Oral Maxillofacial Surg Clin N Am 14 (2002) 297 – 304

Current medical management of sleep-related

breathing disorders
Kent E. Moore, DDS, MDa,*, Mary Susan Esther, MDb
a
Private Practice, Oral and Maxillofacial Surgery, 1718 East Fourth Street, Suite 804, Charlotte, NC 28204, USA
b
Carolinas Sleep Services, Carolinas Medical Center, Mercy Medical Park, 10724 Park Road, Suite 208,
Charlotte, NC 28210, USA

Sleep-disordered breathing, a disorder character-
ized by repeated apnea (cessation of breathing) and
hypopnea (partial cessation of breathing) during sleep,
has been shown to be prevalent in the general pop-
ulation. Obstructive sleep apnea-hypopnea syndrome
(OSAHS) is a common disorder that can adversely
impact longevity and quality of life, and one in which
the oral and maxillofacial surgeon possesses a unique
ability to assist in managing.
Prior to offering surgical therapy, the oral and
maxillofacial surgeon must have a working knowl-
edge of medical options these patients may choose to
pursue. Medical management of OSAHS requires
careful clinical assessment and laboratory evaluation.
Sleep-related breathing disturbances were first des-
cribed polysomnographically in Gustout’s mid-1960s
studies of obese patients with hypercapnia [1]. Sub-
sequent research has shown that obstructive sleep
apnea can occur in nonobese patients as well. In fact,
epidemiological data estimate that 2 – 5% of the pop-
ulation meets the criteria for OSAHS [2]. Community
based studies have confirmed that OSAHS is seen in
2% of women and 4% of men between the ages of
30 and 60 years [3].
OSAHS occurs when there are episodes of pha-
ryngeal narrowing and obstruction combined with
significant daytime symptoms that result from dis-
rupted sleep. Though the basic processes causing
airway narrowing are multifactorial and not com-
pletely understood, this disorder is considered to
* Corresponding author.
E-mail address: kemoore@pol.net (K.E. Moore).
occur over a continuum of severity: the mildest form
of upper airway narrowing produces rapid airflow.
This rapid airflow imparts kinetic energy to the soft
tissues of the upper airway, initially causing stretch-
ing of the compliant portions of the soft tissue upper
airway (ie, the soft palate and lateral pharyngeal
walls), resulting in soft palate elongation and redun-
dancy (ie, secondary elongation), and eventually in
snoring. Further airway narrowing results in increased
upper airway resistance. This increased airway resist-
ance is sensed by the central nervous system, causing
disruption of normal sleep architecture, and forms
the basis for the condition of upper airway resistance
syndrome (UARS) seen most commonly in young,
thin females. Further airway narrowing and frank
obstruction are next on the continuum, causing ob-
structive sleep apnea (OSA). OSA is generally ranked
on a scale of severity, based upon the number of
times a given patient stops breathing over a given
hour of sleep [often called the Respiratory Disturbance
Index (RDI), or Apnea-Hypopnea Index (AHI)]. An
RDI of 0 – 5 events per hour is considered normal. In
most clinics, an RDI of 5 – 20 is considered mild OSA,
20 – 40 or 50 is considered moderately severe OSA,
and an RDI >40 – 50 is considered severe OSA.
Apnea is defined as a cessation of respiratory flow
for at least 10 seconds accompanied by a 2 – 4% drop
in oxygen saturation and usually an associated EEG
arousal [4]. The syndrome of obstructive breathing
requires the combination of daytime symptoms, as
well as an apnea-hypopnea index of at least 5 per
hour of sleep [5]. Therefore, a careful clinical history,
along with the polysomnographic data, is needed.
Factors that increase the risk for OSAHS include

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298 K.E. Moore, M.S. Esther / Oral Maxillofacial Surg Clin N Am 14 (2002) 297–304
obesity, male gender (2 to 3:1 male-female ratio) as
well as family history [6].
Nearly all patents with significant OSAHS snore,
though the absence of snoring does not exclude sleep
apnea [7]. In addition, apneic episodes are reported
by the bed partner in 75% of cases [8]. As snoring
can be loud and lead to restlessness during the night,
it is not surprising that 46% of patients sleep apart
from their partners [9]. Bed partners may report loud
snorts or vocalizations, and patients themselves note
restlessness, often with associated diaphoresis in neck
and upper chest. Nearly 74% of patients complain of
morning dry mouth, and 28% report significant
nocturia [10].
