...

Please check marked references Marin et al, 2005 [1] Case-Control-Study 3b

by user

on
Category: Documents
54

views

Report

Comments

Transcript

Please check marked references Marin et al, 2005 [1] Case-Control-Study 3b
Table e1: Natural course
Please check marked references
Author
Design
EBM
Marin et al, 2005 [1]
Case-Control-Study 3b
Patient population
Results
Comments
N=264 healthy controls ,
Non-fatal CV events and
Follow-up once per
AHI 1.2 ± 0.3,
CV death
year for a mean of
10.1 ± 1.6.
N=377 snorers
Lavie et al, 2007 [2]
Case-Control-Study 3b
AHI 3.5 ± 0.8,
Healthy controls
No follow-up of the
N=403 mild-moderate
20
AHI.
OSA , AHI 18.2 ± 3.5
Snorers
N=235 severe OSA ,
35
AHI 43.3±5.7
Mild-moderate OSA
Treated OSA,
58
AHI 42.4 ± 4.9
Severe OSA 75
AHI<10
Mortality rate per 1000
Median follow-up
N=3227
patient-yrs
period: 4.6 ± 2.2 yrs.
(median RDI 7)
AHI<10
No follow-up of the
AHI 11-20
2.19
AHI.
N=4154
AHI 11-20
(median RDI 15)
4.52
AHI 21-30
AHI 21-30
1
N=2601
5.1
(median RDI 24)
AHI 31-40
AHI 31-40
8.57
N=1204
AHI > 40
(median RDI 35)
10.22
AHI > 40
N=59
(median RDI 59)
He et al, 1988 [3]
Case-Control-Study 3b
Untreated
Cumulative survival
Follow-up period: 5
AHI<=20
5 year:
and 8 yrs
N=142
No follow-up of the
Untreated:
Untreated
AHI<=20
AHI>20
0.96±0.02
AHI.
N=104
Untreated
Treated
AHI>20
Tracheotomy
0.87±0.05
N=33
CPAP: N=25
Treated
UPPP: N=60
Trach: 1
2
CPAP: 1
UPPP: 0.85±0.06
8 year:
Untreated:
AHI<=20
0.96±0.02
Untreated
AHI>20
0.63±0.17
Treated
Trach: 1
CPAP: none
UPPP: 0.78±0.09
Berger et al, 2009 [4]
Case-Control-Study 3b
N=28 snorers, AHI 1.8 ± AHI change (∆AHI)
Follow-up period:
1.6,
5.1±3 yrs
3
49 mild OSA, AHI
Snoring
CV risk associated
9.1±3.3,
11.7±12.8
with BMI and age
not with AHI.
41 moderately severe
OSA,
Mild OSA 12.6±16.4
AHI 21±4.2,
42 severe OSA,
Moderate 8.1±19.6
AHI 52.6±2
Severe OSA -7±28.2
Young et al, 2002 [5]
Population based
2b
N=282 (161 male)
AHI change
study
Wisconsin Sleep
Cohort Study data:
From 2.5 to 5.1 (∆ 2.7±8.2) Follow-up period: 8
yrs
Sign. difference
AHI increase
Obese-not obese: 3.7±1
depended on age,
BMI and snoring but
Older-younger: 2±1
not on gender
Habitual snorer-not : 5.9±1
Redline et al, 2003 [6] Community-based
study
2b
N=486 (197 male)
AHI change
Age: 31.6±17.9 yrs
Follow-up period:
5.38±0.9 yrs using
%RDI>5: from 29 to 42
in-home monitoring
4
%RDI>15: from 10.5 to
AHI increase
16.3
depended on age,
BMI and gender
Mean RDI: from 6±10 to
8.6±14.3
Tishler et al, 2003 [7]
Case-Control-Study 3b
N=286 (180 male)
Follow-up
Cleveland Family
Study:
Age: 36.8±11.9 yrs
AHI:
Follow-up period:
AHI:
0-4.9 N=181
5 yrs using in-home
1.9±1.4
5-9.9 N=58
monitoring
(AHI <5 in all
10-15 N=18
participants)
>15
N=29
AHI incidence over
5 yrs is depended
on age, sex, BMI,
waist-hip-ratio,
cholesterol
Noda et al, 1998 [8]
Case-Control-Study 3b
N=148 (136 male)
Lower survival rate in
Follow-up period:
age 52±12.3 yrs, BMI
middle-aged patients and
10 yrs using
27.2±6.5kg/m2,
in patients with AHI ≥20.
questionnaire
survey.
5
Age groups:
Hypertension is correlated
Young (<40)
with lower survival in total
Prognosis in middle-
Middle aged
and middle-aged groups.
aged population
may depend on the
Elderly (≥65)
role of OSA on
AHI groups:
hypertension, but
<20
not on AHI only.
≥20
Partinen et al, 1988
Case-Control-Study 3b
[9]
N=198 mild to very
Higher mortality and CV
Follow-up period:
severe OSA
risk in the group with
5 yrs using
Age: 51.3±11.3 yrs
weight loss
questionnaire
recommendation.
survey.
recommendation: N=127
OR for vascular death in
No information
Mean AHI 43±30.5
the weight loss group 4.7.
about weight loss.
Weight loss
Tracheotomy: N=71
Higher mortality in
Mean AHI 69±23
the weight loss
group despite lower
AHI and BMI.
Redline et al, 2001
Community based
2b
N=232
Rise in AHI up to 6.2±7.9
(Cleveland Family
6
[10]
study
Persons with an AHI < 5,
Study: Follow-up
AHI 2±1.4
period 5 yrs using
questionnaire
survey.
Age 54±2 yrs, BMI 35±1
kg/m2 ,
AHI increase
depended on BMI,
cardiovascular risk
and diabetes.
Lindberg et al, 1999
Case-Control-Study 3b
N=38 (male) mild OSA
[11]
Rise in AHI from 2.1±4.2 to Follow-up period 10
6.8±7.2
29 untreated
AHI 2.1±4.2
yrs
using PSG.
AHI>5: from 14 to 45%
Rise in AHI
Age 50±10
AHI≥10: from 3 to 28%.
independent on age,
BMI and smoking.
9 treated
AHI 11.8±7.7
Svanborg et al, 1993
[12]
Case-Control-Study
3b
N=42 (35 male) mild to
62% of the patients had a
Follow-up period
very severe OSA
rise in ODI of more than
mean 15.6 (6-32)
age 55 (41-72) yrs
50%.
months
7
using polygraphy
, weight 113±22 kg, BMI
36±6 kg/m2, AHI 37±35,
ODI in PG : 10.1 (1-31)
(follow-up).
6 M weight loss
programme
(baseline) and PSG
ODI in PSG : 20.9 (2-63)h
Rise in ODI
AHI in PSG : 23.5 (6-55)
dependent on AHI
and BMI.
Ancoli-Israel et al,
Prospective
2001 [13]
randomized follow-
2b
up study
N=427
Age > 65 yrs
Change in RDI was
Follow-up period 2
associated with BMI, BMI
yrs
change and hypertension
using PSG.
but not with age.
No RDI data
presented.
Newman et al, 2005
Population-based,
2b
N=2968 (1342 male), age After 5 yrs :
Sleep Heart Health
[14]
prospective cohort
62±10 yrs, weight 87±14
males lost 5 to 10 kg in
Study:
study
kg (males), 75±16 kg
10.3% of the cases,
Follow-up period 5
(females), BMI 29±4
females lost 5 to 10 kg in
yrs. Association
kg/m2 (males), 29±6
11.9% of the cases.
between weight
kg/m2 (females), median
Weight loss of as little as 5 change and
AHI 6.3 (males), 2.8
to 10 kg tended to be
decrease in AHI is
(females)
associated with a greater
stronger in men
8
than 2-fold greater odds of
than in women.
a 15-unit or greater
reduction in the AHI
compared with weight
stability in men.
Pendlebury et al, 1997 Retrospective case
[15]
3b
note study
N=55
AHI increase from
Follow-up period 77
Mild to moderate OSA
21.8±11.5 to 33.4±21.3.
(17-229) weeks
using PSG.
Age: 55.8±10 yrs
AHI changes
BMI: 29.7±5.4 kg/m2
independent on BMI
and age.
Peppard et al, 2000
Prospective
[16]
population-based
cohort study
2b
N=690 (385 male)
10% weight gain with 32%
Follow-up period 4
increase in the AHI
yrs using PSG.
10% weight loss with 26%
AHI changes
AHI: 4.1±9.1
decrease in the AHI
dependent on BMI.
BMI 29±6 kg/m2
10% weight gain with 6-
Age: 46±7 yrs
fold increase in OR
developing moderate-to-
9
severe OSA
Ancoli-Israel et al,
Prospective
1993 [17]
population based
2b
N=24
No changes in AI and RDI
Follow-up period 8.5
over time
yrs
N=32
No changes in RDI, AI or
Follow-up period
(18 male) mild to
HI over time
4.6±0.7 yrs using
study
Mason et al, 1989 [18] Case-Control-Study 3b
moderately severe OSA
PSG
Age 70.3±3.5 yrs
RDI 16.7±11.53
Sahlman et al, 2007
Case-Control-Study 3b
N=28
Rise in AHI from 9±2.7 to
Follow-up period
[19]
(Retrospective
Mild OSA
22.3±18.7
3.9±1.7 yrs using
longitudinal follow-
PSG.
up study)
Age 50.2±7.6 yrs
BMI 31.5±4.5kg/m2
Sforza et al, 1994 [20] Case-Control-Study 3b
N=32
No changes in AHI over
Follow-up period 5.7
10
severe OSA
time in the whole group.
Age: 51±1.8 yrs
No influence of weight gain
yrs using PSG.
on AHI.
BMI:30.7±1.1kg/m2
AHI: 52.2±6
Guilleminault et al,
Case-Control-Study 3b
N=94 (26 male)
2006 [21]
No changes in AHI and
Follow-up period 4.5
RDI
yrs using PSG.
Female 68
Age: 30±4.8 yrs
Worsening in
BMI : 23.4±1.9kg/m2, AHI
subjective
2.2±0.6
complaints but not
RDI: 8.6±3.4
in AHI or RDI.
Male 26
Age: 26.3±3.5 yrs
BMI : 23.7±2.3kg/m2, AHI
2.4±0.6
RDI: 9.5±3.4
11
Hoch et al, 1997 [22]
Case-Control-Study 3b
N=50 healthy volunteers
No changes in AHI over
Follow-up period 3
(23 male)
time
yrs using PSG.
N=40
No changes in AHI over
Follow-up period
(36 male)
time
5±2.8 yrs using
Age:
Young old: 69.3±4 yrs
Old: 81.1±3.5 yrs
BMI:
Young old: 26±4.5 kg/m2
Old: 25.2±3.8 kg/m2
Mean AHI:
Young old: 3.95±3.95
Old: 5.4±7.7
Fisher et al, 2002 [23] Case-Control-Study 3b
PSG.
Age:47±10 yrs
BMI : 28.9±4.8kg/m2
12
RDI: 27±21
Young et al, 2008 [24] Prospective
community based
2b
N=1522
All cause mortality risk with Follow-up period
(839 male)
SDB (HR)
study
13.8 (1.5-18.7) yrs
using PSG.
Age:48±8 yrs
BMI : 28.6 kg/m2
None (AHI<5): Reference
Mild (AHI 5-14.9):1.6
No influence of age,
Moderate (AHI 15-29.9):
BMI or sex on
1.4
mortality
Severe (AHI > 30: 3
13
Table e2: Dietary weight loss in obstructive sleep apnoea syndrome: effect on AHI
Author
Design
EBM
Patient population
Results
Comments
Smith et al, 1985
RCT
1b
N=15 (12 male) very
Weight change –9.6 kg (-
Follow-up after 5 M.
severe OSA, age 59±3
9%), BMI change –3.3
Sleep data taken
(SE) yrs, weight 106±7
kg/m2 (-9%),
from graphs, not
kg, BMI 37 kg/m2, AHI
AHI change NREM
included in the text.
NREM 55±7, AHI REM
-25,8 (-47%), AHI change
57±3, diet instructions
REM –19.4 (-34%)
[25]
Sleep patterns also
improved : decrease in
stage 1 sleep, increase in
stage 2 sleep, deep sleep
unchanged, REM sleep
increased with 5%.
hypersomnolence
decreased
Suratt et al, 1987
Case series,
[26]
prospective study
4
N=8 (5 male) mild to very Weight change –20.6 kg
Although
severe OSA patients, age (-13%), BMI change –6.6
polysomnography
2
49±6 yrs, weight 153±37
kg/m (-13 %)
was performed, no
kg, BMI 53.6 ±13.0
AHI change –32.49 (-36%) sleep data were
14
kg/m2, AHI 90±32 ;
Oxygenation during both
dietary-induced weight
sleep and wakefulness
loss (VLCD)
improved, collapsibility of
reported.
the nasopharyngeal airway
increased
Rubinstein et al,
Case series,
1988 [27]
prospective study
4
N=12 (8 male) moderate
Weight change –24.0 kg
Improvement in
to very severe OSA, age
(-20%), BMI change –9
OSA may be related
49±11 yrs, weight
kg/m2 (-20%), AHI change
to improvement in
117±20 kg, BMI 41±8
–43.0 (-75%)
pharyngeal and
kg/m2, AHI 57±29, diet
glottic function.
instruction or anterior-
Although
banded gastroplasty
polysomnography
was performed, no
sleep data were
reported.
Pasquali et al, 1990
[28]
Case series
4
N=23 (22 male) OSA
Weight change –18.4 kg
A significant
patients, age 46.4±9.2
(-18%), BMI change
correlation was
yrs, weight 105.1±26.4
–6.6 kg/m2(-18%), AHI
found between
kg, BMI 37.5±9.8 kg/m2,
change -33.5 (-50%)
weight loss and
AHI 66±23, low or very
∆AHI (r =-0.55)
low calory diet
Although
15
polysomnography
was performed, no
sleep data were
reported.
Rajala et al, 1991
Case series
4
[29]
N=8 (7 male) mild to very BMI change –6.6 kg/m2
Polygraphy (static
severe OSA patients,
(-12%), ODI change –14.2
charge sensitive
BMI 50.7±8.4, ODI
(-37%)
bed).
Follow-up period 1
46±28, intensified diet
year.
Schwartz et al, 1991 Case-control study
3b
[30]
N=13 male very severe
Weight change –7.3 kg
OSA, age 47±9 yrs,
(-17.4%), BMI change –9.4 3.1±4.2 to –2.4±4.4
weight 129±20 kg, BMI
kg/m2 (-17.4%), AHI
cm H 2 O. Control
42±7 kg/m2, AHI NREM
change –50.8 (-61%)
polysomnography
83±31, diet and CPAP
Pcrit decreased from
was performed
when target weight
was achieved or at
the latest after 25
months. However,
no sleep data were
reported.
Suratt et al, 1992
Case series
4
N=8 (5 male) very severe Weight change –21 kg
Within 2 yrs, all had
16
[31]
OSA, age 40-50 yrs,
(-14%), BMI change –8
returned to their
weight 153±37 kg, BMI
kg/m2 (-14%), AHI change
baseline, pre-VLCD
54±13 kg/m2, AHI 90±32, –28.0 (-30%)
weight. Although
very low calory diet
polysomnography
(VLCD)
was performed, no
sleep data were
reported.
Kiselak et al, 1993
Case series
4
[32]
N=14 severe OSA, age
Weight change –27.2 kg
Polygraphy
43±11 yrs, weight
(-23.7%), AHI change –
(Edentec 4700).
114±20 kg, AHI 42±16,
16.6 (-39.5%)
Blood pressure and
AHI both
diet/behavioural therapy
significantly
declined, soft palate
width decreased,
and vital capacity
increased. Followup period 5 M.
Nahmias et al, 1993
[33]
Case series
4
N=28 (24 male) very
Weight change –22.1 kg
19 patients were
severe OSA, age 49 yrs
(-18%), AHI change –39
considered cured,
(31-68), weight 122±6 kg, (-69%). Sleep quality
i.e. AHI<15. Follow-
%IBW 183±23, AHI 56±3, improved with an increase
up period was 20-76
17
diet/CPAP/VLCD
in stage 2 and REM and a
weeks. Sleep data
decrease in stage 1.
were reported as a
graph.
Rauscher et al, 1993 Case-control study
3b
[34]
N=27 severe OSA
BMI change -2.1 kg/m2 (-
Follow-up period
patients, age 54±2 yrs,
6%)
512±41 days.
BMI 35±1 kg/m2 , %IBW
%IBW change –26.4%IBW Although
155±7, AHI 36±4,
(-17%)
polysomnography
recommendation of
AHI change –1.8 (-5%)
was performed, no
weight loss versus
There was only a small but sleep data were
CPAP.
significant decrease in BMI reported.
in the nasal CPAP control
group.
Only the percentage
change in BMI significantly
contributed to the course of
hypertension.
Kajaste et al, 1994
[35]
Case series
4
N=32 severe OSA, age
After 6 M :
Polygraphy (Static
49±7 yrs, weight 118±14
Weight change –11 kg
Charge Sensitive
kg, BMI 39±4 kg/m2 , ODI (-9.3%)
Bed). Success was
2
39±25, cognitive-
BMI change –3.6 kg/m
defined as a
behavioural weight loss
(-9.3%)
decrease of ODI to
18
programme
ODI change –19.8 (-55.3%) below 10 and a
After 2 yrs :
decrease in ODI
Weight change –4.6 kg
greater than 50%.
(-3.9%)
Follow-up : 6 M, 2
2
BMI change –1.5 kg/m
yrs.
(-3.9%)
ODI change –1 (-2.8%)
Braver et al, 1995
Case series
4
[36]
N=9 mild to very severe
Weight change – 5 kg
Weight loss was
OSA, age 42±13 yrs,
(-4.4%), BMI change –1.6
combined with
2
weight 113±22 kg, BMI
kg/m (-4.4%), AHI change
sleeping on one’s
36±6 kg/m2, AHI 37±35,
–11 (-29.7%)
side, and the
6 M weight loss
administration of a
programme
nasal decongestant.
Follow-up 6 M. No
data on M/F.
Macrostructure of
sleep unchanged.
Noseda et al, 1996
[37]
Case series
4
N=39 (35 male) very
Weight change –3.4 kg (-
3 patients with
severe OSA, age 50±11
3.3 %), BMI change –1.7
gastroplasty were
yrs, weight 103±18 kg,
kg/m2
excluded from
BMI 35±9 kg/m2, AHI
AHI –16.2 (-24.4%)
(-3.3%),
analysis ; only 4
19
66±29,
1 year
VLCD/CPAP
18 patients showed a
patients could be
decrease (≥20% of
weaned from CPAP.
baseline) in AHI, 11 had no Follow-up 1 year.
change, 7 had an increase.
Sleep stage shift index
decreased from 76±29 to
62±28. No changes in
sleep stages.
Kansanen et al,
Case control study
4
1998 [38]
N=15 (14 male)
Weight change –9.2 kg (-8
moderate to severe OSA, %), BMI change –3.1
age 52±9 yrs, weight
kg/m2
114±20 kg, BMI 38±6
11.0 (-37.9%)
Polygraphy (NT901).
Follow-up 3 M.
(-8%), AHI –
kg/m2, AHI 29±19, 3M
VLCD diet
Sampol et al, 1998
[39]
Case series
4
N=24 (predominantly
After 11 M :
Cured OSA were
male) mild to very
BMI change –5.6 kg/m2
evaluated to
severe OSA, BMI
(-17.1%)
ascertain the
32.8±4.6 kg/m2,
AHI –41.3 (-93.2%). %
efficacy of weight
AHI 44.3±27.8, who
stage 1-2 decreased, %
loss in the long-
followed a successful diet stage 3-4 and REM sleep
increased.
and cured more than 5
term. 6 of 13 who
maintained their
20
yrs ago.
After 94 M :
weight presented
BMI change –2 kg/m2 (-
recurrence of OSA,
6%)
as did 8 of 11 who
AHI –17.9 (-40.4%).
had regained
Deterioration of sleep
weight.
quality.
Lojander et al, 1998 Case series
4
[40]
N=24 (23 male)
Weight change –11 kg
moderate to severe OSA, (-10%), BMI change –5
1 year follow-up
period. Only
age 48±7 yrs, weight
kg/m2(-13.9%), ODI –18
polygraphy was
110±11 kg, BMI 36±3
(-60%)
performed (static
kg/m2, ODI4 30±20.
Sleepiness decreased from charge sensitive bed
VLCD and behavioural
47±30 to 37±34 (range
and oximetry
management
visual analogue scale 0-
recordings).
100).
Hakala et al, 2000
[41]
Case series
4
N=13 moderate to severe Weight change –16 kg
Polygraphy (Static
OSA patients, age
(-14.4%), BMI change –3.2 Charge Sensitive
unknown, weight 111
kg/m2(-9.1%), ODI –21
Bed).
(90-129) kg, BMI 35 (30-
(-67.7%). Improved
percentual weight
38) kg/m , ODI4 31 (7-
daytime respiratory
change is different
69). VLCD.
mechanics and gas
from BMI change.
2
Reported
exchange after weight loss. No data on M/F.
21
Peppard et al, 2000
Population-based,
[16]
2b
N=690 (385 male), age
After 4 yrs :
A 10% weight loss
prospective cohort
46±7 yrs, weight 85±19
-20% body weight : AHI-
predicted a 26%
study
kg, BMI 29±6 kg/m2, AHI
48%
decrease in the AHI
4.1±9.1
-10% body weight : AHI-
(data from the
26%
Wisconsin Sleep
-5% body weight : AHI-14% Cohort Study). No
data on sleep
quality.
Kajaste et al, 2004
[42]
Case series
4
N=31 (all male) OSA,
After 6 M :
Polygraphy (Static
age 49±8 yrs, weight
Weight change –19 kg
Charge Sensitive
140±20 kg, BMI 44±5
(-13.6%), BMI change –6
Bed). The greatest
kg/m2, ODI 51±31,
kg/m2(-13.7%), ODI –28
weight loss and
cognitive-behavioural
(-54.9%)
alleviation of OSA
approach and VLCD
After 12 M :
was seen at 6 M,
Weight change –18 kg
after which the
(-12.9%), BMI change –5.5 patients started to
kg/m2 (-12.6%), ODI
gain weight. After 2
change –26 (-50.9%)
yrs, more than one-
After 24 M :
third still showed
Weight change –13 kg
excellent or good
(-9.3%), BMI change –4
results. Adding
22
kg/m2 (-9.1%), ODI change CPAP to part of the
–19 (-37.2%)
patients did not
result in significantly
greater weight loss.
Newman et al, 2005 Population-based,
[14]
2b
N=2968 (1342 male), age After 5 yrs :
Data from the Sleep
prospective cohort
62±10 yrs, weight 87±14
males lost 5 to 10 kg in
Heart Health Study.
study
kg (males), 75±16 kg
10.3% of the cases,
Follow-up period 5
(females), BMI 29±4
females lost 5 to 10 kg in
yrs. Association
kg/m2 (males), 29±6
11.9% of the cases.
between weight
kg/m2 (females), median
Weight loss of as little as 5 change and
AHI 6.3 (males), 2.8
to 10 kg tended to be
decrease in AHI is
(females)
associated with a greater
stronger in men than
than 2-fold greater odds of
in women. No data
a 15-unit or greater
on sleep quality.
reduction in the AHI
compared with weight
stability in men.
Kemppainen et al,
2008 [43]
RCT
1b
N=52 (41 male) mild
After 3 M:
A VLCD diet with a
OSA, Control group :
BMI change -5.4 kg/m2 in
supervised lifestyle
N=26 (20 male), weight
intervention group, versus
intervention versus
94±12 kg, BMI 32±3.1
2
-0.5 kg/m in control group; routine lifestyle
23
kg/m2, AHI 9±3,
AHI change -3±9 in
counselling (control).
Intervention group: N=26, intervention group versus
Significant
weight 103±14 kg, BMI
correlation between
-1±5 in control group.
33±3 kg/m2, AHI 11±4
reduction in AHI and
change in BMI
(r=0.30, p=0.04).
Lam et al, 2007 [44] RCT
1b
Foster et al, 2009
[45]
1b
RCT
N=101 (79 male) mild to
moderately severe OSA,
age 46±1 (SE) yrs,
weight 75±2 kg, BMI
27±1 kg/m2, AHI 21±1.
Randomisation to 3
groups : conservative
measures only (CM),
CPAP group, oral
appliance group (OA).
All received diet
instructions.
Weight change –0.3 kg
(-0.4%) in CM, -1.2 kg
(-1.6%) in CPAP group, -1
kg (-1.4%) in OA; BMI
change –0.2 kg/m2 (-0.7%)
in CM, -0.4 kg/m2 (0.2%) in CPAP, -0.4 kg/m2
(-1.5%) in OA.
AHI CM change +1.2
(+6.2%), AHI change
CPAP –21 (-88.2%), AHI
change OA -10.3 (-49.3%).
Epworth sleepiness scale
improved in all groups (-2, 5, -3 respectively)
N=264 (108 male) mild to In DSE: weight change –
severe diabetic OSA, age 0.6 kg (-0.6%), BMI
change
–0.2 kg/m2 (61±6 (SD) yrs, weight
102±18 kg, BMI 36.7±5.7 0.5%),
AHI change +4.2 (+17.9%).
kg/m2, AHI 23±16.
In ILI: weight change –10.8
Randomisation to 2
BMI change
groups : diabetic support kg (-10.5%),
2
–3.8
kg/m
(-10.3%),
and education (DSE)
Follow-up after 10
weeks.
Patients on CPAP or
OA were
reassessed without
device, after
stopping its use for 1
week. Although
polysomnography
was performed, no
sleep data were
reported.
38.7% had mild
OSA, 35.2% had
moderate OSA, and
26.1% had severe
OSA. ILI was more
effective in reducing
the AHI in men than
in women and more
24
AHI change -5.4 (-23.6%).
[n=139, age 61±6 yrs,
weight 102±17 kg, BMI
36.5±5.7 kg/m2, AHI
23±15] and
intensive lifestyle
intervention (ILI) [n=125,
age 61±7 yrs, weight
103±20 kg, BMI 36.8±5.8
kg/m2, AHI 23±18] .
Johansson et al,
2009 [46]
RCT
1b
effective in
participants with
higher levels of
baseline AHI than in
those with lower
levels of baseline
AHI.
Although
polysomnography
was performed, no
sleep data were
reported.
N=63 (all male) moderate In the intervention group:
Based on
polygraphy
to severe OSA, age 49±7 weight change –18.7 kg
(SD) yrs, weight 112±14 (-16.5%), BMI change –5.7 (WatchPAT100).
2
The intervention
kg, BMI 34.6±2.9 kg/m2, kg/m (-16.5%),
AHI
change
-25
(-67.6%).
group received a
AHI 37±15. 30 were
12 of 30 (40%) improved
very low energy diet
randomised to
by
2
categories
of
AHI,
14
for 7 weeks,
intervention (very low
of 30 (47%) improved by
followed by 2 weeks
calory diet, VLCD) and
one
category,
and
4
of
30
of gradual
33 to control.
(13%) remained in the
introduction of
same category
normal food. The
In controls: weight change control group
+1.1 kg (+1%), BMI
adhered to their
change
+0.3 kg/m2
usual diet during the
(+0.9%),
nine weeks of
AHI change -2 (-5.4%). 1 follow-up.
of 33 (3%) improved by two
AHI categories, 3 of 33
(9%) improved by 1 AHI
category, 24 of 33 (73%)
25
remained static, and 5 of
33 worsened to a higher
AHI category (15%).
Tuomilehto et al,
2009 [47]
RCT
1b
N=72 (53 male) mild
OSA, age 51±9 (SD) yrs,
weight 96±11 kg, BMI
32±3 kg/m2, AHI 10±3.
37 were randomised to
intervention (very low
calory diet, VLCD) and
35 to control.
In the intervention group:
weight change –10.7±6.5
(SD) kg (-11.1%), BMI
change –3.5 kg/m2 (10.9%),
AHI change -4 (-40%).
In the control group:
weight change –2.4±5.6 kg
(-2.5%), BMI change –0.8
kg/m2 (-2.5%),
AHI change +0.3 (+3%).
Follow-up period 1
year. Weight
reduction is a
feasible and
effective treatment
for the majority of
patients with mild
OSA. Although
polysomnography
was performed, no
sleep data were
reported.
26
Table e3: Surgical treatment of obesity in obstructive sleep apnoea syndrome: effect on AHI
Author
Design
EBM
Patient population
Results
Harman et al, 1982
Case series
4
N=4 male OSA, age 36
Weight change –90 kg (-
Follow-up period not
yrs, weight 213±20 kg,
42%) AHI change –76.6 (-
specified.
AHI 80±82, jejunoileal
98%). %Stage 2 and deep
bypass
sleep increased.
N=15 (14 male) OSA
At 2-4 M :
No correlation
patients, age 45±10 yrs,
Weight change –35 kg (-
between the amount
weight 142±31 kg, BMI
25%)
of weight loss and
[48]
Peiser et al, 1984
[49]
Case series
4
2
48±9 kg/m2, excess body BMI change –11.8 kg/m
(-25%)
weight 119±40, AHI
82±44, gastric bypass
(Mason)
%EBW change –54%
Comments
the decrease in AHI.
No data on sleep
quality.
(-45.3%)
AHI change –67 (-82%)
At 4-8 M :
Weight change –57 kg (40%)
BMI change –19.3 kg/m2
(-40%)
27
%EBW change –64 %
(-53.8%)
AHI change –76 (-93%)
Peiser et al, 1985
Case series
4
[50]
N=14 (13 male) OSA
Excess body weight
Follow-up period 6
patients, age 42 yrs,
change –70% (-32%),
M. Most cardiac
excess body weight
AHI change
arrhythmias
222±39%, AHI 85±43,
91%)
–-77.5 (-
disappeared. No
data on sleep
gastric bypass
quality.
Charuzi et al, 1985
Case series
4
[51]
N=13 (12 male) OSA
Excess body weight
Follow-up period 6
patients, age 44±10 yrs,
change –72.5% (-32%)
M. Sleep data taken
excess body weight
AHI change -81 (-91%)
from graphs, not
222±12%, AHI 89±12,
The number of awakenings included in the text.
gastric bypass (Mason)
decreased after surgery
from 9±7 to 4±4 (p<0.01).
Deep sleep augmented by
400% (from 5 to 22%),
while REM sleep increased
almost twofold (from 10 to
20%).
Sugerman et al,
Case series
4
N=28 (23 male)
Weight change –50 kg (-
6 to 12 M follow up
28
1986 [52]
Charuzi et al, 1987
moderate to severe OSA 32%)
Case series
4
[53]
patients, ≥45 kg
AHI change –36 (-82%)
overweight, AHI 44±15,
Increase in deep sleep
gastroplasty/gastric
from 10 to 20% and REM
bypass.
sleep from 10 to 20%.
N=46 (39 male), mild to
Excess weight change –
Follow-up period 6
very severe OSA, age
70%
M. Data on sleep
41±10 yrs, weight
AHI change –51 (-86%).
quality were
139±25 kg, excess body
Significant decrease in
reported as a graph.
weight 116±36%, BMI 48, Stage 2 sleep, significant
increase in deep sleep and
AHI 59±36,
gastroplasty/gastric
REM sleep.
bypass
Rajala et al, 1991
Case series
4
[29]
N=3 male OSA patients,
BMI change –18 kg/m2
Polygraphy (static
BMI 52±9, ODI 45±47,
(–34.3%)
charge sensitive
gastroplasty
AHI change –39.4 (-93%)
bed).
Follow-up period 1
year.
Sugerman et al,
1992 [54]
Case series
4
N=40 OSA patients, BMI
Weight change –57 kg
1 year follow up. No
56±12 kg/m2, weight
(-34.3%), BMI change –19
data on M/F.
166±35 kg, ideal body
kg/m2(-32.7%), IBW
Although
29
weight 244±53%, AHI
change –82%IBW (-
polysomnography
64±39,
33.6%),
was performed, no
gastroplasty/gastric
AHI change –38 (-59.4%).
sleep data were
bypass
Marked improvement in
reported.
arterial blood gases,
pulmonary hypertension,
left ventricular dysfunction,
lung volumes and
polycythemia.
Charuzi et al, 1992
[55]
Case series
4
N=47 (44 male) OSA
% IBW change –73%IBW
Sleep quality
patients, age 41±9 yrs,
(-62%),
improved with higher
weight 139±25 kg, %
AHI change –53 (-86.8%).
sleep efficiency,
ideal body weight
After 1 y 72% had an
shorter REM sleep
116±36%, AHI 61±35,
AHI<10, 40% of the
latency, less
gastroplasty/gastric
patients were cured. 6
wakefulness, and
bypass
patients got a control
increased deep
polysomnography 7 yrs
sleep and REM
postoperatively and
sleep.
revealed that regaining of
weight was associated with
the reappearance of OSA
30
Pillar et al, 1994 [56] Case series
4
N=14 (11 male) OSA
After 4.5 M postop :
After 4.5 M, 42.8%
patients, age 46±9 yrs,
Weight change –34.9 kg
of the patients were
weight 131±23 kg, BMI
(-26.7%), BMI change –12
cured.
45±7 kg/m2, AHI 40±29,
kg/m2 (-26.7%)
7.5 yrs after surgery
gastroplasty/gastric
AHI change –29.0 (-72%)
BMI only slightly
bypass
After 7.5 yrs postop :
increased, while AHI
Weight change –29.2 kg
increased
(-22.2%)
significantly,
BMI change –10 kg/m2
indicating that
(-22.2%), AHI change –16
increase in AHI was
(-40%).
independent of
Improvement in sleep
changes in BMI.
quality : % deep sleep and
REM sleep almost
doubled, without
deterioration on the longterm.
Scheuller et al, 2001 Case series
[57]
4
N=15 (10 male) OSA
Weight change –54.6 kg
Follow-up period 1-
patients, age 35±7 yrs,
(-34.2%), AHI change –86
12 yrs. Although
weight 160±27 kg, AHI
(-88.7%).
polysomnography
97±44, 11 Scopinaro
Scopinaro is more effective was performed, no
31
surgery, 4 gastroplasty
in reducing AHI to normal
sleep data were
values than vertical
reported.
banded gastroplasty.
Rasheid et al, 2003
Case series
4
[58]
N=11 (8 male) mild to
BMI change –22 kg/m2
severe OSA patients, age (-35.5%)
46±1 yrs, weight 155±4
AHI change –33 (-58.9%)
Follow-up period 321 M. Sleep
architecture
kg, BMI 62±3 kg/m2, AHI
improved in all
56±13, gastric bypass
patients (higher
SEI ; shorter REM
latency). Follow-up
data in only 11% of
their study patients.
Guardiano et al,
2003 [59]
Case series
4
N=8 (1 male) mild to very BMI change –15 kg/m2
Follow-up period
severe OSA patients, age (- 31%)
28±20 M. Potential
45±7 yrs, BMI 49±12
AHI change – 41 (–75%).
kg/m2, AHI 55±31, gastric 62% no longer required
bypass
bias due to low
response for repeat
nCPAP. Mean CPAP
polysomnography.
pressure could be
Although
decreased from 9±4 to 3±4 polysomnography
cm H 2 0.
was performed, no
sleep data were
32
reported.
Valencia-Flores et al, Case series
4
2004 [60]
N=28 (13 male ) mild to
BMI change –17.3 kg/m2
1 y follow up period.
very severe OSA
(-30.6%)
46% was cured.
patients, age 38±11 yrs,
% excess body weight
Pulmonary
BMI 56±12 kg/m2, %
change
hypertension
–99 % (-
excess weight 146±53 %, 67.8%)
AHI 54±47,
AHI change –39.7 (-
gastroplasty/gastric
73.5%).
bypass
No difference in sleep
improved.
quality in cured patients.
Lankford et al, 2005
[61]
Case series
4
N=15 (6 male) mild to
Weight change –44.5 kg
3 M follow up. No
very severe OSA
(-32.5%)
post-surgery AHI
patients, age 51±8 yrs,
BMI change –16 kg/m2
available. CPAP
weight 137±21 kg, BMI
(-32.5%)
pressure
48±7 kg/m2, AHI 40±37,
Decrease in optimal CPAP requirements
optimal CPAP pressure
pressure – 2 cm H 2 0 (-18
change
11±3 cm H 2 0, gastric
%)
considerably.
bypass
Although
polysomnography
was performed, no
sleep data were
33
reported.
Busetto et al, 2005
Case series
4
[62]
N= 17 (all male) OSA
Weight change –24 kg
patients, age 26-62 yrs,
(-14%)
weight 168±28 kg, BMI
Study based on
polygraphy (Poly2
BMI change –21.6 kg/m
56±10 kg/m2, AHI 59±18, (-14%)
intragastric balloon
AHI change –45 (-76.4 %)
Mesam). Follow-up
period 6 M. In 59%
AHI was reduced to
<20.
Dixon et al, 2005 [63] Case series
4
N= 25 (17 male)
Weight change –49 kg
1.5 yrs follow-up
moderate to very severe
(-32 %)
period. Lower
OSA patients, age 45±8
BMI change –15.5 kg/m2
CPAP pressures
yrs, weight 154±35 kg,
(-32%), AHI change –48
were needed in
BMI 53±9 kg/m2, AHI
(-78.2 %). Decreased
those who continued
62±32, gastric banding
arousal index with
CPAP.
increased REM sleep and
deep sleep.
Kalra et al, 2005 [64] Case series
4
N=10 adolescents with
Weight change –55 kg
No data on REM
mild to severe OSA, age
(-32 %)
sleep or deep sleep.
17±2 yrs, weight 173±28
BMI change –19.2 kg/m2
Follow-up period
kg, BMI 61±11 kg/m2,
(-32%), AHI change –8
5±1 M. No details
AHI 9.1 (median), gastric (-93 %). Unchanged
bypass
on AHI (no SD).
arousal index.
