass index was 35 and neck circumference 21 inches. Mood was depressed and sad. The patient’s initial diagnosis was major depressive disorder without psychotic features, and therapy was initiated with sertraline.
After 4 months, there was some improvement in depression and his PHQ-9 score decreased in number to 18. Excessive daytime sleepiness and difficulty with concentration persisted. Further questioning revealed a history of snoring that “disturbs the wife,” who had been sleeping in another room. She reported witnessing pauses in his breathing during sleep. His Epworth sleepiness scale core was 18 (normal is <10). Overnight pulse oximetry revealed remarkable desaturations of oxyhemoglobin reaching a nadir of 80%. Subsequent polysomnographic sleep study revealed severe obstructive sleep apnea (OSA) with apnea hypopnea index of 50 per hour, corrected by continuous positive airway pressure (CPAP). With nightly use of CPAP, there was significant improvement in sleep quality as well as mood. He stated, “I have never felt this much better in my life.”
What Is Obstructive Sleep APNEA?
OSA is a condition in which a person, generally an obese loud snorer, frequently stops breathing for 10 seconds or more (apnea) or has shallow breathing (reduced airflow by ≥30%) for 10 seconds or more, which is accompanied by oxygen desaturation of ≥4% (hypopnea).1 This occurs due to obstruction of the upper (oropharyngeal) airway during sleep—when there is reduced motor tone of the pharyngeal muscles. Criteria for The Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-V) requires polysomnographic evidence of at least five obstructive apneas or hypopneas per hour of sleep accompanied by daytime sleepiness, fatigue, or unrefreshing sleep despite adequate opportunities to sleep that are not better explained by a mental disorder or any other sleep disorder. Alternatively, the diagnosis can be made if there are 15 or more obstructive apneas or hypopnea per hour of sleep regardless of accompanying symptoms. Table 1 summarizes various definitions of sleep disordered breathing, and Table 2 describes various signs and symptoms of OSA.
Definition of Sleep-related Breathing Disorders
Signs and Symptoms of Obstructive Sleep Apnea
How Is Obstructive Sleep APNEA Diagnosed?
An overnight polysomnography (PSG) administered by a trained technologist in a sleep laboratory remains the gold standard for diagnosis of OSA. Split-night PSG, in which the first portion of the study is diagnostic and the second portion performed with CPAP titration to determine optimal pressure, is commonly employed.2 In addition, out-of-center (usually in the home) sleep testing is becoming increasingly common, and is used for patients with high likelihood of moderate-to-severe OSA without other comorbid medical conditions.3Figure 1 shows how OSA looks on a typical PSG.
Absent air flow is accompanied by chest and abdominal movements indicating inspiratory effort. Note the “paradoxical” abdominal movement (expansion) coupled with chest retraction indicative of upper airway obstruction. Following apnea, there is a consequent reduction of oxyhemoglobin saturation (SaO2). The electroencephalogram indicates a change of rhythm indicating central nervous system arousal in response to the apnea. This leads to resumption of respiration, return of snoring, and increased SaO2.
During wakefulness there is normal tone in the dilator muscles (mainly tongue) that keeps the airway open. Breathing is under voluntary control during wakefulness. When an individual with a narrowed or crowded upper airway space falls asleep, there is decreased neuronal input to these muscles, which favors collapse of the space.4 A large neck with fatty tissue compressing the airway causes narrowing of the pharyngeal opening, which makes it more likely to collapse when there is reduced neuronal input during sleep. Increasing inspiratory effort in response to this air-flow limitation creates more negative pressure in the airway, sucking it even more closed. Once there is no airflow, oxygen saturation declines, and there is an increase in blood carbon dioxide, which is a stimulant for respiratory drive. Attempts to open the upper airway are usually unsuccessful, leading to increased sympathetic autonomic activity and central nervous system arousal, which reestablishes the tone of the upper airway muscles and generally results in an interruption of sleep that can be detected by the electroencephalogram.5 These central nervous system arousals and fluctuations in oxyhemoglobin saturation (SaO2) are thought to be responsible for the symptoms of obstructive sleep apnea including excessive daytime sleepiness, fatigue, difficulties with concentration, and changes in mood.4,6,7
Prevalence and Course
OSA is a common sleep disorder affecting 2%–15% of middle-aged adults and more than 20% of older individuals. With more awareness of the disease, patients are seeking help at an earlier age.8 With the increase in rates of obesity, the prevalence of OSA has increased significantly.