Daytime sleepiness is, of course, one of the hall-
marks of OSAHS. The severity of this symptom can
vary from subtle to severe. Untreated sleep apnea puts
patients at risk for vehicular accidents [11]. It is
common for patients with sleep apnea to report
opening car windows, drinking caffeinated beverages,
or chewing ice as a help to stay awake. Intellectual
impairment has been noted on neuropsychiatric test-
ing, and patients themselves may note decreased
concentration and job performance [12]. A recent
popular public news telecast nationwide suggested
that the neurocognitive deficits of the sleepy driver
can be at least as severe (if not more so) than that of
the alcohol-impaired driver.
Obstructive sleep apnea-hypopnea syndrome has
been linked to hypertension. Recent prospective data
confirms the association between sleep-disordered
breathing and hypertension and its resulting cardiovas-
cular morbidity [13]. Furthermore, there is evidence
that OSAHS may place patients at an increased risk for
stroke [14]. OSAHS should be looked at as yet another
cardiovascular risk factor for susceptible individuals.
The decision on when, and how, to treat patents
with OSAHS is complex. It must be based on clinical
assessment, including physical examination, medical
history, and polysomnographic data. The decision
must include information about a patient’s sleepiness,
snoring, and disruption of the bed partner’s sleep as
well as assessment of possible adverse cardiovascular
consequences. These factors should all play a role in
determining the proper therapeutic option (both surgi-
cal and nonsurgical) the oral and maxillofacial surgeon
offers to the patient presenting with this disorder.
Effects of medications and associated medical
conditions on sleep-disordered breathing
Once the diagnosis of OSAHS has been estab-
lished, treatment options must be explored. First,
however, possible medical conditions, as well as
pharmacological agents, that could adversely affect
sleep and breathing must be assessed.
Even moderate alcohol intoxication can decrease
hypercapnic ventilatory response to 50% of baseline
[15]. Alcohol can precipitate OSA in vulnerable
individuals. Older, obese subjects are more likely to
be affected than are young healthy subjects. Patients
with mild sleep apnea clearly develop longer and
more frequent obstructive breathing events when they
consume alcohol, and snorers can develop OSA after
alcohol use [16]. Therefore, avoidance of alcohol for
obese snorers and patients with obstructive sleep
apnea is recommended routinely [17].
Smoking is widely known to impact upper airway
physiology detrimentally. The irritation-inflammation-
edema cycle that occurs with repeated use of an
irritant such as smoking is felt to affect a subtle form
of mucosal edema of the upper airway, as well as
increase upper airway mucosal secretions. The com-
bined effect of these reactive conditions, instead of
occurring externally, actually affects closure (or nar-
rowing) of the upper airway. Per Pousille’s equation,
small changes (narrowing) in the radius of the upper
airway tube can potentially effect an exponential
change in airflow and cause a greater chance for ob-
structive upper airway pathology.
Hypnotics can also affect sleep and breathing and
are frequently prescribed. Benzodiazepines are mild
respiratory depressants [18]. Hypercapneic chronic ob-
structive pulmonary disease (COPD) patients appear
to be particularly vulnerable to the respiratory de-
pressant properties. Benzodiazepines, like alcohol,
decrease upper airway muscle tone [19] and in this
way may promote the development of OSA in sus-
ceptible individuals; therefore, they are best avoided
[20]. Newer, non-benzodiazepine agents lack the
myorelaxant and respiratory depressant effects of the
benzodiazepines [21]. In general, however, it is best to
avoid sedative-hypnotic agents in patients with hyper-
capnia and sleep apnea. Narcotics, too, are powerful
respiratory depressants and are best avoided in pa-
tients with significant sleep apnea [22].
Hypothyroidism should also be considered in pa-
tients with a history of OSAHS. Possible mechan-
isms for the increase in sleep apnea seen in patients
with hypothyroidism include obesity, impaired upper
airway muscular function, and macroglossia. Though
screening of all patients with OSAHS for hypo-
thyroidism is not cost-effective, careful assessment
of clinical symptoms is necessary [23]. In hypo-
thyroid patients, it is important to treat their sleep-
disordered breathing during thyroid replacement
[24]. It may take considerable time for normalization
 K.E. Moore, M.S. Esther / Oral Maxillofacial Surg Clin N Am 14 (2002) 297–304
of sleep and breathing, or patients may be suffering
from two disorders.