34
Poitou et al, 2006
Case series
4
[65]
Fritscher et al, 2007
Case series
4
[66]
N= 35 (6 male) moderate Weight change –30.3 kg
Diagnosis based on
to severe OSA patients,
(-22%)
polygraphy (analysis
age 44±2 yrs, weight
BMI change –11.4 kg/m2
of tracheal sounds,
140±5 kg, BMI 51±1
(-22%), AHI change –15
CidelecR). Mean
kg/m2, AHI 25±3, gastric
(-60.4 %)
follow-up period 1
banding/gastric bypass
year.
N= 12 (9 male) severe to Weight change - 51.2 kg
≥1.5 yrs follow-up
very severe OSA
(-33.7 %)
period. 25% was
patients, age 45±7 yrs,
BMI change –21.4 kg/m2
cured, 50%
weight 152±23 kg, BMI
(-38.6 %)
improved. Although
52±10 kg/m2, excess
EBW change –68.8%
polysomnography
body weight 103.8%, AHI (-66.3%)
AHI change – 30.5 (- 65.6
46.5 (33-140), gastric
Haines et al, 2007
[67]
Case series
4
was performed, no
sleep data were
bypass
%)
reported.
N= 101 (predominantly
BMI change –18 kg/m2
Prospective study.
female) mild to very
(-32.1 %)
Follow-up period 6-
severe OSA patients, age AHI change – 36 (- 70.6%). 12 M. Repeat
45±1 yrs, BMI 56±1
SEI increased, with shorter polysomnography in
kg/m2, AHI 51±4 (±SE),
REM latency.
gastric bypass
only 29% of the
included patients
(101/349). No data
35
on M/F.
Marti-Valeri et al,
Case series
4
2007 [68]
N= 30 (8 male) moderate Weight change –61.8 kg
1 year follow-up
to very severe OSA
period. After 1 year
(-43 %)
2
patients, age 44±9 yrs,
BMI change –24.4 kg/m
CPAP was
weight 144±27 kg, BMI
(-43 %)
withdrawn in most
56.5±8.4 kg/m2, AHI
AHI change –46.1 (-
patients. Although
64±38, gastric bypass
72.6 %)
polysomnography
was performed, no
sleep data were
reported.
Lettieri et al, 2008
[69]
Case series
4
N=24 (6 male) severe
Weight change -54 kg
1 year follow-up
OSA patients, age 48±9
(-36.8%)
period. Only 1
yrs, weight 147±29 kg,
BMI change -18.9 kg/m2
patient (4%)
BMI 51.0±10.4 kg/m2,
(-37%)
experienced
AHI 48±34, type of
AHI change -23.4 (-48.9%) resolution of OSA.
bariatric surgery not
The required CPAP
specified
pressure decreased
from 12±4 to 8±2 cm
H 2 O. The only
predictive marker of
the follow-up AHI
36
was the baseline
AHI. Men
experienced much
larger absolute and
relative reductions in
AHI than women.
Cohort represents
only 20% of those
undergoing bariatric
procedures in this
centre.
Rao et al, 2009 [70]
Case series
4
N=46 (36.3% male)
Asian OSA, age 36 (1863) yrs, weight 112 (71204) kg, BMI 45.2 (33-60)
kg/m2, AHI 38.11 (16.6137.7), gastric banding.
Weight change –41.1 kg
(-36.6%) (-66%-120% of
excess body weight), BMI
change -15.2 kg/m2 (33.6%),
AHI change –25 (-65.4%).
%Stage 3-4 and REM
sleep increased. Sleep
efficiency also improved.
OSA showed a cure in 78%
of cases. 20 kg weight loss
was associated with 50%
fall in AHI. 1 kg weight loss
resulted in up to a max of
9.5% reduction of AHI.
Polysomnography
was performed
(thermistors to
evaluate flow).
Follow-up period
12.6±20 M.
37
38
Table e4: Positional therapy
Author
Design
EBM
Patients
Results
Comments
N = 13 overweight men
AHI 49 ± 5 in supine
Not randomised; split-
(BMI 34.5 kg/m2) with
position vs. 20 ± 7 , when
night study to separate
AHI > 35
upper body elevated 60
supine and torso
degrees
upright position.
574 of N = 666 patients
321 patients (55.9%) had
Important, large
1997
had an AHI > 10, a BMI
a supine AHI at least twice collective,
[72]
> 20 kg/m2 and were >
as high as in lateral
retrospective study.
20 yrs of age
decubitus position. These
Proportion of women
patients had a significantly
not defined
Comparison upright or lateral vs. supine position
McEvoy et al, 1986
Individual cohort
[71]
study
Oksenberg et al,
Outcome study
2b
2c
lower BMI (29.4 ± 4.1 vs.
31.9 ± 4.9 kg/m2), a lower
RDI (29 ± 18 vs. 44 ±
30/h) and were two yrs
younger.
Positional therapy (PT)
Cartwright et al,1985 Case series
[73]
4
N = 10 overweight men
AHI in lateral position
Supine position was
(0 – 63% above ideal
(baseline) was 27% of the
prevented in 8 of 10
39
body weight) with supine
value in the supine
patients by the alarm.
position-SAS
position. AHI was
Instructions prevented
significantly reduced from
supine position in 3 of
55 ± 37 to 21 ± 32 ) using
10 patients.
the “positional alarm”.
Distribution of the sleep
stages was unchanged.
No data on daytime
sleepiness.
Kavey et al, 1985
[74]
Case series
4
2
N = 4 (BMI = 25.3 kg/m ,
AI reduced by ball after 3
Small collective; only
age 53 yrs) with OSAS;
to 6 months from 12 to 5;
AI given; Supine
AI 29 (range 7 – 65).
by verbal instructions from
position successfully
46 to 5. No data on
prevented by ball in 2
daytime sleepiness or
of 2 cases, by
sleep.
instructions in 1 of 2
cases.
40
Cartwright et al,
RCT
2b
1984, 1991 [75-76]
N = 30 overweight men
AHI decreased from 33 ±
Diet etc. recommended
(1.2 to 1.3 times ideal
21 to 21 ± 29 in the group
in the verbal instruction
body weight) with OSA,
with the “positional alarm”.
group. 11 of these 15
AHI > 12.5/h
In the group with verbal
patients lost weight
instructions only, AHI
compared to 5 of 15 in
decreased from 27 ± 13 to
the positional alarm
8 ± 10. No data on sleep
group. Supine position
or daytime sleepiness.
was no longer
observed in 8/15 in the
verbal instruction
group vs. 10/15 in the
positional alarm group.
Berger et al, 1997
[77]
Case series
4
N = 13 (11 male), age 52 AHI in lateral decubitus
± 8 yrs; AHI 30 ± 15;
2
BMI 28 ± 4 kg/m
No data on AHI during
position (13 + 9 ) was 25% positional therapy; data
of that in supine position
sleep and daytime
(52 ± 24 ). 24h average
sleepiness lacking.
blood pressure reduced by
4.1 mmHg (average
nighttime BP by 3.9
mmHg) by one month of
positional therapy.
41
Jocic et al, 1999 [78]
RCT, prospective,
2b
single blind
N = 13 mild OSA, age
After 2 weeks of CPAP or
Negative results for
51 ± 9 yrs, AHI 17 ± 8
position therapy each; AHI
CPAP regarding ESS,
improved sign. with
MWT etc. makes
position therapy, but more
interpretation of this
with CPAP (18 vs 9 vs 2).
aspect of the study
No difference in sleep
difficult
crossover
structure, ESS,
Maintenance of
Wakefulness-Test (MWT)
or quality of life
Maurer et al, 2003
Case series
4
[79]
N = 12 mild to
AHI in lateral position
Supine position
moderately severe OSA,
(baseline) was 14% of that successfully avoided in
BMI 27 ± 3 kg/m2, age
in supine position; AHI
12 of 12 patients.
56 ± 12 yrs, AHI 27 ± 12
reduced significantly by
Snoring less
“Supine Position
dependent on body
Avoidance” vest from 27 ±
position.
12 to 8 ± 5. Sleep stages
unchanged.
Zuberi et al, 2004
[80]
Case series
4
N = 22, 11 mild, 8
Triangular pillow with
Special pillow with
moderate and 3 severe
space to place an arm. In
some effect in mild-
OSA. Two
mild-moderate OSA RDI
moderate but not
42
polysomnographies
decreased from 17 to <5.
severe OSA
REM sleep, snoring and
SaO2 improved
significantly
Wenzel et al, 2007
Case series
[81]
24 month follow up
4
N = 14 mild to severe
RDI reduction to 14 ± 9 .
Low compliance with
OSA, BMI 28 ± 5 kg/m2,
Arousal index 23 vs 19. 24 long-term therapy.
age 48 ± 12 yrs, RDI 31
± 28 M later 29% were still
± 13
using the vest. The other
patients refused long term
therapy.
Loord et al, 2007
Case series
[82]
3 months follow up
4
N = 23 mild to
The positioner was a soft
22% drop out after 3
moderately severe OSA
vest attached to a board
months.
with positional sleep
placed under the pillow.
apnoea (AHI> 15 supine
Only 18 (5 women)
and <5 lateral position)
completed 3 months. 61%
Mean AHI= 22, age
had AHI< 10 with
women /men = 60/50 yrs
positioner. ESS decreased
from 12 to 10 (p=0.02)
and AHI 22 vs 14.
Oksenberg et al,
Case series
2006 [83]
6 month follow up
4
N=78 mild to severe
Only 50% returned
Cohort of clear
OSA, age 51 ± 12 yrs;
questionnaire. Of these,
positional sleep
43
BMI 28 ± 4 kg/m2; AHI
38 used tennis ball
apnoea. Only
26 ± 17 (AHI 52 supine
technique (TBT). 24%
questionnaire. High
and 11 lateral)
used TBT only initially, but
drop out rate of 50%
still avoided supine
position. 38% stopped
TBT. Sleep quality,
daytime alertness, and
snoring improved sign.
Comparison positional therapy vs CPAP
Skinner et al, 2004
Randomised
[84]
crossover
2b
N = 14 mild to very
AHI 27±12 vs 21±17 with
CPAP much more
severe OSA; AHI 10-60
elevated posture and 5±3
effective as compared
with CPAP (p=0.008). In 4
to shoulder + head
patients (retrospective)
elevation pillow. No
good improvement with
predictors found
elevation
44
Table e5: Studies of mandibular advancement devices
Author
Design
EBM
Patient population
Results
Comments
1b
27 patients (24 males)
AHI decreased from
Non-customised MAD was
study.
with symptomatic OSA,
20±14 to 10±7 with
used. Better effect on
Monoblock, non-
AHI 15-50 were recruited. MAD (p<0.005) and
sleep apnoeas and
customised MAD vs.
AHI 25±9
daytime sleepiness from
CPAP.
Age 46±11 yrs
Ferguson et al, 1996 RCT, cross-over
[85]
from 18±13 to 4±2 with
CPAP (p<0.005). CPAP CPAP than from MAD.
2
4 months with each
BMI 30±5 kg/m
more effective (p<0.05). Snoring still present with
device.
25 patients finished the
With MAD, 48%
MAD in 6 patients who
2 weeks wash in
study.
received treatment
were treatment or
and
success (AHI<10 and
compliance failures. The
2 weeks wash-out.
relief of symptoms),
patients preferred MAD.
Polysomnography
28% had treatment
(PSG).
failure and 24%
experienced
compliance failure. With
CPAP, 62% received
treatment success and
38% experienced
compliance failure. 6 of
45
7 patients with success
from both devices
preferred MAD.
Ferguson et al, 1997 RCT, cross-over
[86]
1b
24 patients (19 males)
AHI decreased from
Customised adjustable
study.
with symptomatic OSA,
25±15 to 14±15 with
MAD was used. Lower AHI
Adjustable MAD
AHI 15-55 were recruited. MAD (p<0.005) and
with CPAP than with MAD.
vs. CPAP.
Age 44±11 yrs
from 24±17 to 4±2 with
No difference in reported
4 months with each
BMI 32±8 kg/m2
CPAP (p<0.005). Lower symptomatic effects or
device.
ESS 11±3
AHI with CPAP
frequency of use. Snoring
2 weeks wash in
20 patients finished the
(p<0.01). Similar
improved in 100% by
and
study.
decrease in ESS from
CPAP and in 55% with
2 weeks wash-out.
both devices. With
MAD. The patients
PSG
MAD, 55% received
preferred MAD.
treatment success
(AHI<10 and relief of
symptoms), 40% had
treatment failure and
5% experienced
compliance failure. Two
patients had an
increase in AHI. With
46
CPAP, 70% received
treatment success and
30% experienced
compliance failure. 7 of
8 patients with success
from both treatments
preferred MAD.
Hans et al, 1997 [87] RCT, parallel study. 2b
18 patients of 24 (20
RDI changed from
Patients with severe OSA
Non-customised
males) with RDI<30
36±28 to 21±21 with
used a non-customised
MAD vs. non-
finished the protocol.
MAD (p≤0.05) and from device. RDI was
advanced MAD.
Age 52±12 yrs
37±44 to 47±47 with
insufficiently reduced by
Monoblock devices.
MAD (n=10); non-
non-advanced MAD
MAD, but not at all with
2 weeks treatment.
advanced (n=8)
(ns). Increased RDI in
non-advanced MAD. RDI
Limited sleep study.
BMI 29±4; 29±6 kg/m2
1/10 patients with MAD
may increase with non-
ESS 12±4; 13±5
and in 6/8 with non-
advanced MAD.
advanced device. ESS
decreased with MAD
only.
Bloch et al, 2000 [88] RCT, cross-over
2b
24 patients (23 males)
AHI decreased from
Better symptomatic effect
study.
with OSA symptoms and
23±3 (SEM) to 8±2 with from monoblock device.
Monoblock-MAD (M-
AHI≥5 or sleep-disruptive M-MAD and to 9±2 with Patients preferred this
47
MAD) vs. Herbst-
snoring with arousal
H-MAD (p<0.05 for
device. There might be
MAD (H-MAD).
index of >20/h.
each device).
differences in
1 week with each
Age 51±2 (SEM) yrs
Treatment success
effectiveness and
appliance or without
BMI 27±1 kg/m2
(AHI<10) in 75% of
preferences between
any device.
ESS 12±1
patients using M-MAD
appliance designs. The
Adaptation time
and in 67% with H-MAD need for elastics in the
156±14 days
(ns). ESS decreased
Herbst appliance might be
(mean±SEM).
with both devices.
a weakness.
PSG
Better subjective
outcome with M-MAD.
63% of the patients
preferred the M-MAD
and 4% preferred HMAD.
Kato et al, 2000 [89]
Case series.
4
37 of 43 patients with
Each 2-mm mandibular Experimental study
Monoblock MAD
ODI>10 accepted to
advancement produced showing that the
with 2-, 4-, and 6-
participate.
approximately 20%
mm advancement.
ODI 26 (11-72) (95%CI)
improvement in number nocturnal oxygenation and
At least one week
Age 49 (27-67) yrs
and severity of
acclimatisation
BMI 29 (23-40) kg/m2
nocturnal desaturations. was dose-dependently
before trial.
Pharyngeal closing
Advancement of
improvement of both
pharyngeal collapsibility
associated with the degree
48
Measurements of
pressure was evaluated
mandibular position
of mandibular
pharyngeal closing
in 6 patients.
produced dose-
advancement.
pressure.
dependent closing
Oximetry
pressure reduction of all
pharyngeal segments.
Lowe et al, 2000 [90] Case series.
4
38 patients (36 males)
RDI decreased from
Objective measurement of
Adjustable MAD.
with RDI>15 were
33±2 (SEM) to 12±2
compliance is possible for
Compliance monitor.
included.
with MAD (p<0.0001).
MAD´s in accordance with
Age 44 (34-61) (range)
RDI<15 and a
what is achievable for
yrs
resolution of symptoms
CPAP.
BMI 30 (21-39) kg/m2
in 71% of the patients.
The compliance monitor
The index of agreement
was tested in 8 subjects.
was 0.99 between the
compliance monitor
clock time and patients’
reports.
Liu et al, 2001[91]
Case series.
47 patients (42 males)
AHI decreased from
Ordinary cephalograms
Adjustable MAD.
with symptomatic OSA.
40±17 to 17±12 with
that often are available in
PSG
Age 49 (25-80) (range)
MAD (p<0.01). Better
dental practice were used
Upright
yrs
treatment response at
together with physiological
lower age or BMI or in
data to predict treatment
cephalogram in the
4
2
BMI 30 (22-55) kg/m
49
natural head
19 patients completed
patients with smaller
position.
the study.
upper airways. Dental
success for MAD.
and craniofacial
predictors were
identified.
28 patients with AHI≥10
AHI changed from
Short evaluation time. The
study.
and ≥2 OSA symptoms
27±17 (SD) to 14±2
study shows a clear effect
Adjustable MAD
were recruited.
(SEM) with MAD and to from MAD compared with
vs. control splint in
24 patients (19 males)
30±2 with control splint. a control splint. Better
lower jaw.
finished the protocol.
Lower AHI with MAD
effect in milder less obese
One week with each
Age 48±9 yrs
(p<0.0001). Complete
patients. The
device. 1 week
BMI 29±3 kg/m2
success (AHI<5 and
acclimatisation period may
wash-out.
ESS 10±1
resolution of symptoms) be long for MAD.
Mehta et al, 2001
RCT, cross-over
[92]
1b
Acclimatisation:
in 38% of the patients
20±9 (5-40) (range)
and AHI<10 in 54%.
weeks.
Snoring frequency was
PSG
lower with MAD
Cephalogram
(p<0.005). Better effect
on sleep apnoeas in
patients with milder
disease, smaller neck
50
circumference, wider
pharynx or a
backwardly angulated
mandible.
Engleman et al, 2002 RCT, cross-over
[93]
1b
51 of 97 consecutive
AHI decreased from
CPAP more effectively
study.
patients with AHI≥5, and
31±26 to 15±16 with
reduced sleep apnoeas
Monoblock MAD´s
≥2 OSA symptoms
MAD and to 8±6 with
and symptoms and
vs. CPAP.
including ESS≥8 or
CPAP (p=0.001 CPAP
improved quality of life
8 weeks with each
sleepiness while driving
vs. MAD). AHI≤5 was
compared with monoblock
appliance.
were recruited.
Limited sleep study.
48 patients (36 males)
found in 19% with MAD MAD´s in sleepy, mild and
and in 34% with CPAP. more severe OSA
MWT
finished the protocol.
AHI≤10 was found in
Age 46±9 yrs
47% with MAD and in
ESS 14±4
66% with CPAP. Better
patients.
effect from CPAP on
symptoms and quality
of life also in milder
cases. No difference in
objective measurement
of sleepiness. Patients
who preferred CPAP
51
were heavier.
Gotsopoulos et al,
RCT, cross-over
2002 [94]
1b
73 patients (59 males) of
RDI changed from 27±2 Clear effects on
study.
85 with RDI≥10 and ≥2
(SEM) to 12±2 with
respiratory variables
Adjustable MAD
OSA symptoms finished
MAD and to 25±2 with
including snoring from
vs. control splint in
the protocol.
control splint (p<0.0001 MAD compared with
upper jaw.
Age 48±11 yrs
MAD vs. control).
control splint. Subjective
4 weeks with each
BMI 29±5 kg/m2
Complete success
daytime sleepiness
device.
ESS 11±5
(RDI<5) with MAD was
decreased also with
1 week wash-out.
56% had moderate and
achieved in 36% of the
control splint. MAD more
Acclimatisation: 8
29% had severe OSA.
patients. ESS
frequently normalised
(2-22) (range)
decreased with both
ESS. Many patients
weeks.
devices. Lower treated
wanted to continue with
PSG
value with MAD. MSL
the control splint, which
MSLT
was longer with MAD
highlights the need for
than control. Both
objective control of
subjective and objective treatment effects.
snoring frequency and
intensity were lower
with active device
(p<0.0001). 99% of the
patients desired to
52
continue with MAD and
49% with the control
splint. Significantly
more patients reported
side-effects with active
device than with control
splint.
Johnston et al, 2002 RCT, cross-over
[95]
2b
20 patients (16 males) of 21 with AHI changed from
Some effect on sleep
study.
ODI≥10 finished the protocol.
32±21 to 23±23 with
apnoeas from MAD
Monoblock MAD
Age 55±7 yrs
MAD and to 38±25 with compared with a control
vs. control device
BMI 32±6 kg/m2
control device. (p=0.01
device in patients with
in upper jaw.
ESS 14±6 kg/m2
MAD vs. control).
severe OSA. Similar
4-6 weeks with
Treatment success
symptomatic outcome
each device.
(AHI<10) in 33% of the
from the devices. Poor
Limited sleep
patients with MAD. One success rate in the most
study.
of 6 subjects with
severely affected OSA
pretreated AHI>50 had
patients.
53
success. ESS and
reported snoring did not
differ between devices.
Pitsis et al, 2002
RCT, cross-over
2b
23 patients (20 males) of 24
AHI decreased from
Two different degrees of
[96]
study.
recruited completed the protocol. 21±2 (SEM) to 8±1 with mouth openings were
Adjustable MAD
Age 50±10 yrs
4-mm-MAD (p<0.001)
tested and there were no
with 4 mm
BMI 31±5 kg/m2
and to 10±2 with 14-
differences in respiratory
interincisal mouth
mm-MAD (p<0.001). No variables or daytime
opening vs. 14
difference in AHI, ESS
sleepiness between them.
mm.
or reported snoring
The patients preferred the
2 weeks with
between devices. 4-
device with a smaller
each device.
mm-MAD was preferred mouth opening.
1 week wash-out.
by 78% of the patients
Acclimatisation
and 14-mm-MAD by
with 4-mm-MAD.
22% (p<0.007 between
PSG
devices).
Randerath et al,
RCT, cross-over
2002 [97]
20 patients (16 males) with
During the first night,
Insignificant effect from
study.
5≤AHI≤30 were included.
AHI decreased from 18
MAD treatment after 6
Adjustable MAD
Age 57±10 yrs
±8 to 11±8 with MAD
weeks treatment raises the
(p<0.05) and to 4±3
question whether the
vs. CPAP.
PSG during the
1b
2
BMI 31±6 kg/m
with CPAP (p<0.01). No effect from MAD may
54
first night and after
difference in AHI
decline. It is possible that
6 weeks with each
between devices. After
more advancement was
device. No
6 weeks, AHI was
needed. MAD was easier
adjustment of
14±11 with MAD (ns)
to use than CPAP. Similar
MAD.
and 3±3 with CPAP
symptomatic improvement
(p<0.01). Lower with
from MAD and CPAP
CPAP (p<0.01). No
indicates a risk that
effect from MAD in any
patients continue with a
OSA-severity group at 6 suboptimal treatment.
weeks. 30% of patients
had AHI<10 with MAD.
Symptomatic
improvement was
similar with both
devices. Treatment
success with MAD was
related to a higher
weight and lower age.
Rose et al, 2002
RCT, cross-over
[98]
2b
26 patients (22 males) with mild RDI decreased from
Better effect on sleep
study.
OSA were included.
16±5 to 6±3 with K-
apnoeas from Karwetzky
Karwetzky activator
Age 57±5 yrs
MAD and from 16±4 to
activator than Silencor
55
(K-MAD) vs.
BMI 28±3 kg/m2
7±5 with S-MAD
indicates that appliance
Silencor (S-MAD)
16 patients completed the
(p<0.01 for each
stability may be of
6-8 weeks with
protocol.
device). Better effect
importance for the
each device.
from K-MAD (p<0.01).
treatment outcome. Similar
Wash-out 2-3
Similar effects on
symptomatic outcome
weeks.
daytime sleepiness and from both devices.
PSG, limited sleep
snoring from both
study.
appliances. More
problems during S-MAD
treatment in terms of
repairs.
Sanner et al, 2002 Case series.
[99]
4
15 patients (14 males) with
AHI decreased from
Adjustable MAD.
OSA.
20±15 to 7±7 with MAD assessed by MRI during a
PSG
Age 57±9 yrs
(p=0.001). Treatment
Müller manoeuvre while
MRI during a Müller
BMI 31±6
success (≥ 50%
wearing MAD might be
manoeuvre with
13 patients fulfilled the protocol. reduction and AHI<10)
and without MAD in
in 54% of the patients.
supine position.
Five of 7 responders
The airway patency
predictive of treatment
success with MAD.
had no significant
pharyngeal obstruction
during the Müller
56
manoeuvre with MAD,
while 4 of 6 nonresponders had
persistent obstructions.
Skinner et al,
Case series.
2002 [100]
4
14 patients (13 males) of 15 with AHI decreased from
Small study showed that
Adjustable MAD.
OSA 10≤AHI≤40 or CPAP-
34±22 to 10±5
cephalometry had limited
PSG
intolerance finished the study.
(p=0.001). The baseline value for prediction
Cephalogram in
Age 48±11 yrs
distance between the
2
BMI 29±5 kg/m
supine position.
purposes.
hyoid bone and the
6 to 8 weeks
mandibular plane was
treatment.
the only cephalometric
variable associated with
a successful clinical
outcome.
Tan et al, 2002
RCT, cross-over
[101]
2b
24 patients (20 males) of 46 with AHI decreased from
Small study shows similar
study.
10≤AHI<50 were included.
22±10 to 8±11 with
effects from MAD and
Monoblock MAD or
Age 51±10 yrs
MAD and to 3±3 with
CPAP on respiratory
adjustable MAD vs.
BMI 32±7 kg/m2
CPAP (p<0.001 for both variables and daytime
CPAP. 2 months
ESS 13±5
devices). ESS
sleepiness, although high
with MAD or CPAP.
21 patients completed the
decreased with both
success rate with CPAP.
2 weeks wash-out.
protocol.
treatments (p<0.001).
Patients preferred MAD
57
PSG
No difference in AHI or
over CPAP.
ESS between devices.
Treatment success
(AHI<10) with MAD in
67% of the patients and
compliance failure in
4%. Treatment success
with CPAP in 92% of
the patients and
compliance failure in
8%. 17 of 21 (81%)
patients preferred MAD.
Walker-Engström
RCT, parallel
et al, 2002 [102]
1b
95 patients with 5<AI<25 were
AHI decreased from
The first randomised long-
study. Monoblock
included.
18±3 to 5±3 after one
term comparison of
MAD vs. UPPP.
MAD (n=32); UPPP (n=40)
year with MAD
treatment effects from
Follow-up after 4
completed the 4-year follow-up.
(p<0.001) and was 7±3
MAD´s. Better long-term
yrs.
Age 49 (47-52); 51 (49-53) yrs
after 4 yrs (p<0.01 vs.
outcome in patients during
Limited sleep
(±95%CI)
one year). AHI had
treatment with MAD than
study.
BMI 27 (26-28) in both groups.
decreased from 20±3 to in patients who had
10±3 one year after
undergone UPPP.
UPPP (p<0.001) and
Increased AHI between
58
was 14±3 after 4 yrs
one and 4 yrs from both
(p<0.01 vs. one yr).
treatments.
Significantly reduced
AHI after 4 yrs, but
higher treated value
compared with oneyear follow-up for both
treatments. Long-term
AHI higher after UPPP
than with MAD.
Ng et al, 2003
Case series.
[103]
4
10 patients (9 males) with
AHI decreased from
MAD decreased the upper
Adjustable MAD.
AHI≥10 and ≥2 OSA symptoms. 25±3 (SEM) to 13±5
airway collapsibility during
After one week
Age 44±12 yrs
(p<0.05) and upper
wash-out, upper
BMI 31±6 kg/m2
airway closing pressure responders. Upper airway
sleep, particularly in
airway closing
decreased in Stage 2
closing pressure
pressure during
sleep and in slow wave
measurements might be
sleep, with and
sleep with MAD
useful for prediction
without MAD, were
(p<0.05). The reduction purposes.
assessed.
in pharyngeal
PSG
collapsibility was larger
in responders.
59
74 patients with 5≤AI≤25
AHI decreased from
Similar effect from MAD´s
study.
started.
16±3 (95%CI) to 6±4
with 50% compared with
Monoblock MAD
50%-MAD; 75%-MAD
with 50%-MAD
75% mandibular
with 50%
(n=29); (n=26) completed
(p<0.001) and from
advancement after one
mandibular
5±1; 6±1 mm advancement
19±5 to 6±2 with 75%-
year in patients with
advancement vs.
Age 52 (49-55); 54 (52-56) yrs
MAD (p<0.001). No
milder OSA. The authors
75% advancement.
(95%CI) at baseline
difference between
recommend starting MAD
One year
BMI 27 (26-28); 28 (27-29)
devices. Treatment
treatment with 50%
treatment.
kg/m2
success (AHI<10 and
advancement in this
Limited sleep
AI<5) in 79% of the
group of patients.
study.
patients with 50%-MAD
Tegelberg et al,
RCT, parallel
2003 [104]
1b
and in 73% with 75%MAD (ns).
86 men with AI≥20 were
AHI decreased from
Higher success rate from
study.
included. 50%-MAD; 75%-MAD
47±5 to 17±6 with 50%-
75% compared with 50%
Monoblock MAD
(n=37); (n=40) completed.
MAD and from 50±5 to
advancement after 6
with 50%
5; 7 mm advancement
16±6 with 75%-MAD
months in patients with
advancement vs.
Age 54 (52-56); 50 (48-53) yrs
(p<0.001 for both
severe disease, although
75% advancement.
(95%CI) at baseline
devices). No difference
both advancements
6 months
BMI 31±1; 31±1 kg/m2
between them.
reduced the AHI to a
treatment.
(±
Treatment success
similar degree.
Walker-Engström
RCT, parallel
et al, 2003 [105]
1b
95%CI)
60
Limited sleep
(AHI<10 and AI<5) in
study.
31% of the patients with symptomatic outcome
50%-MAD and in 52%
Comparable
from the devices.
with 75%-MAD (p=0.04
between devices).
Patients with normalised
AHI were slimmer. ESS
decreased and no
difference between
devices.
Barnes et al, 2004 RCT, cross-over
[106]
1b
114 patients with AHI 5-30 were AHI changed from 21±1 CPAP was the most
study.
recruited, 80 (63 males) fulfilled
to 14±1 with MAD
effective treatment, but
Adjustable MAD vs.
the protocol.
(p<0.001), to 5±1 with
produced similar effect on
CPAP vs. placebo
Age 46±1 (SEM) yrs
CPAP (p<0.001) and to daytime sleepiness and
tablet.
BMI 31±1 kg/m2
20±1 with placebo (ns)
quality of life as MAD.
3 months with each
ESS 10±1
(p<0.001 MAD vs.
Placebo tablet ineffective
treatment.
placebo; p<0.05 CPAP
on sleep apnoeas and
2 weeks wash-out.
vs. MAD). AHI<10 in
daytime sleepiness.
PSG
49% of the patients with Difficulties to estimate
MWT
MAD. No difference in
effects on
ESS between CPAP
neurobehavioral
61
and MAD. Effects on
functioning because of
quality of life and nightly placebo effects.
diastolic blood pressure
from MAD compared
with placebo. No effect
on objective sleepiness
from MAD. Incomplete
response on
neurobehavioral
functioning from both
MAD and CPAP.
Placebo effects on
some measurements.
Sleepy and non-sleepy
subjects had similar
overall treatment
responses.
Fleury et al, 2004
Case series.
[107]
40 of 44 patients (36 males) with AHI decreased from
Highlights the importance
Adjustable MAD.
OSA completed the protocol.
46±21 to 12±14 with
of the titration procedure,
Titration with
Age 57±9 yrs
MAD (p<0.001). 91% of which was performed
oximetry.
4
2
BMI 28±4 kg/m
the patients needed
based on the combined
62
PSG
ESS 12±4
increased advancement improvement in
from initial 80% of
symptoms and oximetric
maximal protrusion.
recordings.
64% of the patients had
AHI<10 and a
resolution of symptoms
after a mean of 4
advancements.
Gotsopoulos et
RCT, cross-over
1b
67 patients (53 males) of 75 with AHI was reduced about The authors conclude
al, 2004 [108]
study.
AHI ≥10 and ≥2 OSA symptoms 50% with MAD
that oral appliance
Adjustable MAD vs.
were randomised.
compared with the
therapy for obstructive
control splint in
AHI 27±15
control splint.
sleep apnoea over 4
upper jaw.
Age 48±11 yrs
Significant reduction in
weeks results in a
4 weeks with each
BMI 29±5 kg/m2
24-hour diastolic blood
reduction in blood
device.
61 patients fulfilled the protocol.
pressure of 2±1 mmHg
pressure, similar to that
1 week wash-out.
(SEM) from MAD
reported from CPAP.
PSG
compared with the
control splint (p=0.001),
but not in 24-hour
systolic blood pressure.
Awake systolic and
63
diastolic blood-pressure
decreased with 3±1
mmHg (p<0.01). No
significant difference in
blood pressure
measured asleep.
Marklund et al,
Case series.
2004 [109]
4
619 of 630 consecutively treated AHI was reduced from
Large non-randomised
Monoblock MAD.
patients (508 males) were
a mean of 21 (1-74)
study that identifies
Follow-up after
followed-up.
(range) to 8 (0-72)
predictors of treatment
573±521 days.
Age means: 51 yrs in men and
(p<0.001). 72% of the
success in a cohort of
Limited sleep study.
55 yrs in women (p<0.001). 277
patients with an AHI of
consecutively treated
patients had sleep apnoea
≥10 before treatment
patients. 76% of the
recordings with the device.
had an AHI of <10 with
patients used the device
MAD. Treatment
after one year.
success related to
female gender. Men
who had supine
dependent sleep
apnoeas or men who
did not increase in
weight had a better
64
treatment outcome.
Blanco et al, 2005 RCT, parallel
[110]
2b
24 patients (20 males) with
AHI changed from
Small sample size. Some
study.
AHI≥10 and at least two OSA-
34±15 to 10±12 with
effect on AHI also from
MAD and non-
symptoms were randomised.
MAD (p<0.01) and from non-advanced device,
advanced MAD.
MAD; non-advanced MAD
24±12 to 12±8 with
despite no reduction in
Monoblock
(n=8); (n=7)
non-advanced MAD
either supine or lateral
devices.
Age 56±12; 53±13 yrs
(p=0.05). 57% of the
AHI. Positional changes
3 months
BMI 28±4 kg/m2 in both groups.
patients had a complete may have influenced the
treatment.
response (AHI<5 and
PSG
the resolution
results
symptoms) with MAD.
Effect on daytime
sleepiness, snoring and
quality of life only from
MAD.
Kyung et al, 2005
Case series.
[111]
14 patients (12 males) with
AHI decreased from
Advancement of the
Adjustable MAD.
AHI>5 and arousal index >20
45±27 to 11±23 with
mandible with MAD
CT scan and
were included.
MAD (p<0.001). The
produces primarily a
cephalogram
Age 50±16 yrs
retropalatal and
lateral widening of the
during
BMI 25±3 kg/m2
retroglossal cross-
upper airway.
wakefulness.
4
sectional areas
65
increased (p<0.05) with
MAD. The enlargement
of pharynx was greater
in the lateral than in the
sagittal dimension.
Lawton et al, 2005 RCT, cross-over
[112]
2b
49 patients evaluated for AHI changed from 46 (29-68) to The patients had severe
study.
eligibility. 16 patients (12 25 (0-45) with Herbst-MAD and sleep apnoea and an
Herbst-MAD or
males) completed the
to 34 (9-63) with Twin Block-
insufficient treatment
Twin Block-MAD.
protocol.
MAD. No difference in AHI,
response, which makes
2 weeks wash-out.
Age 45 (24-68) (range)
ESS, quality of life or side-
comparison between
Limited sleep
yrs
effects between devices. 56%
devices difficult.
study.
BMI 29 (24-51) kg/m2
of the patients preferred
ESS 10 (2-18)
Herbst-MAD and 31% preferred
Twin Block-MAD.
Naismith et al,
RCT, cross-over
2005 [113]
1b
73 patients (59 males) of AHI changed from 27±15 to
Some aspects of
study.
86 patients with AHI≥10
12±12 with MAD and to 25±15
neurobehavioural
Adjustable MAD vs.
and at least two OSA-
with control splint. (p<0.01
functioning improved with
control splint in
upper jaw.
symptoms completed the between devices). 36% of the
protocol.
patients had an AHI<5 and
4 weeks with each
Age 48±11 yrs
55% had an AHI<10 with MAD. which may be as
device.
Mean BMI 28 and 30
Improvements in self-reported
MAD compared with a
control splint. Factors
important as sleepiness
66
1 week wash-out.
kg/m2 in the
sleepiness, fatigue/energy
such as fatigue, tiredness
Acclimatisation:
randomisation groups.
levels and
and lack of energy
8±4 weeks.
vigilance/psychomotor speed
improved by MAD.
PSG
from MAD.
Coruzzi et al,
Case-control study. 3b
10 OSA patients (6
AHI decreased from 18±1
Improved cardiac
2006 [114]
Monoblock MAD.
males), otherwise
(SEM) to 4±1 with MAD.
automatic modulation
3 months
healthy.
Improved cardiac autonomic
from MAD treatment in
treatment.
Age 48±10 yrs
modulation from MAD
milder, otherwise healthy
Heart rate, blood
BMI 27±1 kg/m2
treatment of OSA-subjects. No OSA patients may have
pressure and
10 matched controls (5
difference in treated values
favourable implications
indices of
males).
between OSA patients and
for the prevention of
control subjects.
cardiovascular disease.
33 of 38 patients (36
MAD-therapy was successful
The study shows a
autonomic cardiac
regulation.
Limited sleep
study.
Dort et al, 2006
Case series.
[115]
Remotely
males) with RDI≥5
at target mandibular protrusion titration procedure for
controlled MAD for
fulfilled the protocol.
in 80% of subjects who had a
MAD´s in accordance
prediction.