Consequences of Obstructive Sleep APNEA
It has been long known that untreated OSA is associated with increased mortality.9 More than half of the individuals with moderate-to-severe OSA report symptoms of excessive daytime sleepiness.10 Motor vehicle accidents are increased significantly for individuals with OSA.11 Untreated OSA is recognized as an independent risk factor for the development of hypertension12 and other cardiovascular diseases.13 A landmark study revealed OSA as an independent, dose-dependent risk factor for hypertension (adjusted odds ratio [OR] of 2).14 On the other hand, treatment of OSA with CPAP improved blood pressure control.14 Although the effect of OSA on neurocognitive impairment has long been known, new data strengthen the relationship between OSA and stroke.15
OSA also appears to be an independent risk factor for insulin resistance and the development of diabetes. The Wisconsin Sleep Cohort Study, with 1,387 individuals, has shown that those with moderately severe OSA were more likely to have diabetes (OR: 2.30).16 This becomes an important issue due to the extremely high rates of diabetes in patients with psychiatric disorders; also many antipsychotic medications are known to increase the risk of diabetes.17,18 Some authors argue that OSA is itself a component of a metabolic syndrome and that there is a bi-directional relationship between OSA and insulin resistance primarily in obese patients.19
OSA and depression have many overlapping symptoms, including fatigue, poor concentration, daytime sleepiness, psychomotor retardation, irritability, and sleep disturbance.20 Differential diagnoses also include other sleep disorders that present as excessive daytime sleepiness: narcolepsy and circadian rhythm disorders. Nocturnal panic attacks may include symptoms of gasping and choking that can resemble sleep-disordered breathing.21 The absence of excessive daytime sleepiness may differentiate nocturnal panic attacks from OSA. Substance use and withdrawal can produce insomnia or excessive daytime sleepiness.
Most treatments for OSA are designed to keep the upper airway open during sleep.1 Weight loss is typically helpful because it reduces the severity of the disease.22 CPAP and other positive airway pressure (PAP) treatments are the mainstay of therapy for moderate-to-severe OSA as well as mild cases accompanied by daytime somnolence.23
CPAP consists of a motorized unit that propels filtered air through a nasal or oronasal interface with positive pressure acting as a pneumatic splint during sleep. The required level of pressure is typically determined during a split-night PSG study,2 but in selected cases may be determined by a self-titrating automated device sensitive to limitation of air flow.23 Optimal treatment should normalize SaO2 and minimize sleep fragmentation.
Other PAP treatments include continuing therapeutic use of automatic titrating CPAP, as noted above, which increases or decreases the pressure based on machine sensitivity to air flow resistance of the upper airway. In some cases, this is advantageous to adjust for different pressure requirements over the course of the night such as in response to position changes. Bi-level PAP delivers pressures that are increased during inspiration and decreased during expiration. This can provide an inspiratory assist, and is often used in patients with neuromuscular problems or with obesity-related hypoventilation. A newer device is adaptive servo ventilation, which will add an inspiratory pressure assist when a patient-triggered breath is absent—such as for patients with central sleep apnea (CSA), which can occur in patients with congestive heart failure,24 some treated with opioid analgesic agents and in occasional patients who develop emerging CSA when obstruction is removed by CPAP.
Adherence to full nightly use of CPAP can be very challenging for patients and varies between 40% and 60%. Table 3 summarizes practical tips that can help solve some of the difficulties compromising CPAP adherence.
