Clinical Practice Guideline



Developed for the

Aerospace Medical Association

by their constituent organization

American Society of Aerospace Medicine Specialists


Overview: The common thread running through most sleep disorders is insufficient quantity or quality of sleep, which leads to excessive daytime sleepiness and diurnal impairment of alertness and cognitive function.  While pathologic sleep disorders command the greatest attention, one of the commonest causes of excessive sleepiness, particularly in young adults, is poor sleep hygiene.  Chronic sleep deprivation due to individual behavior patterns may cause as much debility as a pathologic disorder.  While the definition of sufficient sleep varies, one should generally not work up a complaint of hypersomnolence unless the individual is attempting to get six to eight hours of sleep for a twenty-four hour period, on a reasonably regular schedule.  Careful attention must also be paid to alcohol use, since heavy use may disrupt sleep patterns, and may induce or worsen sleep apnea.


In civilian practice, insomnia is the commonest sleep complaint.  The pattern of disturbance is usually helpful; chronic difficulty initiating sleep is most often associated with anxiety or stress, while early morning awakenings suggest depression.  Frequent brief awakenings throughout the night are more suggestive of sleep-disordered breathing.


While narcolepsy was the classic sleep disturbance, the first description dating back to 1880, it is actually relatively rare.  Narcolepsy is an exception to the rule noted above; narcoleptics tend to have a disrupted pattern of sleep, but the hypersomnolence is not simply related to sleep deprivation.  Instead, narcolepsy appears to be a neurologic disorder characterized by the early onset of rapid eye movement (REM) sleep, with an age of onset usually in childhood or adolescence.  The intrusion of REM patterns into different parts of the sleep-wake cycle may lead to unusual manifestations, such as hypnagogic (predormital) and hypnopompic (postdormital) hallucinations, and sleep paralysis.  While classic, these manifestations usually occur only in about a quarter of narcoleptic patients.  The essential disorder in narcolepsy is nearly uncontrollable attacks of sleepiness leading to brief naps, from which they usually awake feeling refreshed.  Narcoleptics also experience episodic lapses of consciousness typified by automatic behavior and amnesia.  Most subjects if questioned carefully have also had some form of cataplexy, characterized by loss of postural control (e.g., head drooping, knees buckling, even falling) associated with laughter or other emotions.


Obstructive sleep apnea (OSA) has emerged as a major sleep disorder.  The best available estimates of prevalence suggest that among American adults ages 30 to 60, 4% of males and 2% of females are affected.  Prevalence among military aviators is unknown, but because obesity is much less common in that population, the rate is likely to be considerably lower.  The key in OSA lies in the pattern of muscle activity that occurs in different stages of sleep.  While diaphragmatic activity is largely unaffected by sleep stage, muscle tone in the upper airway is considerably depressed in stages III and IV of non-REM sleep, a pattern which continues throughout REM periods.  This loss of muscle tone leads to increased resistance to airflow through the upper airway during inspiration; in expiration, on the other hand, positive intraluminal pressure tends to stent the pharynx open.  A modest amount of obstruction results in snoring, while a greater amount of obstruction may lead to hypopnea (>50% reduction of airflow for >10 seconds) or apnea (total cessation of airflow for >10 seconds).  The disordered breathing causes either awakening or a lighter stage of sleep, which in turn results in fragmented sleep, while apneic episodes of sufficient duration may produce arterial hypoxemia.  More recently it has been recognized that the increase in airway resistance itself, even in the absence of an actual decrease in airflow, may be enough to cause sleep fragmentation, a phenomenon known as the upper airway resistance syndrome (UARS).  While the existence of this entity has been documented by esophageal manometry, with awakenings correlated to excessively negative intrathoracic pressures, the use of an esophageal balloon is too invasive for most clinical situations.  Instead, UARS is usually diagnosed presumptively when the snoring patient with hypersomnolence and sleep fragmentation responds to a diagnostic trial of nasal CPAP during polysomnography.


