Obstructive sleep apnea

Abstract

Obstructive sleep apnea (OSA) affects millions of Americans and is estimated to be as prevalent as asthma and diabetes. Given the fact that obesity is a major risk factor for OSA, and given the current global rise in obesity, the prevalence of OSA will increase in the future. Individuals with sleep apnea are often unaware of their sleep disorder. It is usually first recognized as a problem by family members who witness the apneic episodes or is suspected by their primary care doctor because of the individual's risk factors and symptoms. The vast majority remain undiagnosed and untreated, despite the fact that this serious disorder can have significant consequences. Individuals with untreated OSA can stop breathing hundreds of times a night during their sleep. These apneic events can lead to fragmented sleep that is of poor quality, as the brain arouses briefly in order for the body to resume breathing. Untreated, sleep apnea can have dire health consequences and can increase the risk of hypertension, diabetes, heart disease, and heart failure. OSA management has also become important in a number of comorbid neurological conditions, including epilepsy, stroke, multiple sclerosis, and headache. Diagnosis typically involves use of screening questionnaires, physical exam, and an overnight polysomnography or a portable home study. Treatment options include changes in lifestyle, positive airway pressure, surgery, and dental appliances.

Full text

Neurology International 2011; volume 3:e15
Obstructive sleep apnea
Matthew L. Ho, Steven D. Brass
UC Davis Department of Neurology,
Davis Medical Center, University
of California, California, USA
Abstract
Obstructive sleep apnea (OSA) affects mil-
lions of Americans and is estimated to be as
prevalent as asthma and diabetes. Given the
fact that obesity is a major risk factor for OSA,
and given the current global rise in obesity, the
prevalence of OSA will increase in the future.
Individuals with sleep apnea are often
unaware of their sleep disorder. It is usually
first recognized as a problem by family mem-
bers who witness the apneic episodes or is
suspected by their primary care doctor because
of the individual’s risk factors and symptoms.
The vast majority remain undiagnosed and
untreated, despite the fact that this serious
disorder can have significant consequences.
Individuals with untreated OSA can stop
breathing hundreds of times a night during
their sleep. These apneic events can lead to
fragmented sleep that is of poor quality, as the
brain arouses briefly in order for the body to
resume breathing. Untreated, sleep apnea can
have dire health consequences and can
increase the risk of hypertension, diabetes,
heart disease, and heart failure. OSA manage-
ment has also become important in a number
of comorbid neurological conditions, including
epilepsy, stroke, multiple sclerosis, and
headache. Diagnosis typically involves use of
screening questionnaires, physical exam, and
an overnight polysomnography or a portable
home study. Treatment options include
changes in lifestyle, positive airway pressure,
surgery, and dental appliances.
Introduction
The Greek word apnea means breathless or
loss of breath.
1
Sleep-disordered breathing
(SDB) encompasses a heterogeneous group of
sleep-related disorders that are characterized
by abnormal pauses in breathing during sleep.
There are two major types of SDB: obstructive
sleep apnea (OSA) and central sleep apnea
(CSA). Despite the difference in the actual
cause of each type, in both cases, people with
untreated sleep apnea stop breathing repeat-
edly during their sleep. Of the two types of
sleep apneas characterized, OSA is the most
common type, constituting greater than 85% of
all cases of SBD; CSA is far less common.
2
O
SA is caused by a physical blockage of the
airway; it results from airflow obstruction sec-
ondary to upper airway collapse or anatomic
airway obstruction, even though the respirato-
ry effort is still present. In the case of CSA, the
airway is not blocked; the brain fails to signal
the muscles to breathe and breathing is inter-
rupted by a lack of respiratory effort.
3
T
he clinical picture of OSA has long been
recognized in medical literature. It was first
described in 1918 by William Osler, a 20th cen-
tury physician who coined the term
Pickwickian syndrome in reference to a char-
acter in Charles Dickens's novel The Pickwick
P
apers. The character named Joe has all the
classic symptoms of the condition. Joe is con-
stantly hungry, red faced and always falling
asleep in the middle of doing a task.
The object that presented itself to the eyes of
the astonished clerk, was a boy - a wonderfully
fat boy - habited as a serving lad, standing
upright on the mat, with his eyes closed as if in
sleep.
4
Epidemiology
OSA affects more than twelve million
Americans.