Helpful Hints for Promoting the Use of Positive Airway Pressure
Dental appliances are custom-made devices that are fitted to the upper and lower teeth in order to pull the lower jaw and tongue base forward to enlarge the retropharyngeal opening. Success rates of such mandibular advancement appliances are 30%–80%, depending on the selection criteria, definition of success, and device being used.1
Tracheostomy, very uncommon nowadays, was the original treatment of choice prior to the introduction of CPAP in the 1980s. This cured the disorder by simply bypassing the oropharyngeal airway during sleep. Current surgical options include removal of tissue from the posterior pharyngeal region (uvulopalatopharyngoplasty), tensioning the genioglossus to advance the base of the tongue (genial advancement, hyoid suspension), and maxillo-mandibular advancement, in which both the mandible and maxilla are surgically advanced, enlarging the posterior pharyngeal region. Procedures are selected with respect to the specific patient anatomy with a goal of preventing air-flow limitation and airway collapse during sleep. Success rates of upper airway surgery range between 24% and 86% depending on severity, the patient specifications, and type of surgery performed.25 The most recently developed surgical option is the implantation of an electronic genioglossus muscle stimulating device that coordinates muscle stimulation with inspiratory effort to widen the airway with each breath.26
Relationship with Psychiatric Disorders
Prevalence of depression and anxiety in patients with OSA ranges from 5%–63%.20 In most of these studies, depression is often a variable, either clinically diagnosed or based on self-reported symptoms. In a large retrospective review of the US Veteran’s Health Administration data bank, psychiatric diagnoses in patients with sleep apnea included depressive disorders (21.8%),20 anxiety disorders (16.7%), posttraumatic stress disorder (11.9%), psychotic disorders (5.1%), and bipolar disorders (3.3%).27 Several other studies have reported higher rates of depression in patients with OSA.20 Most patients have difficulty with treatment because of poor adherence to CPAP and some patients with anxiety and posttraumatic stress disorder decline CPAP due to feelings of claustrophobia.28 OSA impacts neurocognitive functioning including vigilance, learning, and memory. Older age, male sex, smoking, obesity, hypertension, diabetes, metabolic syndrome, hypothyroidism, alcoholism, and drug use are all risk factors for further cognitive impairment in patients with OSA.29 At a cellular level, OSA causes cognitive effects via intermittent hypoxemia and systemic inflammation, which causes endothelial dysfunction.29 Frontal and parietal lobe disturbance and decreased hippocampal volume have been implicated in neurocognitive effects of OSA.29 More recently, Castronovo et al.30 showed that white matter changes in patients with severe OSA improved with CPAP use over a 12-month period with improvement in attention, memory, and executive functioning.
OSA is common disorder with serious consequences for cardiovascular, metabolic, and mental health. It is important to recognize that OSA independently affects morbidity and mortality if left untreated. This disorder should be suspected in patients who are obese, snore, hypersomnolent, and have symptoms of depression. Mental health providers can help to assure that OSA is properly evaluated and diagnosed. CPAP is the gold standard treatment; however, in those with mild-to-moderate OSA, a dental appliance may be acceptable. Mental health providers may add considerably to their patient’s quality of life by supporting and encouraging treatment of this disorder.
- Mehra R. Sleep apnea ABCs: airway, breathing, circulation. Cleve Clin J Med. 2014;81(8):479–489. doi:10.3949/ccjm.81gr.14002 [CrossRef]
- Khawaja IS, Olson EJ, van der Walt C, et al. Diagnostic accuracy of split-night polysomnograms. J Clin Sleep Med. 2010;6(4):357–362.
- Collop N. Home sleep testing: appropriate screening is the key. Sleep. 2012;35(11):1445–1446.
- White DP, Younes MK. Obstructive sleep apnea. Compr Physiol. 2012;2(4):2541–2594.