The predominant symptom is typically daytime sleepiness; the greater the degree of sleep apnea, the more likely the individual is to fall asleep, especially when involved in boring or repetitious activity.  He or she may feel an urge to nap, but unlike in narcolepsy these naps are usually not refreshing, since the disordered breathing occurs there as well.  Sleep apnea may be associated with restless nocturnal behavior, choking sensations resolving immediately upon awakening (as opposed to esophageal reflux with aspiration), vivid dreams of strangulation/drowning, and in severe cases with morning headache (due to hypercarbia).  While these symptoms are classic for OSA, the only symptom in moderate cases is typically hypersomnolence of varying degree.  Recent development or worsening of symptoms is frequently due to weight gain.  When symptoms are variable, particularly when a symptomatic patient has a negative polysomnogram, one should pay particular attention to the alcohol history.


Sleep apnea is clearly associated with hypertension.  Sleep apnea patients have a 41% prevalence of systemic hypertension, about double what would be expected.  The cause is unclear, though it may be due to sympathetic overstimulation from multiple arousals.  Nocturnal hypoxia may occasionally result in cardiac arrhythmias, including ventricular tachycardia, a phenomenon primarily seen in older patients.  Those with severe sleep apnea may develop diurnal hypoxia and hypercarbia, and eventually pulmonary hypertension and right-sided congestive heart failure.


Diagnosis of pathologic sleep disorders requires polysomnography (PSG) at a sleep disorders laboratory.  This involves monitoring at least one night’s sleep with electroencephalography, submental electromyography, electro-oculography, measurements of airflow and thoracic/abdominal excursion, and oximetry.  Usually electrocardiography and video monitoring are performed as well.  If the polysomnogram suggests narcolepsy, multiple sleep latency testing needs to be performed the following day.  The overwhelming problem with sleep laboratories is the huge degree of variability of results.  Even accreditation is no guarantee, because standards for interpretation have been difficult to establish.


While multiple treatment options usually exists for sleep apnea, not all are compatible with aviation or worldwide duty.  Positional therapy is likely to be effective only in mild OSA, and even then only when a significant positional component is identified during the sleep study.  Medications have largely been ineffective for OSA, and those that have been tried are not waiverable drugs in and of themselves.  Oral appliances, which attach to the teeth or more rarely the tongue to advance the lower jaw, are frequently effective in moderate OSA, and are fully waiverable.  Nasal continuous positive airway pressure (CPAP), which acts as a pneumatic stent to maintain airway patency, is usually effective for any degree of sleep apnea.  Compliance with long-term use has been a problem.  For active duty personnel, the more immediate problem is that the use of CPAP is incompatible with worldwide qualification, since the device needs a continuous power supply.  Several surgical options are available for OSA, including such procedures as palatoplasty and mandibular advancement; if effective at controlling the problem, any of these is waiverable.  Tracheostomy would obviously not be waiverable, but is no longer performed for OSA.  Narcolepsy is controlled by medications, but neither the disease nor the medications are waiverable for military aviation.


Aeromedical Concerns: Any of the sleep disorders above may result in excessive daytime sleepiness and an inability to maintain the alertness necessary for safety while flying.  Cognitive function and neuromuscular coordination may both be affected by the sleep disorder and/or the treatment modalities used.  When called upon to perform in operational situations with less than optimal sleep, those with OSA are already sleep deprived.  Furthermore, normal individuals when sleep deprived respond by altering sleep patterns, e.g., going into REM early or even immediately, but in the individual with OSA those deeper stages of sleep are fragmented by disordered breathing.  Persons with a sleep disorder may have more than the usual difficulty in adjusting to the circadian rhythm disruption which occurs with travel across time zones.  This would present an additional hazard to a flier who may travel or deploy several time zones away and would still be expected to perform flying duties.


Medical Work-up: If there is a high index of suspicion of a sleep disorder, it is very important that the aviator obtain a sleep study from an accredited sleep center.  Any aviator with a documented sleep disorder will require a thorough aeromedical evaluation prior to returning to flying duties.  That evaluation should include a polysomnography at a sleep laboratory and neuropsychologic testing to evaluate cognitive function.


If an aviator is diagnosed with OSA, it is reasonable to treat him or her with an oral appliance to try to control the problem prior to the waiver evaluation.  However, given the extreme variability in civilian sleep studies, it is difficult to make the same recommendation concerning surgery.  If the aviator does not have symptoms clearly associated with the diagnosis, the disorder should be confirmed at a sleep center before considering a surgical procedure.