5
An epidemiological review by
Young et al. estimates that 1 in 5 adults has at
least mild OSA and 1 in 15 adults has at least
moderate OSA.
6
Sleep apnea can affect anyone
at any age, even children.
7,8
OSA is becoming
increasingly prevalent. However, because of
the lack of awareness by the public and health-
care professionals, the vast majority remain
undiagnosed and untreated. Data from the
Wisconsin sleep cohort study of patients esti-
mate that 93% of women and 82% of men with
moderate-to-severe sleep apnea were undiag-
nosed.
9
A follow-up publication from the
Wisconsin Cohort Study five years later indi-
cated that the prevalence of OSA in people
aged 30-60 years was 9-24% for men and 4-9%
for women.
10,11
Primary risk factors for OSA
include the male gender, those over age 40,
overweight persons or recent weight gain, and
persons with a large neck size or small
chin/jaw (Table 1).
12
Epidemiological studies have consistently
shown that body weight, and in particular BMI,
is the strongest risk factor for OSA. It is esti-
mated that about 70% of those with OSA are
obese and that the prevalence of OSA in obese
men and women is about 40%.
13,14
Twenty-six
percent of patients with a BMI greater than 30
and 33% of those with a BMI greater than 40
have moderate OSA.
15
A large neck circumfer-
ence is also associated with an increased risk
of OSA. In fact, neck circumference of 15.7 in
(40 cm) or greater may have a greater sensitiv-
ity and specificity than BMI in predicting OSA,
regardless of the person’s sex.
16,17
Age is also an important risk factor in the
development of OSA; the prevalence is estimat-
ed to triple in individuals greater than 65 years
of age compared with individuals aged 30-64
years.
18,19
Regarding gender, the male-to-
female ratio in community-based studies is
about 3:1.
20
It is theorized that body fat distri-
bution predispose men to OSA and that sex
hormones play a role in the modulation of
upper airway musculature.
As indicated above, the incidence of OSA
among male and female are 3:1 prior to
menopause. However, the incidence of OSA is
equal amongst males and females following
menopause. There is at least a threefold
increase in risk of OSA among post-
menopausal women compared to pre-
menopausal women.
21,22
In addition, there is a
lower prevalence of OSA among post-
menopausal women who were on hormone
replacement therapy.
23
Interestingly, there
does not appear to be any difference in preva-
lence between males and females prior to
puberty.
Structural factors related to craniofacial
bony anatomy can predispose patients to pha-
ryngeal collapse during sleep, including retrog-
nathia and micrognathia, mandibular hypopla-
sia, and high-arched palate.
24,25
Imaging stud-
ies have demonstrated that patients with OSA
have compromised pharyngeal lumens that
predispose them to collapse.
26
This was inde-
pendently confirmed under general anesthesia
that simulates the total muscle paralysis seen
during REM sleep.
27
Patients with Down syn-
drome, Marfan syndrome, and Prader-Willi
syndrome are particularly at risk due to these
structural factors.
In terms of ethnicity, African American indi-
viduals appear to be more predisposed to OSA
than Caucasians, with an odds ratio of 3 in chil-
Correspondence: Steven Brass, MD, MPH
Director of Neurology Sleep Medicine
4860 Y Street Suite 3700 Sacramento, CA 95817
Tel. +916.734.6785.
E-mail:steven.brass@ucdmc.ucdavis.edu
Key words: apnea, hypopnea, obstructive sleep
apnea, apnea hypopnea index, respiratory distur-
bance index, respiratory event related arousals.
Received for publication: 23 August 2011.
Accepted for publication: 30 August 2011.
This work is licensed under a Creative Commons
Attribution NonCommercial 3.0 License (CC BY-
NC 3.0).
©Copyright M.L. Ho and S.D. Brass, 2011
Licensee PAGEPress, Italy
Neurology International 2011; 3:e15
doi:10.4081/ni.2011.e15
[page 60] [Neurology International 2011; 3:e15]

d
ren younger than 14 and 2 in adults greater
than 25.
28
Individuals of Asian descent, particu-
larly Chinese individuals, have a more crowded
upper airway and retrognathia compared with
C
aucasians. OSA has a prevalence rate similar
in the Asian population sample to those in
Caucasians despite a lower obesity rate. Asians
have an increased risk of developing OSA,
r
egardless of weight or neck circumference, as
well as greater disease severity.
