Dr. Collop is associate professor in the Division of Pulmonary and Critical Care Medicine at the Johns Hopkins University School of Medicine in Baltimore, Maryland. Dr. Neubauer is associate director of the Johns Hopkins Sleep Disorders Center and assistant professor in the Department of Psychiatry at the Johns Hopkins University School of Medicine. He is also medical director of the Psychiatry Mobile Treatment Program at the Johns Hopkins Bayview Medical Center.
Disclosure: Dr. Collop reports no affiliation with or financial interest in any organization that may pose a conflict of interest. Dr. Neubauer is a consultant to and on the speaker’s bureaus of sanofi-aventis and Takeda.
Please direct all correspondence to: David N. Neubauer, MD, Johns Hopkins Bayview Medical Center, 4940 Eastern Ave, Box 151, Baltimore, MD 21224; Tel: 410-550-0066; E-mail: email@example.com.
• Obstructive sleep apnea causes sleep disruption, daytime sleepiness, cognitive impairment, and depressive symptoms.
• Psychotropic medications may exacerbate sleep apnea.
• Depression, anxiety, and psychosis may undermine sleep apnea treatment.
Obstructive sleep apnea (OSA) is a common clinical problem that produces symptoms that overlap with depression. Obesity is the strongest predictor of OSA, although other factors influencing upper airway patency may also predispose individuals to OSA. The key treatment approaches for OSA are nasal continuous positive airway pressure (CPAP) or bilevel positive airway pressure, oral devices, and upper airway surgery. Bariatric surgery may also be beneficial. The presence of OSA with comorbid psychiatric disorders may result in clinical challenges related to diagnoses, evaluations, and treatment adherence. Selected psychiatric medications have the potential to exacerbate OSA due to sedating effects and a propensity for weight gain. Antipsychotics and OSA independently may increase the risk for metabolic abnormalities, including glucose intolerance. Patients with OSA should be evaluated for symptoms of psychiatric disorders, just as psychiatric patients with sleep abnormalities and daytime sleepiness should be assessed for symptoms of OSA.
There are numerous forms of sleep-disordered breathing, including obstructive sleep apnea (OSA), central sleep apnea, and hypoventilation syndromes. This article predominantly focuses on the common problem of OSA. The first part of the article will provide an overview of sleep-disordered breathing and the second part will examine unique issues related to sleep apnea, mental disorders, and psychiatric patients.
Definition and Types
Obstructive sleep-disordered breathing (SDB) exists on a continuum from narrowing of the upper airway to snoring to complete obstruction. Snoring occurs when air is forced through the restricted space of a narrowed airway, causing the surrounding tissues to vibrate. Although snoring has been associated in epidemiologic studies with cardiovascular disease, it is extremely common and is not necessarily “pathologic.” However, as the upper airway decreases in caliber with muscle relaxation, airflow is further restricted and breathing events termed hypopneas can occur. A hypopnea is defined as ≥30% reduction in airflow followed by a 3% to 4% fall in oxyhemoglobin saturation and/or an arousal from sleep. An obstructive apnea is complete collapse of the upper airway during sleep. OSA syndrome is usually defined by an apnea-hypopnea index (apneas + hypopneas/hours of total sleep time or apnea-hypopnea index (AHI) of ≥5 and symptoms of excessive daytime sleepiness, unrefreshing sleep, or chronic fatigue. Furthermore, although OSA accounts for the vast majority of sleep-disordered breathing cases, there are two additional types of apnea that may be noted on a sleep study, namely, central and mixed. Central sleep apnea occurs when there are breathing pauses without respiratory effort lasting ≥10 seconds; mixed apneas are a combination of central and obstructive apneas—usually starting with a central apnea and ending with an obstructive apnea. These events are determined during a sleep study (polysomnography) where brain waves (electroencephalography), muscle tone (electromyography), eye movements (electrooculography), and breathing parameters are monitored.