If narcolepsy is diagnosed or considered, it may be useful to get a second opinion as this often will result in permanent disqualification from all flying duties.


Aeromedical Disposition (military): Aviators with mild documented OSA are waiverable for full flying duties.  Aviators with moderate or severe OSA must be controlled by either an oral appliance or surgery before waiver will be considered.  However, aviators with mild to moderate OSA may be considered for waiver if results of neuropsychologic testing are normal.


Aeromedical Disposition (civilian): In the case of a civilian airman, they may present for examination after they have already been diagnosed with a sleep disorder. If they do, then they need to provide a current status report and a Maintenance of Wakefulness Test (MWT). This is a test where the airman is monitored in a dark room for four periods spread out throughout the day.  There is a twenty and forty minute version and both are acceptable.  The airman cannot use artificial means to stay awake during the test. If the airman falls asleep for more than a total of 90 seconds during the four study periods they are considered to have failed the test for FAA purposes. 


The FAA accepts the following treatments: CPAP, BiPAP, oral fixation device, Uvuloplasty (UPPP), and Nasal septal surgery.  They do not accept any medications such as Provigil nor do they accept the use of tennis balls sewn into pajama top.  


Aeromedical Disposition (NASA): OSA and any sleep disorder that may interfere with the performance of duties are disqualifying for spaceflight duty.


Waiver Experience (military): A military database was queried with data going back to 2001.  There were 128 aviators with waiver requests for the diagnosis of sleep apnea.  Of that total, 48 were disqualified for flying duties, one of whom had earlier been granted a waiver.  This is an approval rate of 62%.


Waiver Experience (civilian):  As of 2007 there are 898 first-class, 873 second-class and 2,184 third-class airmen currently issued with sleep apnea diagnosis.


Waiver Experience (NASA): There are no current waivers for OSA, though a history of OSA would be considered if the astronaut had successfully treated the condition through weight loss or surgery. Other sleep disorders would not be waiverable if they interfere with crew duties.




1.  American Thoracic Society: Medical Section of the American Lung Association.  Sleep apnea, sleepiness, and driving risk.  Am J Respir Crit Care Med.  1994; 150:  1463-73.


2.  Barthel SW, Strome M.  Snoring, obstructive sleep apnea, and surgery.  Med Clin N Am.  1999; 83:  85-96.


3.  Findley L, Unverzagt M, Guchu R, et al.  Vigilance and automobile accidents in patients with sleep apnea or narcolepsy.  Chest.  1995; 108:  619-24.


4.  Fleetham JA, Ferguson KA, Lowe AA, Ryan CF.  Oral appliance therapy for the treatment of obstructive sleep apnea.  Sleep.  1996; 19(10):  S288-S290.


5.  Hudgel DW.  Treatment of obstructive sleep apnea: a review.  Chest.  1996; 109:  1346-58.


6.  Levy P, Pepin JL, Mayer P, et al.  Management of simple snoring, upper airway resistance syndrome, and moderate sleep apnea syndrome.  Sleep.  1996; 19(9):  S101-S110.


7.  Man GCW.  Obstructive sleep apnea: diagnosis and treatment.  Med Clin N Am.  1996; 80:  803-20.


8.  Naegele B, Pepin JL, Levy P, et al.  Cognitive executive dysfunction in patients with obstructive sleep apnea syndrome (OSAS) after CPAP treatment.  Sleep.  1998; 21:  392-7.


9.  Rühle KH, Schlenker E, Randerath W.  Upper airway resistance syndrome.  Respiration.  1997; 64(Suppl I):  29-34.


10.  Valencia-Flores M, Bliwise DL, Guilleminault C, et al.  Cognitive function in patients with sleep apnea after acute nocturnal nasal continuous positive airway pressure (CPAP) treatment: sleepiness and hypoxemia affects.  Journal of Clinical and Experimental Neuropsychology.  1996; 18:  197-210.


11.    Verstraeten E, Cluydts R, Verbraecken J, deRoeck J.  Neuropsychological functioning and determinants of morning alertness in patients with obstructive sleep apnea syndrome.  J International Neuropsychological Society.  1996; 2:  306-14.



Updated: January 19, 2008