29
Pathophysiology
The International Classification of Sleep
Disorders, second edition (ICSD-2) was pub-
lished by the American Academy of Sleep
Medicine to standardize definitions and create
a systematic approach to the diagnosis of sleep
disorders. The ICSD-2 subdivides sleep disor-
ders into eight major categories, one of which
is sleep-disorder breathing (SDB).
30
The ICSD-2 further classifies SDB into three
basic categories: CSA syndromes, OSA syn-
dromes, and sleep-related hypoventilation/
hypoxic syndromes. OSA involves a complete
cessation or a significant decrease in airflow
in the presence of breathing effort. CSA is the
cessation of airflow with an absence of breath-
ing effort. Breathing effort is measured by
abdominal and/or chest movement.
The human airway is composed of soft tis-
sue that can collapse during REM sleep, when
the muscle tone of the body relaxes. Two major
factors likely contribute to OSA pathophysiolo-
gy: i) craniofacial structural abnormalities can
predispose patients to OSA; this has been dis-
cussed previously and has been recognized as
a primary risk factor for OSA; ii) larger soft tis-
sue mass or abnormal tissue deposits can also
increase extraluminal tissue pressure and
lower the threshold for airway collapse (Figure
1). In normal, nonobese individuals without
OSA, muscle relaxation during sleep does not
completely collapse the airway (normal).
However, airway collapse can occur during
muscle relaxation when there is a pathological
i
ncrease in tissue pressure, as a product of
extra soft tissue mass (in a normal-sized
enclosure) and/or structural limitations (small
maxillary or mandibular compartment) with
n
ormal tissue mass (Figure 1).
3
1
C
hronically,
this dysfunction can cause problems with the
regulation of pharayngeal dilator muscle acti-
vation (which plays an important role in main-
t
aining airway patency) in patients with OSA.
OSA is thus characterized by the partial or
total collapse of the pharyngeal airway during
sleep and the need to arouse to resume venti-
l
ation.
3
2
I
n adults, the obstruction typically
occurs at the level of the oropharynx
(uvula/soft palate or tongue).
3
3,34
Chronic
severe OSA can result in prolonged hypoxemia,
sleep deprivation, and other complications.
With most apneic events, the brain briefly
arouses in order for the body to resume breath-
ing, but consequently, sleep is extremely frag-
mented and of poor quality.
Several additional anatomical factors play a
role in OSA. These include the position that the
patient sleeps in, airway reactivity and airway
secretions. Position can have a strong influence
on airway patency. Because the airway is col-
lapsible, gravitational forces can cause the
retropulsion of the tongue and soft palate while
laying supine, thus generating increased posi-
tive tissue pressure and narrowing the airway.
35
For this reason, OSA worsens in the supine
sleeping position for most individuals.
36
Evaluation
Individuals with OSA are rarely aware of
their sleep disorder, even upon arousal.
37
Sleep
a
pnea is usually recognized as a problem by
family members who witness the apneic
episodes or by a primary care doctor because of
the individual’s risk factors and symptoms.
M
ost commonly, patients present with vague
complaints. Clinical symptoms can include
excessive daytime sleepiness (EDS) that usu-
ally begins during quiet activities (eg, reading,
w
atching television), daytime fatigue, feeling
tired despite a full night’s sleep, morning
headaches, personality and mood changes, dry
or sore throat, gastroesophageal reflux, and
s
exual dysfunction.
Snoring is a common finding in individuals
with OSA. Although not everyone who snores
is experiencing sleep apnea, snoring in combi-
nation with obesity has been found to be high-
ly predictive of OSA risk.
38
The volume of the
snoring is not indicative of the severity of
obstruction. However, snoring with witnessed
apneas has a 94% specificity for OSA.
The diagnosis of OSA is based on the evalu-
ation of clinical symptoms and risk factors, as
well as a formal sleep study evaluation
(polysomnography, or a portable home based
test). Individuals should be evaluated appro-
priately with screening questionnaires, as well
as a physical examination.
The Epworth sleepiness scale (ESS) has
been universally adopted as an effective
screening method to monitor for clinical symp-
toms of sleep apnea. This questionnaire is
used to help determine how frequently the
patient is likely to doze off in 8 frequently
encountered situations (e.g., as a passenger in
a car, sitting quietly after lunch, etc). A 2003
study showed that an ESS score of 12 or
greater is considered abnormal and would war-
rant a more formal evaluation.