The prevalence of OSA ranges from 3% to 7.5% in males and 2% to 3% in females.1 It is more common in males, approximately 2–3 times that of females, until menopause, when the prevalence in females increases.2 Interestingly, clinic referrals for OSA display a greater gender discrepancy, with ≥5 times as many men being referred for evaluation than women. Studies suggest OSA may be more common in African Americans at age extremes (<25 years or >65 years) and in Asians at lower body mass indexes (BMI), perhaps due to differences in craniofacial structure.3-5 The prevalence also appears to increase with increasing age, although the severity decreases.6,7
There are several risk factors for OSA, the strongest being obesity. The BMI (weight in kg/height in m2) shows a relationship of BMI >26 kg/m2 and OSA.1 There is a relationship between BMI and AHI as well as between BMI and excessive daytime sleepiness. Weight gain has consistently been associated with an increase in SDB. In one community-based longitudinal study, individuals whose weight increased by 10% were found to have a 32% increase in AHI and were at six times the risk for development of moderate or severe OSA, relative to individuals whose weight remained constant.8
Neck circumference has also been associated with increased risk of OSA,9,10 with a neck circumference of >43 cm in males being highly correlated with OSA.11 Neck circumference may correlate better with OSA than BMI and there may be a relationship between neck circumference and the severity of OSA.
Certain craniofacial features have been shown to increase the risk for OSA, including a high and narrow hard palate, elongated soft palate, small chin, and abnormal distance between upper and lower incisors. Tonsillar enlargement and narrowing of the airway by the lateral pharyngeal walls is also predictive of OSA.11 The Mallampati classification, which was developed by anesthesiologist to determine intubation risk, has also been used to grade degree of upper airway narrowing for OSA patients. Indeed, one study13 showed that on average, for every 1-point increase in the Mallampati score, the odds of having OSA increased >2-fold. Craniofacial structures also differ across racial groups, and these differences have also been associated with higher prevalences of OSA. In part because it decreases muscle tone in the upper airway, drinking alcohol can cause apneic episodes in otherwise normal-breathing individuals, and can worsen the severity of apneic events and oxyhemoglobin desaturation in apnea patients.14 Smoking and exposure to second-hand smoke have been associated with snoring and OSA.11
Numerous clinical instruments have been developed to assist in screening for OSA, including the Berlin questionnaire,15 STOP questionnaire (Table 1),16 and Sleep Apnea Clinical Score (SACS).17 These usually incorporate physical attributes like BMI or neck circumference with questions about snoring and witnessed apneas and/or presence of hypertension. The use of these instruments may assist physicians and other health care providers in determining the need for polysomnography.
Signs and Symptoms
A number of signs and symptoms are associated with OSA. The cardinal symptom of OSA is daytime sleepiness. This is due to the sleep fragmentation resulting from repetitive upper airway obstructions culminating in arousals. Not all patients will exhibit this symptom; some complain of chronic fatigue or tiredness and it has been suggested that the latter occur more in females.18 Differentiating fatigue and tiredness from sleepiness can usually be done by asking how likely someone is to “fall asleep” in certain situations. The Epworth Sleepiness Scale was developed for this purpose and is often used to assist in such determinations (Table 2).19
Snoring is common in OSA and frequently disrupts the bedpartner’s sleep; the bedpartner also may note breathing pauses during sleep. Concern on behalf of the bedpartners, therefore, is a common reason that OSA patients are brought to medical attention. Other common signs and symptoms include awakening with a headache,20 dry throat, gasping, or with a smothering sensation, and impotence.