Pharmacological treatment of sleep apnea has not
proven effective. In the late 1970s, agents such as
protriptyline (a tricyclic antidepressant) were shown
to reduce the number of apneic events by decreasing
the amount of REM sleep and increasing hypo-
glossal nerve activity [25]. Whereas apneas were
reduced in frequency, the total number of sleep and
breathing events remained abnormal. Pharmaco-
logical agents studied and shown not to be of benefit
in treatment include progesterone, tryptophan, and
baclofen [26,27].
Use of supplemental oxygen, position restriction,
and role of weight loss
Other forms of medical treatment for OSAHS that
have been studied include supplemental oxygen.
Oxygen alone is not sufficiently effective in reducing
the frequency of apnea or improving daytime alert-
ness to be a therapeutic option [28]. Oxygen, how-
ever, may have a role as an adjunct to positive airway
pressure in patients who remain hypoxic after cor-
rection of upper airway obstruction. Ongoing studies
need to be completed in order to better understand
the amount of desaturation that necessitates addition
of oxygen.
Restriction of sleeping position may offer signifi-
cant benefit to some patients with OSAHS. Labora-
tory analysis routinely breaks down the presence of
sleep-disordered breathing in both the supine as well
as the nonsupine positions. The supine position, with
resultant occlusion of upper airway based on effects
of gravity on the tongue, can result in apneic or hy-
popneic events. For the oral surgeon, the effect of
positional changes on upper airway volume can most
easily be assessed clinically through the use of both
acoustic pharyngometry, as well as with fiberoptic
nasopharyngoscopy. In many cases, slight cervical
extension of the neck while in the supine position
may affect volumetric expansion of the upper airway.
In this manner, cervical pillows, which allow one to
sleep with slight extension of the head (while in the
supine position), can be of benefit (one such pillow
has shown some merit in minimizing apneic events in
patients with mild OSA). But expecting a patient to
maintain a substantial degree of uncomfortable cer-
vical extension consistently during supine REM sleep
is unrealistic. It is more likely, however, that obese pa-
tients will have OSAS regardless of their position
during sleep [29]. For some patients, sleep and breath-
ing is satisfactory in the lateral position with main-
299
tenance of oxygenation and sleep continuity when
lateral. Use of a small ball, such as a tennis ball,
pinned to the pajama back may help patients to learn
behaviorally to avoid sleeping supine. In addition
sleeping with the head and trunk elevated to a 30°
angle reduces OSAS as it stabilizes the upper airway
[30]. Modification of body position during sleep
should be considered in appropriate patients.
No discussion of the management of OSAHS is
complete without addressing obesity. The effect of
obesity on the upper airway appears to be the result of
mechanical effects on the upper airway (the pharyn-
geal dilator muscles are unable to work efficiently
with increased load) and increased upper airway
resistance. Studies have confirmed that weight reduc-
tion can ameliorate sleep-disordered breathing. It
appears that the degree of improvement is not linearly
related to the amount of weight lost [31]. In fact, it
appears that there must be a critical amount of weight
lost before there can be seen any significant improve-
ment in sleep-disordered breathing. Obese patients
should always be encouraged to lose weight, but
obstructive breathing must be treated while the weight
loss is underway.
Use of nasal continuous positive airway pressure
In part because of the lack of a pharmacological
treatment for OSAHS, nasal continuous positive air-
way pressure (CPAP) is the most established therapy
choice. First used in Australia in 1981, its use in
America became more widespread in l985 [32]. Nasal
CPAP can best be conceptualized as a pneumatic
splint that prevents collapse of the pharyngeal airway.
CPAP successfully eliminates mixed and obstructive
apneas [33]. Titration of the pressure to levels suffi-
cient to eliminate not only the obstruction, but snoring
and snore-arousals as well, can be difficult even for
veteran sleep technicians.
Adjusting to nasal CPAP can be trying, as patients
adapt both to the mask and to the pressure cessation,
as well as the headgear holding the mask in place.
Instructional videos, review of goals of treatment, and
time in the laboratory adjusting to the device can ease
transition to use. Studies confirm the value of patient
education programs to successful CPAP use and
improved compliance [34].