39
However, the
Review
[Neurology International 2011; 3:e15] [page 61]
Table 1. Primary risk factors for obstruc-
tive sleep apnea.
Primary risk factors for sleep apnea
Weight gain or being overweight with a BMI >30
kg/m
2
Neck circumference [≥17in (or 43.2 cm) in men;
≥16in or (40.6 cm) in women]
Age >40
Male gender
Structural factors related to craniofacial anatomy
Ethnicity
Family history of sleep apnea
Figure 1. Reprinted with permission of the American Thoracic Society. Copyright (c) 2011
American Thoracic Society. White D. Pathogenesis of obstructive and central sleep apnea.
Am J Resp Crit Care Med. 2005; 172: 1363-1370. Official Journal of the American
Thoracic Society.

E
SS is still a subjective self assessment meas-
ure and may be inaccurate for a number of rea-
sons. Therefore, if a patient has multiple risk
factors for sleep apnea, the individual should
b
e sent for further evaluation if there is a sus-
picion of sleep apnea despite a low ESS.
Another effective screening tool that has
been used in the primary care population is
t
he Berlin questionnaire.
4
0
S
urvey questions
address snoring behavior, EDS/fatigue, and
history of obesity or hypertension. The sensi-
tivity of the Berlin questionnaire with regards
t
o high-risk patients having sleep apnea was
86%. Another screening tool called the STOP
BANG questionnaire was developed to screen
for the most common risk factors seen specifi-
cally in OSA. The term refers to a mnemonic
that represents 8 factors: Snoring, Tiredness,
Observed apneas, elevated blood Pressure,
BMI (greater than 35 kg/m
2
), Age (greater
than 50), Neck circumference (greater than 40
cm), and Gender (male). Patients receive a
point for each positive risk factor, and those
whose scores are equal to or greater than 3
have a higher likelihood of having OSA. The
sensitivities of the STOP BANG questionnaire
for mild, moderate, and severe sleep apnea
were 83.6%, 92.9%, and 100%, respectively.
The physical examination is frequently nor-
mal in patients with OSA, other than the pres-
ence of obesity, an enlarged neck circumfer-
ence, and/or structural craniofacial bony
abnormalities. There are other medical condi-
tions that may be associated with the develop-
m
ent of OSA, including hypothyroidism and
acromegaly. Both are associated with
macroglossia and increased soft tissue mass in
the pharyngeal region, and patients should be
r
outinely screened for these conditions as well.
Individuals should have a routine evaluation
of their upper airway. The Mallampati score
has been used for years to identify patients at
r
isk for difficult tracheal intubation. It is now
also used commonly by sleep physicians to
evaluate for risk of OSA. The classification pro-
vides a score of 1 thru 4 based on the anatom-
i
c appearance of the airway seen when an indi-
vidual opens his mouth (Figure 2). Studies
have shown that for each 1 score increase in
the Mallampati score, the number of apneic
events increase.
4
2
The next step in the assessment is a formal
sleep evaluation. An overnight polysomnogra-
phy (PSG) is recorded during the normal sleep-
ing hours of a patient. Patients sleep 6 to 8
hours before either awakening spontaneously
or being awokened. The goal of the PSG is to
quantify the amount of time spent in various
stages of sleep during the night and to docu-
ment clinically relevant events such as car-
diopulmonary abnormalities and/or changes in
sleep stages. The standard PSG includes limit-
ed multi-channel recording of an individual’s
electroencephalography (EEG) to assess for
sleep architecture, sleep stages and arousals.
In addition, surface electromyography of the
chin and all four limbs (to assess for move-
ment), electro-oculogram, airflow, pulse
o
ximetry, respiratory effort, electrocardio-
graphic (ECG) tracings, body position, and
snoring are all accumulated.
The portable home-based sleep study has
recently emerged as an alternative to the PSG.
It assesses for oximetry, thoracic and abdomi-
nal movements, and body position. The advan-
tage to this study is that it can be performed
o
vernight in the comfort of the individual’s
home and is more cost effective in comparison
to the formal PSG. In one study, normal
overnight oximetry was very sensitive in
excluding OSA.