Consequences and Associations
Numerous comorbid conditions have been associated with OSA. The association with hypertension has been extensively studied. Large epidemiologic,21,22 clinic-based,23,24 and case control studies25 have consistently shown that the risk for hypertension increases with increasing levels of apnea-hypopnea indices even after correction for a number of frequently encountered comorbid conditions such as obesity, age, and gender. A metanalysis examining 572 patients from 12 randomized, controlled trials did show that use of continuous positive airway pressure (CPAP) resulted in a net decrease of 1.69 mm Hg in 24-hour mean blood pressure, suggesting that treating OSA with CPAP can improve blood pressure.26
In patients who present to the hospital with transient ischemic attacks or stroke, the prevalence of OSA is very high.27,28 Data29 from Yale University showed that the OSA syndrome significantly increased the risk of stroke or death from any cause independent of other risk factors, including hypertension, in a population of >1,000 patients who had undergone sleep studies. Another study30 followed 132 patients after a stroke; those with OSA, both at baseline and after adjustments, were found to have a significantly increased mortality than those with central sleep apnea or no sleep apnea. Other studies31 have also shown that patients with concomitant stroke and OSA have a worse functional outcome.
OSA has also been associated with diabetes and glucose intolerance.32-34 This association is thought to be related to sleep fragmentation and deprivation as well as repetitive hypoxemia accompanying obstructive events.35 However, similar to hypertension, data regarding whether treatment of OSA will result in a change in glucose intolerance or insulin resistance is conflicting.36-38
In addition to hypertension, OSA has been associated with numerous cardiovascular disorders including cardiac arrhythmias, coronary artery disease, congestive heart failure, and pulmonary hypertension. The hypoxemia and hypercapnia that occur repetitively during the night have been shown to lead to systemic inflammation, oxidative stress, sympathetic activation, endothelial dysfunction and hypercoagulability.39 Arrhythmias are very common and include nonsustained ventricular tachycardia, sinus arrest, second-degree heart block, and premature ventricular contractions.40 Patients with severe OSA have been shown to have 2–4-fold higher risk of sleep-related complex arrhythmias.41 OSA also has been found to complicate heart failure in 11% to 37% of patients.42,43 Treatment of OSA independently has been shown to improve ejection fraction as measured by echocardiogram,44 and a recent study45 suggests that treatment of OSA may reduce mortality, although this has not been tested in a randomized trial.
Pulmonary hypertension is noted in ~15% of OSA patients. It is usually mild in nature or occurs only during exercise.46 Again, small trials have shown some improvement in pulmonary artery pressures after treatment with CPAP.47,48
The aim of treatment for OSA is to eliminate obstructed breathing events and snoring, maintain SaO2 >90%, and improve associated symptoms including, but not limited to, daytime sleepiness. OSA treatment options include weight loss, devices (positive airway pressure and oral appliances), and surgery.
It is well documented that even minor amounts of weight loss will decrease AHI in obese OSA patients.49 All obese OSA patients should be counseled on the benefits of weight reduction. Bariatric surgery can result in dramatic weight loss, reduced AHI, and improved arterial blood gases and pulmonary and cardiac function.50,51 These obesity operations are associated with low morbidity and mortality with operative death rates of ~1% and major complication rates of 5% to 8%.52 Bariatric procedures should be considered in morbidly obese patients with life-threatening OSA. However, recent data suggest that despite dramatic weight loss, most patients continue to experience OSA, albeit at a lesser severity.53
Nasal CPAP is the treatment of choice for patients with moderate or severe OSA. It works by creating a “pneumatic splint” in the upper airway and increases functional residual capacity, which improves ventilation perfusion matching and oxygenation.54 Nasal CPAP has been shown to be very successful in the treatment of OSA. It decreases or eliminates excessive daytime sleepiness, improves quality of life (even in mild cases), improves neurocognitive function, and decreases hospitalizations.55-58
Bilevel positive airway pressure (BPAP) varies pressure from inspiration to expiration. It has been shown that lower expiratory pressures can be used with AHI reductions similar to CPAP.59 BPAP, however, was found not to improve compliance compared to CPAP in one study.60 Other studies61,62 in hypercapnic patients with OSA who could not be adequately treated with nasal CPAP showed dramatic improvement in symptoms and arterial blood gases following treatment with BPAP. BPAP should be considered in patients with concomitant hypoventilatory syndromes (obesity hypoventilation or neuromuscular diseases) or those who require excessive CPAP pressures (>16 cm of H2O).