Nasal CPAP titration has as its goal the elimina-
tion of respiratory related arousals in all sleep stages
and positions. Once correct pressure is achieved, the
number of arousals triggered by the sleep-disordered
breathing should be markedly reduced. This leads to a
‘‘rebound’’ of slow wave and REM sleep [35].
300 K.E. Moore, M.S. Esther / Oral Maxillofacial Surg Clin N Am 14 (2002) 297–304
Snoring should be eliminated because it is a sign of
inadequate CPAP pressure. It is apparent that higher
CPAP pressures are generally needed when the pa-
tient is supine or in REM sleep. Successful titration in
REM sleep in the supine position, the most vulner-
able combination of stage and position for obstructive
breathing, is the goal.
Of course, additional factors may have an impact
on CPAP pressures. Alcohol, for example, with its
known neuromuscular effects, would be expected to
result in the need for an increase in CPAP pressure, as
would weight gain [36]. If patients have persistent
sleepiness after treatment of their sleep-disordered
breathing, then review of their sleep history is rec-
ommended. Patients may be suffering from a second,
primary sleep disorder such as narcolepsy. Hyper-
somnolence would need to be assessed with a repeat
evaluation in the laboratory, with CPAP in place to
confirm treatment of sleep-disordered breathing, fol-
lowed by a Multiple Sleep Latency Test to evaluate
daytime fatigue.
Problems related to nasal CPAP include mask
discomfort, nasal congestion, and social considera-
tions (including bed partner tolerance of the device)
and chest discomfort and claustrophobia. The com-
fort of the CPAP mask is critical, and careful fitting of
the mask is crucial to successful treatment. In our
laboratory, technicians spend much time helping the
patient choose an appropriate mask. Claustrophobic
patients, or those who have beards or mustaches are
otherwise difficult to fit, are encouraged to come by
the laboratory prior to their study to have additional
time for choosing an interface system. If a mask does
not fit properly, there is an audible leak of air and
resultant insufficient pressure and ineffective treat-
ment. The patient may not be tightening the headgear
sufficiently at home, whereas in the laboratory the
mask was applied properly. If the air is leaking
toward the eye, then conjunctivitis may result [37].
If the headband or headgear securing the CPAP is too
snug, the increased tension may cause ulceration of
the skin around the bridge of the nose. Nasal prongs
or pillows alleviate some problems regarding com-
fort, but these can irritate the nares as well. Patients
with claustrophobia may need time in the laboratory
for desensitization and graduated exposure in order to
be able to tolerate CPAP.
Persistent nasal congestion is seen in more than
10% of patients on CPAP even after six months of
treatment [38]. It has been found that the relative
humidity of air inhaled through CPAP is 20% lower
than relative humidity of room air [39]. The postu-
lated causes of nasal congestion include unmasking
of allergic rhinitis (particularly in mouth breathers);
vasodilatation of turbinate tissues triggered by muco-
sal receptors, or septal deviation and fixed obstruc-
tion. Efforts to increase nasal patency include the use
of topical steroids, humidification, and topical anti-
histamine sprays. In some patients, correction of
septal deviation (via septoplasty), or enlarged turbi-
nates (via either radiofrequency, volumetric tissue re-
duction, or more traditional surgical turbinectomy)
may be necessary before success with CPAP is ob-
tained. Patients with persistent nasal congestion may
respond to Passover humidifiers attached to CPAP. A
recent study found that among patients with previous
uvulopalatopharyngoplasty, those using drying med-
ications, as well as those over age 60, were more
likely to develop nasopharyngeal dryness. Heated
humidification added to CPAP improved the daily
use rate in this group of patients [40].
Nasal CPAP is effective only when the device is
used, and used consistently. Studies indicate that
even one night off CPAP can lead to the return of
pathologic hypersomnolence [41]. But it is also true
that patients can achieve some benefit from a partial
night’s use. Early studies reporting on patient com-
pliance with nasal CPAP were based purely on
subjective patient reporting; these studies suggested
a relatively high rate of CPAP compliance. Later stud-
ies, done with the use of covert patient monitoring,
revealed a much lower compliance rate (these studies
are generally felt to be a more accurate reflection of
true nasal CPAP compliance). With new CPAP
devices allowing for monitoring of patterns of use,
more information for further study will soon be
forthcoming. Even data on acceptance of CPAP when
attempted in a laboratory setting can be confusing.