RDI 27±18
successful test with the
with CPAP titration. The
PSG
Age 45±10 yrs
remotely controlled MAD and
method points out a
BMI 30±6 kg/m2
failed in 78% of those who had possible prediction
4
67
4
12 patients (11 males)
an unsuccessful test outcome.
method for MAD´s.
AHI decreased from 22±3
The results indicate that
Ng et al, 2006
Case series.
[116]
Adjustable MAD.
with AHI≥10 and ≥2 OSA (SEM) to 9±2 with MAD
primary oropharyngeal
After one week
symptoms.
(p=0.01). All 4 patients with
collapse predict treatment
wash-out, upper
Age 51±9 yrs
primary oropharyngeal collapse success with MAD´s.
airway closing
BMI 28±4kg/m2
had treatment success (AHI<5)
pressure and site
with MAD. Only one of the 8
of collapse during
patients with primary
sleep, with and
velopharyngeal collapse had a
without MAD, were
successful outcome.
assessed.
PSG
De Backer et al,
Case series.
2007 [117]
4
10 OSA patients (8
The results indicated that a
The results suggest that
Monoblock MAD.
males) with AHI<40 (1-
predicted decrease in upper
the outcome of MAD
PSG
31) (range).
airway resistance and an
treatment can be
Upper airway
Age: 44-60 yrs
increase in upper airway
predicted using this upper
imaging techniques
BMI: 24-34 kg/m2
volume correlate with both a
airway modelling
combined with
clinical and an objective
technique.
computational fluid
improvement from MAD.
dynamics for
prediction.
68
Itzhaki et al, 2007
Case-control study. 3b
16 sleepy patients (11
AHI decreased from 30±19 to
[118]
Adjustable MAD.
males) of 25 with AHI≥10 18±11 after 3 months and to
function was found after
After 3 months and
Age 54±8 yrs
20±12 after one year with MAD
one year MAD-
one year.
6 untreated OSA
(p< 0.005 for both). Endothelial
treatment, although
Markers of
patients.
function and levels of oxidative
apnoeic events were not
oxidative stress
Age 43±11 yrs
stress markers improved with
completely eliminated. A
and evaluation of
10 matched controls.
MAD. After one year there were reduction in
endothelial
Age 50 ±4 yrs
no differences compared with
cardiovascular
function.
BMI: 28 kg/m2 in all
reference levels.
complications from
groups.
Improved endothelial
treatment still needs to
be shown.
Lam et al, 2007
RCT, parallel
[44]
101 patients (79 males)
AHI changed from 21±2 (SEM)
study.
of 109 with 5≤AHI≤40
to 11±2 with MAD+C (p<0.001), hygiene and weight
Monoblock MAD
(ESS>9 for patients with
from 24±2 to 3±1 with CPAP+C
control
and conservative
AHI≤20) fulfilled the
(p<0.001) and from 19±2 to
recommendations.
measures (C)
protocol.
21±3 with C only (ns)(p<0.05
CPAP was the most
(sleep hygiene,
Mean age 45-47 yrs, BMI CPAP vs. MAD; p<0.001 MAD
effective treatment.
weight control) vs.
27-28 kg/m2 and ESS 12 vs. placebo). All treatments
Conservative treatment
CPAP+C vs. C
in the randomisation
reduced ESS-scores (p<0.05
only, was ineffective on
only.
groups.
CPAP vs. MAD). Improved
sleep apnoeas and
quality of life from MAD and
weight on a group-level.
10 weeks
1b
All groups had sleep
69
treatment.
CPAP, but not C. Only CPAP-
PSG
users reduced weight. No
differences in blood pressure
effects between the groups.
Hoekema et al,
RCT, parallel
2007 [119]
2b
20 patients (17 males) of The total number of lapses of
The first study of
study.
30 with an AHI of >5
attention during simulated
simulated driving skills
Adjustable MAD vs.
completed the protocol.
driving was significantly higher
during MAD-therapy.
CPAP.
AHI 49±33
in untreated OSA patients
Improved driving
2-3 months
Age 49±11yrs
compared with controls. The
performance from both
treatment.
BMI 33±6 kg/m2
lapses of attention decreased
MAD and CPAP-
PSG
16 control subjects (13
from both MAD and CPAP, with
therapy. The result must
25-min simulated
males) matched for age.
no difference between
be interpreted with some
treatments.
caution when
driving test at
midday.
generalizing to the
actual driving situation.
Hoekema et al,
RCT, parallel
2b
47 of 48 men with an
More signs of sexual
None of the treatments
2007 [120]
study.
AHI of ≥ 5 completed the dysfunction in men with OSA
significantly improved
Adjustable MAD vs.
study.
compared with control subjects.
male sexual functioning
CPAP.
Age 49±9 yrs
No improvement in subjective
after some months
2-3 months
BMI 31±4 kg/m2
reports on sexual functioning or
treatment with MAD or
treatment.
ESS 13±6
testosterone levels from either
CPAP.
70
PSG
48 age-matched control
Testosterone
subjects without any
measurement and
sexual problems.
MAD or CPAP.
questionnaires.
Zeng et al, 2007
Case series.
[121]
4
54 patients (40 males)
The results suggest that flow-
A method that may be
Adjustable MAD.
with OSA and at least
volume curves, in combination
used to predict treatment
PSG
two symptoms were
with BMI, age and baseline AHI effects from MAD´s is
Spirometry
included.
may have a role in the
presented.
Mean age 51 and 53 yrs prediction of treatment
and BMI 28 and 31
response with MAD (>50%
kg/m2 in responders and reduction in AHI).
non-responders,
respectively.
Vanderveken et al, RCT, cross-over
2008 [122]
1b
35 patients (29 males) of AHI changed from 14±12 to 6±8 Significant effect on
study.
38 with AHI≤40 finished
with MAD CM (p<0.01) and to
sleep apnoeas only from
Custom-made
at least one arm.
11±9 with MAD TP (ns).
the custom-made device.
MAD CM vs.
Age 49±9 yrs
Complete success (AHI<5 and
The prefabricated device
thermoplastic
BMI 28±4 kg/m2
reduced snoring) in 49% of the
could not be
MAD TP Monoblock
ESS=8±5
patients with MAD CM and in
recommended as a
devices.
23 patients completed
17% with MAD TP . Compliance
therapeutic option or as
4 months with each
the study.
failure in 6% with MAD CM and
a screening tool.
71
device.
31% with MAD TP . Treatment
1 month wash-out.
failure in 34% with MAD CM and
PSG
37% with MAD TP . 82% of the
patients preferred MAD CM . 63%
of the patients with MAD TP
failure had treatment success
with the custom-made device.
Hoekema et al,
RCT, parallel study. 2b
28 patients (25 males) of Half of the untreated patients
Preliminary data in a
2008 [123]
Adjustable MAD vs.
51 with AHI>20 and
with moderate to severe OSA
small sample indicates
CPAP.
without cardiovascular
without cardiovascular disease
that cardiac function
2-3 months
disease were included.
had left ventricular hypertrophy, improves from effective
treatment.
AHI 52±24
left ventricular dilatation or
MAD- treatment of OSA
PSG
Age 50±10 yrs
elevated natriuretic peptides.
patients with moderate to
Echocardiography
BMI 33±5 kg/m2
Significant improvement in
severe disease.
and measurements
16 patients completed all natriuretic peptides was
recorded during MAD
parts.
of
natriuretic peptides.
treatment.
Hoekema et al,
RCT, parallel study. 1b
228 patients assessed
2008 [124]
Adjustable MAD vs.
for eligibility. 103 patients 8±14 with MAD and from 40±28 than CPAP on sleep
CPAP.
(92 males) with an AHI of to 2±4 with CPAP (p=0.006
≥5 were randomised.
CPAP vs. MAD). Effective
8-12 weeks
AHI decreased from 39±31 to
MAD was less effective
apnoeas, but had similar
symptomatic effects. In
72
treatment.
MAD (n=51); CPAP
treatment (AHI<5 or ≥50%
terms of success rate,
PSG
(n=52)
reduction of AHI to <20 and no
MAD was not considered
Age 49±10 yrs for both
symptoms) in 77% of the
inferior to CPAP in the
groups.
patients with MAD and in 83%
whole sample. In
BMI 32±6; 33±6 kg/m2
with CPAP. AHI<5 in 57% of all patients with severe
ESS 13±6; 14±6
patients, in 84% with mild to
disease CPAP was more
moderate OSA and 31% with
effective.
severe disease. No difference
in ESS or quality of life between
treatments.
Petri et al, 2008
RCT, parallel study. 1b
81 patients (66 males)
AHI changed from 39±24 to
Significant effects on
[125]
Monoblock MAD
out of 93 with AHI of >5
25±28 with MAD (p<0.001),
sleep apnoeas and
vs. non-advanced
fulfilled the study.
from 33±22 to 32±25 with non-
daytime sleepiness from
MAD vs. no
Mean age was in
advanced MAD (ns) and from
MAD compared with
intervention.
between 49-50 yrs, BMI
34±26 to 33±25 with “no
placebo. The first study
4 weeks study.
PSG
2
31 kg/m and ESS 11-12 intervention” (ns).
in the randomisation
AHI<5 and a resolution in
that compares the effects
groups.
symptoms in 29% of the
compared with “no
patients with MAD. ESS
intervention”. No
decreased and quality of life
difference in outcome.
of a non-advanced MAD
improved with MAD.
73
Zeng et al, 2008
Case series.
[126]
4
38 OSA patients (29
Baseline nasal airway
A method that may be
Adjustable MAD.
males) were eligible for
resistance in sitting position was used to predict treatment
PSG
the study.
lower in responders (≥50%
Rhinomanometry
Mean age 51and 55 yrs
reduction in AHI) compared with presented.
and
non-responders.
effects from MAD´s is
BMI 29 and 34 kg/m2 in
the responders and nonresponders, respectively.
Gauthier et al,
RCT, cross-over
2b
16 patients (11 males) of RDI decreased from 10±1 to
2008 [127]
study.
19 fulfilled the protocol.
7±1 with Klearway (p<0.01) and objective and subjective
Adjustable MAD´s,
Age 48±2 (SEM) yrs
to 5±1 with Silencer (p<0.001)
outcome between the
Klearway vs.
BMI 29±1 kg/m2
(p≤0.05 between appliances).
two MAD designs.
Silencer.
No difference in improvement in
3 months with each
symptoms or quality of life or
device.
compliance between devices.
PSG
Klearway was more
Minor differences in
comfortable.
Aarab et al, 2009
Cross-over study.
[128]
2b
17 patients (12 males) of AHI decreased from 22±11 to
The authors recommend
Adjustable MAD.
20 OSA patients finished 6±8 in the most effective jaw
starting the titration
Four randomised
the protocol.
position (p<0.001). The two
procedure at 50%
jaw positions, 0%,
Age 49±9 yrs
most advanced positions were
advancement in order to
74
25%, 50% and
BMI 27±3 kg/m2
most effective on AHI, but also
reduce the initial side-
75% of maximal
ESS=12±6
led to more self-reported side-
effects.
protrusion.
effects.
PSG
Trzepizur et al,
RCT, cross-over
2009 [129]
2b
12 of 17 patients with
AHI decreased from 40 (31-49)
Both appliances
study.
OSA [130].
to 14 (7-18) with MAD and to 2
improved endothelial
Adjustable MAD
Untreated samples
(1-8) with CPAP (p<0.05 for
reactivity with no
vs. CPAP.
without cardiovascular
both). Acetylcholine induced
difference between them,
2 months
disease:
vasodilatation was smaller in
despite that treated AHI
treatment.
9 controls with AHI 6 (4-
OSAS patients than in matched was higher with MAD.
Measurement of
11), median (interquartile controls. The vascular reactivity The first randomised
microvascular
range)
increased with both treatments
reactivity.
12 patients with AHI 32
(p<0.05). No difference between endothelial reactivity
(24-51).
them. The increase correlated
Median age ranged in
with the decrease in nocturnal
between 42 and 56 yrs
oxygen desaturations from
study of effects on
from MAD treatment.
and BMI was in between treatment.
27 and 29.
Ghazal et al, 2009 RCT, parallel
[131]
1b
133 patients were
AHI decreased from 23 (7-32)
Both appliances were
study.
assessed. 103 patients
(median and interquartile range) effective in the short and
Adjustable
with AHI 5-40 were
to 9 (0-16) with IST® and from
longer term, although
75
devices, IST® vs.
randomised.
21 (7-40) to 5 (0-21) with TAPTM there were smaller
TAPTM. Follow-up
IST® (n=51); TAPTM
short-term. Better effect from
after 6 months and
(n=52)
TAPTM. Daytime sleepiness and them. It is possible that
24 months.
Age 51±11; 50±11 yrs.
2
PSG
differences between
quality of life improved with both the longer term
BMI 26±3 kg/m in both
appliances. At long-term follow- effectiveness of a device
groups.
up, AHI was 5 with both
may vary in relation to
ESS 8±2; 10±3
appliances. Snoring and
construction details
45 patients fulfilled the
daytime sleepiness increased
including comfort for the
24 months follow-up.
between the follow-ups.
patients.
Complete long-term response
(AHI<5) in 35% with IST® and
25% with TAPTM. Compliance
failure in 26% with IST® and
42% with TAPTM.
Gagnadoux et al,
RCT, cross-over
2009 [130]
1b
69 patients with AHI 10-
AHI changed from 34±13 to 6
Both appliances
study.
60 were recruited, 59
(3-14) (median and interquartile effectively reduced
Adjustable MAD
were randomised after
range) with MAD and to 2 (1-8)
symptoms and AHI,
vs. CPAP.
successful titration.
with CPAP. CPAP more
although CPAP was
2 months with each
Age 50±9 yrs
effective (p=0.001). Complete
more effective on sleep
device after one-
BMI 27±4 kg/m2
response (≥50% reduction and
apnoeas. A negative
night effective
ESS=11±5
AHI<5) in 73% with CPAP and
result from the titration
76
titration of both
56 completed the
43% with MAD. Subjective and
procedure was a weak
devices.
protocol.
objective sleepiness decreased. predictor for treatment
PSG
No difference between devices. failure. Self-reported
Limited sleep study
Positive and negative predictive compliance was higher
Osler test
values for success from MAD
with MAD and the
titration were 85% and 45%,
majority of the patients
respectively. 70% of the
preferred that treatment.
patients preferred MAD.
Chan et al, 2009
Case series.
4
18 responders (AHI-
The upper airway collapse
Nasendoscopy may
[132]
Adjustable MAD.
reduction≥50%); 17 non- visualised by nasendocopy was become a useful tool for
PSG
responders.
greater in non-responders than
the prediction of
Nasendoscopy
Age 54±12; 56±10 yrs
in responders with MAD in situ
treatment success with
Müller manoeuvre
BMI 29±5; 31±5 kg/m2
during a concomitant Müller
MAD´s.
manoeuvre.
Tsuiki et al, 2009
Case series.
[133]
4
35 patients of 38 who
AHI decreased from 36 to 12 (5- The study shows an
Monoblock MAD.
had used CPAP for 6-13
26) with MAD (p<0.001).
accessible prediction
2-3 weeks
months.
Treatment success (AHI<5 and
method, since many
washout.
Age 55 (41-66) yrs
>50% reduction in AHI) was
patients have tried CPAP
PSG
median (interquartile
associated with a lower CPAP-
before MAD-therapy is
range)
pressure. Patients with CPAP-
initiated. More
pressure ≥11 were unlikely to
prospective testing is
2
BMI 26 (24-29) kg/m
77
respond to MAD therapy.
necessary.
78
Table e6: Studies of tongue retaining devices
Author
Design
EBM
Patient population
Results
Comments
Cartwright et al,
RCT, parallel
1b
60 male patients with
AHI decreased from 27±18 to
TRD reduced sleep
1991 [75]
study.
OSA and positional-
11±15 with TRD (p<0.02).
apnoeas significantly,
TRD vs. posture
dependency (AHI-supine
TRD+PA and HH reduced AHI primarily in supine
alarm (PA) vs.
≥ two times AHI-lateral).
significantly. AHI decreased to position among
TRD+PA vs.
Age ranged between
below 6 in more than half of
patients with positional-
instructions of good
means of 46 and 51 in
the patients in each group.
dependency in this
health habits (HH)
the randomisation
TRD reduced AHI-supine,
early randomised trial.
including
groups.
while AHI-lateral was per
Success was predicted
avoidance of
definition low and unaffected
by a low apnoea
supine sleep
by the device. Disease
frequency in the lateral
position.
severity, AHI-lateral, weight
sleep position.
8 weeks treatment.
and nasal patency related to
PSG
success with TRD or
TRD+PA.
Barthlen et al, 2000
Case series.
4
8 patients (7 males) were No effect from TRD or SPL.
TRD did not reduce
[134]
Non-customised
included.
MAD changed AHI from 72±40 sleep apnoeas in a
MAD vs. TRD vs.
Age 58±22 yrs
to 36±39 (p<0.02). AHI<15 in
soft palate lifter
Follow-up in 8 patients
2 of 5 patients with TRD, none patients with severe
small sample of
79
(SPL) in all patients
with MAD, 5 with TRD
with SPL and in 5 of 8 patients OSA.
in the same order
and 2 with SPL.
with MAD.
8 patients (6 males) who
ODI changed from 41±22 to
Oxygen desaturations
11±9 with TRD (p<0.01).
were reduced with TRD
during 8 months.
PSG
Higurashi et al,
Case series.
4
2002 [135]
TRD
had failed other OSA
3 months
treatments.
in a small sample of
Age 59±8 yrs
patients with severe
2
BMI 25±4 kg/m
Kingshott et al,
Pilot study.
2002 [136]
4
disease.
6 males of 8 TSD users.
AHI changed from 26±17 to
Insufficient treatment
TSD was evaluated
Age 51±4 yrs
15±13 with TSD (p=0.06).
effects of TSD in a
with PSG vs. no
BMI 30±3 kg/m2
Sleep arousals decreased
small sample of
treatment in
(p=0.004). Insufficient effects
patients with moderate
randomised order.
on snoring.
OSA.
32 patients (22 males) of
RDI changed from 16±18 to
The first randomised
Dort et al, 2008
RCT, cross-over
1b
[137]
study.
38 snorers with RDI<30
9±8 with TRD (p=0.006) and
controlled trial of TRD-
Non-customised
completed the protocol.
to 14±15 with control device
treatment. It shows an
TRD vs.
Age 48±10 yrs
(ns). 4 of 5 subjects with
effect on RDI from a
2
nonsuction control
BMI 29±6 kg/m
severe OSA showed an RDI-
device with tongue
device.
ESS 12±5
reduction of at least 50% with
suction compared with
80
One week
TRD. ESS decreased with
a nonsuction control
acclimatisation.
both devices.
device.
22 patients (16 males) of
AHI changed from 27±17 to
Short evaluation time.
One week washout.
Limited sleep
study.
Deane et al, 2009
RCT, cross-over
[138]
study.
27 with AHI>10 and ≥2
12±9 with MAD (p<0.001) and Both devices reduced
TSD vs. adjustable
OSA symptoms
to 13±11 with TSD (p<0.01).
AHI. MAD was
MAD.
completed the study.
The arousal index and ESS
overwhelmingly
One week
Age 49±11 yrs
decreased with both devices.
preferred by the
treatment.
BMI 29±6 kg/m2
91% of the patients preferred
patients.
4 weeks
1b
MAD.
acclimatisation with
each device.
One week washout.
PSG
81
Table e7: Tongue–Muscle-Stimulation
Author
Design
EBM
Patients
Results
Comments
Miki et al, 1989
Apnoea-triggered
4
N=6 (5 male) moderate
AI 39.2 ± 7.7 to 11.7 ± 4.9, No control group
[139]
stimulation
to severe OSA ,age 50.0
oxygen desaturations
± 10.8 yrs, height 165.3
<85% 20.1 ± 10.8 to 4.1 ±
± 5.5 cm, weight 82.9 ±
2.9, minimal saturation
17.7 kg, AI 39.2 ± 18.7.
75.5 ± 3.8% to 82.7 ±
2.9%, SWS 14.3 ± 3.5 to
22.0 ± 4.8%.
Guilleminault et
Submental surface
al,1995 [140]
and intraoral
4
N=7 severe to very
No significant
severe OSA, age 61 ± 8
2
stimulation
improvement in PSG
yrs, BMI 27.2 ± 3 kg/m ,
parameters. Stimulations
RDI 55 ± 6, lowest Sa0 2
induced
80.2 ± 4%.
alpha EEG arousals and
contractions of platysmal
muscles.
Oliven et al,
Sublingual Surface
2001[141]
stimulation
4
N=7 healthy persons,
Tongue protrusion during
6 OSAS patients
day, resistance and
Case studies in OSAS
respiratory disturbances
during sleep. Peak
82
inspiratory flow rate
increased from 319 ± 24
to 459 ± 27 (healthy
persons) and from 58 ± 16
to 270 ± 35 ml/sec
(OSAS) (p<0.001).
Eisele et al, 1997
Nerve stimulation
[142]
4
N=15 healthy patients, 5
Stimulation of
under surgery,
OSAS patients 42.0 ±
genioglossus branch:
intraneural
6.7 yrs., BMI 27.9-46.1
Protrusion and contra-
Insufficient
2
No control group.
stimulation of
kg/m , AHI NREM 108.0
lateral deviation of the
polysomnographic
hyoglossus/glossus
± 43.1
tongue, stimulation of the
data.
during sleep.
hyoglossus: mild
ipsilateral deviation and
Observation of
retrusion.
tongue motions
during surgery,
Threshold of tongue
evaluation
motion lower than apnoea
inspiratory flow
threshold.
during night
Flow increased by 184.5 ±
61.7ml/s under stimulation
of both nerves.
83
Schwartz et al, 1996
Intramuscular
[143]
4
N=9 (8 male) very
Stimulation of retractors
stimulation of the
severe OSA, 42.9 ± 10.8
(n=4): reduction of the
genioglossus
yrs., BMI 40.4 ± 7.2
flow by 239 ± 177 ml/s,
protrusion),
kg/m2, AHI NREM 93.2 ± stimulation of protrusors
stimulation under
hyoglossus,
20.3, all pre-treated with
(n=8): increase of the flow
CPAP.
styloglossus
CPAP. Inclusion criteria
by 217 ± 93 ml/s. CPAP
retractors, triggered
AHI NREM >10,
3,9 ± 3,4 cm H2O, AHI
by inspiration),
exclusion: medical
baseline 65.6 ± 11.5,
measurements of
comorbidity.
under stimulation 9.0 ±
acute effects on
No control group.
Genioglossus
5.8.
inspiratory flow and
52 ± 20 to 23 ± 12
obstructive
disturbances.
Schnall et al, 1995
transcutaneous and 4
N=7 awake healthy
No change under
[144]
transmucosal
persons (6 men), 31.4 ±
transcutaneous
stimulation with and
2.7 yrs., 178.6 ± 3.8 cm,
stimulation. Transmucosal
without artificial
71.9 ± 4.6 kg
stimulation: No change of
pharyngeal
the Rph without artificial
resistance Rph).
resistance but reduction of
Measurement of
the Rph from 11.67 ± 1.9
No control group.
84
acute effects on the
to 6.77 ± 1.3 cm H2O/l/s
pharyngeal
under external resistance
resistance
Decker et al, 1993
Submental surface
[145]
4
N=4 (3 male) healthy
Termination of 22% of
Heterogeneous
stimulation,
persons, 22-28 yrs, 3
apnoeas under surface
population CPAP,
intraneural
men 7 male severe to
stimulation and 23%
intraoral appliance,
stimulation of the
very severe OSA (35-55
apnoeas under intraneural
weight reduction) few
hypoglossus nerve.
yrs., ODI 35-100)
stimulation. Enlargement
data.
of cross-section CT).
Discomfort with much
higher voltage during
sleep as compared to
wake.
Mann et al, 2002
Transcutaneous
[146]
4
N=14 (11 male) healthy
Change of cross-section
stimulation of
patients , 24-50 yrs,
between -25 to 284%.
genioglossus.
Exclusion criteria:
Endoscopical
smokers, disorders of
measurement of
the nervous system,
the pharyngeal
speech or voice.
No control group.
85
cross-section
Schwartz et al,
Direct intraneural
2001 [147]
stimulation of the
4
N=8 male OSA , 36-57
Polysomnography after 1,
No control group.
yrs., BMI 28.4 ± 4.5
3, 6 months, AHI in NREM
No data on arousals.
2
hypoglossus nerve,
kg/m , neck
baseline 52 ± 20.4, under
No significant
unilateral, triggered
circumference 42.1 ±
stimulation 22.6 ± 12.1,
difference in sleep
by inspiration.
2.8 cm, AHI NREM 52 ±
AHI in REM baseline 48.2
profile.
20.4/h, REM 48.2 ± 30.5
± 30.5, stimulation 16.6 ±
Impairment of sleep
17.1, proportion of SWS
efficiency.
baseline 8.7 ±
.4%,stimulation 12.7 ±
11.3, proportion of REM
baseline 11.1 ± 7.7%, St.
14.5 ± 5.7%.
Isono et al, 1999
Induction of
[148]
4
N=7 male OSA , 40-61
Enlargement of the cross-
No control group
apnoeas by
yrs., BMI 18.6-35.7
section under low airway
No polysomnographic
hyperventilation
kg/m2, ODI 7.6-63.4,
pressure by muscle
definition. Huge range
under general
clinical signs of sleep
stimulation, no influence at in BMI and ODI.
anaesthesia.
apnoea.
high pressure levels.
Stimulation of the
86
tongue with
different pressure
level. Correlation
between pressure
and oral pharyngeal
cross-section
endoscopy)
Randerath et al,
Placebo-controlled,
2004 [149]
1b
N=67 mild to severe
Significant improvement of
randomised
OSA, AHI 10-40,
snoring, but not AHI:
tongue-muscle-
treatment group: N=33,
treatment group: snoring
training. Electrical
age, 50.8 ± 12.1 yrs;
baseline, 63.9 ± 23.1
stimulation during
BMI 29.1 ± 4.4 kg/m2,
epochs/h; training, 47.5 ±
daytime
placebo group: n=34,
31.2; P < 0.05, placebo
age, 53.3 ± 11.3 yrs;
snoring baseline 62.4 ±
2
BMI 28.9 ± 4.9 kg/m .
26.1 epochs/h; placebo,
62.1 ± 23.8; NS.).
Oliven et al,
Intraneural
2003 [150]
4
N=5 OSA implanted
Pcrit decreased during
Case series
hypoglossus nerve
electrodes (hypoglossus
HG and GG (Pcrit 3.98 ±
No control group
stimulation
stimulation HG, age 44.8 2.31 to 3.18 ± 1.70
(implanted
± 9.9 yrs, BMI 28.9 ±
cmH 2 O, respectively). No
electrodes),
3.9 kg/m2), 9 patients
change in upstream
87
intramuscular
with fine-wire electrodes
resistance. No influence of
genioglossus
(genioglossus
site of collapse.
stimulation (fine-
stimulation GS, age 46.8
wire electrodes)
± 9.6 yrs, BMI 32.9 ± 7.6
kg/m2)
Oliven et al,
Propofol
2007 [151]
4
N = 32, male, mild to
Pressure/flow,
anesthesia. Hook-
severe OSAS, AHI 29.7
pressure/cross-sectional
wire electrodes,
± 22.8, age 47.5 ± 9.7
area relationship of velo-
inserted
yrs, BMI 29.9 ± 22.8
and oropharynx. The
sublingually for
kg/m2.
genioglossus stimulation:
genioglossus
Reduction of P crit from
stimulation.
1.2 ± 3.3 to -0.7 ± 3,8 cm
No control group
of water. Response
depends on magnitude of
tongue advancements.
88
Table e8: Description of trials of pharmacological agents in the treatment of obstructive sleep apnoea (OSA)
Author
Design
Atkinson 1985 [152]
RCT, crossover:
Patient population
Results
Comments
Ten adults (8 male) with
Desatuartion index
Not possible to
sleep apnoea diagnosed
decreased by 25% (p<
segregate the results of
saline infusion,
on PSG (but 3 had
0.05)
subjects with OSA
duration 2 x single
central apnoeas)
nights
Mean age 45.7 yrs
RCT, crossover:
Eight adult males with
No difference between
Primary outcome was
severe OSA on PSG
verum and placebo, AHI
genioglossus activity in
75.2 and 73.7 respectively
NREM which was
IV naloxone vs
Berry 1999 [153]
Paroxetine 40 mg
EBM
2b
2b
nocte vs placebo 2
alone
x single nights
increased by
paroxetine
Bortolotti 2006 [154]
RCT, parallel study:
Twenty adult subjects (17 Self reported ‘attacks’ of
The attacks may well
male), mean age 55.4
apnoea were reduced by
have been
BD versus placebo.
yrs. All had co-existent
omeprazole. Sleep studies laryngospasm rather
4 weeks baseline 6
gastro-oesophageal
were not repeated on
than OSA. There is
weeks intervention
reflux
treatment.
noevidence of benefit
Omeprazole 20 mg
2b
on sleep parameters
Brownwell 1982[155] RCT, crossover:
Protriptylline 20 mg
nocte versus
1a*
Five adult males, severe
No improvement in AHI or
*Results analysed with
OSA on PSG, AI: 64.4.
sleep continuity but
Stepanski and Whyte.
subjective report of
89
placebo, duration 2
reduced daytime
x 2 weeks, 2 weeks
sleepiness.
washout
Carley 2007[156]
RCT 3 way
Twelve adults: 7 males
The AHI was 22.3 on
mean age 39, mean AHI
placebo and 13.5 and 11.4 commercial studies did
mirtazipine 4.5mg,
22 and 5 females, mean
respectively on Mirtazipine not reproduce these
15mg and placebo,
age 43, AHI 24 )
4.5 and 15mg respectively
crossover:
2b
7 days in each
(p=0.004). There was no
condition in random
significant difference in
order
ODI or Stanford sleepiness
Subsequent
effects on AHI
scale between placebo and
verum.
Cook 1989[157]
RCT, crossover
medroxyprogestero
2b
Ten adult men. Age
No improvement in
range: 31 to 67 yrs;
respiratory indices
ne 50 mg tds, 1
severe OSA on PSG
week vs placebo (3
(AHI: 77.3 on placebo)
week washout)
Diamond 1982 [158]
RCT, crossover
Naloxone 2mg at
half-hourly intervals
2b
Four adults with OSA. No No improvement in
Statistical methods
baseline data or entry
were not reported in
criteria reported.
respiratory indices
the study
90
versus placebo
duration unclear
Espinoza 1987 [159] RCT, crossover
Ten adult males; mean
No improvement in
age 52.6 yrs; AHI 76.4;
respiratory measures.
versus saline (both
Inclusion criteria: >15
Active treatment reduced
intravenous). 2 x
apnoeas/hr; daytime
sleep efficiency
single nights
hypersomnolence
RCT, crossover
Twelve adults (10 male)
AHI was reduced by
Mean AHI: 32.9. mean
naltrexone compared with
versus placebo. 2
age 60.2 yrs;
placebo (29.1 versus 37.6,
single nights. No
Inclusion criteria: >10
P < 0.009) but total sleep
washout period
AHI.
time fell (P < 0.04) and
Aminophyline
Ferber 1993 [160]
Naltrexone 50mg
2b
2b
described.
Single blind
arousals from sleep
increased.
Grote 1995 [161]
Hedner 1996 [162]
RCT, parallel
1b
Fifty-five adult males,
No differences found in
groups Cilazapril
mean age 50.2 yrs; RDI
respiratory measures
2.5mg QD versus
47.2. Inclusion criteria:
between cilazapril and
placebo. Duration 2
Co-existing arterial
placebo
x 8 days
hypertension and OSA
RCT crossover,
Thirteen adults (11
Difference scores reported
91
Sabeluzole 10 mg
2b
males); mean age: 49
only, no overall positive
BD versus placebo,
yrs. Inclusion criteria:
effect of the drug.
duration 2 x 4
previously diagnosed
weeks, 2 week
moderate to severe OSA
washout
Hedner 2003 [163]
RCT crossover
study. Intravenous
2b
Ten adult males, obese
AHI was reduced by 13.6
The greatest fall in AHI
patients excluded, (BMI
(95% CI 2.2 to 25.1) but
was seen in REM sleep
physiostigmine
26.8); Mean age 48.3 yrs; only normalised in one
and in the thinner
(0.12mcg/kg/minute
AHI: 54.4
subjects
subject. Total sleep time
) versus placebo.
also reduced, by 74
Study duration: 2
minutes (95 CI 33.9 to
single nights
114.9).
Heitmann 1998 [164] RCT, parallel group
trial. Mibefradil
Fifty-three adult males
1b
No significant impact on
recruited (data on 48 who respiratory or sleep
50mgs QD versus
completed were
placebo. Study
reported). Mean age:
duration: 8 days
50.7 yrs. AHI: 62.43
parameters
Inclusion criteria: 23-69
yrs; mild-moderate
hypertension; OSA
92
diagnosed by PSG and
symptoms
Issa 1992 [165]
RCT crossover
clonidine 0.2 mg
2b
Eight adult males, mean
No significant impact on
Dosage may have
AHI 27
AHI, minimal oxygen level
been suboptimal as
improved
REM sleep only
nocte, 10 days each
limb
Jokic 1998 [166]
supressed in 2 subjects
RCT crossover
10 male adults (mean
AHI and arousals lower on
The compound was not
study, topical airway 2b
age: 49) mild and
active treatment, mean
thought to be safe for
lubricant
moderate OSA (median
differences of -10 (p =
long term use as it was
(phosphocholinami,
AHI: 16).
0.0003) and -8 (p = 0.001)
based on a mineral oil
0.4ml) administered
Inclusion criteria: OSA
respectively.
with risk of lipoid
twice overnight
diagnosed by overnight
pneumonia on
versus placebo
PSG; AHI ≥10
aspiration
Single nights x 2
Kraiczi 1999 [167]
RCT crossover
Twenty adult males,
There was clinically
No benefit was found
study Paroxetine 20 1b
mean age 52.1 yrs.
unimportant but statistically on a complex
mg/day versus
Three withdrawals. ODI
significant fall in AHI,
assessment of
placebo. Study
25.4 (SD 13). Inclusion
(placebo 36.3 vs
symptoms
duration: 2 x 6
criteria: ODI ≥10/hr; 25-
paroxetine 30.2, p = 0.021)
weeks treatment
65 yrs
93
arms, 4 weeks
washout
Marshall 2008 [168]
Two separate
studies:
1b
Study1: placebo
controlled 3 way
cross over with 6
dose sequences of
7.5 to 45 mg of
mirtazapine
Mendelson
Study 2: 3 arm
randomised parallel
group study placebo
vs 15mg
mirtazapine vs
15mg mirtazapine
with CD0012
RCT crossover
1991[169]
Buspirone 20 mg
1b
Study 1: Twenty adults
randomised (15 male) 2
drop outs; mean age 47
(no SD quoted) yrs, AHI
24 (SD 8.0)
Study 2: 64 adults (56
male) randomised, 15
drop outs; arm 1 n=13
mean AHI 27.4 (SD 11),
arm2 n=26 mean AHI
23.7 (SD 9.8), arm 3 n=
25 mean AHI 23.6 (SD
10.8).
There were no significant
improvements in measures
of OSA in either trial. In
trial 1 on some doses the
AHI was significantly
raised. In both trials
subjects withdrew due to
increased lethargy on
verum. In both studies
there was clinically
significant weight gain on
verum
Compared to Carley
2007 there were fewer
women and subjects
were less obese
5 adult males. Mean age: There was a fall in AHI on
The description of the
45.4 yrs; AHI 30.8
treatment (placebo 30 and
methods is sketchy. It
versus placebo
buspirone 20) but this was
is not clear whether
Study duration:
not significant. No
subjects were blinded.
single night? (not
differences found in
specified)
oxygenation or sleep
2b
parameters
Mulloy 1992 [170]
RCT crossover,
12 adult males (3
Total sleep time was
The paper reports a
94
Theophylline 800
2b
withdrawals). Age range
significantly reduced by the significant fall in total
mg nocte versus
35 to 64 yrs. Mean AHI
drug, mean difference of -
number of
placebo
59
76 (95% CI -100.88 to -
desaturations,
51.12) minutes. The ODI
recalculating as ODI
Study duration:2 x 4
Rasche 1999 [171]
weeks (washout not
Inclusion critieria: AHI
was 51.5 and 49 per hour
shows that is acheived
specified
>/=15
of sleep for placebo and
at the expense of sleep
treatment respectively
time
20 adults (16 male).
No beneficial effects were
Subjects with asthma
Mean age 53 yrs. Mean
found on any of the
or COPD excluded.
salmeterol with
AHI 35.6 (SD 25.3.
respiratory parameters
placebo. Study
Inclusion criteria: AHI >5; measured
duration: 2 x 3
history of excessive
nights (no washout)
daytime sleepiness; ≥ 18
RCT crossover
comparing
2b
yrs of age; adequate
inhaler technique.
Stepanski 1988 [172] RCT crossover,
Protriptylline 10 to
1a*
Eight adult males. Mean
No improvement in AHI or
*Results analysed with
age 44.9; AHI 87.3
sleep continuity but
Brownwell and Whyte
20mg nocte versus
subjective report of
placebo. Study
Inclusion criteria: AHI ≥
reduced daytime
duration: 3 weeks
10 and sleepiness
sleepiness
95
Stradling 2003 [173]
RCT crossover,
10 adults (9 male) with
No impact of ondansetron
The dose used was
moderate OSA. Mean
on any of the respiratory
less ( per kg) than in
(16mg) Nocte
age: 53 yrs.
parameters reported
animal studies but the
versus placebo, 2 x
Inclusion criteria:
maximum licensed for
single nights , 1
Symptomatic OSA; < 4%
use in humans
week washout
SaO2 dips of 10-40
Controlled trial,
Four adults (ages 29 to
There were differences in
Not specified to be
55yrs). No data on AHI
AHI between drug and
randomised
given.
placebo but very small
Ondansetron
Suratt 1986 [174]
crossover of
2b
2b
Doxapram
(0.5mg/kg lean body
study and no statistical
mass bolus,
Inclusion criteria: not
followed by 1mg/ml
stipulated
tests were performed.
infusion overnight)
versus placebo.