43,44
However, the main limita-
tion of the portable home sleep study is that it
d
oes not have the EEG component; it is there-
fore not able to assess an individual’s sleep
architecture and will not be able to assess
arousals based on changes in sleep stages and
can therefore underestimate the prevalence of
OSA. It is thus indicated for use as an alterna-
tive to PSG for the diagnosis of OSA in patients
with a high pretest probability of moderate to
severe OSA and no other comorbid sleep disor-
ders or major comorbid medical disorders.
45
Patients should be excluded if they have con-
gestive heart failure, chronic obstructive pul-
monary disease, neuromuscular disease, use
certain medications (potent narcotics), or may
have another suspected causes for sleepiness.
Diagnosis
The American Academy of Sleep Medicine
(AASM) defines an apnea as a cessation in air-
flow lasting at least 10 sec; apneic episodes
can last anywhere from 10 sec to min, and may
occur multiple times per hour.
46
Hypopnea is
defined as a recognizable transient reduction
(but not complete cessation) of breathing for
at least10 sec. This differs from apnea in that
there remains some flow of air. In the context
of sleep disorders, a hypopnea event is only
considered to be clinically significant if there
is a 30% or more reduction in flow with an
associated 4% or greater desaturation in O2
level, lasting for 10 seconds or longer, or if it is
associated with an arousal or fragmentation of
sleep. Apneas and hypopneas are both consid-
ered in assessing the severity of a person’s
sleep disorder.
47
The Apnea-Hypopnea Index (AHI) is an
index used to assess the severity of sleep
apnea based on the total number of apneas and
hypopneas occurring per hour of sleep. In gen-
eral, an individual is considered to have an
OSA syndrome if they demonstrate an AHI of at
least 5 with the presence of daytime symptoms
or AHI of 15 or more independent of symptoms.
The AHI can also be used to stratify the sever-
ity of the disease; an AHI of 5-15 is classified
as mild, 15-30 is considered moderate, and
greater than 30 is considered severe.
48
Review
[page 62] [Neurology International 2011; 3:e15]
Figure 2. Mallampati
score. Author Jmarchn.
January 29, 2011.
Permission is granted to
copy, distribute and/or
modify this document
under the terms of the
GNU Free Documenta -
tion License, Version 1.2
or any later version pub-
lished by the Free Software
Foundation. [online]
Available from: http://en.
wikipedia.org/wiki/Malla
mpati_score.

A
nother measure that is often used is the
Respiratory Disturbance Index (RDI). Like the
AHI, RDI measures respiratory events; howev-
er, it also includes respiratory event related
arousals (RERAs). RERAs are arousals from
sleep that do not technically meet the defini-
tions of apneas or hypopneas, but do disrupt
sleep. Some research studies have found that
3
0% of symptomatic patients would have been
left untreated if the AHI were used rather the
RDI.
4
9
Please see Figure 5 for a simplified
guideline for the evaluation, diagnosis and
appropriate treatment options for OSA man-
agement.
Complications and comorbidities
Untreated, OSA can have a profound effect
on the body and can contribute to multiple
health problems (Table 2). It is associated with
cardiovascular disease,
50,51
hypertension,
52-54
stroke,
55
arrhythmias, and insulin resistance.
Patients with OSA have a 30% higher risk of
heart attack or death than those unaffected.
5
8
Hypertension that is primarily caused by OSA
(in contrast to essential hypertension) is dis-
tinctive in that the blood pressure does not
drop significantly when the individual is sleep-
ing.
59
OSA that remains untreated can also
have a negative effect on memory. Research
has recently shown that individuals with OSA
have mammillary bodies that were nearly 20
percent smaller on MRI.
60
This decreased tis-
sue mass may be related to the memory prob-
lems seen in chronic OSA.
OSA can have broader cognitive impair-
ments, including sustained attention, working
memory, visuospatial learning, motor perform-
ance, and executive functioning.
61,62
In partic-
ular, patients with OSA have been shown to
have impaired judgment, prolonged reaction
time and vision problems, all of which can
compromise work and driving ability.
63
OSA
increases motor vehicle accident risk by 2- to
3-fold, independent of EDS or AHI score.
64
Behavior and mood can also be profoundly
affected by a lack of the adequate restful sleep
seen in sleep apnea, including irritability,
aggressiveness, lack of attentiveness, as well
as depression.
