A Psychiatrist's Primer on Sleep Apnea
A Psychiatrist's Primer on Sleep Apnea
Sleep apnea, a medical disorder with significant health and behavioral
effects, is of particular interest to psychiatrists for its capacity
to mimic or exacerbate symptoms of psychiatric disturbances such
as depression, anxiety and panic disorder.
Apnea presents with cessation of breathing for at least 10 seconds
during sleep. Three types of apneas have been described. In obstructive
sleep apnea (OSA), cessation of breathing (gas exchange) occurs
despite persistent respiratory efforts. In central apnea, there
is no respiratory effort and thus no gas exchange. Mixed apnea
usually begins with absent effort and terminates with obstruction.
Although most patients with obstructive and mixed apnea complain
of excessive sleepiness, some OSA patients report midnocturnal
awakenings. These patients may awaken with a startle or sense
of panic, and complain of anxiety and insomnia at night as well
as daytime sleepiness. Brief central apneas at sleep onset are
fairly common and usually clinically unimportant. Sleep onset
may be disrupted by central apnea, generating nonre-storative
sleep and complaints of insomnia.
The majority of OSA patients are men age 50 and older. Virtually
all report a history of loud, continuous snoring. Though they
may be unaware of pauses in breathing, spouses or family members
will describe gasping, choking or snorting breakthroughs for air
concurrent with brief arousals. Although most such patients are
moderately obese, relatively few have a classic Pickwickian habitus,
and some are at or below a normal weight for their height. Thin
individuals with significant apnea are likely to show upper airway
abnormalities. These include, e.g., hypertrophic tonsils and adenoids,
a low-set palate or palatal webbing, a large uvula, a large tongue
or a small mandible.
Obstructive sleep apnea (OSA) is a very common disorder. A recent
report by Young and colleagues generated a conservative estimate
of 9 percent prevalence in working-age men and 4 percent in working-age
women. In addition to sleepiness, OSA symptoms include restless
sleep, headache, intellectual deterioration, impotence and mood
changes, such as irritability, emotional lability and depression.
Many obstructive apnea patients deny the severity of their symptoms.
Serious medical complications may develop in persistent apnea.
Complications can include pulmonary and systemic hypertension,
congestive heart failure and cardiac arrhythmias. The pathogenesis
of this disorder probably relates both to disrupted nocturnal
sleep and to brain and systemic anoxia. Even with severe disturbance,
marked improvement and even complete cure may be attained with
Sleep position often influences OSA. Most patients snore more
loudly in the supine position; bed partners often "encourage"
them to move to their side while asleep.
Cartwright showed that some patients who have repetitive apneas
while sleeping on their backs may breathe normally when they sleep
on their side.
Polysomnography (PSG) is a diagnostic procedure for sleep apnea,
performed in a sleep disorders center. Although PSG is expensive,
it provides critical diagnostic information. Typical PSG monitoring
for sleep apnea would include recordings of electroencephalogram
(EEG), electrocardiogram (EKG), eye movements or electrooculogram
(EOG), body muscle tone (EMG) and body movement, respiratory effort
from the chest and abdomen, airflow, snoring and blood oxygen
New diagnostic approaches have become available in recent years.
Some use new technology; others have been developed in response
to economic pressures of the managed care environment. Technology
now allows patients to be recorded in a home or hospital setting
without a technician in attendance, with remote monitoring capability
via modem. Other limited recording approaches include montages
without EEG or other typical "scoring" channels, or
use of oximetry alone as a screening device.
Various medications have been explored as treatments for OSA.
Acetazolamide (Diamox) has respiratory stimulant properties, but
is apparently not effective in the treatment of OSA. Whyte and
associates showed that despite a reduction in apnea/hypopnea frequency
with acetazolamide, there was no symptomatic benefit, and paresthesias
were common. Medroxyprogesterone (Amen and others) also has some
respiratory stimulant properties. Although it has been suggested
as a treatment for OSA, studies performed by Cook and colleagues
suggest that it provides little if any therapeutic benefit.
Protriptyline (Vivactil), a tricyclic antidepressant generally
described as a more "stimulating" agent than other tricyclics,
has been used in the treatment of several sleep disorders including
narcolepsy and OSA. Brownell and colleagues proposed rapid eye
movement (REM) sleep suppression to explain improvement in OSA
severity, but Stepanski and associates interpreted improvement
in oxygenation, respiratory events and arousals as not being caused
by REM suppression.
Although mechanisms of protriptyline effects on sleep apnea are
not known, Bonora and others focused on its capacity to raise
skeletal muscle tone in sleep and, perhaps particularly in REM,
preventing airway collapse and decreasing apnea severity. Séries
and Cormier demonstrated that protriptyline treatment produced
improvements in oxygen and carbon dioxide levels in patients with
chronic obstructive pulmonary disease, suggesting a possible primary
respiratory stimulant effect.
Nortriptyline (Pamelor) and desipramine (Norpramin) may provide
alternatives to protriptyline. Sunderrajan and colleagues described
effects of nortriptyline treatment in a 61-year-old male with
severe renal disease. Treatment of depression with nortriptyline
at a dose of 125 mg provoked severe hyperventilation. Medication
was stopped and restarted with similar results. In patients intolerant
of protriptyline side effects, we have used nortriptyline with
reported improvement in snoring and OSA symptoms.
A study comparing fluoxetine (Prozac) with protriptyline in 12
OSA patients was performed by Hanzel and colleagues. Both drugs
decreased the proportion of REM sleep time and decreased the number
of apneas in non-REM sleep. For the entire group, no sig-nificant
improvement was seen for either drug in oxygenation, desaturation
events or arousals. Wide variability was seen in response to each
medication, but six of the 12 patients had a good response to
one or both medications. Fluoxetine was better tolerated overall.