Some studies have reported acceptance rates (agree-
ment to use CPAP at home) of 80%, whereas others
are as low as 58% [42,43]. It does appear that pa-
tients’ perception of improvement, not the severity of
the obstructive breathing itself, is the most predictive
measure of compliance [44]. Equally evident is the
fact that patients overestimate their CPAP use [45]. It
appears that about half of patients will be consistent
users of CPAP, and Weaver et al showed that, by as
early as day 4 of treatment, nonusers could be sepa-
rated from nightly users [46]. Follow-up early after
starting CPAP is important to help patients adjust to
CPAP and to address initial difficulties.
Studies do demonstrate that hypersomnolence
prior to treatment is predictive of good compliance.
Of course, this makes common sense, as the patient’s
response to CPAP would be positive reinforcement
for continued usage. In fact, one recent study by
Barbe et al found that in patients with significant
OSAHS but with no subjective sleepiness CPAP
 K.E. Moore, M.S. Esther / Oral Maxillofacial Surg Clin N Am 14 (2002) 297–304
offered no improvement in cognitive function, quality
of life, or arterial blood pressure [47]. This article does
not, however, take into account such factors as effect
on bed partner’s sleep, nor does it include objective
measurement of sleepiness. When, then, should pa-
tients be treated? Again, careful clinical assessment is
required, taking into account not only hypersomno-
lence and its associated risk for vehicular or industrial
accidents, but also social factors such as unacceptable
levels of snoring and potentially reduced cardiovas-
cular risk factors [48].
When CPAP is not tolerated, it is important first to
determine the specific cause for the discontinued use.
A complete upper airway examination, looking for
structural abnormalities, should be performed. Kribb
et al have demonstrated that only 46% of patients
were able to use CPAP for 4 hours each night at least
70% of the time [49]. Clearly, such objective meas-
ures indicate that CPAP compliance is less than
optimal [50].
Bilevel positive airway pressure
Bilevel positive airway pressure (BiPAP) devices
have the capability to allow for a separate pressure for
inspiration and expiration. It has been shown that
patients with OSA need a lower expiratory pressure
than that needed to prevent upper airway occlusion
during inspiration [48]. As would be expected, the
continuous pressure level of CPAP and the inspir-
atory pressure of BiPAP for a given patient would be
the same. This makes intuitive sense, as identical lev-
els would be needed to maintain inspiratory potency.
Sanders et al found that a reduction in expiratory
pressure could be achieved, with mean expiratory
pressures being 37% lower than inspiratory pressures
[51]. BiPAP can be delivered in three ways: (1)
through a spontaneous, or patient-triggered mode,
(2) through a spontaneous/timed mode, or (3) a timed
mode alone. Only the spontaneous mode is usually
indicated for OSA; the spontaneous/timed mode can
be used in patients with significant neuromuscular
disease, whereas the timed mode allows BiPAP to
function as a controlled ventilator. BiPAP, because of
its increased cost as compared with CPAP, is reserved
for those patients who are intolerant of CPAP or who
would benefit from lower expiratory pressures. Pa-
tients experiencing chest wall discomfort, or those
sensing difficulty in exhaling against pressure or a
smothering sensation, may benefit from BiPAP [52].
Studies have demonstrated a similar long-term com-
pliance rate for CPAP and BiPAP, though the initial
301
acceptance rate of BiPAP is higher [53]. If patients
are more likely to accept the treatment initially, use
will be increased overall.
Autotitrating CPAP
Currently available, and being ever more fine-
tuned, are CPAP devices that detect changes in flow
and automatically adjust the pressure. These devices
can detect changes in upper airway resistance (such as
can be seen after alcohol use) and make the necessary
pressure adjustments. Several methodological prob-
lems with autotitrating devices have been found,
however. The devices appear to be confused by leaks
about the cap mask, with resultant over pressure of
CPAP as the device tries to compensate [54]. The
devices appear to have a median pressure of 70 – 80%
of peak ‘‘auto set’’ as compared with manual pressure.
For most patients, though changes in position and
sleep stage may require minor changes in CPAP
pressure, these changes are insignificant and auto
PAP offers little advantage. Additionally, auto PAP
does not offer an advantage to patients with nasal
congestion [54]. Further investigations are underway
to establish guidelines on when use of auto PAP may
be beneficial.