65
There has been increasing recognition of
OSA as a comorbid condition in a number of
neurological disorders, including epilepsy,
stroke, multiple sclerosis, and headache. OSA
appears to be more prevalent in patients with
epilepsy than in the general population and
untreated OSA may theoretically worsen
seizure control by increasing seizure burden
through sleep disruption/deprivation.
66
OSA
also increases the risk of stroke and appears to
compromise rehabilitation following strokes.
67
It is theorized that OSA may directly cause
d
irect neural injury or cause extension of vas-
c
ular penumbra via hypoxia and ischemia in
stroke.
6
8
There appears to be a higher incidence of
OSA in the multiple sclerosis (MS) population,
but this has been poorly studied in small
prospective series. It is unclear at this time if
this comorbidity association is due to MS
lesions, symptomatic medications used for
p
ain and spasticity, etc.
6
9
C
hronic and morning
h
eadaches are a relatively common symptom
in OSA, and OSA may aggravate the frequency
and severity of migraines.
7
0
OSA treatment has
been shown to reduce cluster headache fre-
quency in patients with OSA and comorbid
cluster headaches.
71
The conclusion regarding
OSA as a comorbid condition in some neuro-
logical disorders is that neurologists should be
mindful of the fact that OSA is more prevalent
in their patient population and that practition-
ers should routinely screen for OSA in their
patients.
Treatment options
The most common first step in the treat-
ment of mild OSA is behavioral or lifestyle
modification, including losing weight, avoid-
ing alcohol, sleep aids or muscle relaxants, and
quitting smoking.
7
2
Weight loss in overweight
patients has been shown to decrease apneic
episodes,
72,73
both directly and by reducing
neck fat and nasopharyngeal crowding.
75,76
If an individual’s apneic episodes are mild
and occur mainly during supine sleep, then
patients are advised to take measures to avoid
sleeping supine.
77,78
The most common posi-
tion that apneic and hypopnic episodes are
observed during sleep is in the supine posi-
tion. These patients may also benefit from
sleeping at a 30-degree incline.
79
Both these
steps may help prevent the tongue and palate
from falling backwards and prevents the gravi-
tational collapse of the airway.
Along with lifestyle modifications, there are
other treatment options of OSA.
Positive airway pressure
For moderate to severe sleep apnea, the use
of a continuous positive airway pressure
(CPAP) is the first line therapy.
80
CPAP uses
continuous pressurized air flow to keep the
individual’s airway open during sleep. The
amount of pressure used is initially titrated
during the PSG (split test) based on the
patient’s comfort and lowest pressure required
to decrease apneic and hypopneic episodes.
CPAP therapy is the most effective treatment
option in reducing apneas in OSA.
81
It has
been shown to improve AHI, RDI, sleep archi-
tecture, EDS, neurobehavioral performance
and cardiovascular morbidity (hypertension).
However, noncompliance is common and may
be as high as 40%, due mainly to discom-
fort.
82,83
Newer models of CPAP devices humidify the
air, which decreases dry mouth and makes
usage more comfortable.
84
In addition, newer
models have automatic positive airway pres-
sure options. This modality automatically
titrates the amount of pressure delivered to the
patient to the minimum required to maintain
an unobstructed airway on a breath-by-breath
basis by measuring the resistance in the
patient's breathing, thereby giving the patient
the precise pressure required at a given
time.
85
BiPAP (variable/bilevel positive airway pres-
sure) provides two levels of pressure: a higher
inspiratory positive airway pressure (IPAP)
and a lower expiratory positive airway pres-
sure (EPAP) for easier exhalation. This modal-
ity appears to be better tolerated and individu-
als may find it easier to use; it is used in cases
when patients cannot tolerate CPAP, for
patients with chronic CO
2
retention as well as
sleep apnea, and for patients with neuromus-
cular disease who need some assistance with
nocturnal ventilation. BiPAP may also be more
useful in CSA.
86
Dental appliances
Dentists specializing in sleep dentistry can
make a custom-made mouthpiece that shifts
the lower jaw forward, thereby maintaining an
open airway (in theory). This approach can be
successful in individuals with mild to moder-
ate OSA but has been proven less effective for
severe cases.
