Clinical observations have shown that patients who present with psychological characteristics indicating depression, may suffer from obstructive sleep apnea.

Humans spend approximately a third of their lives sleeping, yet most do not think much about the quality of their sleep (or the fact that poor sleep can impair day-to-day activities and the level of their performance). Feeling chronically tired, fatigued, sleepy, irritable, disinterested, unmotivated, and even depressed may be the consequences of a sleep disorder, not just the results of stress, age, or weight gain–all of which seem to be typical excuses for feeling tired all the time.

The National Sleep Foundation1 conducted a poll in 1998 to survey US residents’ knowledge and attitudes concerning sleep, sleep habits, and sleep disorders. Findings showed that many had little or no idea of the importance of sleep. A striking 86 percent of the adult population polled failed a 12-question sleep-knowledge test. The poll also found that 32 percent of respondents slept 6.5 hours or less per night during the work week, and 64 percent slept less than the recommended 8 hours.1 It is not surprising that 63 million US adults suffer from moderate to severe levels of daytime sleepiness, and 58 million experience excessive daytime sleepiness to a point that interferes with daily activities.2 It is amazing that only 17 percent of those who reported routinely feeling sleepy during the day consulted a physician.2

One would think that the major industrial disasters that have been officially cited as having fatigue-related contributing factors would create more awareness of sleep disorders.2 Sleep disorders, sleep deprivation, and sleepiness have added $15.5 billion to the annual US health care bill,2 and this figure does not take into account the indirect cost of sleepiness in terms of decreased productivity, work-related accidents, and property loss. The total is an unbelievable $150 billion,3 and the costs of suffering and loss of life are unknown.

Fortunately, with the founding of the American Sleep Disorders Association in 1987 (followed by the founding of the Sleep Research Society and the National Sleep Foundation), progress is being made toward paying off a very serious national sleep debt. Sleep medicine is now a recognized specialty within the American Medical Association, and a national research center on sleep disorders has been established within the National Heart, Lung, and Blood Institute. As a result of sleep awareness efforts, there has been increased funding for sleep-related research at the national level, and support has been given to federal public awareness campaigns about sleep and the consequences of sleep deprivation.2 Incentives have been provided for federally funded education programs about sleep that target primary care practitioners, researchers, accident investigators, and law-enforcement officials.2 Additional legislative support has enabled medical schools to increase training in sleep.

Despite these measures, an estimated 70 million US residents suffer from sleep problems, with approximately 40 million having a diagnosable and treatable sleep disorder, yet 95 percent remain undiagnosed.3 Sadly, the result is a population of exhausted, sleepy people who needlessly struggle through the day and are at risk of falling asleep in potentially dangerous situations.

The fairly rapid growth of sleep disorders centers in recent years has been helpful in providing services to evaluate, diagnose, and treat a range of more than 80 sleep disorders. One of the most common sleep disorders is obstructive sleep apnea (OSA), a serious and potentially life-threatening breathing disturbance during sleep. Approximately 30 million US residents suffer from OSA,3 which is characterized by varying degrees of snoring interrupted by partial or complete upper-airway obstruction caused by a combination of physical, structural, and anatomic features.

Upper-airway obstruction is more common in a person who has a short neck with a circumference of more than 17 in for men or 16 in for women. A thick tongue, a narrow soft palate, a small or crowded posterior pharyngeal opening, an elongated or wide uvula, large tonsils, and an overbite can be additional risk factors. Sleep position, sleep stage, and alcohol/sedative use play a role in snoring and OSA. For instance, a person who is sleeping on his or her back in rapid eye movement or dream sleep and who has had an alcoholic beverage before bedtime is more likely to snore and have apneic events. This is primarily because the muscles of the upper airway and tongue and the tissues of the soft palate are more likely to become relaxed and unstable and to collapse in the airway while the individual is supine. In addition, during this stage of sleep, muscles are essentially paralyzed, even without the extra sedative effect of alcohol. This is not to say that all of those who use alcohol and sleep on their backs during dream sleep will have OSA, but these factors certainly do increase that possibility, especially in known snorers.