Study duration: 2
consecutive 1 night
treatment periods
Whyte 1988 [175]
RCT crossover trial
Ten adult subjects (8
Protriptyline: no fall in AHI
*Results analysed with
male), 34 to 67 yrs old.
and in contrast to
Brownwell and Whyte
of Protriptyline
1a* for
20mg nocte, 2
protriptyl AHI 50 (sd 26).
Brownwell and Whyte no
96
weeks
line,
Acetazolamide 250
subjective report of
Inclusion criteria: AHI >
reduced daytime
Of three subjects
15 with 2 from EDS
sleepiness.
offered long term
mg bd 1 week and
2b for
then 250 mg qds 1
acetazol snoring , unsatisfying
Acetazolamide: significant
treatment with
week versus
amide
fall in AHI with active drug
acetazolamide, only 1
placebo 2 tabs at
of -24 (95% CI -44.33 to -
could tolerate the drug
night
3.67) per hour but no less
sleep or awakenings
self reported daytime
sleepiness.
Guimarães KC et al,
Oropharyngeal
1989 [176]
exercises vs. sham
PuhanMA et al,
Muscle exercise by
2006 [177]
Didgeridoo playing
Oropharyngeal exercise
Unclear which exercise
significantly improved
was most relevant.
yrs, BMI 30.3 ± 3.4
neck
circumference (39.6 ± 3.6
kg/m2, neck
vs. 38.5 ± 4.0 cm), snoring
circumference 39.6 ± 3.6
frequency and intensity,
daytime sleepiness (ESS
cm, AHI 22.4 ± 4.8
14 ± 5 vs.8± 6), sleep
quality score, AHI 22.4 ±
4.8 vs. 13.7 ± 8.5. No
significant change in the
control group.
1b
N=31, OSA, age 25-65
1b
N=25, 21 male, Age:
didgeridoo 49.9 ±6.7 vs.
control 47.0 ± 8.9, BMI
25.8 ± 4.0 vs. 25.9 ± 2.4,
AHI 22.3 ± 5.0 vs. 19.9 ±
Improvement under
didgeridoo in daytime
sleepiness, AHI
(difference − 6.2, − 12.3 to
− 0.1, P = 0.05). No effect
97
4.7.
on the quality of sleep.
Table e9: External Nasal Dilators
Author
Design
EBM
Patient population
Results
McLean et al, 2005
RCT
1b
10 patients with nasal
Treatment with topical
obstruction and OSA
decongestant and external
[178]
dilator strip reduced nasal
resistance, improved
sleep architecture, and
reduced OSA severity
(change in AHI 12 (95%
CI: 3-22); p < 0.02)
Todorova et al, 1998
Case series
4
[179]
30 patients with primary
Maximum snoring intensity
habitual snoring
was reduced in 22 of 30
snorers. Sleep
architecture remained
almost unchanged.
Ulfberg et al, 1997
[180]
Case series
4
35 habitual snorers
Snoring decreased
(graded by bed partner) (p
98
< 0.001) and Epworth
Sleepiness Scale
decreased (graded by the
patient) (p = 0.001)
Liistro et al, 1998
Case series
4
10 non-apnoeic snorers
[181]
No influence on sleep and
snoring as measured by
polysomnography
Wenzel et al, 1997
Case series
4
[182]
30 patients with OSA, 20 In 90% of OSA patients,
snorers
daytime sleepiness
remained unchanged,
33% described improved
sleep quality. Polygraphic
data remained
unchanged.
Bahammam et al,
1999 [183]
RCT
1b
18 patients with Upper
Nasal cross-sectional area
Airway Resistance
increased (p < 0.001),
Syndrome
oxygen desaturation time
decreased (12.2 ± 2.2%
vs. 9.1 ± 1.3%; p = 0.04).
No change in sleep
architecture, MSLT,
99
cardiorespiratory
parameters. Stage 1 sleep
was reduced from 8.6 */0.8% to 7.1 ± 0.7% (p =
0.034).
Gosepath et al, 1999 Case series
[184]
4
26 patients with an RDI
19 patients showed
> 10/h
reduction of RDI
100
Table e10: Internal Nasal Dilators
Author
Design
EBM
Patient population
Results
Lorino et al, 1999
Case series
4
17 healthy subjects
Nasal resistance decreased from 1.65 ± 0.54 cm
[185]
Metes et al, 1992
H 2 O/L/s to 1.02 ± 0.27 cm H 2 O/L/s (p < 0.001).
Case series
4
[186]
72 awake snorers and
Nasal respiratory airflow resistance of awake
10 heavy snorers while
snorers decreased from 0.164 ± 0.128 to 0.065 ±
asleep
0.037 Pa/cm3/sec. During sleep no effect on
snoring, apnoeas, hypopnoeas, and oxygen
saturation.
Petruson et al, 1988
Case series
4
16 subjects
Airflow increased from 0.68 to 0.84 L/sec.
Case series
4
15 patients without nasal No effect on apneas, hypopneas, or oxygen
[187]
Hoffstein et al, 1993
[188]
pathology
saturation. Snoring was reduced during slow wave
sleep (9.4 ± 7.0 to 4.1 ± 7.0 snores/min; p < 0.05)
Shinkawa et al, 1998 Case series
4
18 Japanese snorers
[189]
72.2% experienced subjective improvement in
snoring, based on degree of the bed partner’s
disturbance.
Höijer et al, 1992
[190]
Case series
4
11 patients with habitual
Nasal airflow increased by 18%, apnea index was
snoring and/or OSA
reduced from 18 (range, 1.8 to 60) to 6.4 (range,
1.3 to 15) /h. Minimum oxygen saturation increased
101
from 78 (range, 68 to 89) to 84 (range, 76 to 88) %.
Snoring noise was reduced.
Schönhofer et al,
2000 [191]
Case series
4
26 patients with OSA
In 4 out of 21 analysed patients, RDI was reduced
to < 50% of the baseline value, and RDI of < 10/h.
102
Table e11: Impact of nasal obstruction in the development of obstructive sleep apnoea
Author
Design
Rubin AH et al, 1983 Case series
EBM
Patient population
Results
Comments
4
9 male OSA patients with
Non significant post-operative
Selection bias since
positive ENT findings (not
reduction in Apnoea Index
post-operative
further specified), age
from 38±26 to 27±19
polygraphy was
47±13 yrs, BMI n.a., were
56% of patients who
performed in clinical
included
underwent submucosal
responders only
[192]
Polygraphic measurements resection reported improved
prior to and between 2 and sleep quality (not measured)
6 months postoperative
submucosal resection w/o
turbinectomy
Caldarelli DD et al,
1985 [193]
Case series
4
23 male OSA patients with No significant postoperative
nasal obstruction due to
change in Apnoea-Index from
septum deviation, age
44±29 pre to 41±41
50±7yrs, weight 100±20kg, 8 pts. (34%) were responders
were included
with > 50% improvement in
Polysomnography prior to
the Apnoea-Index
and approx. 9 weeks after
submucosal resection of
the nasal septum and
103
inferior turbinates
Dayal VS et al, 1985 Case series
4
[194]
6 male OSA patients with
No significant postoperative
Snoring and daytime
septum deviation, age
reduction in AHI from 47±25 to somnolence improved
46±15yrs, BMI n.a., were
28±15
included
Non-significant modest
Polysomnography prior to
improvements in SaO 2 mean
and between 4 and 44
and “movement arousals”
in all patients
months postoperative
nasal septum surgery (not
further specified)
Series F et al, 1992
[195]
Case series
4
20 OSA patients (18 male) No significant postoperative
Significant relationship
with chronic nasal
change in AHI from 40±6/hr
between nasal
obstruction, age 53±2 yrs,
pre to 37±6/hr
resistance and AHI at
BMI 34±1.7kg/m2, were
No changes in total apnoea
baseline;
included
time (%TST) or SaO 2 indices
AHI normalisation in 4
Polysomnography 1 to 3
Significant postoperative
pts with normal
months prior to and
improvement in stage REM
posterior soft tissue;
between 2 and 3 M
(%TST) from 11±1 to 14±1%
Hypersomnolence
postoperative nasal
(p<0.05)
improved in 14 pts.
surgery (septoplasty in all
Significant postoperative
(80%)
pts. and submucosal
improvements in nasal
104
resection with turbinectomy resistance
in 18 pts.)
Series F et al, 1993
Case series
4
[196]
14 OSA (12 male) patients Postoperative AHI reduction
Significant
with chronic nasal
from 17±1 to 6.5±1 in patients
improvements in nasal
obstruction, age 50±3 yrs,
with normal cephalometric
resistance irrespective
BMI 29±1 kg/m2 were
measurements
of cephalometric
included
Significant improvements in
findings
Polysomnography and
sleep architecture in pts. with
cephalometric
normal cephalometric
measurements prior to and measurements
between 2 and 3 months
No significant postoperative
posoperative nasal surgery AHI change from 18±2 to 25±3
(septoplasty in all pts. and
in those with abnormal
submucosal resection with
cephalometric measurements
turbinectomy in most
patients)
Friedman M et al,
2000 [197]
Case series
4
50 OSA patients (41 male) No significant postoperative
Improvements in
with nasal obstruction, age change in RDI from 32 to 39
subjective nasal
range 20-71 yrs (no mean
(no means reported)
breathing and daytime
values reported), BMI
No significant postoperative
energy levels in most of
2
35kg/m were included
change in SaO 2 min from 82% the patients
105
Polysomnography prior to
to 84% post
and 6 weeks postoperative Snoring improved or
septum surgery and
disappeared in 35% of
bilateral inferior
patients
turbinectomy including
Significant postoperative
postoperative CPAP
reduction in therapeutic CPAP
titration
pressure from 9.3cmH2O to
6.7cmH2O
Verse T et al, 2002
Case series
4
[198]
26 patients (25 male) with
No significant postoperative
Significant
snoring and nasal
change in AHI from 32±25 pre postoperative reduction
congestion, age 52±8 yrs,
to 29±24 post-operative
in ESS score from 12±5
BMI 29±4 kg/m2, were
No change in oxygen
to 8±5
included
desaturation index
Polysomnography prior to
Significant postoperative
and between 3 and 50
reduction in arousal index
months post-operative
from 31±19 to 23±17
septo(rhino)plasty
19 patients had an AHI>10
Kalam I,
2002 [199]
Case series
4
21 patients with snoring
Postoperative reduction in
This study lacks further
and nasal obstruction with
apnoea index from 14±3 to
details on patient
an AHI < 25 and BMI
11±3 (p<0.005 according to
characteristics
106
<30kg/m2 were included
the manuscript, however, the
Septoplasty w/o mucosal
statistical report is confusing)
resection of inferior
turbinate was performed
Pre- and postoperative
polysomnography was
performed
Kim ST et al ,
Case series
4
2004 [200]
21 patients (15 male) with
Postoperative reduction in RDI No significant
nasal obstruction, age
from 39±14 pre to 29±14
2
difference in snoring
39±5 yrs, BMI 28±2 kg/m
Postoperative reduction in ODI duration after nasal
were included
from 48±17 pre to 33±16
surgery
Polysomnography prior to
and 1 M postoperative
All pts. underwent
septoplasty and 11 pts.
underwent turbinectomy
Nakata S et al, 2005 Case series
[201]
4
12 male OSA patients with No significant postoperative
CPAP tolerance
daytime sleepiness
change in AHI from 56±18 to
increased and CPAP
intolerant to CPAP due to
48±20
pressures required
nasal obstruction, age
Significant postoperative
decreased
2
54±9 yrs, BMI 27±4 kg/m
improvement in SaO 2 min from
107
Virkkula P et al, 2006 Case series
4
[202]
were included
68±12% to 75±7%
Patients underwent
Significant improvement in
submucosal resection w/o
ESS score from 12±4 pre to
inferior turbinectomy
3±1
Polysomnography prior to
Improvements in nasal
and rhinomanometry
resistance
40 male patients with
No significant postoperative
No significant
suspected OSA and nasal
AHI change from 14±16 to
improvements in
obstruction, age 44±9 yrs,
15±19
snoring time
2
BMI 28±3 kg/m , and ESS
No significant change in ODI,
6±4 were included
total sleep time, sleep
Polysomnography prior to
architecture or % sleep time
and between 63 to 176
with SaO 2 <90%
days postoperative
Significant reduction in total
Patients underwent
nasal resistance
septoplasty w/o partial
inferior turbinectomy
Koutsourelakis I et
Randomised,
al, 2008 [203]
sham controlled
2b
49 OSA patients (30 male) No significant postoperative
Responders (n = 4) had
with fixed nasal
change in AHI from 31±17 to
lower BMI and lower
obstruction, age 38±8 yrs,
31±18 in treatment arm
baseline nasal
Significant postoperative
breathing epochs.
2
BMI 30±3 kg/m were
108
included
reduction in ESS from 13.4±3
Sleep characteristics
Polysomnography 1month
to 11.7±3
not reported
prior to and between 3 and No significant changes in ODI
4 M postoperative
Significant improvements and
septoplasty and inferior
nasal resistance and nasal
turbinectomy or sham
breathing epochs
surgery
Nakata S et al, 2008 Case series
4
[204]
49 male OSA patients with No significant postoperative
Significant
nasal obstruction due to
improvements in sleep
change in AHI from 44±22 to
deviated nasal septum und 42±22
chronic rhinitis, age 46±12
Significant improvements in
yrs, BMI 26±4 kg/m2, were
nasal resistance, SaO 2 min
included
(76±11% vs.79±8%, p<0.01),
Polysomnography prior to
apnoe-hypopnea duration, and
and after inferior
ESS score (12±4 vs. 3±1,
turbinectomy w/o
p<0.001)
quality
submucous resection of
the nasal septum
Li HY et al, 2008
[205]
Case series
4
51 OSA patients (50 male) No significant postoperative
Significant
with nasal obstruction, age change in AHI from 37±29 to
improvements in 6 out
39±10 yrs, BMI 26±3 kg/m
2
38±33
of 8 quality of life
109
Polysomnography prior to
No significant postoperative
and 3 M after
change in SaO 2 min from
septomeatoplasty
78±12 to 79±12
subscores of the SF-36
Significant postoperative
reduction in ESS score from
10 (CI 9.8-12.1) to 8 (CI 6.9 to
9.5), p<0.01
Li HY et al, 2009
[206]
Particular casecontrol study
3b
66 OSA patients with
chronic nasal obstruction
(44 patients underwent
surgery, 22 served as
controls)
Polysomnography and
rhinomanometry prior to
and 3 months after
septomeatoplasty
No significant changes in
polysomnographic parameters
in neither group
Improvements in daytime
sleepiness (ESS) and nasal
resistance with surgery
110
Table e12: Effects of intranasal steroids on sleep disordered breathing
Author
Design
EBM Patient population
Results
Comments
Brouilette RT
Randomised, triple-blind, 2b
25 children (14 male),
Treatment associated AHI
No changes in
et al,
placebo-controlled,
age 3.8±0.4 yrs, BMI
reduction from 11±2/hr to 6±2/hr
tonsil size,
2001 [207]
parallel-group trial of
n.a., AHI 11±2, with
(n=13, p<0.05); Number of O 2
adenoidal size or
nasal fluticasone (50mcg
adenotonsillar
desaturations and respiratory
symptom scores
per nostril twice daily for
hypertrophy, symptoms
related arousals decreased more Children with
1 week followed by once
of OSA, and AHI > 1
in fluticasone group
daily for 5 weeks)
Kiely JL et al,
Randomised, double-
2004 [208]
severe OSA
were excluded
2b
13 patients (number of
Treatment associated median -
No treatment
blind, placebo-controlled,
males n.a.), age 47±9
6.5 (CI -29.5 to 1.8) AHI
associated
cross-over trial of nasal
yrs, BMI 30±5 kg/m2,
reduction;
changes in sleep
fluticasone (100 µg per
median AHI 26 (IQR 27), Significant reduction in nasal
nostril twice daily)for 4
and co-existing rhinitis
architecture
airflow resistance and improved
daytime alertness in treatment
weeks
arm
No changes in oxygenation
indices or symptom scores
Mansfield LE
Open clinical trial of
et al, 2004
nasal budesonide (64 µg
4
14 children (8 male),
Treatment associated AHI
Oxygen
mean age 5.9yrs (range
reduction from 7.6 to 0.9 (SD
saturation indices
111
[209]
per nostril once daily) for
4-9yrs), BMI n.a., mean
n.a.);
not reported; no
6 weeks;
AHI 7.6 (SD n.a.), and
Significant improvements in
adverse drug
Home PSG recordings
allergic rhinitis > 2 yrs
subjective sleep quality and nasal reactions
prior to and after
symptoms;
treatment
No changes in sleep stages
Alexopoulos
Open clinical trial of
EI et al, 2004
[210]
4
27 snoring children (15
Treatment associated AHI
Sustained
nasal budesonide (50 µg
male), median age 7
reduction from 5±2 to 3±1;
symptomatic
per nostril twice daily) for
(range 2-14 yrs), BMI
Significant improvements in
improvements at
4 weeks; PSG 2 weeks
n.a.; AHI 5±2, and
oxygen saturation indices,
9 month follow
after treatment end;
chronic nasal obstruction respiratory arousal index, and
up; no adverse
symptomatic follow up
due to adenoidal
symptom scores
drug reactions
after
hypertrophy
22 children (12 male)
Treatment associated AHI
No adverse drug
and residual sleep
reduction from 3.9±1/hr to
reactions
disordered breathing
0.3±0.3/hr;
monteleukast and nasal
(AHI 1-5) after previous
Significant reduction in SaO2min
budesonide (32mcg per
adeno-tonsillectomy, age and respiratory arousal index in
nostril once daily)
6.3±1.3yrs, BMI 19±1
the treatment arm; No changes in
kg/m2, AHI 3.9±1
these parameters in control
9 months
Kheirandish L Open label clinical trial
et
with a control group; 12
al, 2006 [211] week treatment with
3b
group;
112
No changes in sleep efficiency,
sleep time, or mean SaO 2
Kheirandish-
Double blind,
48 children (28 male)
Treatment associated AHI
Gozal L et al,
randomised, crossover
with diagnosed mild
reduction from 3.7±0.3 to 1.3±0.2; of treatment for 8
2008 [212]
trial of intranasal
OSA, age 8.0±0.3yrs,
Significant improvements in sleep weeks did not
budenoside (32 µg per
BMI z-score 0.75±0.05,
architecture, mean SaO 2, and
result in rebound
nostril) or placebo for 6
AHI 3.7±0.3/hr
adenoidal size; No such
of sleep apnoea
weeks
2b
Discontinuation
improvements in the control
group
113
Table e13: Tonsillectomy and tonsillotomy in adults
Author
Design
EB
Patient population
Results
Comments
4 OSA patients (3 male) with
Postoperative Apnea-Index
Improved postoperative
M
Orr WC et al,
Case
1981
series
4
[213]
tonsillar hypertrophy, age 37±19 yrs, reduction from 42±34/hr to
sleep quality and
weight 107±28 kg
improvements in mean
9±14/hr (p=0.06)
Polygraphy prior to and between 1
apnea duration
and 30 M after tonsillectomy
Rubin AH et al,
Case
1983
series
4
[192]
Moser RJ et al,
Case
1987
series
[214]
4
4 male OSA patients with tonsillar
Postoperative Apnea-Index
Selection bias since
hypertrophy, age 45±12 yrs, BMI
reduction from 60±22/hr to
post-operative
n.a.
32±23/hr (p= 0.07)
polygraphy was
Polygraphy prior to and between 2
performed in clinical
and 6 M after tonsillectomy
responders only
5 male OSA patients with
Non-significant postoperative Only 3 patients were
adenotonsillar hypertrophy, age
Apnea-Index change from
37±10 yrs, weight 88±19 kg.
14±4 to 9±7
Polygraphy prior to and between 2
Trend towards improved
and 23 M after tonsillectomy
overnight oxygen saturation
restudied within 12 M
and reduction in apnea
duration time
114
Houghton DJ et al, Case
1997
4
series
[215]
Miyazaki S et al,
Case
1998
series
4
[216]
Verse T et al,
Case
2000 [217]
series
4
5 male OSA patients with tonsillar
Postoperative AHI reduction
One of these patients
hypertrophy, age 43±4 yrs, BMI
from 54±10 to 3±4
had lymphoma of the
32±8 kg/m2 were included
tonsils
Polygraphy prior to and within 3 M
No postoperative
after tonsillectomy
complications reported
10 OSA patients (5 male) with
Postoperative AHI reduction
Interpretation of the
tonsillar hypertrophy mean age 39
from 14±20 to 3±4
findings difficult as
yrs, mean BMI 24.8 kg/m2 (SD not
Trend towards improved
some of the patients
reported) were included
overnight SaO 2 min and
also underwent partial
Daytime polysomnography and
overnight oesophageal
uvulectomy, however,
overnight SaO 2 monitoring was
pressure recordings
the data are not
performed prior to and between 3
presented by procedure
and 6 M postoperative tonsillectomy
type.
11 OSA patients (8 male) with
Postoperative AHI reduction
tonsillar hypertrophy, age 43±14 yrs, from 39±28 to 8±13
80% of patients
demonstrated a
BMI 31±4 kg/m2
Postoperative ODI reduction reduction in the AHI
Polysomnography prior to and
from 44±31 to 18±17
>50% and had a
between 3 and 6 M postoperative
No changes in sleep
postoperative AHI<20
tonsillectomy
efficiency or sleep
architecture
Martinho FL et al,
Case
4
7 OSA patients (5 male) with
Postoperative AHI reduction
2 patients within this
115
2006
series
tonsillar hypertrophy who were
[218]
from 81±26 to 23±18
intolerant to a CPAP trial, age 36±10 Postoperative improvement
yrs, BMI 36±6 kg/m2
in SaO 2 min from 69±14% to
Polysomnography prior to and
83±3%
between 7 and 13 weeks
Improvements in %TST in
postoperative tonsillectomy
slow wave sleep from 6±6%
cohort also underwent
partial uvulectomy
to 16±5%
Nakata S et al,
Case
2006
series
4
30 OSA patients (28 male) with
Postoperative AHI reduction
Success in all with a
tonsillar hypertrophy, age 33±7 yrs,
from 69±28 to 30±24
BMI < 25kg/m2.
BMI 30±6 kg/m2 Polysomnography 3 Postoperative improvements 8 out of 13 CPAP users
[219]
M prior to and
in SaO 2 min from 81±9% to
prior to surgery stopped
6 M postoperative tonsillectomy
93±6%, Arousal Index from
CPAP treatment
68±50 to 32±20, and ESS
postoperatively due to
score from 12±4 to 5±4
improvements in
Significant reduction in
sleepiness
therapeutic CPAP pressure
in users
Nakata S et al,
Case
2007[220]
series
4
20 OSA patients (17 male) with
Postoperative AHI reduction
Significant
tonsillar hypertrophy intolerant to
from 56±22 to 21±14
postoperative reduction
CPAP, age 33±6 yrs, BMI 28±5
Postoperative improvements in nasal resistance in
kg/m
2
in SaO 2 min from 74±10% to
patients
116
Polysomnography prior to and 6 M
84±7%, and ESS from 11±4
postoperative tonsillectomy
to 5±4
117
Table e14: Tonsillectomy and tonsillotomy in children
Author
Design
EBM Patient population
Results
Comments
Frank Y et al,
Case
4
14 children with symptoms of OSA and
Postoperative reduction in total
Diagnostic criteria for
1983
series
clinically determined upper airway
number of apnoeas and
apnoeas and
obstruction, age range 2-14 yrs;
hypopnoeas from 226/night to
hypopnoeas according
Polysomnography prior to and 4 to 6 weeks
24/night (p<0.01)
to the late 70’s
postoperative adenotonsillectomy available
Non-significant trend towards
Improvements in
in 7 children (gender distribution and body-
improvements in sleep efficiency
symptoms of OSA in all
weight was not specified in this group)
and number of awakenings/sleep
children
Stradling JR et al, Particula 3b
61 snoring children with recurrent tonsillitis
Postoperative reduction in 4%
7 had tonsillectomy
1990
r case-
were included, age 4.7±1.7 yrs (range 2-14
SaO 2 dip rate from median 3.6/hr alone,
[222]
control
yrs), 54% male, 31 healthy children matched (0.3 to 23) to median 1.5/hr (0.3
46 had
study
for age and sex served as controls;
adenotonsillectomy,
[221]
to 4.3)
Overnight oximetry and video-recording prior Postoperative reduction in
and 8 had
to and 6 months postoperative (adeno-)
overnight movement time, pulse
adenoidectomy alone
tonsillectomy
rate and OSA symptoms; Rapid
No changes in any of
increase in growth rate
the parameters in
postoperative
controls at the followup visit
Zucconi M et al,
Case
4
14 children with snoring and AHI > 1 on
Postoperative AHI reduction from
No cure of OSA
118
1993
series
[223]
nocturnal PSG, age range 2-15 yrs, gender
11±9 to 3±2
symptoms in 5 children
and weight n.a.
Postoperative improvement in
who underwent
Polysomnography prior to and after (mono-)
SaO 2 min from 81±12% to 89±4% adenoidectomy only
tonsillectomy w/or adenoidectomy
SaO 2
No significant changes in sleep
architecture
Suen JS et al,
Case
1995
series
4
[224]
26 children (age range 1-14 yrs) with
Postoperative reduction in RDI
Preoperative RDI < 19/
suspected OSA and RDI > 5 underwent
from 18±11 to 4.5±9.4
predicted postoperative
polysomnography prior to and 6 weeks
RDI fell below 5 in 21 subjects
RDI < 5
postoperative adenotonsillectomy
(80% success rate)
Significant improvements in
median and minimum SaO 2 , total
sleep time, and number of
arousals
Ali NJ et al,
Particula 3b
12 children (6 male) with moderate OSA,
Postoperative reduction in > 4%
Significant
1996
r case-
age range 6-12 yrs; 11 matched children (6
SaO 2 dip rate from median 2.9/hr improvements in
[225]
control
male) with non-obstructive snoring served
(1.6 to 11.3) to median 1.4/hr (3-
behaviour,
study
as controls, age range 6-12 yrs
7.6) in the OSA group;
psychological
Overnight oximetry including videorecording No postoperative change in
functioning, and % time
was performed prior to and 3-6 months after children with non-obstructiving
spent moving during
adenotonsillectomy
the recording night in
snoring only
119
both groups
Helfaer MA et al,
Case
1996
series
4
[226]
15 children with adenotonsillar hypetrophy
Postoperative reduction in AHI
Total sleep time and
and OSA (AHI 1-15/hr), age 5.1±0.8yrs,
from 5±1/hr to 2±1/hr
sleep efficiency was
weight 24±3.7kg,
Significant postoperative
reduced on first
Pre- and postoperative polysomnography on improvements in SaO 2 min during postoperative night
Nishimura T et al, Case
1996
4
series
[227]
REM sleep
35 children with OSA and adenotonsillar
Postoperative AHI reduction from
hypertrophy, (mean age 4.9 yrs) underwent
mean 13 to 3
pre- and postoperative polysomnography
Wiet GJ et al,
Case
1997
series
4
[228]
Shintani T et al,
Case
1998
series
[229]
the ICU on the first postoperative night
4
31 children/patients (age range 1.5-20 yrs)
Postoperative AHI reduction from
No specific PSG data
with OSA (AHI >5) underwent PSG prior to
23 to 6
available on 12
and after adenotonsillectomy
Significant improvements in
additional patients with
oxygenation indices
morbid obesity
134 children (92male) with OSA, age
Postoperative AHI reduction from
No differences in
4.4±1.5 yrs (range 1-9 yrs) who underwent
25±13 to 8±5
outcome across
adenoidectomy w/o tonsillectomy were
Postoperative improvement in
different age groups
included in this report;
SaO 2 min from 79±12% to
Patients with grade 2
Pre and postoperative (2 M after surgery)
86±6%SaO 2
and 3 tonsillar
polygraphy data available in 74 children who
hypertrophy had higher
underwent adeno-bilateral-tonsillectomy and
postoperative AHI
had pre-operative AHI>10. No data available
reduction than those
120
on the other group
with hypertrophy grade
1
Bar A et al,
Case
1999
series
4
[230]
13 children (11 male) with OSA, age 6±3
Postoperative reduction in RDI
Serum insulin growth
yrs, underwent polygraphy before and 5±3
from 8±9 to 1±2
factor-I levels
M (range 3 to 12 M) postoperative
Significant postoperative increase increased
adenotonsillectomy
in %time spent in slow wave
postoperatively
sleep
Nieminen P et al, Particula 3b
21 snoring children with symptoms of OSA
Postoperative AHI reduction from
Increase in OSA
2000
r case-
and AHI>2 (73% had previous
7±1 to 0.3±1.1
symptom score in
[231]
control
adenoidectomy), age 5.6± 2.1 yrs (range 3-
Postoperative ODI reduction from controls, however, no
study
10 yrs);
5±7 to 0.2±0.6
changes in sleep
PSG prior to and 6 M postoperative
Significant improvements in OSA
parameters in controls
adenotonsillectomy
symptom scores
at follow-up
30 children (age range 4-12 yrs) with
Postoperative AHI reduction from
19 patients underwent
symptoms of upper airway obstruction
27 to 6 (SD n.a.)
adenoidectomy, 8
undergoing adenoidectomy and/or
Significant postoperative
adenotonsillectomy,
tonsillectomy (no further details on patient
improvements in total apnoea
and 3 children
characteristics available)
duration, SaO 2 min and ODI
underwent
37 children with AHI < 2 served as controls
Jain A et al,
Case
2002
series
[232]
4
PSG was performed prior to and 6-8 weeks
tonsillectomy as a
after surgery
single procedure
121
Mora R et al,
Case
2003
series
4
[233]
Tal A et al,
Case
2003
series
4
[234]
Guilleminault C,
Case
2004
series
4
[235]
40 children (23 male) with OSA and tonsillar Postoperative reduction in RDI
Resolution of OSA in
hypertrophy, age range 2-14 yrs
from 27 to 2 (SD n.a.)
37 cases
Polygraphy prior to and 1 M postoperative
Significant postoperative increase Significant reduction in
adenotonsillectomy
in SaO 2 mean from 79% to 95%
36 children (25 male) with OSA (RDI > 1),
Postoperative reduction in median Decision for surgery
median age 6.9 yrs (age range 2-12 yrs)
RDI from pre 4.1 (range 0-85) to
was based on clinical
Polygraphy prior to and median 3.7 M
0.9 (range 0-13)
and PSG findings
postoperative adenotonsillectomy
Modest but significant
4 children (11%) there
postoperative improvements in
was residual OSA with
SaO 2 mean and arousal index
RDI >5 after surgery
Postoperative AHI reduction from
Significant
17 children (12 male; age range 24 M to 12
OSA symptom scores
yrs) with adenotonsillar hypertrophy and AHI 26±4 to 2±3
postoperative AHI
> 10 underwent PSG prior to and 3-4 M
Postoperative increase in
reduction in 202
postoperative adenotonsillectomy
SaO 2 min
additional children with
baseline AHI < 10,
detailed data not
available on this group
Mitchell RB et al,
Case
2004
series
[236]
4
29 children (22 male) with severe OSA and
Postoperative reduction in RDI
Significant
RDI > 30, mean age 7.1 yrs (range 1-17
from 64 (95% CI: 52-76) to14
postoperative
yrs), 14 children (48%) had a BMI >95th
(95%CI: 9-19); 22 children (76%)
improvements in QoL
122
percentiles
had postoperative RDI >5
PSG prior to and mean 5.8 M postoperative
indicating persistent OSA
OSA scores
adenotonsillectomy
Mitchell RB, et al
Case
2004
series
4
Case
2005
series
Postoperative reduction in RDI
age 9.3 yrs (range 3-17 yrs), mean BMI 28.6 from 30 (95% CI 19-49) to 11
[237]
Mitchell RB et al,
30 children (26 male) with RDI > 5, mean
4
kg/m2 (range 19-47)
(95% CI 5-18)
PSG prior to and 6 M postoperative
Significant postoperative
adenotonsillectomy
improvements in QoL OSA scores
20 children (15 male) with adenotonsillar
Postoperative reduction in RDI
hypertrophy (mean age 2.2 yrs, range 1.1 to from 34 to 12
25% of children had
postoperative
3 yrs) underwent PSG prior to and
65% of children had postoperative complications such as
postoperative adenotonsillectomy
RDI>5
laryngospasms
Chervin RD et al, Particula 3b
78 children (41 male) scheduled for
Postoperative AHI reduction from
Between group
2006
r case-
adenotonsillectomy, age 8±2 yrs (range 5-13 7±12 to 1.2±1.9 in adeno-
differences
[239]
control
yrs), BMI 20±5 kg/m2;
disappeared after
study
27 controls (age 9±2 yrs, BMI 19±3 kg/m2)
[238]
tonsillectomy groups
surgery at the follow-up
who underwent surgery not related to the
Significant postoperative
8 children (21%) in the
upper airway served as controls
improvements in arousal index
surgical treatment arm
PSG was performed prior to and 12 M
and SaO 2 min
had residual OSA
123
postoperative;
Li HY et al, 2006
Case
[240]
series
4
40 children (36 male) with suspected OSA
Postoperative AHI reduction from
Attention and Child
and tonsillar hypertrophy, age 8±2 yrs
11±11 to 1.7±2.1
Behaviour Checklist
(range 5-12 yrs), BMI 18.6±4 kg/m
Postoperative improvement in
Scores improved
PSG prior to and 6 M postoperative
SaO 2 mean from 96±2% to 97±1% significantly
2
adenotonsillectomy
Tauman R et al,
Particula 3b
110 children (60% male), age 6.4±3.9 yrs
Postoperative AHI reduction from
Complete resolution of
2006
r case-
(range 1-16 yrs), 71% of these children had
22±29 to 6±9
OSA (AHI<1) in 25% of
[241]
control
a history of allergy
Postoperative reduction in
children only; 29% had
study
22 age, sex, and body-mass-index matched
Arousal Index from 22±22 to
postoperative AHI >5
controls
12±10
Obesity associated
Postoperative increase in
with lower
PSG prior to and 5±3 M postoperative
SaO 2 min from 78±18% to
postoperative AHI
adenotonsillectomy
86±10%
reduction
No difference in sleep parameters
between controls and children
who had complete resolution of
OSA
Pavone M et al,
Case
2006 [242]
series
4
5 children (4 males) with Prader Willi
Postoperative AHI reduction from
4 children had
Syndrome and OSA due to adenotonsillar
median 12 (9-20) to 1.6 (0.6-4.7
postoperative
hypertrophy, median age 4.4 yrs (range 1-14 Significant postoperative
complications such as
124
yrs), median BMI 18kg/m2 (range 18-42
improvements in SaO 2 min and
laryngospasm or
kg/m2)
%TST spent < 90%SaO 2
hemorrhage
199 snoring children (~55% male), age
Postoperative AHI reduction from
46% of children had
range 19 M to 4yrs;
median 7.6 (range 2 to 35) to
AHI>1 after surgery;
Polysomnography (> 90%) or polygraphy
median 3.8 (range 0-22)
Mallampati score and
prior to and 12 to 20 weeks postoperative
Postoperative improvement in
deviated septum were
(adeno-) tonsillectomy
SaO 2 min from 90±2% to 93±3%
predictors for
SaO 2
persistent sleep
Polygraphy prior to and 3-43 M after surgery
adenotonsillectomy
Guilleminault C et Case
al, 2007
4
series
[243]
apnoea after surgery
Mitchell RB et al,
Case
2007
series
4
[244]
79 children (40 male) with OSA and an
Postoperative AHI reduction from
Tonsillar size
AHI>5, mean age 6.3 yrs (range 3 to 16 yrs) pre 27±22 to 3±5
correlated with
PSG prior to and mean 5.2 M (range 1 to 9
Significant postoperative
preoperative AHI
M) postoperative adenotonsillectomy
improvements in SaO 2 mean,
20% of children had
SaO 2 min, %TST < 92%SaO 2 ,
persistent OSA after
and Arousal Index
surgery
Improvements in QoL scores
Surgery successful in all cases
with preoperative AHI < 10
Mitchell RB et al,
Particula 3b
33 obese children (23 male, mean age 7.3
Postoperative AHI reduction from
25 obese children
125
2007
r case-
yrs, age range 3-17 yrs) and 39 normal
mean 31 to 6 (SD n.a.) in obese
(76%) and 11 controls
[245]
control
weight children (20 male, mean age 6 yrs,
children;
(28%) had persistent
study
age range 3-15 yrs) with OSA and AHI >2
Postoperative AHI reduction from
OSA after surgery
were studied;
mean 18 to 2 (SD n.a.) in normal
Preoperative BMI and
Polysomnography prior to and 5 M
weight;
AHI were predictors for
postoperative adenotonsillectomy
Significant postoperative
persistent OSA after
improvements in arousal index
surgery
and SaO 2 min in both groups
Dillon JE et al,
Particula 3b
40 children (22 male) with adenotonsillar
Postoperative reduction in OAI
Significant
2007
r case-
hypertrophy and OSA (OAI >0.5, age
from 5.6±8.0 to 0.2±0.3 in OSA
postoperative reduction
[246]
control
7.8±1.8 yrs, BMI n.a.
group
in attention and
study
38 children (19 male) with adenotonsillar
No postoperative change in OAI
disruptive behaviour
hypertrophy and OAI <0.5, age 8.4±1.7 yrs,
in both other groups
disorder rating scales
BMI n.a.