87
In one study comparing CPAP
to dental appliance in mild to moderate OSA,
dental appliances decreased AHI from 21
(baseline) to 14, compared to a decreased AHI
of 5 in patients using CPAP.
88
Surgery
Surgical treatment for OSA needs to be indi-
vidualized in order to address all anatomical
areas of obstruction. The most frequently uti-
Review
[Neurology International 2011; 3:e15] [page 63]
Table 2. Long term health problems associ-
ated with untreated obstructive sleep
apnea.
Health problems associated with sleep
apnea
Hypertension
Stroke
Diabetes
Heart failure
Cardiac arrhythmia
Myocardial infarction
Obesity
Depression
Worsening of Attention Defficit Hyperactivity
Disorder (ADHD)

l
ized surgery treatment is the uvu-
lopalatopharyngoplasty (UPPP or UP3). These
surgeries aim to address pharyngeal obstruc-
tion by removing tissue in the back of the
t
hroat, including part of the uvula, the soft
palate, the tonsils, the adenoids and pharynx
(Figure 3). In a retrospective review compar-
ing CPAP to surgery, there appeared to be
s
uperior results with CPAP compared to
UPPP.
89
Further studies have not been conclu-
sive that this surgery has been effective at
treating severe OSA.
90
M
axillomandibular advancement (MMA) is
another type of surgery that has been used to
treat OSA. This procedure aims to advance the
maxilla and mandible, thereby pulling forward
the anterior pharyngeal tissues attached to the
maxilla, mandible and hyoid to structurally
enlarge the retrolingual and retropalatal
spaces (Figure 4).
91
It is considered the most
e
ffective surgery for OSA patients, because it
increases the posterior airway space.
92
In a
study in 2008, it was noted that MMA surgery
led to a significant increase in general produc-
t
ivity, social outcome, activity level and sex.
9
3
In addition, there are specialized tech-
niques that are available for correction of spe-
cific regions or obstruction, including the
n
asal passages (septoplasty and turbinate sur-
gery), the soft palate (implantation of Dacron
pillars) and the tongue. However, there have
not been clinical trials or current evidence to
s
upport the use of these techniques in the
treatment of OSA.
Pharmacological management
Medications are generally not a part of the
primary treatment of OSA. Modafinil is
approved by the FDA for use in patients with
OSA who have residual daytime sleepiness.
A
rmodafinil, the R-enantiomer of modafinil, is
now FDA approved for use as well. The
American Academy of Sleep Medicine (AASM),
in a clinical review of medical therapies for
OSA, recommended Modafinil as a standard
treatment of residual excessive daytime
sleepiness in patients with OSA despite maxi-
mal management of CPAP. Protriptyline was
not recommended as a primary treatment for
OSA, although it was acknowledged that it may
induce moderate improvement in the AHI in
patients with OSA and may be used as a second
line treatment option. Aminophylline, theo-
p
hylline, SSRIs and estrogen were not recom-
mended for treatment of patients with OSA
given that there was no consistent evidence of
their effectiveness.
94
Conclusions
In the context of the current epidemic of
obesity, the prevalence and consequences of
OSA will likely increase in the coming years.
Given the aging population, the number of
neurological patients with OSA and comorbid
stroke, epilepsy, headache, and cognitive
decline will also likely rise. OSA can signifi-
cantly affect physical health, mental health and
emotional well-being. Fortunately, screening
methods for sleep apnea have improved, and
there are now very effective means of diagno-
sis and treatment. Treatment can lead to a ben-
eficial impact on a patient’s health and quality
of life. Several treatment options exist, and
research into additional options continues.
The medical community faces many hurdles
regarding the development of adequate early
screening and appropriate treatment of OSA.
An important next steps in understanding and
treating OSA is to be proactive and develop bet-
ter screening methods and properly treat
patients at risk (Figure 5).
It is imperative that the medical communi-
ty understand that the effects of OSA is far-
reaching, and early detection/treatment will
be beneficial to individual patients, as well as
a cost-effective public health measure to
reduce morbidity and mortality. Physicians of
all specialties should screen for the presence
of sleep disturbances and consider referral to
a sleep specialist when indicated.
Neurologists, in particular, should be mindful
of comorbid OSA in their patient population,
since prompt identification and treatment of
OSA may reduce health risk and improve neu-
rological functioning.
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