Diagnostically, OSA is considered medically significant if airflow is partially or completely stopped for a minimum duration of 10 seconds, repeated at least five times per hour of sleep.4 Whether the event is hypopneic or apneic, the result is usually brief oxygen desaturation (a minimum drop of 2 percent, not always to a saturation level of less than 90 percent) along with an associated arousal from sleep.4 The more often these respiratory abnormalities occur, the less restorative the sleep becomes, increasing the potential for fatigue, sleepiness, and other daytime manifestations. A consequence less frequently recognized by the person who has OSA is an increased cardiovascular workload, which increases the risk of hypertension, myocardial infarction, cerebrovascular accident, and congestive heart failure.5

The usual clinical picture of a person with OSA is an overweight, middle-aged male who snores and gasps during sleep. It has been estimated that 2 percent to 4 percent of middle-aged men and 1 percent to 2 percent of middle-aged women have OSA.6 This is probably an underestimate, partly due to missing those who do not fit the stereotypical description. Some of the most severe cases of OSA have been observed in thin people with high, narrow hard palates, overbites, or underbites.7 Presenting complaints may include frequent nocturnal awakenings (often in association with nocturia or gastro-esophageal reflux), morning headaches, daytime fatigue/sleepiness, and decreased libido. Weight gain seems to be a problem for those with OSA, with a reported two thirds being obese (20 percent over ideal body weight).7 Many OSA patients are hypertensive, and some continue to experience poorly controlled blood pressure even while using antihypertensive medications. In severe cases, increased lower-extremity edema and shortness of breath during the day may indicate the progression of congestive heart failure and, in some situations, cor pulmonale.

After referral, most sleep centers will schedule an initial consultation to determine whether a sleep disorder should be suspected. If so, overnight polysomnography in an outpatient laboratory setting is arranged, followed by a return visit to discuss results. If OSA is diagnosed, treatment will depend on its severity. Conservatively, all patients are encouraged to sleep on their sides, to avoid alcohol and sedative medication, to maintain a routine sleep schedule with 8 hours of sleep per night, and to follow a healthy diet and exercise program. Most cases of OSA can be treated noninvasively using continuous positive airway pressure (CPAP) or bilevel/variable positive airway pressure (BPAP/VPAP). Invasive surgery involving the soft palate and uvula (uvulopalatopharyngoplasty, UPPP, or laser-assisted uvulopalatoplasty, LAUP) may be treatment considerations. The UPPP success rate is about 50 percent.8 Of those who do not respond to UPPP, the site of obstruction is usually below the soft palate and uvula. The result may be improved snoring with silent apneas. In these and other select cases (provided CPAP/BPAP/VPAP therapy is refused or not tolerated), more extensive surgery of the maxilla, mandible, and hyoid bone may be considered, to correct jaw abnormalities or to open a narrow posterior pharyngeal airway at the base of the tongue.8

Diagnosing OSA is actually very simple. The difficult part is recognizing it initially and seeking appropriate evaluation. Because of the insidious nature of OSA, its effects often go unnoticed until sleepiness begins to interfere with work performance, family life, social activities, and/or the ability to stay awake while driving. As OSA progresses, sleepiness becomes difficult to control and daytime manifestations such as cognitive dysfunction, poor concentration, decreased alertness, memory loss, impaired judgement, anxiety, paranoia, irritability, and depression may appear.7,9 Unfortunately, these symptoms overlap with those of other medical and psychological disorders, and an underlying sleep disorder is often missed.

Depression is fairly common and is likely to occur during the third and fourth decades of life, at about the same time as OSA. Similarities in the clinical presentation of both disorders include insomnia, frequent awakenings, fragmented sleep, and sleep loss.10 Likewise, fatigue, sleepiness, poor concentration, decreased motivation, lack of energy, and loss of interest seem to be shared symptoms. Given these components in common, there is probably an extraordinarily high amount of misdiagnosis (and, in consequence, misdirected therapy). It would be beneficial for clinicians to recognize the relationship between OSA and depression before diagnosing a depressive disorder presumptively and, perhaps, prescribing antidepressant medication inappropriately. Unfortunately, consideration of an OSA diagnosis may emerge only after an unsuccessful response to treatment for depression.11

In view of the strongly related symptoms of OSA and depression, it stands to reason that a person with OSA may experience depression as well. Few systematic controlled studies have been published, but clinical observations have shown that OSA patients often present with certain psychological characteristics.