No data on oxygen saturation or
in children with
27 children (19 male) with surgery unrelated sleep architecture available
adenotonsillar
to the upper airways, age 9.3±2.0 yrs
hypertrophy unrelated
Polysomnography prior to and 10-15 M
to OSA severity
postoperative adenotonsillectomy
Gozal D et al,
Case
2007 [247]
control
study of
4
26 children (16 male) with OSA and
Postoperative AHI reduction from
adenotonsillar hypertrophy, age 6.9±0.6 yrs, 11.9±2.2 to 1.9±0.7
2
BMI 17.1±0.6 kg/m
Postoperative improvements in
Significant
postoperative
improvements in
126
limited
8 children (5 male) matched for age and sex respiratory arousal index %REM
endothelial function in
quality
served as controls at baseline, age 6.8±0.5
sleep, %Slow Wave Sleep,
OSA group
yrs, BMI 16.8±0.5 kg/m2
SaO 2 min, and %TST < 90%SaO 2
Polysomnography prior to and 4-6 M
postoperative adenotonsillectomy
Guilleminault C et Case
4
17 children with cyanotic breath holding
Postoperative AHI reduction from
Resolution of cyanotic
al, 2007
control
spells and signs of upper airway obstruction, 2.1±1.2 to 0.7±0.8 in 13 children
breath holding spells in
[248]
study of
age range 13-14 M, BMI n.a.
that underwent surgery;
all children who
limited
Polysomnography prior to and 4-5 M
Significant postoperative
underwent surgery
quality
postoperative adenotonsillectomy
improvements in SaO 2 min and
Persisting symptoms
snoring time
and sleep disordered
breathing in 4 children
that did not undergo
surgery
Gozal D et al,
Particula 3b
37 obese (18 male) children with
Postoperative obstructive AHI
2008
r case-
adenotonsillar hypertrophy, age 7.9±0.4 yrs, reduction from 19.2±2.9 to
was associated with
[249]
control
BMI z-score 2.4±0.08
5.5±0.7 in the obese children
significant
study
25 non-obese (15 male) children with
Postoperative obstructive AHI
improvements in lipids
adenotonsillar hypertrophy, 6.6±0.5 yrs, BMI reduction from 12.9±1.3 to
Adenotonsillectomy
and inflammatory
z-score -0.02±0.2
1.9±0.2 in the non-obese children markers in both groups
Polysomnography prior to and 6-12 M
Significant improvements in
127
postoperative adenotonsillectomy
SaO 2 min and arousal index in
both groups
Walker P et al,
Case
2008
series
4
[250]
34 children with adenotonsillar hypertrophy,
Postoperative reduction in the
4 children (12%) had
mean age 3 yrs (range 0.9-5 yrs), mean
RDI from 15.5 to 3 (SD n.a.)
persistently severe
14.2 kg (range 7-31kg), 8 children had co-
Significant improvements in
OSA postoperatively
existing medical morbidities, such as Down
SaO 2 min and arousal index
syndrome, hydrocephalus, or epilepisy
2 children developed secondary
postoperative hemorrhage, no
Apostolidou MT
Case
et al, 2008
series
4
[251]
Polysomnography prior to and 9.8 M
other relevant complications were
postoperative (adeno-)tonsillectomy
reported
22 obese (15 male) children with
Postoperative obstructive AHI
adenotonsillar hypertrophy, age 5.8±1.8 yrs, reduction from 9.5±9.7 to 1.9±1.6
(<1/hr) was achieved in
BMI z-score 2.6±0.6
in the obese children
23% of obese and 25%
48 non-obese (30 male) children with
Postoperative obstructive AHI
of non-obese children
adenotonsillar hypertrophy, 6.9±2.6 yrs, BMI reduction from 6.0±5.4 to 1.9±1.4
Guilleminault C et Case
al, 2008
series
4
Normalisation of AHI
z-score 0.09±1.1
in the non-obese children
Polysomnography prior to and 5.7±3.4 M
Improvements in SaO 2 min and
postoperative adenotonsillectomy
respiratory arousal index
16 children with OSA and adenotonsillar
Postoperative AHI reduction from
hypertrophy, age range 4.7-9 yrs, BMI n.a.
11±3 to 5±5
(p>0.05)
128
[252]
Polysomnography prior to and 3 M
Postoperative improvements in
postoperative adenotonsillectomy w/o
RDI and SaO 2 min
inferior turbinectomy (n=9)
Amin R et al,
Particula 3b
40 children (24 male) with OSA (AHI >1) and Postoperative AHI reduction from
BMI gain over 1yr was
2008
r case-
adenotonsillar hypertrophy, age 10±2 yrs,
9.2±14 to 1.4±2 after 6 weeks
associated with
[253]
control
45% had BMI >95% percentile
Significant increase in the AHI
significant increase in
study
30 children without OSA, matched for age
over time with an AHI >3 in 22%
risk of OSA recurrence
and sex served as controls, 10% had
and 50 % of the children with
No significant change
BMI>95% percentile
OSA at 6 M and 1yr interval,
in any parameters in
Polysomnography prior to and 6 weeks, 6 M, respectively
and 1 year postoperative
Recurrence of OSA was
adenotonsillectomy
associated with increased blood
controls
pressure
De la Chaux R et Case
al, Int J 2008
4
20 children (15 male) with OSA (AHI >5),
2
series
age 4±2 yrs (range 2-9 yrs), BMI 15±3 kg/m
[254]
Postoperative reduction in AHI
No postoperative
from 15±9 to 1.1±1.6
complications; Children
Postoperative improvements in
were discharged on the
Polysomnography prior to and postoperative SaO 2 mean and SaO 2 min
laser tonsillotomy w/o adenoidectomy
3rd postoperative day
(71±11% vs. 91±3%SaO 2 )
No postoperative changes in
sleep stages and total sleep time
Sullivan S et al,
Case
4
399 children (age < 10yrs) underwent
Postoperative AHI reduction from
Lower AHI reduction in
129
2008
series
polysomnography prior to and 3 to 4 M
[255]
Tunkel DE et al,
Case
2008
series
4
[256]
8.6±9 to 1.8±2
those with co-existing
postoperative adenotonsillectomy
enlargement of the
No further baseline characteristics available
inferior nasal turbinates
14 children (7 male) with OSA (RDI 5-15),
Postoperative AHI reduction from
Significant
mean age 71 M (range 28-113 M), BMI n.a.
median 7.9 (IQR 5-17) to 0.1 (IQR improvements in all
Polysomnography prior to and median 6
0-3.6)
weeks postoperative intracapsullar
Postoperative improvement in
tonsillectomy and adenoidectomy
SaO 2 mean from 88.5±4% to
OSA-18 QoL scales
93.9±3%
Significant reduction in arousal
index
Friedman M et al, Case
2009
4
series
[257]
3b
159 children and adolescents (84male) with
Postoperative reduction in AHI
Friedman tongue
OSA, age 8.5±3.1 yrs (range 4-18 yrs), 40% from mean 18 to 3 (SD not
position III or IV and
of the population was considered overweight reported)
elevated preoperative
Polysomnography prior to and 6±1 M
55% had postoperative AHI<1
AHI were predictors of
postoperative intracapsullar coblation
Significant postoperative
lower postoperative
tonsillectomy
improvements in SaO 2 min
AHI reduction
44 healthy snoring children (27 male)
Postoperative AHI reduction from
Kohler MJ et al,
Case-
Plos One 2009
control
age 6.6±2.6yrs (range 3-12yrs), BMI z-score median 0.8 (IQR 0-50) to 0.36
[258]
series
0.84±1.3
(IWR 0-4.7) in surgical group
48 age and gender matched non-snoring
No significant improvements in
130
controls
neurocognitive parameters
Polysomnography and neurocognitive
relative to controls
testing prior to and 6 months after surgery
131
Table e15: Patient characteristics and follow-up data in studies on radiofrequency of tonsils
Author
N
Mean age (range)
Follow-up
Tonsil reduction (%)
AHI
ESS (0-24)
Snoring (0-10)
Nelson, 2000
9
- (24-47)
12 weeks
70.8
-
7.7 -> 4.4
6.8 -> 2.4
12
34 (24-51)
1 year
-
-
7.8 -> 2.5
6.5 -> 1.3
22
32 (14-47)
12 weeks
53.6
-
-
-
31
20.7 (16-25)
1 year
-
-
-
-
[259]
Nelson, 2001
[260]
Friedman et al,
2003 [261]
Ericsson et al,
2007 [262]
132
Table e16: Monitoring of side effects after radiofrequency surgery of tonsils
Author
N
Post-op bleeding
Pain day 1
no-mild
Pain day 7
moderate-severe
no-mild
moderatesevere
Nelson, 2000
9
0
5
4
9
0
22
0
22
0
-
-
12
0
“most”
“none”
-
-
31
0
-
-
25
6
[259]
Friedman et al,
2003 [261]
Nelson, 2001
[260]
Ericsson et al,
2007 [262]
133
Table e17: UPPP results in prospective studies
Author
Design
EBM
Patient population
Results
Comments
Berger et
Non
3b
25 OSA (22 male), age With UPPP, RDI
Follow-up after a
al, 2003
randomised,
49±11 yrs, BMI 28±3
revealed an
mean of 12 M.
[263]
prospective,
kg/m2, AHI 26±18,
improvement, but did
case controlled
underwent a modified
not reach statistical
procedure of LAUP
significance (26±18
and were compared to
vs 19±21,
a matched control
respectively) (P=.09).
group of 24 patients
Fourteen patients
operated by classic
(58%) had a
UPPP
successful surgery
defined by a
decrease in RDI
>50%
134
Shin et al,
RCT
2009 [264]
2
UPPP: 16 male severe
Subjective sleep
Polysomnographic
comparing
to very severe OSA,
quality from the PSQI
mean follow-up
classic (UPPP)
age: 46 yrs, mean BMI
was significantly
interval of 10 M (8-
(n=16) versus
24.9 kg/m2 (20-31),
improved in both
18).
modified
AHI 54±14
groups. ESS was
UPPP
MUPPP: 16 severe to
significantly improved
(MUPP) (n=16)
very severe OSA,
in both groups. 20 on
age: 46 yrs, mean BMI
32 patients were
24.9 kg/m2 (21-30),
post-operatively
AHI 56±23
evaluated by PSG. In
UPPP group AHI
decrease from 54 ±
14 to 35 ± 25. In
MUPPP group AHI
decrease from 56 ±
23 to 35 ± 27.
Surgical successes
were 30 % in the
UPPP group and 40
% in the modified
UPPP group.
135
Pang et al,
RCT
2007 [265]
2
45 (41 male) severe
Apnoea-hypopnoea
comparing
OSA, BMI 28.7±?, age
index improved from
Mean follow-up of 6.5
classic (UPPP)
42 yrs (24-47), with
38± 6 to 20 ± 8 in the
M
(n=22) versus
small tonsils, body
uvulopalatopharyngo
No data on
expansion
mass index less than
plasty group (P
sleepiness
2
sphincter
30 kg/m , of Friedman
<0.005). Lowest
pharyngoplast
stage II or III, or type I
oxygen saturation
y (ESP) (n=23)
Fujita.
improved from 75 ±
6% to 87 ± 2% in the
uvulopalatopharyngo
plasty group (P
<0.005). Success
rate was 68.1% in
136
uvulopalatopharyngo
plasty.
Li et al,
Case series.
2006[266]
4
N=110 (105 male)
Overall success rate
Anatomy-based
Prospective
severe OSA, age
of UPPP was 78%.
staging system
design with a
43±9.4 yrs;
Success rates for
predicted UPPP
retrospective
AHI 44 ± 29; BMI 27.1
patients with
outcomes more
review.
± 3.3 kg/m2
anatomy-based
effectively than did
stages I, II, III, and IV
AHI.
(Friedman
classification) were
100%, 96%, 65%,
and 20%,
respectively (p <
.001). Changes in
apnoea-hypopnoea
index were
significantly
correlated with
Friedman tongue
position (FTP).
Kinoshita et Prospective
4
N = 15 (14 male)
CRP improved from
137
al, 2006
moderate to very
0.21 ± 0.17 mg/dL to
[267]
severe OSA, age 43
0.10 ± 0.16 mg/dL.
±9 yrs, BMI
AHI reduced from 48
27.9 ± 2.8 kg/m2, AHI
± 24 to 16 ±15 .
48±24
Lee et al,
2009 [268]
Prospective
4
15 Healthy subjects
UPPP success in
30 OSA
47% of patients
Patient characteristics:
(14/30).
Successful UPPP
Successful treatment
(n=14): 12 male,age
of OSA by UPPP led
34 ±6 yrs, BMI
to restoration of
27.4 ± 1.6 kg/m2, RDI
endothelial function:
34.1±9.4
Flow mediated
UPPP failure (n=16):
vasodilation
14 male, age 37 ±6
increased from 5.2 ±
yrs, BMI
5.0 % preoperatively
138
27.6 ± 1.5 kg/m2, RDI
to 10.0±4.7
34.4±9.9
postoperatively in
UPPP successes (p <
0.027).
Walker-
RCT
Engström
1
95 male mild to
At 4 yrs, AHI reduced
In the UPPP group,
comparing
moderately severe
from 18 ±3 to 7±3 in
AHI significantly
et al, 2002
dental
OSA randomized. 49
the dental appliance
deteriorated between
[102]
appliance vs
assigned to dental
group compared to
1 year and 4 yrs
UPPP
appliance, 46 to
20±3 to 14 ±3.
follow-up from 10±3
UPPP. 4 yrs follow-up.
63% of the patients in to 14±3.
the dental-appliance
group attained an
AHI<10 after 4 yrs, a
proportion that was
significantly higher
than that among the
patients in the UPPP
group, 33%.
139
Cahali et al, RCT
2004 [269]
Patient characteristics:
AHI improved in the
comparing
lateral pharyngoplasty
lateral
classic (UPPP)
(12 men), BMI
pharyngoplasty group evaluation after at
(n=12) versus
29.3.1 kg/m2, AHI 41.6/ but not in the
Lateral
and classic UPPP (8
uvulopalatopharyngo
pharyngoplast
men), BMI
plasty group (from 35
Significant ESS
to 30). ESS
improvements in both
significantly
groups (median
decreases in the two
reductions of 11 and
groups.
10 in lateral PP and
y (n=15)
2
2
30.1 kg/m , AHI 34.6/h
Post operative
least 6 M
UPPP groups
respectively).
140
Kezirian et
Prospective
al,, 2006
[270]
4
3,130 patients
Serious life-
study with
operated from 1991 to
threatening
retrospective
2001. 97% were men
complications
analysis
aged 50±11 yrs
including intubation
difficulties, bleedings
and acute upper
airway obstruction
occurred with a 1.5%
incidence. Mortality
rate was 0.2%.
Higher AHI and
comorbidities were
significantly
associated with
complications
141
Table e18: Laser assisted uvulopalatoplasty
Author
Design
EBM
Patient population
Results
Comments
Ferguson et al,
RCT comparing
1
N=46 mild to moderately
21% reduction in mean
Follow-up period 7 M
2003 [271]
LAUP to
severe OSA (21 LAUP,
AHI after LAUP (from
conservative
24 conservative
19 to 15) with a
treatment
treatment)
significant difference in
age 45 ± 8 yrs ;
final AHI in favor of
2
BMI 36 ± 4.5 kg/m
LAUP compared to
AHI: LAUP: 19±4;
conservative treatment
Control 16 ±4;
(P = 0.04).
ESS: LAUP: 11±4;
No significant between-
Control: 10 ±5.
group difference in the
Epworth Sleepiness
Scale or the Calgary
Sleep Apnoea Quality
of Life Index.
Snoring intensity and
frequency were
significantly decreased.
142
Larrosa et al, 2004 RCT, parallel
[272]
groups.
Laser-assisted UPP
versus sham
procedure.
1
N = 28 mild OSA, Whole
population: age:
44±7 yrs; BMI: 27.1±2.9
kg/m-2; AHI: 15±13;
AHI LAUP: 14; control:
17;
ESS: LAUP: 10; control:
11.
No differences were
3 M follow-up.
observed in body
weight, sleepiness,
quality of life, subjective
and objective intensity,
and frequency of
snoring, and
apnoea/hypopnoea
index between the
groups after treatment
(14± 8 vs 15±18).
143
Table e19: Radiofrequency surgery of the soft palate
Author
Design
Device and
EBM Patient population
Results
4
12 patients, 1 only
Statistically significant
receiving 2 of 3
reduction of AHI from
treatments (n=12)
31.2 to 25.3 at short
Comments
Technique
Brown et al,
2001 [273]
case series monopolar,
interstitial
term follow up (6 weeks)
16.7% success rate (AHI
reduced more than 50%
and below 20)
Blumen et al,
2002 [274]
case series monopolar,
4
intersitial
78 patients, 49 drop outs
Statistically significant
High number of drop
(n=29)
reduction of AHI from
outs after the first
19.0 to 9.8 after 8.5
treatment sessions
months
65.5% success rate (AHI
reduced more than 50%
and below 20)
Atef et al, 2005 randomised Coblation, RF[275]
UPP
3b
75 in RF group, 11 drop
Statistically ignificant
Randomised: RF against
outs (n=64)
reduction in the
LAUP
subgroups with 3 or
144
more treatment sessions
at short- (3m) and longterm (18m) follow up*
Bassiouny et
randomised Coblation,
al, 2007 [276]
3b
interstitial
20 in interstitial group, no
Statistically significant
randomised: intersitial
drop outs
reduction at 3 months,
vs. RAUP
reduction in mean AHI
from 15.3 to 9.8
40% success rate (AHI
reduced more than 50%
and below 20)
randomised Coblation, RAUP
3b
20 in RAUP group, no
Statistically significant
randomised: intersitial
drop outs
reduction at 3 months,
vs. RAUP
reduction in mean AHI
from 17.2 to 8.1
50% success rate (AHI
reduced more than 50%
and below 20)
Bäck et al.
Randomise Bipolar RF,
32 patients with mild to
No significant reduction
2009 [277]
d, Placebo- interstitial
moderate sleep apnea (17 in AHI in RF-group from
controlled
RF and 15 placebo)
single step intervention
only
11.0 to 13.0
145
*success rates at short term (long-term) follow-up according to subgroup: one session: 0 (0)%, two sessions: 27.2 (9)%, three
sessions: 90 (55)%, four sessions: 70 (60)%, five sessions: 88.2 (82.2)%
146
Table e20: Uvulopalatal flap for OSA
Authors
Design
EBM
Study population
Results
Comments
Hsieh et al, 2005
Case series
4
N=6 severe to very
RDI pre: 517 ± 13
fixed combination of
severe OSA (6
RDI post: 12 ± 23
surgeries
male), b/a MLS
Success: 83.3 %
follow-up: 6 M
[278]
EUPF + MLG
MLS effective for
age: 43 ± 8 yrs
OSA
BMI pre: 27.5 ± 2.0
kg m-2
BMI post: no data
Li et al, 2005 [279]
Retrospective case
series
4
N= 85 OSA, b/a
similar results and
lower hospitalisation
EUPF + nasal
complication rates
costs in the single
septoplasty
stage surgery group
Group 1
follow-up: 7 ± 1 M
Group 1: single
RDI pre: 35 ± 15
EUPF + nasal
stage
RDI post: 12 ± 9
septoplasty effective
N=55 moderate to
Success: 81.8 %
for OSA
severe OSA(53
male)
Group 2
147
age: 40 ± 7 yrs
RDI pre: 39 ± 20
BMI pre: 25.9 ± 2.2
RDI post: 11 ± 8
kg m-2
Success: 73.3 %
BMI post: no data
Group 2: two stages
N=30 moderate to
very severe OSA
(29 male)
age: 41 ± 7 yrs
BMI pre: 26.7 ± 1.5
kg m-2
BMI post: no data
Li et al, 2005 [280]
Case series
4
N=50 mild to very
RDI pre: 45 ± 29
isolated procedure
severe OSA (49
RDI post: 13 ± 20
follow-up 6 M
male), b/a EUPF
Success: 84 %
EUPF effective for
age: 43 ± 9 yrs
OSA
BMI pre: 26.6 ± 3.9
kg m-2
BMI post: 25.8 ± 5.1
kg m-2
148
Li et al, 2004 [281]
Individual case-
3b
control study
N=12 severe to very
Type 1
follow-up: 6 months
severe OSA, b/a
RDI pre: 51 ± 13
MLS
RDI post: 8 ± 14OK
EUPF is effective in
EUPF + MLG
Success: 83.3%
resolving palatal
6/12 type I
Type 2
obstruction
obstruction
RDI pre: 56.± 13
6/12 type II
RDI post: 63 ± 15
obstruction
Success: 0%
age: 45 ± 7 yrs
BMI pre: 26.5 ± 2.6
kg m-2
BMI post: no
significant change
Li et al, 2004 [282]
Case series
4
N=84 mild to very
Mental Health 5
isolated procedure
severe OSA (81
questionnaire (MH5)
EUPF effective for
male),
Pre: 61.8 ± 16.0
OSA
b/a EUPF
Post: 70.0 ± 15.8
improvement in MP5
age: 44 ± 9 yrs
RDI pre: 47 ± 30
independent from
BMI pre: 26.8 ± 3.6
RDI post: 15 ± 22
ESS or RDI
kg m
-2
BMI post: 26.7 ± 3.6
ESS pre: 11 ± 4
ESS post: 7 ± 4
149
Li et al, 2004 [283]
Case series
4
kg m-2
Success: 79.8%
N= 55 mild to very
SF-36, SOS
isolated procedure
severe OSA (52
ESS pre: 12 ± 5
follow-up: 6 M
male), b/a EUPF
ESS post: 8 ± 4
increased QOL after
age: 45 ± 10 yrs
RDI pre: 44 ± 30
surgery
BMI pre: 26.4 ± 4.1
RDI post: 12 ± 19
kg m-2
Success: 82.0%
BMI post: 25.8 ± 5.1
kg m-2
Li et al, 2004 [281]
Case series
4
N=105 mild to very
RDI pre: 45 ± 29
isolated procedure
severe OSA (101
RDI post: 15 ± 22
follow-up: 12 M
male), b/a EUPF
Success: 80.0%
Friedman Staging
N=33 mild to very
RDI pre: 42 ± 28
isolated procedure
severe OSA (32
RDI post: 13 ± 18
follow-up 6 M
male),
Success: 81.8%
EUPF effective for
age: 43 ± 9 yrs
Li et al, 2003 [284]
Case series
4
b/a EUPF
OSA
age: 44 ± 9 yrs
BMI pre: 26.7 ± 3.9
kg m-2
150
Neruntarat 2003
Case series
4
[285]
N=56 OSA (50
(VAS 10) no PSG
isolated procedure
male), b/a flap
Snore pre: 8.2 ± 3.4
follow-up: 14 M
age: 48 ± 10 yrs
Snore post: 2.6 ± 1.4 EUPF effective for
BMI pre: 26.5 ± 2.4
snoring
kg m-2
BMI post: 26.8 ± 3.5
kg m-2
Neruntarat 2003
Case series
4
[286]
Neruntarat 2003
[287]
Case series
4
N=31 severe to very
RDI pre: 48 ± 11
MLS with fixed
severe OSA (28
RDI post: 14 ± 6
combination of
male), b/a MLS
Success: 70 %
surgeries
GG-A + HS + flap
Snore pre: 8.1 ± 0.6
follow-up 8 M
age: 46 ± 6 yrs
Snore post: 3.4 ± 0.9 MLS effective for
BMI pre: 28.8 ± 3.2
ESS pre: 15 ± 2
kg m-2
ESS post 8 ± 2
N=32 severe to very
RDI pre: 45 ± 9
MLS with fixed
severe OSA (30
RDI post:15 ± 6
combination of
male), b/a MLS
Success: 78.0%
surgeries follow-up
HS + flap
Snore pre: 8.5 ± 1.8
8M
age: 39 ± 6 yrs
Snore post: 3.5 ± 1.7 MLS effective for
BMI pre: 29.3 ± 2.4
ESS pre: 14 ± 2
kg m-2
ESS post 8 ± 2
OSA
OSA
151
Powell et al, 1996
Individual case-
[288]
control study
3b
N=80 mild to very
Flap:
MLS with various
severe OSA, b/a
RDI pre: 29 ± 27
combinations of
MLS
RDI post: no data
surgeries
N=59 OSA (49
success: no data
UPPP and Flap
male) b/a flap + GG- UPPP:
show comparable
A + HS
RDI pre: 36 ± 32
results in concern to
age: 44 ± 12 yrs
RDI post: no data
efficacy, amount of
BMI pre: 30.2 ± 5.9
success: no data
tissue removed and
kg m-2
complications.
BMI post: 29.6 ± 5.7
kg m-2
N=21 OSA (18
male) b/a UPPP +
GG-A + HS
age: 47 ± 13yrs
BMI pre: 31.7 ± 7.8
kg m-2
BMI post: 30.8 ± 7.6
kg m-2
152
Table e21: Uvulopalatal flap as an isolated procedure for OSA
Authors
N
follow-up [months]
AHI
AHI post
success [%]
EBM
pre
Li et al, 2003 (170)
33
6
42
13
81.8
4
Li et al, 2004 [281]
84
no data
47
15
no data
4
Li et al, 2004 [282]
105
12
45
15
80
4
Li et al, 2004 [283]
55
6
44
12
82
4
Li et al, 2005 [279] 50
6
45
13
84
4
all
6 - 12
45
14
81.52
C
327
153
Table e22: Pillar method
Author
Design
Nordgard S et Case series
EBM Patient population
Results
Comments
4
25 patients (age 51.7±9.8, BMI
AHI was significantly reduced
Patients only included if
27.2±1.9 kg/m2, gender not
in mean from 16.2±4.6 to
<50% of obstructive
al, 2006; [289] (single
centre)
mentioned) with mild to moderately 12.1±9.1, HI from 14.1±4.8 to
events were classified as
severe OSA (AHI 10-30) and
8.7±5.5, ESS from 9.7±3.6 to
lower (retrolingual)
BMI<30 kg/m , no drop outs.
5.5±3.5,success rates (a)
events; the sum of AI and
Polygraphy with pharyngeo-
48%, (b) 36%, (c) 36%
HI differs from AHI.
2
esophageal pressure
measurements prior to and
between 3 to 4 months after
surgery
Friedman M et Case series
al, 2006; [290] (single
centre)
4
26 patients with mild to moderately
AHI was significantly reduced, Patients after failed
severe OSA (AHI 5-40) and
ESS from 13.2±2.9 to 8.7±1.8, UPPP with persistent
BMI<40 kg/m2 , 3 drop outs, 23
success rate 22% (AHI
palatal obstruction.
patients (18 males) remaining,
reduced more than 50% and
Postoperative BMI
mean BMI 29.8±3.2 kg/m2, mean
below 20)
missing. Neither raw data
age 48.7±7.4 yrs.
nor mean values for
PSG prior and 3-6 months after
respiratory parameters
154
surgery
Walker RP et
Case series
4
al, 2006; [291] (5 centres)
given.
63 patients with mild to moderately
AHI was significantly reduced
Better outcome in
severe OSA (AHI 10-30) and
in mean from 25.0±13.9 to
patients with Mallampati I
2
BMI<32 kg/m , 10 drop outs, 53
22.0±14.8, ESS from 11.0±5.1 and II compared to
patients (44 males) remaining,
to 6.9±4.5, BMI unchanged,
Mallampati III and IV. 9
mean BMI 28.4±2.9 kg/m2, mean
success rates (a) 23%, (b)
patients included despite
age 50.2±11.7 yrs. PSG prior and 3 19%, (c) 15%
BMI>32 or AHI>30.
months after surgery
Significant number of
drop outs.
Goessler U et Case series
4
16 patients (14 males) with mild to
AHI was significantly reduced
in mean from 16.5±4.4 to
al,
(single
moderately severe OSA (AHI 10-
2007; [292]
centre)
30) and BMI< 30 kg/m2 , mean BMI 11.2±10.2,
26.6 (range 21.5-30.0) kg/m2, mean ESS from 7.2±2.5 to 4.6±3.2,
age 51 (range 34-64) yrs, no drop
success rates (a) 63%, (b)
outs. PSG prior and 3 months after
38%, (c) 38%
surgery
Nordgard S et Case series
al,
2007; [293]
(2 centres)
4
41 patients with mild to moderately
AHI was significantly reduced
Follow-up of the 41
severe OSA (AHI 10-30) and
in mean from 16.5±4.5 to
patients of the studies of
BMI<30 kg/m2, 15 patients
12.3±12.7, ESS from 8.3±4.7
Nordgard (2006) and
excluded. Subset of 26 patients (18 to 5.4±4.0, success rates (a)
males) with mean BMI 27.2±2.3
58%, (b) 50%, (c) 50%
Goessler (2007).
Significant number of
155
kg/m2, mean age 53.4±9.4 yrs,
drop outs.
PSG prior and in mean 435±90
days after surgery
Walker RP
Case series
2007 [294]
(4 centres)
4
53 patients with mild to moderately
AHI was reduced in mean
No raw data given, SD
severe OSA (AHI 10-30) and
from 19.7 to 18.3, ESS from
cannot be calculated.
BMI<32 kg/m2, 31drop outs, 22
11.7 to 8.4, BMI unchanged,
Patients stratified
patients (16 males) remaining,
success rates (a) 23%.
according to initial
mean BMI 27.8±2.8 kg/m2, mean
AHI<10 was maintained in 5 of decrease (13 patients) or
age 53.3±11.9 yrs,. PSG prior and
7 patients (71%).
increase (9 patients) of
in median 438.5 (interquartile range
AHI in the study of
121) days after surgery
Walker (2006). Very high
number of drop outs.
Friedman M et Randomised, 1b
62 patients with mild to moderately
AHI was significantly reduced
Amount of delta sleep
al, 2008; [295] placebo-
severe OSA (AHI 5-40) and
in mean from 23.8±5.5 to
significantly more in the
2
controlled,
BMI<32 kg/m , 31 implant (18
15.9±7.6 (implant) vs.
placebo group, quality of
double-blind
males) vs. 31 placebo (15 males),
20.1±4.0 to 21.0±4.8
life (SF-36) significantly
(single
mean age 48.1±11.2 vs. 39.0±9.9
(placebo), ESS from 12.7±2.7
better in the treatment
centre)
yrs, mean BMI 29.3±1.9 kg/m2 vs.
to 10.2±3.1 vs. 11.7±2.7 to
group.
28.7±2.3 kg/m2; 2 implants and 5
11.1±2.7, success rate 45%
placebo drop-outs, 29 implants vs.
vs. 0% (AHI reduced more
26 placebo remaining, PSG prior
than 50% and below 20)
156
and 3 months after surgery
Steward DL et Randomised 1b
100 patients with mild to severe
AHI was slightly increased in
SD not available.
al, 2008; [296] placebo-
OSA (AHI 5-40) and BMI<32 kg/m2, mean from 17.2 to 20.1
Significant increase of
controlled
50 implant (39 males) vs. 50
(implant) vs. a significant
time spent supine in both
trial, double-
placebo (40 males), no drop-outs,
increase from 16.7 to 25.7
treatment (48-56%) and
blind
mean age 47 vs. 52, mean BMI
(placebo), change of AHI
placebo (37-
(three
27.4 kg/m2 vs. 27.8 kg/m2, PSG
significantly better in implant
46%),;significant
centres)
prior and 3 months after surgery
group, ESS changed from
correlation of change in
10.6 to 8.7 vs. 10.7 to 9.2, BMI proportion of supine
unchanged, success rate 26% position during sleep and
vs. 10% (AHI reduced more
change in AHI. FOSQ
than 50% and below 20)
results superior in the
treatment group.
Success rates are given for three different definitions if not mentioned otherwise: (a) postoperative AHI<10, (b) AHI reduction greater
than 50%, (c) AHI reduction greater than 50% and postoperative AHI<10.
157
Table e23: Radiofrequency surgery of the tongue base
Author
Design
EBM Patient population
Results
Comments
Powell et al,
case
4
N=18 patients
statistically significant reduction of mean AHI
data for the subgroup of
1999 [297]
series
(female/male ration not
from 47.0 to 20.7 at short term follow up (4
patients with obstructive
given) with sleep
months, OSA group only)
sleep apnoea
disordered
46.7% success rate (AHI reduced more than
breathing/snoring (15 with
50% and/or below 20)
obstructive sleep apnoea,
n=15), mean AHI (OSA
group only): 47±30.8,
mean age: 44.9±8.68 y,
mean BMI: 30.2±5.5 kg/m2
Woodson et al,
case
2001 [298]
series
3b
N=73 patients with
statistically significant reduction of mean AHI
obstructive sleep apnoea
from 40.5 to 32.8 at short term follow up (6
(17 drop outs; n=56),
weeks)
mean AHI: 40.5±21.5,
20% success rate (AHI reduced more than
mean age: 47.1±9.5 y,
mean BMI: 30.6±4.1 kg/m
50% and below 20)
2
158
Stuck et al, 2002
case
[299]
series
3b
N=18 patients (16 male)
reduction in AHI from 32.1 to 24.9 (statistically
with obstructive sleep
not significant, 1 month follow up)
apnoea, mean AHI:
33% success rate (AHI reduced more than
32.1±13.7, mean age:
50% and below 20)
49.3±8.46 y, mean BMI:
29.2±2.68 kg/m2
Li et al, 2002
case
[300]
series
4
N=18 patients (17 male)
reduction in AHI from 39.5 to initially 17.8
long-term follow up of
with obstructive sleep
(statistics not given). At long-term follow up
previously unpublished
apnoea (2 drop outs,
(28 months) AHI of 28.7 (no statistical
data, no statistical
n=16), mean AHI:
comparison to baseline), no success rates
comparison to baseline
39.5±32.7, mean age:
given
given
N=20 patients (15 male)
statistically significant reduction of mean AHI
modified technique with
with obstructive sleep
from 35.1 to 15.1 after 3 month follow up
transoral approach to the
44.9±8.7 y, mean BMI:
30.2±5.5 kg/m2
Riley et al, 2003
case
[301]
series
3b
apnoea (1 drop out, n=19), 63.2% success rate (AHI reduced more than
mean AHI: 35.1±18.1,
50% and below 20)
dorsal tongue and
mean age: 49.5±10.7 y,
tongue (genioglossus
mean BMI: 30.0±5.8 kg/m2
insertion)
additionally to the ventral
159
Table e24: Hyoid suspension for OSA
Authors
Baisch et al, 2006
[302]
Bowden et al, 2005
[303]
Design
particular cohort
study
particular casecontrol study
Dattilo + Drooger
2004 [304]
den Herder et al,
2005 [305]
particular casecontrol study
retroperspective
Hsu et al, 2001[306] case study
EBM
Study
population
3b
Results
With HS
AHI pre: 38.3
AHI post: 18.9
Success: 59.7 %
N=83 b/a MLS
Without HS
AHI pre: 28.6
67/83 with HS
AHI post: 21.7
16/83 without HS Success: no data
N=29 b/a MLS
HS (29) + UPPP
AHI pre: 36.5
(28)
AHI post: 37.6
type 2
obstruction
Success: 17.2 %
3b
N=45 b/a MLS
UPPP, AT, HS,
GG-A
3b
N=31 b/a HS
4
N=13 MLS
UPPP + GA +
2b
AHI pre: 38.7
AHI post: 16.2
Success: 70.3 %
AHI pre: 32.1
AHI post: 22.2
Success: 51.6 %
AHI pre: 52.8
AHI post: 15.6
Comments
MLS with various
different combinations
of surgeries
MLS is effective for
OSA
HS is effective within
the MLS concept
follow-up: 1 month
follow-up 12 months
HS alone does not
provide results similar
to GG-A
follow-up 2 months
MLS with various
different combinations
of surgeries
MLS is effective for
OSA
isolated procedure
follow-up: 6 months
HS is effective
MLS with fixed
combination of
160
HS
Success: 76.9 %
N=37 b/a MLS
UPPP (all) +
GG-A (23) + HS
(16) + RFT TB
(27)
Jacobowitz O. 2006
[307]
Neruntarat 2003
[285]
particular casecontrol study
retroperspective
case study
Neruntarat 2003
[286]
retroperspective
case study
Neruntarat 2003
[287]
retroperspective
case study
3b
With HS
AHI pre: 48.8
AHI post: 19.3
Success: 62.5 %
Without HS
16/37 with HS
AHI pre: 44.8
AHI post: 11.6
21/37 without HS Success: 85.7 %
4
N=31 b/a MLS
Flap + GG-A +
HS
AHI pre: 48.2
AHI post: 14.5
Success: 73.3 %
4
N=46 b/a MLS
Flap + GG-A +
HS
4
N=32 b/a MLS
Flap + HS
AHI pre: 47.9
AHI post: 18.6
Success: 65.2 %
AHI pre: 44.5
AHI post: 15.2
Success: 78.0 %
surgeries
follow-up 12.6 months
MLS is effective for
OSA
MLS with various
different combinations
of surgeries
MLS is effective for
OSA
follow-up: 3 months
MLS with fixed
combination of
surgeries
follow-up: 8.0 months
MLS is effective for
OSA
MLS with fixed
combination of
surgeries
follow-up 39.4 months
MLS is effective for
OSA
MLS with fixed
combination of
surgeries
161
Ramirez et al, 1996
[308]
particular casecontrol study
3b
AHI pre: 49.0
N=12 b/a MLS
UPPP + GG-A + AHI post: 23.0
HS
Success: 41.7 %
Richard et al, 2007
[309]
particular casecontrol study
3b
Riley et al, 1994
[310]
particular casecontrol study
3b
AHI pre: 48.7
N=12 b/a MLS
UPPP + GG-A + AHI post: 28.8
HS + RFT TB
Success: 45.0 %
AHI pre: 44.7
AHI post: 12.8
N=15 b/a HS
Success: 53.3 %
4
N=239 b/a MLS
Phase I (UPPP,
GG-A, HS)
Phase II (24)
4
N=223 b/a MLS AHI pre: 48.3
UPPP + GG-A + AHI post: 9.5
HS
Success: 60.1 %
Riley et al, 1993
[311]
Riley et al, 1993
[312]
retroperspective
case study
retroperspective
case study
Phase I
Success: 60.7%
Phase II
Success: 100%
follow-up: 8.1 months
MLS is effective for
OSA
MLS with fixed
combination of
surgeries
follow-up 6.0 months
MLS is effective for
OSA
MLS with fixed
combination of
surgeries
MLS is effective for
OSA
isolated procedure
follow-up: 3 to 6 months
HS effective for OSA
staged protocol for
surgery of OSA
with CPAP data
protocol is effective for
OSA
MLS with fixed
combination of
surgeries
follow-up 9.0 months
MLS is effective for
OSA
162
Riley et al, 1989
[313]
Riley et al,1989
[314]
Riley et al, 1986
[315]
Sorrenti et al, 2004
[316]
retroperspective
case study
retroperspective
case study
retroperspective
case study
Retroperspective
case series
4
N=80
group A
GG-A, HS
group B
MMO
4
N=55 b/a MLS
UPPP (42) +
GG-A + HS
4
N=5 b/a GG-A +
HS
4
N=8 MLS
UPPP + open
tongue base
resection + HS
AHI pre: 58.0
AHI post: 23.2
Success: 67.3 %
AHI pre: 73.6
AHI post: 21.0
Success: 80.0 %
AHI pre: 55.1
AHI post: 9.7
ESS pre: 14.3
ESS post: 5.3
Success: 100 %
AHI pre: 35.2
AHI post: 27.4
Success: 40.0 %
Stuck et al, 2005
[317]
particular casecontrol study
3b
N=14 b/a HS
No changes in
MMO superior to MLS
MLS with fixed
combination of
surgeries
follow-up 3.0 months
MLS is effective for
OSA
fixed combination of
surgeries
Type 3 obstruction
follow-up: 3 months
GG-A + HS effective for
tongue base
obstruction
Fixed combination of
surgeries
requires temporary
tracheostomy
Follow-up: 3 months
isolated HS
HS is only effective in a
subgroup of patients
no relevant changes in
airway diameters
follow-up: 2 months
163
Verse T et al, 2006
[318]
particular cohort
study
particular caseYin et al, 2007 [319] control study
2b
MRT imaging
with HS
AHI pre: 38.9
AHI post: 20.7
N=60 b/a MLS
Success: 51.1 %
Flap + HS + RFT without HS
AHI pre: 27.8
TB (45)
AHI post: 22.9
Flap + RFT TB
(15)
Success: 40.0 %
3b
AHI pre: 63.8
N=18 b/a MLS
UPPP + GG-A + AHI post: 21.4
HS
Success: no data
MLS effective for OSA
HS effective part within
the concept
follow-up 4,3 months
MLS fixed combination
of surgeries
MLS effective for OSA
follow-up: 6 months
MLS is effective for
OSA
164
Table e25: Effectiveness of isolated hyoid suspension for OSA
Author
N
follow-up [months]
AHI pre AHI post
Success [%]
ESS pre
ESS post
EBM
15
3-6
44.7
12.8
53.3
no data
no data
3b
31
6
32.1
22.2
52
7.6
4.3
3b
[317]
14
2
35.2
27.4
40
9.1
6.1
3b
all
60
2-6
36.0
21.1
49.5
8.1
4.9
B
Riley et al, 1994
[310]
den Herder et al,
2005 [305]
Stuck et al, 2005
165
Table e26: Laser midline glossectomy
Author
Fujita
[320]
Design
1991 Case
EBM
Patient population
4
12
patients
(11
Results
Comments
male), AHI dropped from 56.3 ± 22 to Included patients were UPPP
series,
severe OSA, age 45 yrs, 37.0 ± 25 after 5-15 months.
consecutive
BMI
patients
(responders) and 37.9 ± 6.3 postoperative
30.6
±
kg/m2 42%
4.6
kg/m2(nonresponders),
success
(≥
reduction
AHI AHI)
56.3 ± 22.0
failures.