Alternative interface systems
Recent innovations (combining oral appliance tech-
nologies with CPAP or BiPAP designs) are intended
to minimize the inherent problems associated with
nasal CPAP interfaces, troublesome headgear, and
patient claustrophobia.
CPAP Pro1 is a nasal CPAP interface, which
utilizes a maxillary dental mouthpiece to hold a
specially designed connector (this connector supports
the tubing that attaches to nasal pillows). If properly
fitted and oriented, this appliance has the potential to
eliminate headgear completely. This appliance is
currently being offered with a quick-setting gel poly-
mer (so that the patient can make his or her own
maxillary tray), or, as a professional kit, so that a
more permanent and durable oral appliance can be
fitted and placed by the dentist. This appliance can
also be combined with an oral appliance (such as a
Klearway1 or Herbst1 appliance) that affects man-
dibular advancement/ protrusion. The main benefit
for their combined use with CPAP Pro is in their
ability to maintain closure of the mandible, and to
prevent oral leakage of the positive pressure ventila-
tion. It is debatable whether the effect of mandibular
302 K.E. Moore, M.S. Esther / Oral Maxillofacial Surg Clin N Am 14 (2002) 297–304
protrusion will be of dramatic benefit (with this
combined appliance) so as to lower the pressures
required for elimination of obstructive upper airway
pathology because ventilation through the relatively
high-resistance nasal airway is still required.
Oral Positive Airway Pressure (or OPAP1) has
recently received FDA approval as an alternative in-
terface system for patients requiring positive pressure
ventilation. This custom-fitted oral appliance is de-
signed to connect directly with the CPAP tubing,
permitting oral positive pressure ventilation while
bypassing the nasal airway. This one-piece appliance
is also designed to permit fixed-position mandibular
advancement, thereby potentially affecting expansion
of the tongue-base region of the upper airway. In this
case, one possible advantage to this design, because
of the forward mandibular posturing, is the potential
for lower required airway pressures for adequate
ventilation and elimination of OSA, as the high-
resistance nasal airway is bypassed. Potential prob-
lems with this system, however, include those
patients who have undergone previous uvulopalato-
pharyngoplasty- with the potential for nasal venting,
as well as the drying effect on the oral cavity and
pharyngeal airway.
With each of the above alternative interfaces (as
well as with oral appliances in general), retention of
the appliance is critical. Also, as with all oral appli-
ances used in the treatment of OSA, risks of alteration
of the existing occlusion, TMJ dysfunction, and dam-
age to existing dental restorations is possible. Com-
pliance data with these newer interface systems is
lacking at this time.
Oral appliances
Although this topic is covered in detail in another
article here, oral appliances have definitely found a
place within the medical management of varying
levels of upper airway obstructive pathology. The
reader is referred to the accompanying article; mem-
bership within the Academt of Dental Sleep Medicine
(www.dentalsleepmed.org) offers another excellent
opportunity for those doctors wishing to learn more
about this form of treatment.
Summary
Sleep and breathing disorders are common. As-
sessment by the oral and maxillofacial surgeon
should include thorough physical examination and
assessment of clinical symptoms both during sleep
and wakefulness, as well as review of polysomno-
graphic data. Treatment then focuses on nasal CPAP
as the most widely accepted therapeutic option. CPAP
is not always well tolerated, however; suboptimal
compliance and complications often lead to its discon-
tinuation. Optimizing CPAP treatment may require
changes in the mask style or switching to BiPAP
(particularly for patients with hypoventilation or re-
fractory nasal congestion). The interface system may
need to be changed entirely, as with OPAP1, in order
for a patient to tolerate CPAP. More conservative
treatment approaches include weight loss, position re-
striction, and oral appliances, effective options for
patients with largely positional or only mild breathing
obstruction. These options must be thoroughly inves-
tigated prior to initiating a course of irreversible surgi-
cal therapy. Pharmacological options have as yet been
of no benefit.
Obviously, future investigations must be directed
toward better diagnostic tools for assessment of sleep
apnea, especially as it relates to distortion of the
upper airway when patients are in the supine position
during sleep. It is hoped that newer treatments,
offering improvement in overall tolerance and com-
pliance, will derive from these efforts.
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