A variety of oral appliances have been invented to treat OSA. These devices alter the oral cavity to increase airway size and improve patency. Oral appliances have been shown to result in significant decreases in AHI (usually >50%) and improvement in oxygenation, although some patients do not improve and may worsen.63 Subjective improvement in sleepiness has also been consistently shown.64 When nasal CPAP has been compared to an oral appliance, the appliance does not reduce the AHI as much as nasal CPAP; however, patients had fewer side effects and preferred the oral appliance.65,66 In general, the higher the AHI, the less benefit obtained with oral appliances.63,67,68
Side effects of these devices include excessive salivation, transient discomfort after awakening, temporomandibular joint discomfort, and changes in occlusive alignment. Although complications are common, most are minor and appear to be infrequent.69,70 Minor changes have been noted on dental exams after prolonged use of the appliances.71
Regarding surgical procedures for OSA, a tracheotomy is the only procedure that is consistently effective; however, due to its morbidity, it usually is performed in situations in which the patient has life-threatening OSA with cor pulmonale, arrhythmias, and/or severe hypoxemia that cannot be controlled with nasal CPAP.
Uvulopalatopharyngoplasty (UPPP) is a surgical procedure which enlarges the airway by removing redundant tonsillar tissue, trimming tonsillar pillars, and excising the uvula and posterior soft palate. The “cure” rate of UPPP is usually quoted as <50%72 and one study73 showed that 31% of patients actually had worse OSA after undergoing UPPP. Use of an anatomy-based staging system has been shown to improve treatment outcomes.74
Maxillomandibular advancement (MMA) has being used as a treatment for OSA. In this procedure, both the maxilla and mandible are advanced with a sliding osteotomy; the mandible advancement is more than the maxilla to increase the posterior airway. The success rates of this surgery vary; in most cases, MMA is conducted as part of a stepwise program, usually following an ineffective UPPP.75,76 Other surgical procedures are also available for OSA such as Pillar implants, laser-assisted UPP, and genioglossus suspension. However, none has a high success rate or evidence for long-term efficacy.
The Relationship of OSA with Psychiatric Symptoms and Disorders
The considerable overlap in symptoms of sleep-disordered breathing and psychiatric disorders generates numerous challenges in relation to the identification, evaluation, diagnosis, and treatment of individuals experiencing the effects of diseases in one or both of these clinical realms.77 Psychiatric disorders and sleep-disordered breathing independently may result in significant impairment in daytime functioning, health-related quality of life, cognitive performance, and many other parameters of mental health. The negative synergistic effects resulting from comorbidity may be exacerbated further by inadequate treatment of either and potentially by the effects of certain psychotropic medications. The mental health impairments of sleep-disordered breathing foster misdiagnosis and missed opportunities for optimal treatment of comorbid conditions.
Patients with OSA, whether or not it is identified, may complain of disrupted nighttime sleep, excessive daytime sleepiness, fatigue, poor concentration and memory, irritability, an impairment in daytime functioning, an inability to enjoy usual activities, and a general sense of discouragement.78 They may express feelings of discouragement and depression, and may question the value of living with their burdensome and often unexplained symptoms. Does the OSA mimic a major depressive episode (MDE) or does the constellation of mood disorder symptoms demonstrate comorbidity of OSA and major depressive disorder (MDD)? Both are possible.
Exactly how sleep apnea impairs cognitive and emotional functioning has not been fully explained. Clearly, repeated sleep disruptions and a decrease in the total sleep time can cause daytime sleepiness with poor attention and concentration, and perhaps lead to low energy, irritability, and moodiness. It has been suggested that OSA-related sleep stage alterations, such as decreased slow-wave and rapid eye movement (REM) sleep, and recurrent oxyhemoglobin desaturations further exacerbate mental impairment and increase the risk for depressive disorders. Furthermore, shared predispositions may contribute to the high prevalence of OSA and depressive symptoms. Schroeder and O’Hara79 note that serotonin has key roles in the neurobiology of depression and arousal, but also in the control of upper airway muscle tone during sleep. Decreased serotonin activity may increase the risk of developing depressive symptoms and, perhaps, increase the probability of pharyngeal collapsibility during sleep.