50% Nonresponders were more
of obese and
lateral
had greater
wall
contributing
bulge,
to
airway
narrowing
Mickelson 1997 Case series 4
12
patients
(11
male), AHI decreased from 73.3 ± LMG
and
[321]
severe OSA, age 48.8 ± 14.2 17.9 to 46.6 ± 28.8 after 2.4 epiglottoplasty
partial
in
patients
yrs, BMI 36.0 ± 8.8 kg/m2, months
who failed previous UPPP
AHI 73.3 ± 17.9
(with
25% success (AHI < 20)
or
without
tonsillectomy, septoplasty or
turbinate reduction).
No
differences
responders
and
between
non
responders
6 patients had temporary
tracheotomy, the others had
166
a permanent tracheotomy
Hsieh
2005 Case series 4
[278]
6 patients, severe OSA, age AHI decrased from 50.7 ± 12.6 LMG
was
performed
43.3 yrs (range 33-54), BMI to 11.6 ± 23.0 at 6 months simultaneously with EUPF in
27.5
kg/m2
(range
23.9- follow-up.
patients with retropalatal and
30.5), AHI 50.7 ± 12.6
hypopharyngeal obstruction.
None required tracheotomy.
Andsberg 2000 Case series 4
22 severe OSA patients, 21 AI
[322]
male, age 50 yrs (range 37- (range 5-89) to 18 (0-84) at 1 excision of a section of the
73), mean weight 88 kg, AI year
35 (range 5-89)
was
reduced
from
postoperative.
35 UPPP combined with simple
16 dorsum of the tongue
subjects had long-term (8.4 BMI was normal in 13, 2
yrs) follow-up, with AI change were
from 39 (7-89) to 21 (0-74)
10%
overweight,
3
were 20% overweight and 4
were
30%
overweight.
Weight remained unchanged
during the follow-up.
167
Table e27: Other approaches for tongue base reduction (plasty – resection)
Author
Design
EBM
Patient population
Results
Comments
Chabolle
Case series, 4
10 male patients, severe OSA, AHI dropped from 70.0 ± 18
4 patients were UPPP
1999 [323]
retrospectiv
47.5 (range 35-57 yrs), BMI 32 to 27.0 ± 37.0 after 3
failure, 8 had UPPP (3
e study
± 5 kg/m2, AHI 70 ±18
months, 80% success (≥
revisions) and 3 patients had
50% reduction of AHI and
inferior turbinectomy or
AHI < 20)
septum repositioning,
satisfactory improvement in
snoring and daytime
sleepiness.
Sorrenti 2006 Case series, 4
10 male severe OSA patients,
AHI dropped from 54.7 ±
UPPP, tongue base
[324]
retrospectiv
51.7 ± 7 yrs, BMI 31.01 ± 2.5
11.5 to 9.4 ± 5.4 after 14.6
reduction and
e non
kg/m2, AHI 54.7 ± 11.5
months. Low SaO 2 improved hyoepiglottoplasty
randomised
from 77 ± 6.2% to 90.7 ±
In patients with Type II
study
3%.
obstruction
Success 100% (AHI<20, >
Temporary tracheotomy
50% reduction in AHI and
improvement of subjective
symptoms)
Woodson
Case series, 4
22 patients (21 male), severe
AHI dropped from 58.6 ±
15 patients were UPPP
168
1992 [325]
consecutive
OSA, age 48 ± 15 yrs, BMI 32
36.6 to 16.3 ± 17.2 after 6
failures, 8 patients had
patients
± 5.6 kg/m2(responders) and
weeks.
combined LP and UPPP (or
33.3 ± 9.5
Success rate was 79% in the revision pharyngoplasty).
kg/m2(nonresponders), AHI
LP alone group versus 75%
Success rate was 79% in the
58.6 ± 36.6
in the UPPP + LP group
LP alone group versus 75%
(≥ 50% decrease in AHI and in the UPPP + LP group. All
AHI < 20 events)
patients had a temporary
tracheotomy
27% perioperative
complication rate
Li 2004 [326]
Prospective 2b?
12 consecutive male severe
Group 1: AHI decreased
Patients had Type II
Case series
OSA patients, age 44.5 ± 6.5
from 50.7 ±12.6 to 8 ±14.3.
obstruction
BMI and
yrs, BMI 26.5 ± 2.6 kg/m2
MeanSaO 2 increased from
Group 1: obstruction at the
RDI
Group 1 n=6
76.3% ± 11.6% to 88.8
uvulopalatal complex and
matched
Group 2 n=6
±3.2%, the effect size of this tongue base treated with
comparative
change was 1.47.
EUPF with subsequent LMG
study
Success rate = 83.3% (>
Group 2: obstruction at the
between 2
50% reduction in AHI and
uvulopalatal complex and
treatment
postoperative AHI< 20)
lingual tonsil treated with
modalities
Group 2: RDI increased from EUPF and LT
169
56.2 ±12.6 to 62.8 ±14.7 and
MeanSaO 2 increased from
75.6 ±10.5% to 76 ±14.4%.
No patient in this group was
treated successfully
Follow-up time: at least 6
months
Djupesland
Case series 4
1992 [327]
20 male severe OSA patients, AHI dropped from 54 (range
Uvulopalatopharyngoglossop
age 50 yrs (range 22-68 ),
lasty= UPPP + partial tongue
10-98) to 31 (range 0-61)
weight 96.6 kg (range 72-120), after 8.7 months
resection and glossopexia.
AHI 54 (range 10-98)
50% success (>50%
18 patients reported
reduction in AHI)
improvement in daytime
sleepiness, alertness and
vigilance. 4 continued to
snore every night. 18
patients had a significant
weight loss from 96.6 to 87.8
kg after 9 months.
Miljeteig 1992 Case series 4
26 severe OSA patients, mean AI dropped from a mean of
UPPGP=Uvulopalatopharyn
[328]
age 45 yrs, mean weight 91
30 to 9 and ODI from a
go-plasty combined with
kg, mean AI 30, mean ODI 13
mean of 13 to 4, 6-12
bilateral resections at the
170
months after surgery.
tongue base
Success 67% (> 50%
Sex and AHI not specified,
reduction AI)
more than 90% of patients
reported good or excellent
results with respect to
snoring, morning sleepiness
and mental ability.
Faye-Lund
1992 [329]
Case series 4
8 OSA patients, age 55.7 ± 5.8 Total number of apnoeas
yrs,
partial tongue resection and
dropped from 123.4 ± 79.0 to anterior suspension of the
55.9 ± 71.5, total number of
tongue (glossopexia) after
hypopnoeas dropped from
failed UPPGP
120.5 ± 105.5 to 62.4 ±
6 patients had weight loss
104.4
(range 8-20 kg)
at 12-24 months
AHI and BMI were not
postoperatively.
reported
171
Table e28: Tongue suspension (Repose )
Author
Design
EBM
Patient
Results
Comments
14 severe
AHI decreased from 35.4 ±
Patients failed palatal
Uncontrolled case
OSA, 47.1 ±
13.73 to 24.5 ± 14.5 after 2
surgery
series
8.0 yrs, BMI
months
In 7 patients with positional
28.0 ± 3.9
3 out of 14 (21%) success (≥
data, side AHI decreased but
population
Woodson 2001 [330] Open enrollment
4
2
kg/m , AHI
50% reduction in AHI and AHI not supine AHI.
35.4 ± 13.7
< 15)
Improvement in snoring,
Epworth sleepiness score
and quality of life (FOSQ)
after 2 months
Woodson 2000
Open enrolment,
[331]
4
9 severe
AHI dropped from 33.2 ± 13.5
Isolated tongue-base
prospective
OSA
to 17.9 ± 8.1 after 2 months.
obstruction, mostly after
uncontrolled case
patients, 15
failed UPPP.
series
male, age
ESS, energy and fatigue
45.6 ± 8.3
measured by the MO-SF36,
yrs, BMI 28.2
2
Vigilance measured by
± 4.0 kg/m ,
FOSQ were improved at 2
AHI 33.2 ±
months follow-up. Snoring
13.5
was still rated as bothersome
172
by bedpartners without
significant improvement
DeRowe 2000 [332] Case series,
Thomas 2003 [333]
16 patients
AHI dropped from 35 ± 16.5 to Tongue suspension as a
retrospective data
(15 male),
17 ± 8 after 2-3 months
collection
severe OSA,
No data on BMI but patients
age 35-74
with BMI > 35 were excluded
yrs, AHI 35 ±
Snoring improved in 14
16.5
patients
Prospective
4
2b
single procedure
17 severe
57% success for Repose
Palatopharyngoplasty
randomised trial,
OSAS, 9
after 4 months (>50%
combined with mandibular
mandibular
randomised
reduction in AHI and AHI < 20) osteotomy or tongue
osteotomy versus
to the tongue
suspension (Repose).
Repose
suspension
Patients had Type II
group
obstruction.
Age 50.8 ±
Significant improvement in
16.1 yrs, BMI
ESS and snoring scores.
30.9 ± 6.2
Mean data on postop AHI not
2
kg/m , AHI
reported.
46.0 ± 22.0
Tongue suspension was
slightly more effective than
tongue advancement for
173
daytime sleepiness and
snoring.
Miller 2002 [334]
15 severe
AHI dropped from 38.7 ± 12.3
UPPP and Repose tongue
series, retrospective
OSA
to 21.0 ± 7.4 and SaO 2 min
suspension, 19 patients
analysis
patients, 11
improved from 82 to 88% after enrolled, pre-post op data
male, age
6 months
available for 15 patients.
48.8 ± 9.5
Success 20% (> 50%
Patients had Type II
yrs, BMI 31.
reduction AHI and AHI < 20).
obstruction.
Uncontrolled case
4
2
3 ± 4.9 kg/m ,
No significant changes in
AHI 38.7 ±
posterior airway space.
12.3.
Terris 2002 [335]
Non randomized,
4
19 severe
67% success (> 50%
Only 12 patients had
prospective study,
OSA
reduction in AHI and AHI <20
postoperative PSG, group
case series
patients, 16
or > 50% reduction in AI and
characteristics of these are
male, 44.9 ± AI< 10)
not reported
14.2 yrs, AHI AHI improved from 32.4 to 14. ESS and snoring were
42.8 ± 24.8
4 and AI from 7.4 to 0.9 in the
significantly improved
responders (n=8)
Cephalometric analysis
revealed a significant
improvement of the airway at
the tongue base, the palate
174
and the lateral pharyngeal
wall
Sorrenti 2003 [336]
Retrospective
4
15 male
RDI dropped from 44.5 to 24.
UPPP and tongue
analysis,
severe OSA
2, 4-6 months after surgery
suspension (Repose) 4
uncontrolled case
patients, 50.
40% success (> 50%
patients underwent nasal
series
5 yrs (range
reduction in AHI or AHI < 20
surgery.
36-66), BMI
and disappearance of
Patients had Type II
28.27 (range
subjective symptoms:
obstruction. 80% reported
22.6-34.4)
sleepiness and snoring
marked decrease in snoring
2
kg/m , AHI
and improvement of sleep
44.5 (range
with less EDS.
23-63)
Vicente 2006 [337]
Non randomised,
4
55 patients
AHI dropped from 52.4 ± 14.9
Patients underwent UPPP,
prospective study,
(51 male),
to 14.1 ± 23.5 after 3 yrs
Repose and nasal
case series
severe
follow-up.
reconstruction (n=21) and
OSAS, age
78% success (> 50%
tonsillectomy (n=17).
47.3 ± 4.5
reduction in AHI, AHI < 20 and 1 patient lost to follow-up.
yrs, BMI 29.6 ESS < 11)
2
Patients had type II
± 4.8 kg/m ,
obstruction.
AHI 52.8 ±
BMI at baseline was
14.9
correlated with postsurgery
175
change in AHI (r= 0.554,
p<0.001)
Kühnel 2005 [338]
Prospective, non
4
randomised study
28 male
AHI dropped from a mean of
Nasal surgery and
severe OSA
41 (range 2-125) to a mean of reconstructive palatal
patients,
31 (range 1-102) 12 months
surgery were performed “ as
mean 50 yrs
after surgery
required”
(range 26-
Mean ESS score was 12
71), BMI 31
preoperatively, 9 after 3
kg/m2, AHI
months and 11 at 12 months
mean 41
The change in retrolingual
(range 2-125)
space was nonsignificant
when assessed by
endoscopy and significant on
lateral cephalometry.
Omur 2005 [339]
Retrospective
4
22 severe
AHI dropped from 47.5 ± 15.7
All patients underwent
analysis,
OSA
to 17.3 ± 14.2, 14.0 ± 2.3
simultaneous UPPP and a
uncontrolled case
patients, age months after surgery
series
44.4 ± 7.9
81.8% success (> 50%
suspension.
yrs, BMI
reduction in AHI and AHI <
Sex not specified
30.27 ± 3.81
20).
Successful improvement of
2
kg/m , AHI
modified tongue base
snoring (VAS ≤ 3) in 72.7%.
176
47.5 ± 15.5
Patients had type II
obstruction
Abbreviations:
AI: apnoea index
AHI: apnoea/hypopnoea index
DR: desaturation rate
EDS: excessive daytime sleepiness
ESS: Epworth sleepiness score
EUPF: extended uvulopalatal flap
FOSQ: Functional Outcomes of Sleep Questionnaire
LMG: Laser midline glossectomy
LP: lingualplasty
LT: lingual tonsillectomy
PPGP: Palatopharyngoglossoplasty
TBRHE: tongue base reduction with hyoepiglottoplasty
Type II obstruction: palatal and tongue base obstruction
UA: upper airway
UPPGP: Uvulopalatopharyngoglossoplasty
UPPP: uvulopalatopharyngoplasty
177
Table e29: Genioglossus advancement
Author
Design
EBM
Patient population
Results
Comments
10 non obese patients, mild
OSAS, hypopharynx
obstruction (narrow PAS),
Dos
1
Santos
prospective
Junior JF case series
retrognatia (Macnamara's
4
cephalometric analysis).
Monobloc genioplasty.
[340]
UPPP 8/10, septoplasty
2/10. Post op PSG from 4 to
AHI from 12,4±4,6 to 4,4±5,7.
60% AHI<5 and 70% with 50%
reduction. SaO2 from 82,8±9,0 to
88,4±3,1. Mean advancement 9
mm. PAS from 7,9±2,4 to
10,8±2,6. One local infection.
various surgical
techniques. Short
term evaluation.
Evaluation of
hypopnea ?
6 months.
31 non obese patients (23
Validity of PSG data
males) with AHI<35. Mean
2
Foltan R
retrospective
[341]
case series
4
age 53,2. Mortise
23 success (74%). AHI from 20,9 ? Lot of
genioplasty + hyoid
to 10,3. Basal SaO2 from 95,1 to complications.
myotomy. Succes AHI<20
96,1. 2 fractures, one hyoid
Associated
and reduced of 50%. Post- fistula
procedures (GA +
op PSG from 3 to 16
HS)
months (mean 7,5)
178
3
Liu SA
prospective
[342]
case series
4
44 patients (AHI>40).
52,3% success. Preoperative AI
UPPP+genioglossus
predictive of success (if AI<25).
advancement. Post-op PSG
: 3 months
AHI ???
35 patients. Genial bone
AHI from 59,2±17,1 to 15,9±7,5.
advancement trephine
SaO2min from 80,1±8,4 to
system + UPPP. 24 pre and 88,3±7,1%. 67% success
4
Miller FR retrospective
[343]
case series
4
Short term
evaluation.
Associated
procedures (GA +
HS)
More effective on
post PSG. 13/24 hyoid
(16/24), moderate (AHI<40) 88% moderate patients.
suspension associated.
(7/8), severe 56% (9/16). No
Associated
Success AHI<20 and
difference with or without hyoid
procedures (GA +
reduced of 50%. PSG post suspension.3 plate exposures, 2 UPPP)
from 3 to 6 months (mean
hematomas of the floor of mouth.
4,7)
BMI from 30,5±2,9 to 29,7±3,2
31 patients (28 males).
46,2±5,8 yrs. BMI 28,8±3,2.
5
Neruntara retrospective
t C [344]
case series
4
GGA + Hyoid suspension +
7 UPPP. Post PSG 6 to 10
months. Success AHI<20
AHI from 48,2±10,8 to 14,5±5,8.
SaO2min from 81,8±3,8 to
88,8±2,9. 70,1% succes(22/31).
Assciated procedures
(GA + HS ± UPPP)
and reduced of 50%.
179
AHI pre, short term, long term :
47,9±8,4; 14,2±3,9; 18,6±4,1.
6
Neruntara retrospective
t C [344]
case series
46 patients with GGA + HS. SaO2min 81,2±2,9; 88,8±2,7;
4
40,1±4,2 yrs, 28,9±2,1. 37
87,2±3,1. BMI increased in
to 46 months follow-up.
recurrence ???. 65,2% long term
success; 6 short term success,
Control of post-op
BMI. Associated
procedures (GA +
HS)
failed in long term.
Associated
7
Thomas
AJ [333]
17 patients. UPPP +
randomized
crossover
2b
surgical trail
tongue suspension: 57% success procedure.
randomised GA (8 patients) (post op PSG for 7 patients). GA: Comparison of GA
or tongue suspension (9
50% success (4 patients). In both and tongue
patients).
groups good subjective results.
suspension.
Incomplete PSG data
20% success (reduction of 50%
and AHI<20). AHI from 38,7±12,3
8
Miller FR retrospective
[343]
case series
15/19 patients with
4
complete PSG data. UPPP
+ Tongue suspension.
to 21,0±7,4. Pain and dysarthria
for all patients. 5 complications :
2 sialadenitis, 1 floor of the
mouth floor hematoma, 1
extrusion of suture, 1 removal of
Associated
procedure (UPPP +
tongue suspension).
Significant rate of
complications.
suture for globus sensation in the
180
base of tongue base.
40 patients. 33 UPPP + GA 33 patients: BMI 32,6±6,95;
9
Hendler
retrospective
BH [345] case series
4
(mortised genioplasty,
mean age 47. AHI fom 60,2±29,9
minimum 10 mm
to 28,75±27,38. Moderate OSAS Various surgical
advancement); 7
(AHI 21 to 40) 86% success
techniques. Better if
maxillomandibular
(6/7); if AHI<50 71% (10/14); if
no severe OSA and
advancement (4 preventive AHI>50 32% (6/19). If BMI<30,
patient not obese.
tracheotomy). Postop PSG: 63% success; if BMI>30 43%
6 months.
success.
181
16 patients (15 men). 35 to
10
DeRowe retrospective
A [332]
case series
74 yrs old. Tongue
4
suspension (Repose
system). Postop PSG: 2 to 3
months
AHI from 35 to 17. 4/14 AHI<20
and 50% reduction (28,6%
success). 2 local infections (need
removal of device), 1 hematoma,
1 late mouth floor cyst. Painful for
Short term
evaluation. Low rate
of objective success
2 weeks
182
Table e30: Efficiency of MMA on AHI in OSA patients
Author
N
Age
BMI
Sex
Use of
PreAHI
SaO2<9
SWS
PostAHI
SaO2<90
SWS
Succe
EB
(yrs old)
(kg/m²)
(% of
CPAP
(/h)
0%
before
(/h)
%
after
ss
M
males)
before
before
after
MMA
(% of
(% of TST)
(%)
TST)
Waite
23 45
1989
(35 –
[346]
64)
Riley
30 43
1989
(18 –
[314]
63)
Hochba
n 1997
38 44
(±12)
NA
91
Yes
63
NA
NA
(±29)
31
NA
Yes
(±5)
28
72
Yes
(±3)
44
NA
NA
65
4
NA
NA
97
2b
0,4*
16*
97
2b
NA
9 -NS
100
2b
NA
NA
90
4
(±17)
NA
NA
(±23)
93
15
9
(±7)
12
9
(±17)
2
(±6)
[347]
Prinsell
1999
50 42
(±9)
30
88
Yes
(±4)
59
NA
6
(±28)
5***
(±5)
[348]
Li 2000
[349]
40 47
(±10)
31
(±6)
83
Yes
70
(±28)
NA
NA
9
(±5)
183
Wagner 21 45
29,7
2000
(± 4,9)
(± 10)
95
Yes
58
27
15
17
9*
27*
70
4
(±23)
(±22)
(+/16)
(±12)
(±17)
(+/17)
59
17
4
11***
1***
8*
75
4
NA
NA
86
4
NA
NA
82
4
NA
NA
87
4
10
2
NA
84
4
(±7)
(±5)
8****
7*
15****
89
4
[350]
Bettega
20 44
2000
27
(±12)
(±3)
Hendler 7
47
36.3
2001
(±6.22)
(±6.95)
90
Yes
(±29)
(±9)
[351]
86
NA
90
NA
NA
(±31)
16****
(±23)
[345]
Goh
11 43
2003
(32 –
[352]
56)
Dattilo
15 44
2004
(31 –
[304]
55)
Smatt
2005
18 47
(±6)
NA
100
No
65
NA
NA
(±19)
NA
80
Yes
76
(±7)
NA
NA
(±45)
29
83
Yes
(±4)
11
13
(±12)
54
11
(±21)
(±20)
45
20
NA
[353]
Dekeist
er 2006
25 48
(±7)
28
(±3)
100
Yes
(±15)
8
(±7)
184
[354]
29 44±3
29,5±2,
8
7 kg/m²
yrs old
90±7%
96 %
60±13/h
17,9±6,
8±4%
5%
(N=154)
9±4/h
3,8±3,9%
14±8%
88,3±
(N=104)
(N=154)
11,0%
B
(N=104)
Definition of abbreviations:
-
NS : no significant
-
* : p < 0,05; **: p<0,01; *** : p<0,001; ****: p < 0,0001
-
SWS : slow wave sleep (stages III and IV)
-
TST: Total sleep time
-
BMI : body mass index (kg/m²)
-
NA: not available
185
Table e31: Cephalometric data of patients selected for MMA
Author
Waite 1989
N
23
SNA(°)
SNA(°)
before
after
before
after
(mm)
MMA
MMA
MMA
MMA
NA
NA
SNB(°) SNB(°)
NA
NA
EVP
EVP
ELP
ELP
(mm)
(mm)
(mm)
before after
before
after
MMA
MMA
MMA
MMA
NA
NA
NA
+ 8 mm
[346]
Riley 1989
4
(0 - 14)
30
77,5°
81,9°
73,7°
82,4°
(67-82)
(69-88)
(69-83)
(75-83)
38
NA
NA
NA
NA
NA
50
79°
86°***
75°
82°***
NA
(±4)
(±4)
(±4)
(±5)
78,9°
84,5°
74,8°
80,4°
(+/3,7)
(±4)
(+/5,4)
(+/4,4)
78,8°
NA
75,7°
NA
[314]
Hochban 1997
EBM
NA
NA
3,8mm
9,76mm
2b
(2-8)
(7-12)
NA
NA
NA
2b
NA
5mm
12mm***
2b
(±2)
(±3)
3,7mm
10,1mm
(±6)
(± 2,1)
NA
+11,5mm
[355]
Prinsell 1999
[348]
Li 2000 [349]
Wagner 2000
40
21
[350]
Bettega 2000
(±4,8)
NA
NA
NA
NA
(±3,3)
4
4
(8 – 17)
20
NA
NA
NA
NA
NA
NA
NA
NA
4
7
NA
NA
NA
NA
NA
NA
NA
NA
4
[351]
Hendler 2001
186
[345]
Goh 2003 [352]
11
NA
NA
NA
NA
NA
NA
NA
NA
4
Dattilo 2004
15
NA
NA
NA
NA
NA
NA
NA
NA
4
18
NA
NA
NA
NA
NA
NA
NA
NA
4
25
80°
86° NS
78°
81°NS
5 mm
10mm** 8mm
14mm***
4
(±5)
(±5)
(±5)
(±5)
(±2)
(±2)
(±3)
(±3)
10mm
4,9±2,0mm 11,35±2,10mm B
[304]
Smatt 2005
[353]
Dekeister 2006
[354]
298 78,8±0,9° 84,7±1,9° 75,2±1,4°
(N=166)
(N=145)
(N=166)
81,4±0,9 5mm
(N=145)
(N=25) (N=25)
(N=145)
(N=145)
Definition of abbreviations:
-
SNA: position of the maxillar
- SNB: position of the mandible
-
EVP: space behind the soft palate
-
NS : no significant
-
* : p < 0,05; **: p<0,01; *** : p<0,001; ****: p < 0,0001
- ELP: space behind the tongue
- NA : not available
187
Table e32: Effect of DOG in mandibular micrognathia
Author
Design
EBM Patient population
Results
Comments
Cohen et
retrospective
al,1998
4
case series.
[356]
N=16 mild OSA, 8 candidates to
tracheostomy,
8
Mean advancement 25 mm (18 to
tracheostomised. 12 males / 4
35)
females
Impossible to evaluate the effect
7/8
decannulation
and
1/8
Aged from 14 weeks to 16 yrs.
of distraction alone because of
postoperative tracheostomy
soft tissue procedures.
14 bilateral mandibular external
RDI decreased from 7,1 to 1,7,
distraction,
2
unilateral.
LSAT from 0,7 to 0,89.
Immediate advancement + bone
graft (except tracheostomised).
Li KK et al, prospective
4
2002 [357] case serie
N=5 adults with severe to very
severe OSA: 4 mandibular Mean advancement: 8,1 mm (5,5 to
advancement (3 bilateral), 1 12,5)
Mean follow up: 12 M (6 to 18 M)
bimaxillary – 3 males / 2 females
RDI decreased from 49,3 (26-87,5)
Aged from 26 to 68 yrs
to 6,6 (0-13,3); LSAT from 79,8% Date of postoperative PSG ?
Procedure advise for patients
(61-87) to 85,8% (79-90)
Internal devices removed 3
unsuitable
to
undergo
months after the end of Few local complications. Good conventional MMA.
activation.
UPPP
and skeletal stability. All patients cured
genioglossus advancement for from OSAS (RDI<15)
one patient.
188
N=28 very severe
males/ 9 females
Wang X et
retrospective
al,
2003
4
case serie
[358]
OSA.
19 Mean advancement 20,4 mm (9 to
30)
Aged from 3 to 60 yrs (mean 21,2 RDI decreased from 58,0 to 3,15;
y).
LSAT from 77,0 to 90,3%.
PSG post-op within 1 week after OSAS (no symptoms,
LSAT>85%).
distraction completion
Monasterio
prospective
O et al,
4
case serie
2002 [359]
Mean follow up: 18,1 M (3 to 61).
23 bilateral internal mandibular No complications. Good skeletal
distraction, 5 unilateral.
stability. 23/28 patients cured from
RDI<5,
N=18 mild to moderately severe
Mean advancement 12 mm (7 to
OSA (3 tracheostomised + 4
19).
candidates)
RDI from 22 (AI 18,3 ; HI 8,5) to 0.
Age from 8 to 150 days. 17 Pierre
Average 0 2 saturation from 76% to Neonatal distraction.
Robin sequence.
93%.
tongue protraction
Transfacial mandibular distraction
3/3 decannulated + 0/4 need anterior pin ?
with 2 pins pulling tongue
tracheostomy
anteriorly.
Resolution of gastroesophageal
Post-op evaluation: 2 to 4 months
reflux.
after consolidation.
Effect of
by the
189
N=17 patients (candidates for
tracheostomy)
Advancement 12 to 15 mm.
Wittenborn
prospective
W et al,
4
case serie
2004 [360]
Age from 5 to 120 days.14 Pierre 2/17 need tracheostomy
Robin sequence.
55% improvement of obstructive Neonatal distraction. Follow-up 8
External or internal unidirectional apnoea (94% if late tracheostomy to 48 M (mean 16,5).
mandibular distraction.
excluded) and 36% improvement of
Post-op evaluation: 2 to 4 Ms LSAT, 5% improvement of sleep
after consolidation. 10 pre and efficiency.
post-op PSG
N=5 tracheostomised children
Steinbache
retrospective
r DM et al,
4
case serie
2005, [361]
Age 2 to 14 yrs.
Unidirectional
mandibular distraction.
Mean advancement 23 mm (11-31
mm).
Postop
PSG
with
occluded Mean follow-up 3,2 yrs (1,5m to
tracheostomy port. No postop 5yrs). Failure of soft tissue
bilateral obstructive event. LSAT from 76% procedures before distraction.
(68-82 %) to 98% (96-99 %).
4/5 decanulated
Denny A et uncontrolled
al,
2005 clinical
4
[362]
pilot study
N=11 neonates (candidates to
tracheostomy) 5 males / 6
0/11 need tracheostomy.
females
Neonatal
distraction.
Age of 3 to 45 days (mean 18,5). 7 "normal" postop PSG 1 week to 1 Unconsistent PSG data.
month post distraction.
External distraction.
6 preop
PSG.
190
N=12 children with mild to
moderately severe OSA (some Mean advancement 28 mm (25-31
are candidates to tracheostomy) mm) on the left and 29 mm (26-32
mm) on the right side
– 5 males/7 females
Rachmiel
prospective
A et al,
4
case serie
2005 [363]
All patient cured. Good stability
.
RDI
decreased
from
21,3
±
4,7
to
Aged 1 to 7 yrs. Clinical
after one year.
1,4
±
0,
!
at
1
month
and
1,8
±
0,4
diagnosis of OSAS.
at 1 year. LSAT from 79,5 ± 2,4 to Mean enlargement of UA volume
External unidirectional bilateral 97,2± 0,8 at 1 month and 96,1± 0,7 on CT 71,9 %.
mandibular distraction.
at 1 year.
Post op PSG 1 month and over a 0 need tracheostomy.
year after distraction.
N=10 children with mild OSA - 5
males/ 5 females
Mean advancement 15 mm.
Mitsukawa
retrospective
et al, 2007
4
case serie
[364]
Aged 1 month to 4 yrs with OSAS
and
micrognathia
(2 RDI decreased from 12,6 (9,6-18,8) All patient cured. Good stability
to 1,5 (0,5_3,6). MeanSAT from
tracheostomised)
after one year.
93,4 (86-97) to 99,2 (98-100).
Internal
bilateral
mandibular
2/2 decannulated
distraction.
PSG post at one year.
Shen et al, Retrospectiv
4
2009 [365] e case serie
N=6 neonates
tracheostomy)
(candidates
to
0/6 need trachestomy
Neonatal
cured
distraction.100
Aged from 1 to 21 days
191
%
Looby et
Prospective
al,
2009
4
case serie
[366]
N=17 neonates with mild OSA Mean advancement 18.1 mm (12Neonatal distraction. Follow-up 1
25 mm)
(candidates for tracheostomy)
to 11 yrs.
RDI
decreased
from
10,5
(0-43,1)
Mean age 105 days (11-310 d)
to 2,21 (0-12,9). LSAT from 83 to 209% improvement of CT
retrolaryngeal cross-sectionnal
90
area.
Internal distraction device
1/17 need tracheostomy
N=67 severe OSA (41 trach + 26 Mean advancement 22 mm (10-32
candidates)
mm)
Genecov
Retrospectiv
et al, 2009
4
e case serie
[367]
Mean age 1,2 yrs (5 days to 6 AHI decreased from 35-50 to 5-15 Follow-up 1 to 3 yrs. Lack of
yrs).
in 65 patients (2 remains >35 AHI) PSG detailed datas.
33 internal devices and 34 38/41 decannulated and 1/26 need
tracheostomy
external
192
Table e33: Effect of DOG in midfacial advancement (Lefort III or monobloc)
Author
Design
EBM Patient population
Results
Comments
55 children (13 tracheostomised)
Mathijssen Retrospecti
et al, 2006 ve case
4
[368]
serie.
Mean age 4,5 - 6 yrs (4 m to 18
yrs)
Follow-up 3 to 4,5 yrs.
8/13 decannulation
No PSG datas available.
19 Lefort III + 36 monobloc
Flores et
al, 2009
[369]
Retrospecti
ve case
4
serie
Retrospecti
Xu et al,
ve case
4
2009 [370]
serie
20 children (2 tracheostomised and
Mean advancement 16 mm (6,2 to
10 severe OSA) – 10 males / 10
26,1)
females
mean increase of 9,1 mm in
1 decanulated + 3 improvement of nasopharyngeal space
Mean age 5,7 yrs (3 to 12 yrs)
AHI
Lefort III advancement
11 children
Mean advancement 20,2 mm (± 8) Follow-up 5,4 M.