- Greenstone M, Hack M. Obstructive sleep apnoea. BMJ. 2014;348:g3745. doi:10.1136/bmj.g3745 [CrossRef]
- Lugaresi E, Cirignotta F, Montagna P. Pathogenic aspects of snoring and obstructive apnea syndrome. Schweiz Med Wochenschr. 1988;118(38):1333–1337.
- Mills PJ, Dimsdale JE. Sleep apnea: a model for studying cytokines, sleep, and sleep disruption. Brain Behav Immun. 2004;18(4):298–303. doi:10.1016/j.bbi.2003.10.004 [CrossRef]
- Marshall NS, Wong KK, Liu PY, Cullen SR, Knuiman MW, Grunstein RR. Sleep apnea as an independent risk factor for all-cause mortality: the Busselton Health Study. Sleep. 2008;31(8):1079–1085.
- He J, Kryger MH, Zorick FJ, Conway W, Roth T. Mortality and apnea index in obstructive sleep apnea. Experience in 385 male patients. Chest. 1988;94(1):9–14. doi:10.1378/chest.94.1.9 [CrossRef]
- Ishman SL, Benke JR, Cohen AP, Stephen MJ, Ishii LE, Gourin CG. Does surgery for obstructive sleep apnea improve depression and sleepiness?Laryngoscope. 2014;124(12):2829–2836. doi:10.1002/lary.24729 [CrossRef]
- George CF, Smiley A. Sleep apnea & automobile crashes. Sleep. 1999;22(6):790–795.
- Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med. 2000;342(19):1378–1384. doi:10.1056/NEJM200005113421901 [CrossRef]
- Vizzardi E, Sciatti E, Bonadei I, D’Aloia A, Curnis A, Metra M. Obstructive sleep apnoea-hypopnoea and arrhythmias: new updates. J Cardiovasc Med (Hagerstown). 2014;[Epub ahead of print] doi:10.2459/JCM.0000000000000043 [CrossRef]
- Dernaika TA, Kinasewitz GT, Tawk MM. Effects of nocturnal continuous positive airway pressure therapy in patients with resistant hypertension and obstructive sleep apnea. J Clin Sleep Med. 2009;5(2):103–107.
- Valham F, Mooe T, Rabben T, Stenlund H, Wiklund U, Franklin KA. Increased risk of stroke in patients with coronary artery disease and sleep apnea: a 10-year follow-up. Circulation. 2008;118(9):955–960. doi:10.1161/CIRCULATIONAHA.108.783290 [CrossRef]
- Reichmuth KJ, Austin D, Skatrud JB, Young T. Association of sleep apnea and type II diabetes: a population-based study. Am J Respir Crit Care Med. 2005;172(12):1590–1595. doi:10.1164/rccm.200504-637OC [CrossRef]
- Citrome L, Collins JM, Nordstrom BL, et al. Incidence of cardiovascular outcomes and diabetes mellitus among users of second-generation antipsychotics. J Clin Psychiatry. 2013;74(12):1199–1206. doi:10.4088/JCP.13m08642 [CrossRef]
- Vanderlip ER, Chwastiak LA, McCarron RM. Integrated care: nonfasting screening for cardiovascular risk among individuals taking second-generation antipsychotics. Psychiatr Serv. 2014;65(5):573–576. doi:10.1176/appi.ps.201400015 [CrossRef]
- Vgontzas AN, Bixler EO, Chrousos GP. Sleep apnea is a manifestation of the metabolic syndrome. Sleep Med Rev. 2005;9(3):211–224. doi:10.1016/j.smrv.2005.01.006 [CrossRef]
- Ejaz SM, Khawaja IS, Bhatia S, Hurwitz TD. Obstructive sleep apnea and depression: a review. Innov Clin Neurosci. 2011;8(8):17–25.
- Edlund MJ, McNamara ME, Millman RP. Sleep apnea and panic attacks. Compr Psychiatry. 1991;32(2):130–132. doi:10.1016/0010-440X(91)90004-V [CrossRef]
- Young D, Collop N. Advances in the treatment of obstructive sleep apnea. Curr Treat Options Neurol. 2014;16(8):305. doi:10.1007/s11940-014-0305-6 [CrossRef]
- Ballard RD. Management of patients with obstructive sleep apnea. J Fam Pract. 2008;57(8 Suppl):S24–30.