Problems arise when a mood disorder or related psychiatric condition is diagnosed, but the possibility of sleep-disordered breathing is not considered as a possible contributor to nighttime sleep disruption or daytime fatigue and sleepiness. Although selected symptoms may improve with antidepressant therapy, the patient could be labeled as treatment resistant due to limited improvement in core daytime and nighttime symptoms. Accordingly, sleep-disordered breathing should always be in the differential diagnosis of patients with complaints of disrupted nighttime sleep or excessive daytime sleepiness. This is especially important since psychotropic medications may both directly and indirectly exacerbate sleep apnea.
General Population Studies
Representative population studies have explored the presence of sleep-disordered breathing and symptoms representing psychiatric and medical disorders. Ohayon80 performed a large-scale, Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition,81 diagnosis-based structured telephone survey of 18,980 randomly selected individuals in four European countries. The presence of OSA specifically was reported by 2.1% of the subjects, and in general 4.6% reported any type of breathing-related sleep disorder, although these were not objectively confirmed by polysomnography. An MDE was diagnosed in 4.3% of the overall sample. Psychotic symptoms, such hallucinatory or delusional experiences, were reported by 4.8% of the individuals as occurring at least several days per week. The prevalence of breathing-related sleep disorders were markedly elevated among subjects with MDEs with psychotic features (19.6%) and in those with MDEs without psychotic features (17.7%). A breathing-related sleep disorder was present in 6.2% of the subjects with psychotic symptoms who did not have an MDD diagnosis. The MDD diagnoses and presence of psychotic symptoms independently remained strongly associated with the disordered breathing when multifactorial analyses controlled for obesity and hypertension.80
A population-based epidemiologic study by Peppard and colleagues82 found the presence of a causal link with a sleep-related breathing disorder increasing the probability of depressive symptoms. The sleep-related breathing disorder diagnoses and severity ratings were based on sleep laboratory polysomnographic recordings and the presence of depression determined by Zung depression rating scores in 788 men and 620 women participating in the Wisconsin Sleep Cohort Study. Statistical models adjusting for numerous variables (eg, age, BMI, antihypertensive use) demonstrated that depression (Zung score ≥50) was associated, respectively, with odds ratios of 1.6, 2.0, and 2.6 for subjects with minimal, mild, and moderate or worse sleep-related breathing disorders. A longitudinal analysis82 showed that an increase of one level of disordered breathing severity was associated with a 1.8-fold increase for developing depression.
Surveys of OSA Patients
The presence of psychiatric symptoms also has been surveyed in populations of patients diagnosed with OSA in a large number and wide variety of studies.83 For example, Sharafkhaneh and colleagues84 analyzed Veterans Health Administration healthcare records of >4 million patients and identified sleep apnea diagnoses in 118,105 of the individuals. The records indicated the presence of psychiatric symptoms with disproportionately higher prevalence rates. Comorbid diagnoses among the sleep apnea patients included depression (21.8%), anxiety (16.7%), posttraumatic stress disorder (PTSD; 11.9%), psychosis (5.1%), and bipolar disorder (3.3%).
McCall and colleagues85 examined depressive symptoms using the Beck Depression Inventory in 92 men and 29 women who had been diagnosed with moderate-to-severe OSA. At least mild degrees of depression were present in 44.6% of patients, representing 62% of the women and 39% of the men. At least a moderate level of depression was found in 11.6% of patients, including 28% of the women and 6% of the men. A significant relationship between daytime sleepiness and depression was not evident in the patient population.