Mean age 10,2 yrs (5 to 16 yrs)
In 2 patients evaluated by PSG :
Increase of 64,3% in upper
AHI decreased from 22,2 (14,4-30) airway volume (especially
behind velum)
pre-op to 2,75 (1,1-4,4) post-op
Lefort III advancement
193
Table e34: Efficiency of MLS on AHI in OSA patients
Author
N
Velar
surgery
Lingual
surgery
Nose
surgery
Eun 2008
[371]
Benazzo
2008 [372]
Richard
2007 [309]
Vicente
2006 [337]
Verse 2006
[318]
Jacobowitz
2006 [307]
Baisch
2006 [302]
Liu 2005
[342]
Bowden
2005 [303]
Li 2004
[326]
Verse 2004
[373]
Miller 2004
[343]
Dattilo
2004 [304]
Kao 2003
[374]
Thomas
2003 [333]
Friedman
2003 [375]
90
UPPP
RTBR
No
Follow
up
(mont
hs)
6
109
UPPP
HS
Yes
6
22
UPPP
NA
NA
55
24
83
UPPP
RTBR/
HS/GA
HS/GA
RTBR
HS
31%
(N=17)
43%
(N=26)
No
36
37
UPPP/
Flap
UPPP/
Flap
UPPP
RTBR
HS /GA
HS
44
UPPP
GA
36%
(N=30)
No
3.6
(±2.3)
36
29
UPPP
HS
No
12
12
UPPP
Partial glossectomy
No
6
46
Flap
No
24
UPPP
RTBR/
HS
GA
No
36
37
UPPP
GA / HS
No
1,5
42
UPPP
RTBR
Yes
13
17
UPPP
Partial glossectomy
No
3
143
UPPP
RTBR
No
6
60
4,7
PreAHI
(/h)
PostAHI
(/h)
Succes
s
(%)
E
B
M
20
(±9)
37
(±19)
49
(±20 )
53
(± 15)
36
(±20)
47
(±25)
36
(±21)
62
(±14)
37
(±28)
51
(±13)
36
(± 22 )
53
(±17 )
39
(± )
38.2
16 - NS
(±15)
19
(±16)
29****
(± 20 )
14**
(±23)
21 - NS
(±20)
15
(±17)
19****
(±20)
29,6***
(±18,1)
38 - NS
(±29)
8**
(±14)
25**
(±22 )
16 ****
(± 7 )
16
(± )
12.7***
40%
4
65,7%
4
45%
4
78%
4
48,25%
2b
76%
4
60%
4
52,3%
2b
17%
4
83%
4
39%
4
67%
4
70,3%
4
83,3%
4
41.7
(±18.6)
43,9/h
(±23.7)
NA
54,5%
4
28,1/h
(±20.6)
41%
4
194
Neruntarat
2003 [285]
Neruntarat
2003 [286]
Vilaseca
2002 [376]
Nelson
2001 [260]
Hendler
2001 [345]
Hsu 2001
[306]
Bettega
2000 [351]
Andsberg
2000 [322]
Lee 1999
[377]
Chabolle
1999 [323]
Elasfour
1998 [378]
Mickelson
1997 [321]
Ramirez
1996 [308]
Johnson
1994 [379]
Riley 1993
[312]
Djupesland
1992 [327]
Woodson
1992 [325]
32
Flap
HS
No
8,1
44,5/h
15,2/h
78%
4
49
Flap
GA
No
39,4
47,9/h
18,6/h
65,2%
4
20
UPPP
GA /HS
No
6
60,5/h
44,6/h
35%
4
13
UPPP
RTBR
No
2
29,5/h
18,8/h
50%
4
33
UPPP
GA
No
6
60,2/h
28,8/h
45,5%
4
13
UPPP
GA/HS
No
12,6
52,8/h
15,6/h
76,9%
4
44
UPPP
GA /HS
No
6
45,2/h
42,8/h
22,7%
4
22
UPPP
No
100
35/h
18/h
75%
4
33
UPPP
Partial
glossectomy
GA
Yes
4-6
55,2/h
21,7/h
66,7%
4
10
UPPP
Partial glossectomy
No
3
2b
UPPP
No
3-21
44,4%
4
12
UPPP
No
2.5
73/h
47/h
25%
4
12
UPPP
Partial
glossectomy
Partial
glossectomy
HS /GA
27/h
(±37)
29,2/h
80%
18
70/h
(±18)
65/h
No
6
49/h
23/h
41,7%
4
9
UPPP
GA
No
39
58.7/h
14.5/h
77,8%
4
223
UPPP
GA /HS
No
9
48.3/h
9.5/h
60,1%
4
19
UPPP
No
8.7
54/h
31/h
31,6%
4
22
UPPP
No
1.5
Nose
12.3±1
9.9
month
s
16.3/h***
(±17.2)
20±10/h
2b
UPPP
(93%)
Flap
(7%)
58.6/
(+/36.6)
44±12/h
77%
1431
patients
Partial
glossectomy
Partial
glossectomy
Glossectomy
(9.2%)
HS/GA
(65.05%)
61±
19%
C
17.9%
N=257
195
RTBR
(25.92%)
Definition of abbreviations:
-
NS : no significant
NA ; not available
-
**: p<0,01
*** : p<0,001
* : p < 0,05
****: p < 0,0001
196
Table e35: Efficiency of MLS on nocturnal oxymetry and sleep stage in OSA patients
Authors
N
Mean
SaO2
after
MLS
(%TST
95%*
(±3,2)
NA
SaO2<90%
before
MLS
(% TST)
SaO2<90%
after MLS
(% of TST)
SWS
before
MLS
(%TST)
SWS
after
MLS
(%TST)
REM
before
MLS
(%TST)
REM
after
MLS
(%TST
EBM
NA
NA
NA
NA
NA
NA
NA
NA
15,2%
(±6,5)
NA
16,2%*
(±6,2)
NA
4
109
Mean
SaO2
before
MLS
(%TST)
94%
(±2,1)
NA
Eun 2009
[380]
Benazzo
2008 [372]
Richard
2007 [309]
Vicente
2006 [337]
Verse
2006 [318]
Jacobowitz
2006 [307]
Baisch
2006 [302]
Liu 2005
[342]
Bowden
2005 [303]
Li 2004
[326]
Verse
2004 [373]
Miller 2004
[343]
Dattilo
2004 [304]
Kao 2003
[374]
Thomas
2003 [333]
90
22
NA
NA
NA
NA
NA
NA
NA
NA
4
55
NA
NA
NA
NA
NA
4
92,37%
(±2,6)
NA
93,4%
(±2,1)
NA
5,1%**
(±12,4)
NA
NA
60
28,5%
(±18,6)
NA
NA
NA
NA
NA
2b
NA
NA
NA
NA
NA
NA
4
93.4%**
(±2.6)
NA
NA
NA
NA
NA
NA
NA
4
44
92.3%
(±3.3)
NA
NA
NA
NA
NA
NA
NA
2b
29
NA
NA
NA
NA
NA
NA
NA
NA
4
12
NA
NA
NA
NA
NA
NA
NA
NA
4
46
93.2%*
(±2 .2)
NA
NA
NA
NA
NA
NA
NA
4
24
92.4%
(±2.3)
NA
NA
NA
NA
NA
NA
NA
4
37
NA
NA
NA
NA
NA
NA
NA
NA
4
42
91.4%
NA
NA
NA
NA
NA
NA
4
17
NA
92.7% NS
NA
NA
NA
NA
NA
NA
NA
4
37
83
4
197
Friedman
2003 [261]
Neruntarat
2003 [287]
Neruntarat
2003 [286]
Vilaseca
2002 [376]
Nelson
2001 [260]
Hendler
2001 [345]
Hsu 2001
[306]
Bettega
2000 [351]
143
NA
NA
NA
NA
NA
NA
NA
NA
4
32
NA
NA
NA
NA
NA
NA
NA
NA
20.1%*
(±3.7)
NA
9.1%
(±4.2)
NA
18.2%**
(±6.7)
NA
4
49
12.5%
(±2.8)
NA
20
NA
NA
NA
NA
25% *
(±26)
NA
6%
(±5,5)
NA
8%- NS
(±7)
NA
15.6%
(±5)
NA
15.7%
(±8)
NA
4
13
40%
(± 26)
NA
33
NA
NA
NA
NA
NA
NA
NA
NA
4
13
NA
NA
NA
NA
NA
NA
NA
NA
4
44
93.2%
(±3)
94.7%*
(±2.2)
53 min
(± 85)
25 min- NS
(± 70)
4%
(±7)
16%
(±7)
20%*
(±8)
4
Andsberg
2000 [322]
Lee 1999
[377]
Chabolle
1999 [323]
Elasfour
1998 [378]
Mickelson
1997 [321]
Ramirez
1996 [308]
Johnson
1994 [379]
Riley 1993
[312]
22
NA
NA
NA
NA
NA
5 %NS
(± 5)
NA
NA
NA
4
33
NA
NA
NA
NA
NA
NA
NA
NA
4
10
95%
(±1.5)
NA
9%
(±8)
NA
5%
(±5)
NA
13%
(±9)
NA
20%
(±12)
NA
6%
(±8)
NA
16%
(±11)
NA
2b
18
94%
(±2)
NA
12
NA
NA
NA
NA
NA
NA
NA
NA
0.6%
(±2.8)
NA
9.4%
(±6.1)
NA
7.25%
(±5.2)
NA
4
12
1.8%
(±4.3)
NA
9
NA
NA
NA
NA
NA
4
64%
71.9%
42,7 min*
(± 37,6)
NA
NA
223
114,3 min
(± 43,9)
NA
4.4%
(±5.6)
8.5%
(±7.7)
11.9%
(±5.8)
17.7%
(±5.6)
4
19
NA
NA
NA
NA
NA
NA
NA
NA
4
22
78,6%
(±9,7)
87,3%**
(±7,3)
NA
NA
NA
NA
NA
NA
2b
Djupesland
1992 [327]
Woodson
1992 [325]
4
4
4
4
198
1431
81.8
±5.4%
(N=620)
85.7
±7.4%
(N=620)
28.9
±15.7%
(N=85)
9.7
±11.5%
(N=85)
5.4
±4.7%
(N=341)
9.2
±8.0%
(N=341)
12.8
±3.9%
(N=431)
17.2
±4.1%
(N=431)
C
Definition of abbreviations:
-
NS : no significant
NA ; not available
-
**: p<0,01
*** : p<0,001
* : p < 0,05
****: p < 0,0001
199
Table e36: Anthropometric and clinical data of patients selected for MLS
Authors
Eun 2009 [380]
Benazzo 2008 [372]
Richard 2007 [309]
Vicente 2006 [337]
Verse 2006 [318]
N
90
109
22
55
60
Jacobowitz 2006 [307] 37
Baisch 2006 [302]
83
Age
BMI
Sex
Use of CPAP EBM
(yrs old)
(kg/m²)
(% of males) Before MLS
45,6
26
90%
(±11)
(±3)
(N=81)
51,3
28,2
(±9,4)
(±3,1)
50,3
No
4
NA
Yes
4
27,7
91%
Yes
4
(±7)
(±3,4)
(N=20)
47,3
29,6
93%
Yes
4
(±4,5)
(±4,8)
(N=51)
51,9
28,5
93%
Yes
2b
(±10)
(±3)
(N=56)
47.6
29.9
78%
Yes
4
(±12.1)
(±4.1)
(N=29)
52
28.2
95%
Yes
4
200
Liu 2005 [342]
Bowden 2005 [303]
Li 2004 [326]
Verse 2004 [373]
Miller 2004 [343]
Dattilo 2004 [304]
44
29
12
46
24
37
(±9.6)
(±3.3)
(N= 79)
41,2
28
100%
(9 - 66)
(±3,3)
(N=44)
53.9
34.1
100%
(±6)
(±6.4)
(N=29)
44,5
26,5
(±6,5)
(±2,6)
51.8
Yes
2b
Yes
4
NA
No
4
28.37
91%
Yes
4
(±7)
(±2.9)
(N=42)
43.1
30.5
88%
Yes
4
(±8.9)
(±2.9)
(N=24)
48.3
NA
76%
NA
4
Yes
4
Yes
4
(N=32)
Kao 2003 [374]
42
(18 – 60)
NA
100%
(N=42)
Thomas 2003 [333]
17
47.5
29.8
NA
201
Friedman 2003 [375]
Neruntarat 2003 [286]
Neruntarat 2003 [287]
Vilaseca 2002 [376]
Nelson 2001 [381]
143
32
49
20
13
(±13)
(±4.5)
47.0
31.5
73%
(±11.7)
(±4.8)
(N=104)
39.2
29.3
94%
(±5.7)
(±2.4)
(N=30)
41
30
100%
(±4)
(±2)
(N=49)
44.7
27.8
100%
(±5.7)
(±3.3)
(N=20)
51,5
27,9
92%
Yes
4
Yes
4
Yes
4
Yes
4
NA
4
NA
4
Yes/No
4
Yes
4
(N=12)
Hendler 2001 [345]
Hsu 2001 [306]
33
13
47
32.6
85%
(±10.5)
(±6.95)
(N=28)
47.4
31.4
85%
(N=11)
Bettega 2000 [351]
44
47
26.3
86%
202
Andsberg 2000 [322]
Lee 1999 [377]
22
33
(±11)
(±2.9)
(N=38)
50
88 kg
95%
(37 – 73)
(average weight) (N=21)
41
NA
(28 – 59)
Chabolle 1999 [323]
10
47.5
Mickelson 1997 [321]
Ramirez 1996 [308]
Johnson 1994 [379]
Riley 1993 [312]
18
12
12
9
223
4
NA
4
Yes
2b
NA
4
(N=28)
32
(35 – 57)
Elasfour 1998 [378]
85%
NA
100%
(N=10)
44
26
90%
(31 – 66)
(±3)
(N=26)
48.8
36
92%
(±14.2)
(±8.8)
(N=11)
52
35
100%
(±17)
(±9)
(N=12)
46.7
32.7
100%
(±3)
(±1.3)
(N=9)
51.8
29.2
NA
Yes
Yes
4
Yes
4
Yes
4
203
Djupesland 1992 [327] 19
Woodson
22
1992 [325]
(±9.8)
(±5.2)
50
96.6 kg
100%
(22 – 68)
(72 – 120)
(N=19)
48
32
NA
(±15)
(±5,6)
1431 49.5±3.8
34.5±2.7 kg/m²
(N=1389) (N=1088)
91.3±7.8%
NA
4
Yes
2b
C
(N=1048)
Definition of abbreviations:
-
NS : no significant
NA ; not available
-
**: p<0,01
*** : p<0,001
* : p < 0,05
****: p < 0,0001
204
Table e37: Cephalometric data of patients selected for MLS
Authors
N
SNA(°)
before
MLS
SNA(°)
after
MLS
SNB(°)
before
MLS
SNB(°)
after
MLS
ELP(mm)
before
MLS
ELP(mm)
after MLS
MPH
(mm)
after MLS
EBM
NA
4
NA
MPH
(mm)
before
MLS
17,4mm
(±5,9)
NA
Eun 2009
[380]
Benazzo
2008 [372]
Richard
2007 [309]
Vicente
2006 [337]
Verse
2006 [318]
Jacobowitz
2006 [307]
Baisch
2006 [302]
Liu 2005
[342]
Bowden
2005 [303]
Li 2004
[326]
Verse
2004 [373]
Miller 2004
[343]
Dattilo
2004 [304]
Kao 2003
[374]
Thomas
2003 [333]
90
NA
NA
9,2mm
(±3,6)
NA
NA
NA
82°
(+/64,9)
NA
NA
109
82,7°
(±5)
NA
NA
4
22
NA
NA
NA
NA
NA
NA
NA
NA
4
55
NA
NA
NA
NA
NA
NA
NA
NA
4
60
NA
NA
NA
NA
NA
NA
NA
NA
2b
37
85.6°
(+/5.4)
NA
NA
NA
4
NA
24.4mm
(±6.4)
NA
NA
NA
6.9mm
(±1.7)
NA
NA
NA
81.6°
(±4)
NA
NA
4
83,3°
(+/3,4)
NA
78,2°
(±5,1)
NA
78,1°
(±5)
NA
9,1mm
(±2,1)
NA
11,3mm***
(±2)
NA
23,6mm
(±7,5)
NA
21,3mm***
(±7,7)
NA
2b
29
83,4°
(+/3,6)
NA
12
NA
NA
NA
NA
NA
NA
NA
NA
4
46
NA
NA
NA
NA
NA
NA
NA
NA
4
24
NA
NA
NA
NA
NA
4
NA
NA
NA
NA
12.6mm****
(±2.8)
NA
NA
37
7.9mm
(±2.3)
NA
NA
NA
4
42
NA
NA
NA
NA
NA
NA
NA
NA
4
17
NA
NA
NA
NA
NA
NA
NA
NA
4
83
44
4
205
Friedman
2003 [375]
Neruntarat
2003 [286]
Neruntarat
2003 [287]
Vilaseca
2002 [376]
143
NA
NA
NA
NA
NA
NA
NA
NA
4
32
81.9°
(±2)
82,1°
(+/1,5)
78,1°
(± 4)
81.7)
(±3)
82,2°
(+/1,6)
78,1°
(±4)
80.3°
(±2)
80,5°
(±2,2)
76,6°
(±3)
80.1°
(±4)
80,2°
(+/3,4)
77,7° *
(±3)
6.8mm
(±3)
5,2mm
(±1,3)
10,9 mm
(± 4)
8.6mm**
(±3)
9,2mm***
(±1,4)
12,8 mm
(± 4)
22.1mm**
(±2)
22,4mm***
(±1,9)
42,5mm
(+/9)
4
Nelson
2001 [381]
Hendler
2001 [345]
Hsu 2001
[306]
Bettega
2000 [351]
Andsberg
2000 [322]
Lee 1999
[377]
Chabolle
1999 [323]
Elasfour
1998 [378]
Mickelson
1997 [321]
Ramirez
1996 [308]
Johnson
1994 [379]
Riley 1993
[312]
Djupesland
1992 [327]
Woodson
1992 [325]
13
NA
NA
NA
NA
NA
NA
19.7mm
(±3)
19,5mm
(±4,1)
35,3
mm
(± 10)
NA
NA
4
33
NA
NA
NA
NA
NA
NA
NA
NA
4
13
81.5°
81.5°
79.8°
80°
4.6mm
9.8mm
25.4mm
22.8mm
4
44
NA
NA
NA
NA
NA
NA
NA
NA
4
22
NA
NA
NA
NA
NA
NA
NA
NA
4
33
NA
NA
NA
NA
NA
NA
NA
NA
4
10
82°
(±3)
NA
82°
(±3)
NA
82°
(±3)
NA
10mm
(±4.5)
NA
14.5mm
(±5)
NA
16.5
(±4.5)
NA
12
NA
NA
NA
NA
NA
NA
28mm
(±4.5)
19,4mm
(±3)
NA
2b
18
82°
(±3)
NA
NA
4
12
NA
NA
NA
NA
NA
NA
4
NA
NA
NA
8.5mm
(±2.1)
NA
NA
19
78,4°
(±1)
77.5°
(±5.2)
NA
30mm
(±6)
26,6mm
(±4)
NA
27mm
(±8)
NA
223
82,9°
(±1)
NA
13mm
(±6)
NA
4
9
7mm
(±2)
8,4mm
(±1)
5.5mm
(±1.6)
NA
NA
NA
4
22
79.8°
(+/3,7)
NA
78,4°
(±4)
NA
NA
NA
25
(±8)
NA
4
49
20
NA
NA
4
4
4
4
206
1431
82.4
±2.0°
(N=326)
82.0
±1.8°
(N=168)
81.0
±1.9°
(N=549)
80.4
±1.6°
(N=153)
7.9
±2.0mm
(N=563)
9.7
±2.2mm
(N=425)
19.8
±5.1mm
(N=359)
24.9
±8.3mm
(N=180)
C
Definition of abbreviations:
-
NS : no significant
NA ; not available
-
**: p<0,01
*** : p<0,001
* : p < 0,05
****: p < 0,0001
207
References
1.
Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or
without treatment with continuous positive airway pressure: an observational study. Lancet. 2005 Mar 19-25;365(9464):1046-53.
2.
Lavie P, Herer P, Lavie L. Mortality risk factors in sleep apnoea: a matched case-control study. J Sleep Res. 2007 Mar;16(1):128-34.
3.
He J, Kryger MH, Zorick FJ, Conway W, Roth T. Mortality and apnea index in obstructive sleep apnea. Experience in 385 male patients.
Chest. 1988 Jul;94(1):9-14.
4.
Berger G, Berger R, Oksenberg A. Progression of snoring and obstructive sleep apnoea: the role of increasing weight and time. Eur Respir J.
2009 Feb;33(2):338-45.
5.
Young T, Peppard PE, Gottlieb DJ. Epidemiology of obstructive sleep apnea: a population health perspective. Am J Respir Crit Care Med.
2002 May 1;165(9):1217-39.
6.
Redline S, Schluchter MD, Larkin EK, Tishler PV. Predictors of longitudinal change in sleep-disordered breathing in a nonclinic population.
Sleep. 2003 Sep;26(6):703-9.
7.
Tishler PV, Larkin EK, Schluchter MD, Redline S. Incidence of sleep-disordered breathing in an urban adult population: the relative
importance of risk factors in the development of sleep-disordered breathing. JAMA. 2003 May 7;289(17):2230-7.
8.
Noda A, Okada T, Yasuma F, Sobue T, Nakashima N, Yokota M. Prognosis of the middle-aged and aged patients with obstructive sleep
apnea syndrome. Psychiatry Clin Neurosci. 1998 Feb;52(1):79-85.
9.
Partinen M, Jamieson A, Guilleminault C. Long-term outcome for obstructive sleep apnea syndrome patients. Mortality. Chest. 1988
Dec;94(6):1200-4.
10.
Redline S, Larkin E, Schluchter M, Aylor J, Clark K, Graham G, et al. Incidence of sleep disordered breathing (SDB) in a population-based
sample. Sleep. 2001;24:511.
11.
Lindberg E, Elmasry A, Gislason T, Janson C, Bengtsson H, Hetta J, et al. Evolution of sleep apnea syndrome in sleepy snorers: a
population-based prospective study. Am J Respir Crit Care Med. 1999 Jun;159(6):2024-7.
12.
Svanborg E, Larsson H. Development of nocturnal respiratory disturbance in untreated patients with obstructive sleep apnea syndrome.
Chest. 1993 Aug;104(2):340-3.
13.
Ancoli-Israel S, Gehrman P, Kripke DF, Stepnowsky C, Mason W, Cohen-Zion M, et al. Long-term follow-up of sleep disordered breathing
in older adults. Sleep Med. 2001 Nov;2(6):511-6.
14.
Newman AB, Foster G, Givelber R, Nieto FJ, Redline S, Young T. Progression and regression of sleep-disordered breathing with changes in
weight: the Sleep Heart Health Study. Arch Intern Med. 2005 Nov 14;165(20):2408-13.
15.
Pendlebury ST, Pepin JL, Veale D, Levy P. Natural evolution of moderate sleep apnoea syndrome: significant progression over a mean of 17
months. Thorax. 1997 Oct;52(10):872-8.
208
16.
Peppard PE, Young T, Palta M, Dempsey J, Skatrud J. Longitudinal study of moderate weight change and sleep-disordered breathing.
JAMA. 2000 Dec 20;284(23):3015-21.
17.
Ancoli-Israel S, Kripke DF, Klauber MR, Parker L, Stepnowsky C, Kullen A, et al. Natural history of sleep disordered breathing in
community dwelling elderly. Sleep. 1993 Dec;16(8 Suppl):S25-9.
18.
Mason WJ, Ancoli-Israel S, Kripke DF. Apnea revisited: a longitudinal follow-up. Sleep. 1989 Oct;12(5):423-9.
19.
Sahlman J, Pukkila M, Seppa J, Tuomilehto H. Evolution of mild obstructive sleep apnea after different treatments. Laryngoscope. 2007
Jun;117(6):1107-11.
20.
Sforza E, Addati G, Cirignotta F, Lugaresi E. Natural evolution of sleep apnoea syndrome: a five year longitudinal study. Eur Respir J. 1994
Oct;7(10):1765-70.
21.
Guilleminault C, Kirisoglu C, Poyares D, Palombini L, Leger D, Farid-Moayer M, et al. Upper airway resistance syndrome: a long-term
outcome study. J Psychiatr Res. 2006 Apr;40(3):273-9.
22.
Hoch CC, Dew MA, Reynolds CF, 3rd, Buysse DJ, Nowell PD, Monk TH, et al. Longitudinal changes in diary- and laboratory-based sleep
measures in healthy "old old" and "young old" subjects: a three-year follow-up. Sleep. 1997 Mar;20(3):192-202.
23.
Fisher D, Pillar G, Malhotra A, Peled N, Lavie P. Long-term follow-up of untreated patients with sleep apnoea syndrome. Respir Med. 2002
May;96(5):337-43.
24.
Young T, Finn L, Peppard PE, Szklo-Coxe M, Austin D, Nieto FJ, et al. Sleep disordered breathing and mortality: eighteen-year follow-up
of the Wisconsin sleep cohort. Sleep. 2008 Aug 1;31(8):1071-8.
25.
Smith PL, Gold AR, Meyers DA, Haponik EF, Bleecker ER. Weight loss in mildly to moderately obese patients with obstructive sleep
apnea. Ann Intern Med. 1985 Dec;103(6 ( Pt 1)):850-5.
26.
Suratt PM, McTier RF, Findley LJ, Pohl SL, Wilhoit SC. Changes in breathing and the pharynx after weight loss in obstructive sleep apnea.
Chest. 1987 Oct;92(4):631-7.
27.
Rubinstein I, Colapinto N, Rotstein LE, Brown IG, Hoffstein V. Improvement in upper airway function after weight loss in patients with
obstructive sleep apnea. Am Rev Respir Dis. 1988 Nov;138(5):1192-5.
28.
Pasquali R, Colella P, Cirignotta F, Mondini S, Gerardi R, Buratti P, et al. Treatment of obese patients with obstructive sleep apnea
syndrome (OSAS): effect of weight loss and interference of otorhinolaryngoiatric pathology. Int J Obes. 1990 Mar;14(3):207-17.
29.
Rajala R, Partinen M, Sane T, Pelkonen R, Huikuri K, Seppalainen AM. Obstructive sleep apnoea syndrome in morbidly obese patients. J
Intern Med. 1991 Aug;230(2):125-9.
30.
Schwartz AR, Gold AR, Schubert N, Stryzak A, Wise RA, Permutt S, et al. Effect of weight loss on upper airway collapsibility in
obstructive sleep apnea. Am Rev Respir Dis. 1991 Sep;144(3 Pt 1):494-8.
31.
Suratt PM, McTier RF, Findley LJ, Pohl SL, Wilhoit SC. Effect of very-low-calorie diets with weight loss on obstructive sleep apnea. Am J
Clin Nutr. 1992 Jul;56(1 Suppl):182S-4S.
209
32.
Kiselak J, Clark M, Pera V, Rosenberg C, Redline S. The association between hypertension and sleep apnea in obese patients. Chest. 1993
Sep;104(3):775-80.
33.
Nahmias J, Kirschner M, Karetzky MS. Weight loss and OSA and pulmonary function in obesity. N J Med. 1993 Jan;90(1):48-53.
34.
Rauscher H, Formanek D, Popp W, Zwick H. Nasal CPAP and weight loss in hypertensive patients with obstructive sleep apnoea. Thorax.
1993 May;48(5):529-33.
35.
Kajaste S, Telakivi T, Mustajoki P, Pihl S, Partinen M. Effects of a cognitive-behavioural weight loss programme on overweight obstructive
sleep apnoea patients. J Sleep Res. 1994 Dec;3(4):245-9.
36.
Braver HM, Block AJ, Perri MG. Treatment for snoring. Combined weight loss, sleeping on side, and nasal spray. Chest. 1995
May;107(5):1283-8.
37.
Noseda A, Kempenaers C, Kerkhofs M, Houben JJ, Linkowski P. Sleep apnea after 1 year domiciliary nasal-continuous positive airway
pressure and attempted weight reduction. Potential for weaning from continuous positive airway pressure. Chest. 1996 Jan;109(1):138-43.
38.
Kansanen M, Vanninen E, Tuunainen A, Pesonen P, Tuononen V, Hartikainen J, et al. The effect of a very low-calorie diet-induced weight
loss on the severity of obstructive sleep apnoea and autonomic nervous function in obese patients with obstructive sleep apnoea syndrome. Clin
Physiol. 1998 Jul;18(4):377-85.
39.
Sampol G, Munoz X, Sagales MT, Marti S, Roca A, Dolors de la Calzada M, et al. Long-term efficacy of dietary weight loss in sleep
apnoea/hypopnoea syndrome. Eur Respir J. 1998 Nov;12(5):1156-9.
40.
Lojander J, Mustajoki P, Ronka S, Mecklin P, Maasilta P. A nurse-managed weight reduction programme for obstructive sleep apnoea
syndrome. J Intern Med. 1998 Sep;244(3):251-5.
41.
Hakala K, Maasilta P, Sovijarvi AR. Upright body position and weight loss improve respiratory mechanics and daytime oxygenation in
obese patients with obstructive sleep apnoea. Clin Physiol. 2000 Jan;20(1):50-5.
42.
Kajaste S, Brander PE, Telakivi T, Partinen M, Mustajoki P. A cognitive-behavioral weight reduction program in the treatment of
obstructive sleep apnea syndrome with or without initial nasal CPAP: a randomized study. Sleep Med. 2004 Mar;5(2):125-31.
43.
Kemppainen T, Ruoppi P, Seppa J, Sahlman J, Peltonen M, Tukiainen H, et al. Effect of weight reduction on rhinometric measurements in
overweight patients with obstructive sleep apnea. Am J Rhinol. 2008 Jul-Aug;22(4):410-5.
44.
Lam B, Sam K, Mok WY, Cheung MT, Fong DY, Lam JC, et al. Randomised study of three non-surgical treatments in mild to moderate
obstructive sleep apnoea. Thorax. 2007 Apr;62(4):354-9.
45.
Foster GD, Borradaile KE, Sanders MH, Millman R, Zammit G, Newman AB, et al. A randomized study on the effect of weight loss on
obstructive sleep apnea among obese patients with type 2 diabetes: the Sleep AHEAD study. Arch Intern Med. 2009 Sep 28;169(17):1619-26.
46.
Johansson K, Neovius M, Lagerros YT, Harlid R, Rossner S, Granath F, et al. Effect of a very low energy diet on moderate and severe
obstructive sleep apnoea in obese men: a randomised controlled trial. BMJ. 2009;339:b4609.
47.
Tuomilehto HP, Seppa JM, Partinen MM, Peltonen M, Gylling H, Tuomilehto JO, et al. Lifestyle intervention with weight reduction: firstline treatment in mild obstructive sleep apnea. Am J Respir Crit Care Med. 2009 Feb 15;179(4):320-7.
210
48.
Harman EM, Wynne JW, Block AJ. The effect of weight loss on sleep-disordered breathing and oxygen desaturation in morbidly obese men.
Chest. 1982 Sep;82(3):291-4.
49.
Peiser J, Lavie P, Ovnat A, Charuzi I. Sleep apnea syndrome in the morbidly obese as an indication for weight reduction surgery. Ann Surg.
1984 Jan;199(1):112-5.
50.
Peiser J, Ovnat A, Uwyyed K, Lavie P, Charuzi I. Cardiac arrhythmias during sleep in morbidly obese sleep-apneic patients before and after
gastric bypass surgery. Clin Cardiol. 1985 Oct;8(10):519-21.
51.
Charuzi I, Ovnat A, Peiser J, Saltz H, Weitzman S, Lavie P. The effect of surgical weight reduction on sleep quality in obesity-related sleep
apnea syndrome. Surgery. 1985 May;97(5):535-8.
52.
Sugerman HJ, Fairman RP, Baron PL, Kwentus JA. Gastric surgery for respiratory insufficiency of obesity. Chest. 1986 Jul;90(1):81-6.
53.
Charuzi I, Fraser D, Peiser J, Ovnat A, Lavie P. Sleep apnea syndrome in the morbidly obese undergoing bariatric surgery. Gastroenterol
Clin North Am. 1987 Sep;16(3):517-9.
54.
Sugerman HJ, Fairman RP, Sood RK, Engle K, Wolfe L, Kellum JM. Long-term effects of gastric surgery for treating respiratory
insufficiency of obesity. Am J Clin Nutr. 1992 Feb;55(2 Suppl):597S-601S.
55.
Charuzi I, Lavie P, Peiser J, Peled R. Bariatric surgery in morbidly obese sleep-apnea patients: short- and long-term follow-up. Am J Clin
Nutr. 1992 Feb;55(2 Suppl):594S-6S.
56.
Pillar G, Peled R, Lavie P. Recurrence of sleep apnea without concomitant weight increase 7.5 years after weight reduction surgery. Chest.
1994 Dec;106(6):1702-4.
57.
Scheuller M, Weider D. Bariatric surgery for treatment of sleep apnea syndrome in 15 morbidly obese patients: long-term results.
Otolaryngol Head Neck Surg. 2001 Oct;125(4):299-302.
58.
Rasheid S, Banasiak M, Gallagher SF, Lipska A, Kaba S, Ventimiglia D, et al. Gastric bypass is an effective treatment for obstructive sleep
apnea in patients with clinically significant obesity. Obes Surg. 2003 Feb;13(1):58-61.
59.
Guardiano SA, Scott JA, Ware JC, Schechner SA. The long-term results of gastric bypass on indexes of sleep apnea. Chest. 2003
Oct;124(4):1615-9.
60.
Valencia-Flores M, Orea A, Herrera M, Santiago V, Rebollar V, Castano VA, et al. Effect of bariatric surgery on obstructive sleep apnea and
hypopnea syndrome, electrocardiogram, and pulmonary arterial pressure. Obes Surg. 2004 Jun-Jul;14(6):755-62.
61.
Lankford DA, Proctor CD, Richard R. Continuous positive airway pressure (CPAP) changes in bariatric surgery patients undergoing rapid
weight loss. Obes Surg. 2005 Mar;15(3):336-41.
62.
Busetto L, Enzi G, Inelmen EM, Costa G, Negrin V, Sergi G, et al. Obstructive sleep apnea syndrome in morbid obesity: effects of
intragastric balloon. Chest. 2005 Aug;128(2):618-23.
63.
Dixon JB, Schachter LM, O'Brien PE. Polysomnography before and after weight loss in obese patients with severe sleep apnea. Int J Obes
(Lond). 2005 Sep;29(9):1048-54.
211
64.
Kalra M, Inge T, Garcia V, Daniels S, Lawson L, Curti R, et al. Obstructive sleep apnea in extremely overweight adolescents undergoing
bariatric surgery. Obes Res. 2005 Jul;13(7):1175-9.
65.
Poitou C, Coupaye M, Laaban JP, Coussieu C, Bedel JF, Bouillot JL, et al. Serum amyloid A and obstructive sleep apnea syndrome before
and after surgically-induced weight loss in morbidly obese subjects. Obes Surg. 2006 Nov;16(11):1475-81.
66.
Fritscher LG, Canani S, Mottin CC, Fritscher CC, Berleze D, Chapman K, et al. Bariatric surgery in the treatment of obstructive sleep apnea
in morbidly obese patients. Respiration. 2007;74(6):647-52.
67.
Haines KL, Nelson LG, Gonzalez R, Torrella T, Martin T, Kandil A, et al. Objective evidence that bariatric surgery improves obesity-related
obstructive sleep apnea. Surgery. 2007 Mar;141(3):354-8.
68.
Marti-Valeri C, Sabate A, Masdevall C, Dalmau A. Improvement of associated respiratory problems in morbidly obese patients after open
Roux-en-Y gastric bypass. Obes Surg. 2007 Aug;17(8):1102-10.
69.
Lettieri CJ, Eliasson AH, Greenburg DL. Persistence of obstructive sleep apnea after surgical weight loss. J Clin Sleep Med. 2008 Aug
15;4(4):333-8.
70.
Rao A, Tey BH, Ramalingam G, Poh AG. Obstructive sleep apnoea (OSA) patterns in bariatric surgical practice and response of OSA to
weight loss after laparoscopic adjustable gastric banding (LAGB). Ann Acad Med Singapore. 2009 Jul;38(7):587-7.
71.
McEvoy RD, Sharp DJ, Thornton AT. The effects of posture on obstructive sleep apnea. Am Rev Respir Dis. 1986 Apr;133(4):662-6.
72.
Oksenberg A, Silverberg DS, Arons E, Radwan H. Positional vs nonpositional obstructive sleep apnea patients: anthropomorphic, nocturnal
polysomnographic, and multiple sleep latency test data. Chest. 1997 Sep;112(3):629-39.
73.
Cartwright RD, Lloyd S, Lilie J, Kravitz H. Sleep position training as treatment for sleep apnea syndrome: a preliminary study. Sleep.
1985;8(2):87-94.
74.
Kavey NB, Blitzer A, Gidro-Frank S, Korstanje K. Sleeping position and sleep apnea syndrome. Am J Otolaryngol. 1985 Sep-Oct;6(5):3737.
75.
Cartwright R, Ristanovic R, Diaz F, Caldarelli D, Alder G. A comparative study of treatments for positional sleep apnea. Sleep. 1991
Dec;14(6):546-52.
76.
Cartwright RD. Effect of sleep position on sleep apnea severity. Sleep. 1984;7(2):110-4.
77.
Berger M, Oksenberg A, Silverberg DS, Arons E, Radwan H, Iaina A. Avoiding the supine position during sleep lowers 24 h blood pressure
in obstructive sleep apnea (OSA) patients. J Hum Hypertens. 1997 Oct;11(10):657-64.
78.
Jokic R, Klimaszewski A, Crossley M, Sridhar G, Fitzpatrick MF. Positional treatment vs continuous positive airway pressure in patients
with positional obstructive sleep apnea syndrome. Chest. 1999 Mar;115(3):771-81.
79.
Maurer JT, Stuck BA, Hein G, Verse T, Hormann K. [Treatment of obstructive sleep apnea with a new vest preventing the supine position].
Dtsch Med Wochenschr. 2003 Jan 17;128(3):71-5.
80.
Zuberi NA, Rekab K, Nguyen HV. Sleep apnea avoidance pillow effects on obstructive sleep apnea syndrome and snoring. Sleep Breath.
2004 Dec;8(4):201-7.
212
81.
Wenzel S, Smith E, Leiacker R, Fischer Y. [Efficacy and longterm compliance of the vest preventing the supine position in patients with
obstructive sleep apnea]. Laryngorhinootologie. 2007 Aug;86(8):579-83.
82.
Loord H, Hultcrantz E. Positioner--a method for preventing sleep apnea. Acta Otolaryngol. 2007 Aug;127(8):861-8.
83.
Oksenberg A, Silverberg D, Offenbach D, Arons E. Positional therapy for obstructive sleep apnea patients: A 6-month follow-up study.
Laryngoscope. 2006 Nov;116(11):1995-2000.
84.
Skinner MA, Kingshott RN, Jones DR, Homan SD, Taylor DR. Elevated posture for the management of obstructive sleep apnea. Sleep
Breath. 2004 Dec;8(4):193-200.
85.
Ferguson KA, Ono T, Lowe AA, Keenan SP, Fleetham JA. A randomized crossover study of an oral appliance vs nasal-continuous positive
airway pressure in the treatment of mild-moderate obstructive sleep apnea. Chest. 1996 May;109(5):1269-75.
86.