Jennum and Sjol12 investigated the relationship between snoring, OSA, and cognitive complaints and found OSA to correlate positively with concentration problems, but not with memory complaints. Beutler et al,13 using the Minnesota Multiphasic Personality Inventory, found higher depression scores in a group of patients with severe OSA. Cassel14 studied patients with OSA and concluded that fatigue, sleepiness, and impaired alertness should be considered effects of OSA, not of depression. Research15 on OSA and quality of life found that OSA patients have decreased quality of life, characterized by sickness-related behavior, impaired function due to ill health, and poor psychologic adjustment to illness.

As it is a common manifestation of OSA and depression, daytime sleepiness was reviewed in order to evaluate the tendency to fall asleep under certain circumstances. The Epworth Sleepiness Scale (ESS) is widely used in sleep centers to assess a patient’s subjective level of sleepiness. The ESS is a rating scale for eight situations routinely encountered in daily activities. Research16 using this tool revealed that the sleepiest subjects were to be found among those with OSA.

Self-reported depressive symptoms, mood ratings, and treatment outcomes in sleep-disorder patients have been studied, and findings17 have revealed that the depression found in OSA patients is not a primary depression; rather, it is a medical depression. In a study18 of 55 patients with OSA, 45 percent were found to have scores, on a self-reported depression scale, that were consistent with depression. The investigators concluded that the severity of apnea appeared to be related to that of depressive symptoms, which could be alleviated by appropriate treatment of the apnea.

Kaplan,11 in a study of the link between OSA and depression, reported the overlapping symptoms of the two disorders as confusion, lethargy, poor concentration, memory loss, mood swings, irritability, and anger. Kaplan wrote, “OSA itself can cause depression . . . patients feel that they are in a continual tired haze, losing control of their lives and fearing senility or madness.”11 This may seem extreme, but it may be all too true in severe cases of OSA.

Nearly all descriptions of OSA’s behavioral sequelae found in the literature focus largely on cognition and the effects of daytime sleepiness. Research results have been contradictory, and population variables have been unappreciated. The most consistent findings19,20 related to the CPAP treatment of OSA were reported improvements in cognition, personality, psychosocial factors, and depression. Most studies, however, failed to determine the existence of a psychopathologic disorder or even to identify a level of impairment. Rather, they showed certain psychopathologic characteristics in OSA patients and a decline in symptoms after the initiation of CPAP therapy.

This result was confirmed by unpublished 1997 data from Audubon Hospital-Sleep Disorders Center, Louisville, Ky. Data were obtained retrospectively from 349 patient charts; these data included a respiratory disturbance index (for OSA diagnosis), depression scores from the Beck Inventory (BI), ESS scores, body mass index (BMI), and CPAP treatment levels. If available, ESS and BI scores for the period after CPAP initiation were obtained.

This study was unable to correlate OSA and depression. The research did, however, support previous findings regarding the predominant characteristics of OSA patients: male gender, a mean age of 45 to 50 years, an increased BMI, and significant subjective sleepiness. Depression and sleepiness scores also improved after CPAP treatment, suggesting that patients with OSA have a tendency for their depressive manifestations and sleepiness to return to baseline levels following treatment for OSA.

Overall, the majority of OSA patients do not suffer from clinical depression (using the criteria of Beck et al21) as a result of having OSA. This does not imply that these patients lack symptoms and characteristics associated with depression; rather, they do not reach a pathological level. Because depression and OSA may initially present in the same manner, a focused physical examination may be the determining factor, with emphasis placed on assessing the nasal/oropharyngeal airway, neck, jaw, and overall body habitus. By asking the patient (and his or her bed partner) a few simple questions about sleep–in addition to using subjective screening tools such as depression and sleepiness scales–during routine physical examinations, clinicians will find that sleep disorders may be detected easily. This certainly would be a large contribution toward paying off the national sleep debt.

Pamela A. McCullough, MSN, ARNP, is an adult nurse practitioner at Norton Audubon Hospital-Sleep Disorders Center, Louisville, Ky.

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