Schizophrenia and OSA
The relationship of schizophrenia and sleep-disordered breathing is complicated by numerous factors. People with schizophrenia prior to treatment have increased risk for developing obesity and metabolic dysfunction (eg, type 2 diabetes and metabolic syndrome), which may be exacerbated further as a result of psychiatric medications. Weight gain significantly increases the likelihood of OSA. Moreover, sleep-disordered breathing independently increases the risk of type 2 diabetes and hypertension. Profound increases in morbidity and excess mortality may be especially problematic among schizophrenia patients.
Metabolic abnormalities, such as impaired carbohydrate metabolism and an increased risk for the development of type 2 diabetes, are more likely to be present among schizophrenic patients compared with the general population. Increased visceral adiposity and the predisposition for diabetes has been demonstrated in research studies86,87 conducted prior to the introduction of antipsychotics and with newly diagnosed and untreated schizophrenic patients.
Weight gain among schizophrenia patients may be exacerbated with the use of antipsychotics, especially atypical agents clozapine and olanzapine.88 It has been argued that atypical antipsychotic-induced weight gain relates to antihistaminic effects from selective activation of hypothalamic adenosine monophosphate-activated protein kinase.89
The relationship of obesity and antipsychotic use in primary care settings was examined in a longitudinal, retrospective analysis90 of 42,437 patients, of which 1.3% were taking an antipsychotic. The medications were approximately equally divided among the typical and atypical antipsychotics. Significantly increased obesity, diabetes, hypertension, and dyslipidemia all were associated with the use of antipsychotics.
Several studies have explored the presence of OSA in populations of patients diagnosed with schizophrenia. Winkelman and Lajos91 retrospectively evaluated 397 psychiatric inpatient consultations to the Sleep Disorder Program at McLean Hospital. They found that the rate of OSA was disproportionately higher among male and female schizophrenia patients, in contrast with those diagnosed with depression, bipolar disorder, PTSD, and substance abuse. The severity of the OSA also was greater for the schizophrenia patients. The authors91 speculate that medication-related weight gain, poor nutrition, and inadequate exercise contributed to the higher severity in the schizophrenia patients. An increased prevalence of sleep apnea was also found by Ancoli-Israel and colleagues,92 who prospectively studied 52 older schizophrenia patients (mean age=59.6 years) with home recordings of their sleep electroencephalograph, respirations, and leg movements. A relatively high percentage of these patients (48%) had at least 10 respiratory events per hour.
OSA Treatment in Psychiatric Patients
The strategy recommended for the treatment of OSA depends upon the patient’s clinical characteristics, including physical features (eg, upper airway anatomy, obesity), sleep laboratory testing results, and the ability of the individual to adhere to the therapy. The symptoms of patients with major mental illnesses also may influence the decisions regarding treatment approaches. Many psychiatric patients will benefit from weight loss and related strategies to improve any metabolic abnormalities. Longitudinal monitoring of weight, waist circumference, blood pressure, fasting plasma glucose, and the fasting lipid profile are recommended for patients on antipsychotics.
The treatment of OSA may be associated with a broad spectrum of beneficial effects in relation to psychiatric symptoms and cognitive functioning. Most obviously, improvements in nighttime sleep quantity and quality should promote alertness and help facilitate greater physical activity. However, psychiatric and other cognitive parameters also may improve with effective treatment of OSA.
The potential benefits of OSA treatment on psychiatric symptoms have been examined in several studies of different therapeutic modalities. Generally, the results support improvement in depressive symptoms, but there is limited literature regarding psychotic symptoms. Millman and colleagues93 surveyed 55 OSA patients with the Zung Self-Rating Depression Scale and found that 45% had scores signifying depression (≥50). The patients in the depression group had higher rates of sleep apnea. There also was a significant decline in the depression score for the group of 11 OSA patients initially in the depressed group that were treated with nasal CPAP.
In a Japanese study,94 measures of mood, daytime sleepiness, and quality of life were assessed in 38 control subjects and 132 patients with severe OSA. At baseline, the OSA patients had worse scores in all of these parameters. The OSA patients were treated with nasal CPAP and were reassessed after 8 weeks of treatment. The CPAP use was associated with significant improvements in mood, sleepiness, and quality of life.