- Wang J, Wang Y, Feng J, Chen BY, Cao J. Complex sleep apnea syndrome. Patient Prefer Adherence. 2013;7:633–641.
- Khan A, Ramar K, Maddirala S, Friedman O, Pallanch JF, Olson EJ. Uvulopalatopharyngoplasty in the management of obstructive sleep apnea: the mayo clinic experience. Mayo Clin Proc. 2009;84(9):795–800. doi:10.4065/84.9.795 [CrossRef]
- White DP. New therapies for obstructive sleep apnea. Semin Respir Crit Care Med. 2014;35(5):621–628. doi:10.1055/s-0034-1390074 [CrossRef]
- Sharafkhaneh A, Giray N, Richardson P, Young T, Hirshkowitz M. Association of psychiatric disorders and sleep apnea in a large cohort. Sleep. 2005;28(11):1405–1411.
- Hurwitz TD, Khawaja I. Treatment of obstructive sleep apnea may be an important adjunct to therapy of posttraumatic stress disorder not to be overlooked. Sleep. 2010;33(11):1435–1436.
- Lal C, Strange C, Bachman D. Neurocognitive impairment in obstructive sleep apnea. Chest. 2012;141(6):1601–1610. doi:10.1378/chest.11-2214 [CrossRef]
- Castronovo V, Scifo P, Castellano A, et al. White matter integrity in obstructive sleep apnea before and after treatment. Sleep. 2014;37(9):1465–1475.
Definition of Sleep-related Breathing Disorders
||Cessation of airflow for at least ≥10 seconds
||Reduction of airflow with resultant oxygen desaturation of ≥4%
|Apnea hypopnea index
||Average frequency of apnea and hypopnea events per hour of sleep
|Obstructive sleep apnea
||AHI of ≥15 or ≥5 associated symptoms such as excessive daytime sleepiness, impaired cognition, mood disorders, insomnia, hypertension, heart disease, or history of stroke
|Central sleep apnea
||AHI of ≥5 with ≥50% of the respiratory events occurring without any inspiratory effort—associated with symptoms of either excessive daytime sleepiness or disrupted sleep
Signs and Symptoms of Obstructive Sleep Apnea
Witnessed apneas or snort arousals
Excessive daytime sleepiness
Difficulty maintaining sleep
Restless or unrefreshing sleep
Large neck circumference
Chronic heart failure
Helpful Hints for Promoting the Use of Positive Airway Pressure
|Unable to Tolerate Pressure
Set CPAP machine to gradually increase pressure (“ramp up”) or use auto-titrating CPAP
|Dry Nose or Mouth/Congestion
Use an in-line heated humidifier (water reservoir with a heating plate). The air from the flow generator passes over the heated water to increase the humidity to the patient
Try using normal saline nasal spray or gel. These products are available over-the counter and should be used at least twice daily
For severe congestion, the use of nasal steroids and/or ENT consultation should be considered
Use chin strap or full-face mask if patient keeps the mouth open during sleep
Practice using the positive airway device during the day. Put the mask on and start the flow generator while watching television or listening to music
Use the ramp feature and expiratory pressure relief
Short-acting sedative hypnotics may be helpful while the patient is becoming accustomed to using CPAP
Use nasal pillows (small cones that fit into the nostrils and do not cover the nose or mouth)
The flow generators are quite quiet, but if noise is an issue, the unit can be moved up to 12 feet away from the bed by adding extra tubing
Keep the face and the mask clean
If irritation persists, a mask refit may be needed
If leaks are large and adjustment of the headgear does not resolve the problem, contactthe durable medical equipment company for a mask refit
|Unable to Fall Asleep with Mask
Avoid daytime naps
Consider short-term use of a hypnotic medication