Schwartz and colleagues95 studied OSA patients treated with nasal CPAP and who demonstrated a significant disordered-breathing response to the treatment. Their mood was assessed with the Beck Depression Inventory at the beginning of CPAP treatment and with short-term (4–6 weeks) and long-term (~1 year) follow up. The study found significant and sustained improvement in mood in the patients continuing to use CPAP regularly.
Strakowski and colleagues96 found improvements in manic symptoms in four patients described as having treatment-resistant mania and OSA when treated with nasal CPAP. At the opposite end of the mood spectrum, Krahn and colleagues97 reported a case study of a severely depressed and suicidal man whose psychiatric symptoms resolved rapidly with the initiation of nasal CPAP for his newly diagnosed severe OSA.
While most psychiatric outcome studies have investigated the potential benefits of CPAP in OSA patients, a few reports have examined surgical approaches. In a prospective longitudinal Taiwanese study98 of 84 OSA patients, mental health scales were completed by the patients before and after extended uvulopalatal flap procedures. The baseline mental health scores of the patients were below the national average, but improved to a moderate degree postoperatively. Li and colleagues98 reported a case study of a 30-year-old man with recurrent psychotic episodes and intellectual impairment. There was a complete resolution of the OSA with a tonsillectomy and at a 2-year postoperative visit there had been a full remission of the psychotic symptoms, but persistent intellectual impairment.
OSA Treatment Challenges Among Psychiatric Patients
The first obvious challenge of OSA treatment among psychiatric patients is case identification. Sleep disturbances and daytime symptoms associated with OSA often are assumed to be psychiatric in origin by patients, as well as by their families and healthcare providers. Furthermore, excessive daytime sleepiness may be attributed to effects of sedating antipsychotic, antidepressant, anxiolytic, and mood-stabilizing medications. Disabled patients not following a regular schedule will not necessarily experience daytime sleepiness and impairment as a practical problems requiring treatment and, therefore, may not seek help. Patients with poor insight and motivation, perhaps exacerbated by their illnesses, may not pursue or even may resist efforts to evaluate possible sleep disorders with sleep laboratory testing and subsequently cooperate with recommended treatments. Symptoms of both anxiety and depression have been associated with decreased CPAP use.99 Educational efforts with patients and their families should help optimize the management of people with OSA and comorbid psychiatric disorders. Wells and colleagues100 noted that the subjective benefits and CPAP may be diminished in patients with depressive symptoms and, therefore, may undermine adherence with nightly CPAP use. Broad-based support and encouragement may be necessary to promote CPAP adherence with selected patients.101
The treatment of patients at risk for sleep-disordered breathing with antipsychotics necessitates a careful risk-benefit analysis. The antipsychotic risks of weight gain and metabolic abnormalities must be weighed against their therapeutic efficacy in patients with mood disorders or with schizophrenia and related psychotic disorders. Medication-related sedation and weight gain independently can exacerbate OSA. Weight loss strategies, appropriate nutritional guidelines, and routine laboratory screening for metabolic abnormalities may all be beneficial for patients prescribed antipsychotics, particularly those with the greatest risk for weight gain, abnormal carbohydrate metabolism, and hyperlipidemia.
Sleep-disordered breathing is a common problem in the general population that in some cases shares overlapping symptoms with mood, anxiety, and psychotic disorders. The result may be a complex clinical presentation with diagnostic confusion and significant treatment challenges. Mental health professionals should be mindful of possible sleep-disordered breathing in patients with disrupted sleep or daytime sleepiness. Patients with chronic mental illnesses should be screened for possible sleep disorders. Conversely, healthcare professionals managing patients with sleep apnea should evaluate patients for symptoms associated with psychiatric disorders. Optimized management of both sleep and psychiatric disorders likely will be necessary to allow patients the maximum opportunity for recovery. PP
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