Ferguson KA, Ono T, Lowe AA, al-Majed S, Love LL, Fleetham JA. A short-term controlled trial of an adjustable oral appliance for the
treatment of mild to moderate obstructive sleep apnoea. Thorax. 1997 Apr;52(4):362-8.
87.
Hans MG, Nelson S, Luks VG, Lorkovich P, Baek SJ. Comparison of two dental devices for treatment of obstructive sleep apnea syndrome
(OSAS). Am J Orthod Dentofacial Orthop. 1997 May;111(5):562-70.
88.
Bloch KE, Iseli A, Zhang JN, Xie X, Kaplan V, Stoeckli PW, et al. A randomized, controlled crossover trial of two oral appliances for sleep
apnea treatment. Am J Respir Crit Care Med. 2000 Jul;162(1):246-51.
89.
Kato J, Isono S, Tanaka A, Watanabe T, Araki D, Tanzawa H, et al. Dose-dependent effects of mandibular advancement on pharyngeal
mechanics and nocturnal oxygenation in patients with sleep-disordered breathing. Chest. 2000 Apr;117(4):1065-72.
90.
Lowe AA, Sjoholm TT, Ryan CF, Fleetham JA, Ferguson KA, Remmers JE. Treatment, airway and compliance effects of a titratable oral
appliance. Sleep. 2000 Jun 15;23 Suppl 4:S172-8.
91.
Liu Y, Lowe AA, Fleetham JA, Park YC. Cephalometric and physiologic predictors of the efficacy of an adjustable oral appliance for
treating obstructive sleep apnea. Am J Orthod Dentofacial Orthop. 2001 Dec;120(6):639-47.
92.
Mehta A, Qian J, Petocz P, Darendeliler MA, Cistulli PA. A randomized, controlled study of a mandibular advancement splint for
obstructive sleep apnea. Am J Respir Crit Care Med. 2001 May;163(6):1457-61.
93.
Engleman HM, McDonald JP, Graham D, Lello GE, Kingshott RN, Coleman EL, et al. Randomized crossover trial of two treatments for
sleep apnea/hypopnea syndrome: continuous positive airway pressure and mandibular repositioning splint. Am J Respir Crit Care Med. 2002 Sep
15;166(6):855-9.
94.
Gotsopoulos H, Chen C, Qian J, Cistulli PA. Oral appliance therapy improves symptoms in obstructive sleep apnea: a randomized,
controlled trial. Am J Respir Crit Care Med. 2002 Sep 1;166(5):743-8.
95.
Johnston CD, Gleadhill IC, Cinnamond MJ, Gabbey J, Burden DJ. Mandibular advancement appliances and obstructive sleep apnoea: a
randomized clinical trial. Eur J Orthod. 2002 Jun;24(3):251-62.
96.
Pitsis AJ, Darendeliler MA, Gotsopoulos H, Petocz P, Cistulli PA. Effect of vertical dimension on efficacy of oral appliance therapy in
obstructive sleep apnea. Am J Respir Crit Care Med. 2002 Sep 15;166(6):860-4.
213
97.
Randerath WJ, Heise M, Hinz R, Ruehle KH. An individually adjustable oral appliance vs continuous positive airway pressure in mild-tomoderate obstructive sleep apnea syndrome. Chest. 2002 Aug;122(2):569-75.
98.
Rose E, Staats R, Virchow C, Jonas IE. A comparative study of two mandibular advancement appliances for the treatment of obstructive
sleep apnoea. Eur J Orthod. 2002 Apr;24(2):191-8.
99.
Sanner BM, Heise M, Knoben B, Machnick M, Laufer U, Kikuth R, et al. MRI of the pharynx and treatment efficacy of a mandibular
advancement device in obstructive sleep apnoea syndrome. Eur Respir J. 2002 Jul;20(1):143-50.
100. Skinner MA, Robertson CJ, Kingshott RN, Jones DR, Taylor DR. The efficacy of a mandibular advancement splint in relation to
cephalometric variables. Sleep Breath. 2002 Sep;6(3):115-24.
101. Tan YK, L'Estrange PR, Luo YM, Smith C, Grant HR, Simonds AK, et al. Mandibular advancement splints and continuous positive airway
pressure in patients with obstructive sleep apnoea: a randomized cross-over trial. Eur J Orthod. 2002 Jun;24(3):239-49.
102. Walker-Engstrom ML, Tegelberg A, Wilhelmsson B, Ringqvist I. 4-year follow-up of treatment with dental appliance or
uvulopalatopharyngoplasty in patients with obstructive sleep apnea: a randomized study. Chest. 2002 Mar;121(3):739-46.
103. Ng AT, Gotsopoulos H, Qian J, Cistulli PA. Effect of oral appliance therapy on upper airway collapsibility in obstructive sleep apnea. Am J
Respir Crit Care Med. 2003 Jul 15;168(2):238-41.
104. Tegelberg A, Walker-Engstrom ML, Vestling O, Wilhelmsson B. Two different degrees of mandibular advancement with a dental appliance
in treatment of patients with mild to moderate obstructive sleep apnea. Acta Odontol Scand. 2003 Dec;61(6):356-62.
105. Walker-Engstrom ML, Ringqvist I, Vestling O, Wilhelmsson B, Tegelberg A. A prospective randomized study comparing two different
degrees of mandibular advancement with a dental appliance in treatment of severe obstructive sleep apnea. Sleep Breath. 2003 Sep;7(3):119-30.
106. Barnes M, McEvoy RD, Banks S, Tarquinio N, Murray CG, Vowles N, et al. Efficacy of positive airway pressure and oral appliance in mild
to moderate obstructive sleep apnea. Am J Respir Crit Care Med. 2004 Sep 15;170(6):656-64.
107. Fleury B, Rakotonanahary D, Petelle B, Vincent G, Pelletier Fleury N, Meyer B, et al. Mandibular advancement titration for obstructive
sleep apnea: optimization of the procedure by combining clinical and oximetric parameters. Chest. 2004 May;125(5):1761-7.
108. Gotsopoulos H, Kelly JJ, Cistulli PA. Oral appliance therapy reduces blood pressure in obstructive sleep apnea: a randomized, controlled
trial. Sleep. 2004 Aug 1;27(5):934-41.
109. Marklund M, Stenlund H, Franklin KA. Mandibular advancement devices in 630 men and women with obstructive sleep apnea and snoring:
tolerability and predictors of treatment success. Chest. 2004 Apr;125(4):1270-8.
110. Blanco J, Zamarron C, Abeleira Pazos MT, Lamela C, Suarez Quintanilla D. Prospective evaluation of an oral appliance in the treatment of
obstructive sleep apnea syndrome. Sleep Breath. 2005 Mar;9(1):20-5.
111. Kyung SH, Park YC, Pae EK. Obstructive sleep apnea patients with the oral appliance experience pharyngeal size and shape changes in
three dimensions. Angle Orthod. 2005 Jan;75(1):15-22.
112. Lawton HM, Battagel JM, Kotecha B. A comparison of the Twin Block and Herbst mandibular advancement splints in the treatment of
patients with obstructive sleep apnoea: a prospective study. Eur J Orthod. 2005 Feb;27(1):82-90.
214
113. Naismith SL, Winter VR, Hickie IB, Cistulli PA. Effect of oral appliance therapy on neurobehavioral functioning in obstructive sleep apnea:
a randomized controlled trial. J Clin Sleep Med. 2005 Oct 15;1(4):374-80.
114. Coruzzi P, Gualerzi M, Bernkopf E, Brambilla L, Brambilla V, Broia V, et al. Autonomic cardiac modulation in obstructive sleep apnea:
effect of an oral jaw-positioning appliance. Chest. 2006 Nov;130(5):1362-8.
115. Dort LC, Hadjuk E, Remmers JE. Mandibular advancement and obstructive sleep apnoea: a method for determining effective mandibular
protrusion. Eur Respir J. 2006 May;27(5):1003-9.
116. Ng AT, Qian J, Cistulli PA. Oropharyngeal collapse predicts treatment response with oral appliance therapy in obstructive sleep apnea.
Sleep. 2006 May 1;29(5):666-71.
117. De Backer JW, Vanderveken OM, Vos WG, Devolder A, Verhulst SL, Verbraecken JA, et al. Functional imaging using computational fluid
dynamics to predict treatment success of mandibular advancement devices in sleep-disordered breathing. J Biomech. 2007;40(16):3708-14.
118. Itzhaki S, Dorchin H, Clark G, Lavie L, Lavie P, Pillar G. The effects of 1-year treatment with a herbst mandibular advancement splint on
obstructive sleep apnea, oxidative stress, and endothelial function. Chest. 2007 Mar;131(3):740-9.
119. Hoekema A, Stegenga B, Bakker M, Brouwer WH, de Bont LG, Wijkstra PJ, et al. Simulated driving in obstructive sleep apnoeahypopnoea; effects of oral appliances and continuous positive airway pressure. Sleep Breath. 2007 a Sep;11(3):129-38.
120. Hoekema A, Stel AL, Stegenga B, van der Hoeven JH, Wijkstra PJ, van Driel MF, et al. Sexual function and obstructive sleep apneahypopnea: a randomized clinical trial evaluating the effects of oral-appliance and continuous positive airway pressure therapy. J Sex Med. 2007 b
Jul;4(4 Pt 2):1153-62.
121. Zeng B, Ng AT, Darendeliler MA, Petocz P, Cistulli PA. Use of flow-volume curves to predict oral appliance treatment outcome in
obstructive sleep apnea. Am J Respir Crit Care Med. 2007 Apr 1;175(7):726-30.
122. Vanderveken OM, Devolder A, Marklund M, Boudewyns AN, Braem MJ, Okkerse W, et al. Comparison of a custom-made and a
thermoplastic oral appliance for the treatment of mild sleep apnea. Am J Respir Crit Care Med. 2008 Jul 15;178(2):197-202.
123. Hoekema A, Voors AA, Wijkstra PJ, Stegenga B, van der Hoeven JH, Tol CG, et al. Effects of oral appliances and CPAP on the left
ventricle and natriuretic peptides. Int J Cardiol. 2008b Aug 18;128(2):232-9.
124. Hoekema A, Stegenga B, Wijkstra PJ, van der Hoeven JH, Meinesz AF, de Bont LG. Obstructive sleep apnea therapy. J Dent Res. 2008a
Sep;87(9):882-7.
125. Petri N, Svanholt P, Solow B, Wildschiodtz G, Winkel P. Mandibular advancement appliance for obstructive sleep apnoea: results of a
randomised placebo controlled trial using parallel group design. J Sleep Res. 2008 Jun;17(2):221-9.
126. Zeng B, Ng AT, Qian J, Petocz P, Darendeliler MA, Cistulli PA. Influence of nasal resistance on oral appliance treatment outcome in
obstructive sleep apnea. Sleep. 2008 Apr 1;31(4):543-7.
127. Gauthier L, Laberge L, Beaudry M, Laforte M, Rompre PH, Lavigne GJ. Efficacy of two mandibular advancement appliances in the
management of snoring and mild-moderate sleep apnea: a cross-over randomized study. Sleep Med. 2009 Mar;10(3):329-36.
215
128. Aarab G, Lobbezoo F, Hamburger HL, Naeije M. Effects of an oral appliance with different mandibular protrusion positions at a constant
vertical dimension on obstructive sleep apnea. Clin Oral Investig. 2009 Jun 18.
129. Trzepizur W, Gagnadoux F, Abraham P, Rousseau P, Meslier N, Saumet JL, et al. Microvascular endothelial function in obstructive sleep
apnea: Impact of continuous positive airway pressure and mandibular advancement. Sleep Med. 2009 Aug;10(7):746-52.
130. Gagnadoux F, Fleury B, Vielle B, Petelle B, Meslier N, N'Guyen XL, et al. Titrated mandibular advancement versus positive airway
pressure for sleep apnoea. Eur Respir J. 2009 Oct;34(4):914-20.
131. Ghazal A, Sorichter S, Jonas I, Rose EC. A randomized prospective long-term study of two oral appliances for sleep apnoea treatment. J
Sleep Res. 2009 Sep;18(3):321-8.
132. Chan AS, Lee RW, Srinivasan VK, Darendeliler MA, Grunstein RR, Cistulli PA. Nasopharyngoscopic evaluation of oral appliance therapy
for obstructive sleep apnoea. Eur Respir J. 2009 Sep 24.
133. Tsuiki S, Kobayashi M, Namba K, Oka Y, Komada Y, Kagimura T, et al. Optimal positive airway pressure predicts oral appliance response
to sleep apnoea. Eur Respir J. 2009 Oct 19.
134. Barthlen GM, Brown LK, Wiland MR, Sadeh JS, Patwari J, Zimmerman M. Comparison of three oral appliances for treatment of severe
obstructive sleep apnea syndrome. Sleep Med. 2000 Oct 1;1(4):299-305.
135. Higurashi N, Kikuchi M, Miyazaki S, Itasaka Y. Effectiveness of a tongue-retaining device. Psychiatry Clin Neurosci. 2002 Jun;56(3):331-2.
136. Kingshott RN, Jones DR, Taylor DR, Robertson CJ. The efficacy of a novel tongue-stabilizing device on polysomnographic variables in
sleep-disordered breathing: a pilot study. Sleep Breath. 2002 Jun;6(2):69-76.
137. Dort L, Brant R. A randomized, controlled, crossover study of a noncustomized tongue retaining device for sleep disordered breathing. Sleep
Breath. 2008 Nov;12(4):369-73.
138. Deane SA, Cistulli PA, Ng AT, Zeng B, Petocz P, Darendeliler MA. Comparison of mandibular advancement splint and tongue stabilizing
device in obstructive sleep apnea: a randomized controlled trial. Sleep. 2009 May 1;32(5):648-53.
139. Miki H, Hida W, Chonan T, Kikuchi Y, Takishima T. Effects of submental electrical stimulation during sleep on upper airway patency in
patients with obstructive sleep apnea. Am Rev Respir Dis. 1989 Nov;140(5):1285-9.
140. Guilleminault C, Powell N, Bowman B, Stoohs R. The effect of electrical stimulation on obstructive sleep apnea syndrome. Chest. 1995
Jan;107(1):67-73.
141. Oliven A, Schnall RP, Pillar G, Gavriely N, Odeh M. Sublingual electrical stimulation of the tongue during wakefulness and sleep. Respir
Physiol. 2001 Sep;127(2-3):217-26.
142. Eisele DW, Smith PL, Alam DS, Schwartz AR. Direct hypoglossal nerve stimulation in obstructive sleep apnea. Arch Otolaryngol Head
Neck Surg. 1997 Jan;123(1):57-61.
143. Schwartz AR, Eisele DW, Hari A, Testerman R, Erickson D, Smith PL. Electrical stimulation of the lingual musculature in obstructive sleep
apnea. J Appl Physiol. 1996 Aug;81(2):643-52.
216
144. Schnall RP, Pillar G, Kelsen SG, Oliven A. Dilatory effects of upper airway muscle contraction induced by electrical stimulation in awake
humans. J Appl Physiol. 1995 May;78(5):1950-6.
145. Decker MJ, Haaga J, Arnold JL, Atzberger D, Strohl KP. Functional electrical stimulation and respiration during sleep. J Appl Physiol. 1993
Sep;75(3):1053-61.
146. Mann EA, Burnett T, Cornell S, Ludlow CL. The effect of neuromuscular stimulation of the genioglossus on the hypopharyngeal airway.
Laryngoscope. 2002 Feb;112(2):351-6.
147. Schwartz AR, Bennett ML, Smith PL, De Backer W, Hedner J, Boudewyns A, et al. Therapeutic electrical stimulation of the hypoglossal
nerve in obstructive sleep apnea. Arch Otolaryngol Head Neck Surg. 2001 Oct;127(10):1216-23.
148. Isono S, Tanaka A, Nishino T. Effects of tongue electrical stimulation on pharyngeal mechanics in anaesthetized patients with obstructive
sleep apnoea. Eur Respir J. 1999 Dec;14(6):1258-65.
149. Randerath WJ, Galetke W, Domanski U, Weitkunat R, Ruhle KH. Tongue-muscle training by intraoral electrical neurostimulation in patients
with obstructive sleep apnea. Sleep. 2004 Mar 15;27(2):254-9.
150. Oliven A, O'Hearn DJ, Boudewyns A, Odeh M, De Backer W, van de Heyning P, et al. Upper airway response to electrical stimulation of
the genioglossus in obstructive sleep apnea. J Appl Physiol. 2003 Nov;95(5):2023-9.
151. Oliven A, Tov N, Geitini L, Steinfeld U, Oliven R, Schwartz AR, et al. Effect of genioglossus contraction on pharyngeal lumen and airflow
in sleep apnoea patients. Eur Respir J. 2007 Oct;30(4):748-58.
152. Atkinson RL, Suratt PM, Wilhoit SC, Recant L. Naloxone improves sleep apnea in obese humans. Int J Obes. 1985;9(4):233-9.
153. Berry RB, Yamaura EM, Gill K, Reist C. Acute effects of paroxetine on genioglossus activity in obstructive sleep apnea. Sleep. 1999 Dec
15;22(8):1087-92.
154. Bortolotti M, Gentilini L, Morselli C, Giovannini M. Obstructive sleep apnoea is improved by a prolonged treatment of gastrooesophageal
reflux with omeprazole. Dig Liver Dis. 2006 Feb;38(2):78-81.
155. Brownell LG, West P, Sweatman P, Acres JC, Kryger MH. Protriptyline in obstructive sleep apnea: a double-blind trial. N Engl J Med. 1982
Oct 21;307(17):1037-42.
156. Carley DW, Olopade C, Ruigt GS, Radulovacki M. Efficacy of mirtazapine in obstructive sleep apnea syndrome. Sleep. 2007 Jan
1;30(1):35-41.
157. Cook WR, Benich JJ, Wooten SA. Indices of severity of obstructive sleep apnea syndrome do not change during medroxyprogesterone
acetate therapy. Chest. 1989 Aug;96(2):262-6.
158. Diamond E, Druz W, D'souza V, Sharp JT. Effect of naloxone in obstructive sleep apnea. Am Rev Respir Dis. 1982;125:235.
159. Espinoza H, Antic R, Thornton AT, McEvoy RD. The effects of aminophylline on sleep and sleep-disordered breathing in patients with
obstructive sleep apnea syndrome. Am Rev Respir Dis. 1987 Jul;136(1):80-4.
160. Ferber C, Duclaux R, Mouret J. Naltrexone improves blood gas patterns in obstructive sleep apnoea syndrome through its influence on sleep.
J Sleep Res. 1993 Sep;2(3):149-55.
217
161. Grote L, Heitmann J, Penzel T, Cassel W, Ploch T, Peter JH, et al. Arterial hypertension and sleep apnoea: effect of the angiotensinconverting enzyme (ACE) inhibitor cilazapril on continuously measured blood pressure during sleep and wakefulness. J Sleep Res. 1995
Jun;4(S1):112-6.
162. Hedner J, Grunstein R, Eriksson B, Ejnell H. A double-blind, randomized trial of sabeluzole--a putative glutamate antagonist--in obstructive
sleep apnea. Sleep. 1996 May;19(4):287-9.
163. Hedner J, Kraiczi H, Peker Y, Murphy P. Reduction of sleep-disordered breathing after physostigmine. Am J Respir Crit Care Med. 2003
Nov 15;168(10):1246-51.
164. Heitmann J, Grote L, Knaack L, Kohler U, Hinder M, Peter JH. Cardiovascular effects of mibefradil in hypertensive patients with
obstructive sleep apnea. Eur J Clin Pharmacol. 1998 Nov-Dec;54(9-10):691-6.
165. Issa FG. Effect of clonidine in obstructive sleep apnea. Am Rev Respir Dis. 1992 Feb;145(2 Pt 1):435-9.
166. Jokic R, Klimaszewski A, Mink J, Fitzpatrick MF. Surface tension forces in sleep apnea: the role of a soft tissue lubricant: a randomized
double-blind, placebo-controlled trial. Am J Respir Crit Care Med. 1998 May;157(5 Pt 1):1522-5.
167. Kraiczi H, Hedner J, Dahlof P, Ejnell H, Carlson J. Effect of serotonin uptake inhibition on breathing during sleep and daytime symptoms in
obstructive sleep apnea. Sleep. 1999 Feb 1;22(1):61-7.
168. Marshall NS, Yee BJ, Desai AV, Buchanan PR, Wong KK, Crompton R, et al. Two randomized placebo-controlled trials to evaluate the
efficacy and tolerability of mirtazapine for the treatment of obstructive sleep apnea. Sleep. 2008 Jun 1;31(6):824-31.
169. Mendelson WB, Maczaj M, Holt J. Buspirone administration to sleep apnea patients. J Clin Psychopharmacol. 1991 Feb;11(1):71-2.
170. Mulloy E, McNicholas WT. Theophylline in obstructive sleep apnea. A double-blind evaluation. Chest. 1992 Mar;101(3):753-7.
171. Rasche K, Duchna HW, Lauer J, Orth M, Kotterba S, Bauer TT, et al. Obstructive Sleep Apnea and Hypopnea Efficacy and Safety of a
Long-Acting beta2-Agonist. Sleep Breath. 1999;3(4):125-30.
172. Stepanski EJ, Conway WA, Young DK, Zorick FJ, Wittig RM, Roth T. A double-blind trial of protriptyline in the treatment of sleep apnea
syndrome. Henry Ford Hosp Med J. 1988;36(1):5-8.
173. Stradling J, Smith D, Radulovacki M, Carley D. Effect of ondansetron on moderate obstructive sleep apnoea, a single night, placebocontrolled trial. J Sleep Res. 2003 Jun;12(2):169-70.
174. Suratt PM, Wilhoit SC, Brown ED, Findley LJ. Effect of doxapram on obstructive sleep apnea. Bull Eur Physiopathol Respir. 1986 MarApr;22(2):127-31.
175. Whyte KF, Gould GA, Airlie MA, Shapiro CM, Douglas NJ. Role of protriptyline and acetazolamide in the sleep apnea/hypopnea syndrome.
Sleep. 1988 Oct;11(5):463-72.
176. Guimaraes KC, Drager LF, Genta PR, Marcondes BF, Lorenzi-Filho G. Effects of oropharyngeal exercises on patients with moderate
obstructive sleep apnea syndrome. Am J Respir Crit Care Med. 2009 May 15;179(10):962-6.
177. Puhan MA, Suarez A, Lo Cascio C, Zahn A, Heitz M, Braendli O. Didgeridoo playing as alternative treatment for obstructive sleep apnoea
syndrome: randomised controlled trial. BMJ. 2006 Feb 4;332(7536):266-70.
218
178. McLean HA, Urton AM, Driver HS, Tan AK, Day AG, Munt PW, et al. Effect of treating severe nasal obstruction on the severity of
obstructive sleep apnoea. Eur Respir J. 2005 Mar;25(3):521-7.
179. Todorova A, Schellenberg R, Hofmann HC, Dimpfel W. Effect of the external nasal dilator Breathe Right on snoring. Eur J Med Res. 1998
Aug 18;3(8):367-79.
180. Ulfberg J, Fenton G. Effect of Breathe Right nasal strip on snoring. Rhinology. 1997 Jun;35(2):50-2.
181. Liistro G, Rombaux P, Dury M, Pieters T, Aubert G, Rodenstein DO. Effects of Breathe Right on snoring: a polysomnographic study. Respir
Med. 1998 Aug;92(8):1076-8.
182. Wenzel M, Schonhofer B, Siemon K, Kohler D. [Nasal strips without effect on obstructive sleep apnea and snoring]. Pneumologie. 1997
Dec;51(12):1108-10.
183. Bahammam AS, Tate R, Manfreda J, Kryger MH. Upper airway resistance syndrome: effect of nasal dilation, sleep stage, and sleep position.
Sleep. 1999 Aug 1;22(5):592-8.
184. Gosepath J, Amedee RG, Romantschuck S, Mann WJ. Breathe Right nasal strips and the respiratory disturbance index in sleep related
breathing disorders. Am J Rhinol. 1999 Sep-Oct;13(5):385-9.
185. Lorino AM, Lofaso F, Dahan E, Coste A, Harf A, Lorino H. Combined effects of a mechanical nasal dilator and a topical decongestant on
nasal airflow resistance. Chest. 1999 Jun;115(6):1514-8.
186. Metes A, Cole P, Hoffstein V, Miljeteig H. Nasal airway dilation and obstructed breathing in sleep. Laryngoscope. 1992 Sep;102(9):1053-5.
187. Petruson B. Improvement of the nasal airflow by the nasal dilator Nozovent. Rhinology. 1988 Dec;26(4):289-92.
188. Hoffstein V, Mateika S, Metes A. Effect of nasal dilation on snoring and apneas during different stages of sleep. Sleep. 1993 Jun;16(4):3605.
189. Shinkawa A, Sakai M. A clinical study of the nasal dilator Nozovent in Japanese subjects. Tokai J Exp Clin Med. 1998 Mar;23(1):13-7.
190. Hoijer U, Ejnell H, Hedner J, Petruson B, Eng LB. The effects of nasal dilation on snoring and obstructive sleep apnea. Arch Otolaryngol
Head Neck Surg. 1992 Mar;118(3):281-4.
191. Schonhofer B, Franklin KA, Brunig H, Wehde H, Kohler D. Effect of nasal-valve dilation on obstructive sleep apnea. Chest. 2000
Sep;118(3):587-90.
192. Rubin AH, Eliaschar I, Joachim Z, Alroy G, Lavie P. Effects of nasal surgery and tonsillectomy on sleep apnea. Bull Eur Physiopathol
Respir. 1983 Nov-Dec;19(6):612-5.
193. Caldarelli DD, Cartwright RD, Lilie JK. Obstructive sleep apnea: variations in surgical management. Laryngoscope. 1985 Sep;95(9 Pt
1):1070-3.
194. Dayal VS, Phillipson EA. Nasal surgery in the management of sleep apnea. Ann Otol Rhinol Laryngol. 1985 Nov-Dec;94(6 Pt 1):550-4.
195. Series F, St Pierre S, Carrier G. Effects of surgical correction of nasal obstruction in the treatment of obstructive sleep apnea. Am Rev Respir
Dis. 1992 Nov;146(5 Pt 1):1261-5.
219
196. Series F, St Pierre S, Carrier G. Surgical correction of nasal obstruction in the treatment of mild sleep apnoea: importance of cephalometry in
predicting outcome. Thorax. 1993 Apr;48(4):360-3.
197. Friedman M, Tanyeri H, Lim JW, Landsberg R, Vaidyanathan K, Caldarelli D. Effect of improved nasal breathing on obstructive sleep
apnea. Otolaryngol Head Neck Surg. 2000 Jan;122(1):71-4.
198. Verse T, Maurer JT, Pirsig W. Effect of nasal surgery on sleep-related breathing disorders. Laryngoscope. 2002 Jan;112(1):64-8.
199. Kalam I. Objective assessment of nasal obstruction in snoring and obstructive sleep apnea patients: experience of a Police Authority
Hospital. Ann Saudi Med. 2002 May-Jul;22(3-4):158-62.
200. Kim ST, Choi JH, Jeon HG, Cha HE, Kim DY, Chung YS. Polysomnographic effects of nasal surgery for snoring and obstructive sleep
apnea. Acta Otolaryngol. 2004 Apr;124(3):297-300.
201. Nakata S, Noda A, Yagi H, Yanagi E, Mimura T, Okada T, et al. Nasal resistance for determinant factor of nasal surgery in CPAP failure
patients with obstructive sleep apnea syndrome. Rhinology. 2005 Dec;43(4):296-9.
202. Virkkula P, Bachour A, Hytonen M, Salmi T, Malmberg H, Hurmerinta K, et al. Snoring is not relieved by nasal surgery despite
improvement in nasal resistance. Chest. 2006 Jan;129(1):81-7.
203. Koutsourelakis I, Georgoulopoulos G, Perraki E, Vagiakis E, Roussos C, Zakynthinos SG. Randomised trial of nasal surgery for fixed nasal
obstruction in obstructive sleep apnoea. Eur Respir J. 2008 Jan;31(1):110-7.
204. Nakata S, Noda A, Yasuma F, Morinaga M, Sugiura M, Katayama N, et al. Effects of nasal surgery on sleep quality in obstructive sleep
apnea syndrome with nasal obstruction. Am J Rhinol. 2008 Jan-Feb;22(1):59-63.
205. Li HY, Lin Y, Chen NH, Lee LA, Fang TJ, Wang PC. Improvement in quality of life after nasal surgery alone for patients with obstructive
sleep apnea and nasal obstruction. Arch Otolaryngol Head Neck Surg. 2008 Apr;134(4):429-33.
206. Li H, Lee L, PC W, TJ F, NH C. Can nasal surgery improve obstructive sleep apnea: subjective or objective? Am J Rhinol Allergy.
2009;Nov-Dec(23(6)):e51-5.
207. Brouillette RT, Manoukian JJ, Ducharme FM, Oudjhane K, Earle LG, Ladan S, et al. Efficacy of fluticasone nasal spray for pediatric
obstructive sleep apnea. J Pediatr. 2001 Jun;138(6):838-44.
208. Kiely JL, Nolan P, McNicholas WT. Intranasal corticosteroid therapy for obstructive sleep apnoea in patients with co-existing rhinitis.
Thorax. 2004 Jan;59(1):50-5.
209. Mansfield LE, Diaz G, Posey CR, Flores-Neder J. Sleep disordered breathing and daytime quality of life in children with allergic rhinitis
during treatment with intranasal budesonide. Ann Allergy Asthma Immunol. 2004 Feb;92(2):240-4.
210. Alexopoulos EI, Kaditis AG, Kalampouka E, Kostadima E, Angelopoulos NV, Mikraki V, et al. Nasal corticosteroids for children with
snoring. Pediatr Pulmonol. 2004 Aug;38(2):161-7.
211. Kheirandish L, Goldbart AD, Gozal D. Intranasal steroids and oral leukotriene modifier therapy in residual sleep-disordered breathing after
tonsillectomy and adenoidectomy in children. Pediatrics. 2006 Jan;117(1):e61-6.
220
212. Kheirandish-Gozal L, Sans Capdevila O, Kheirandish E, Gozal D. Elevated serum aminotransferase levels in children at risk for obstructive
sleep apnea. Chest. 2008 Jan;133(1):92-9.
213. Orr WC, Martin RJ. Obstructive sleep apnea associated with tonsillar hypertrophy in adults. Arch Intern Med. 1981 Jul;141(8):990-2.
214. Moser RJ, 3rd, Rajagopal KR. Obstructive sleep apnea in adults with tonsillar hypertrophy. Arch Intern Med. 1987 Jul;147(7):1265-7.
215. Houghton DJ, Camilleri AE, Stone P. Adult obstructive sleep apnoea syndrome and tonsillectomy. J Laryngol Otol. 1997 Sep;111(9):82932.
216. Miyazaki S, Itasaka Y, Tada H, Ishikawa K, Togawa K. Effectiveness of tonsillectomy in adult sleep apnea syndrome. Psychiatry Clin
Neurosci. 1998 Apr;52(2):222-3.
217. Verse T, Kroker BA, Pirsig W, Brosch S. Tonsillectomy as a treatment of obstructive sleep apnea in adults with tonsillar hypertrophy.
Laryngoscope. 2000 Sep;110(9):1556-9.
218. Martinho FL, Zonato AI, Bittencourt LR, Soares MC, Silva RF, Gregorio LC, et al. Obese obstructive sleep apnea patients with tonsil
hypertrophy submitted to tonsillectomy. Braz J Med Biol Res. 2006 Aug;39(8):1137-42.
219. Nakata S, Noda A, Yanagi E, Suzuki K, Yamamoto H, Nakashima T. Tonsil size and body mass index are important factors for efficacy of
simple tonsillectomy in obstructive sleep apnoea syndrome. Clin Otolaryngol. 2006 Feb;31(1):41-5.
220. Nakata S, Miyazaki S, Ohki M, Morinaga M, Noda A, Sugiura T, et al. Reduced nasal resistance after simple tonsillectomy in patients with
obstructive sleep apnea. Am J Rhinol. 2007 Mar-Apr;21(2):192-5.
221. Frank Y, Kravath RE, Pollak CP, Weitzman ED. Obstructive sleep apnea and its therapy: clinical and polysomnographic manifestations.
Pediatrics. 1983 May;71(5):737-42.
222. Stradling JR, Thomas G, Warley AR, Williams P, Freeland A. Effect of adenotonsillectomy on nocturnal hypoxaemia, sleep disturbance, and
symptoms in snoring children. Lancet. 1990 Feb 3;335(8684):249-53.
223. Zucconi M, Strambi LF, Pestalozza G, Tessitore E, Smirne S. Habitual snoring and obstructive sleep apnea syndrome in children: effects of
early tonsil surgery. Int J Pediatr Otorhinolaryngol. 1993 Apr;26(3):235-43.
224. Suen JS, Arnold JE, Brooks LJ. Adenotonsillectomy for treatment of obstructive sleep apnea in children. Arch Otolaryngol Head Neck Surg.
1995 May;121(5):525-30.
225. Ali NJ, Pitson D, Stradling JR. Sleep disordered breathing: effects of adenotonsillectomy on behaviour and psychological functioning. Eur J
Pediatr. 1996 Jan;155(1):56-62.
226. Helfaer MA, McColley SA, Pyzik PL, Tunkel DE, Nichols DG, Baroody FM, et al. Polysomnography after adenotonsillectomy in mild
pediatric obstructive sleep apnea. Crit Care Med. 1996 Aug;24(8):1323-7.
227. Nishimura T, Morishima N, Hasegawa S, Shibata N, Iwanaga K, Yagisawa M. Effect of surgery on obstructive sleep apnea. Acta
Otolaryngol Suppl. 1996;523:231-3.
228. Wiet GJ, Bower C, Seibert R, Griebel M. Surgical correction of obstructive sleep apnea in the complicated pediatric patient documented by
polysomnography. Int J Pediatr Otorhinolaryngol. 1997 Aug 20;41(2):133-43.
221
229. Shintani T, Asakura K, Kataura A. The effect of adenotonsillectomy in children with OSA. Int J Pediatr Otorhinolaryngol. 1998 Jun
1;44(1):51-8.
230. Bar A, Tarasiuk A, Segev Y, Phillip M, Tal A. The effect of adenotonsillectomy on serum insulin-like growth factor-I and growth in children
with obstructive sleep apnea syndrome. J Pediatr. 1999 Jul;135(1):76-80.
231. Nieminen P, Tolonen U, Lopponen H. Snoring and obstructive sleep apnea in children: a 6-month follow-up study. Arch Otolaryngol Head
Neck Surg. 2000 Apr;126(4):481-6.
232. Jain A, Sahni JK. Polysomnographic studies in children undergoing adenoidectomy and/or tonsillectomy. J Laryngol Otol. 2002
Sep;116(9):711-5.
233. Mora R, Salami A, Passali FM, Mora F, Cordone MP, Ottoboni S, et al. OSAS in children. Int J Pediatr Otorhinolaryngol. 2003 Dec;67
Suppl 1:S229-31.
234. Tal A, Bar A, Leiberman A, Tarasiuk A. Sleep characteristics following adenotonsillectomy in children with obstructive sleep apnea
syndrome. Chest. 2003 Sep;124(3):948-53.
235. Guilleminault C, Li KK, Khramtsov A, Pelayo R, Martinez S. Sleep disordered breathing: surgical outcomes in prepubertal children.
Laryngoscope. 2004 Jan;114(1):132-7.
236. Mitchell RB, Kelly J. Outcome of adenotonsillectomy for severe obstructive sleep apnea in children. Int J Pediatr Otorhinolaryngol. 2004
Nov;68(11):1375-9.
237. Mitchell RB, Kelly J. Adenotonsillectomy for obstructive sleep apnea in obese children. Otolaryngol Head Neck Surg. 2004 Jul;131(1):1048.
238. Mitchell RB, Kelly J. Outcome of adenotonsillectomy for obstructive sleep apnea in children under 3 years. Otolaryngol Head Neck Surg.
2005 May;132(5):681-4.
239. Chervin RD, Ruzicka DL, Giordani BJ, Weatherly RA, Dillon JE, Hodges EK, et al. Sleep-disordered breathing, behavior, and cognition in
children before and after adenotonsillectomy. Pediatrics. 2006 Apr;117(4):e769-78.
240. Li HY, Huang YS, Chen NH, Fang TJ, Lee LA. Impact of adenotonsillectomy on behavior in children with sleep-disordered breathing.
Laryngoscope. 2006c Jul;116(7):1142-7.
241. Tauman R, Gulliver TE, Krishna J, Montgomery-Downs HE, O'Brien LM, Ivanenko A, et al. Persistence of obstructive sleep apnea
syndrome in children after adenotonsillectomy. J Pediatr. 2006 Dec;149(6):803-8.
242. Pavone M, Paglietti MG, Petrone A, Crino A, De Vincentiis GC, Cutrera R. Adenotonsillectomy for obstructive sleep apnea in children with
Prader-Willi syndrome. Pediatr Pulmonol. 2006 Jan;41(1):74-9.
243. Guilleminault C, Huang YS, Glamann C, Li K, Chan A. Adenotonsillectomy and obstructive sleep apnea in children: a prospective survey.
Otolaryngol Head Neck Surg. 2007 Feb;136(2):169-75.
244. Mitchell RB. Adenotonsillectomy for obstructive sleep apnea in children: outcome evaluated by pre- and postoperative polysomnography.
Laryngoscope. 2007 Oct;117(10):1844-54.
222
245. Mitchell RB, Kelly J. Outcome of adenotonsillectomy for obstructive sleep apnea in obese and normal-weight children. Otolaryngol Head
Neck Surg. 2007 Jul;137(1):43-8.
246. Dillon JE, Blunden S, Ruzicka DL, Guire KE, Champine D, Weatherly RA, et al. DSM-IV diagnoses and obstructive sleep apnea in children
before and 1 year after adenotonsillectomy. J Am Acad Child Adolesc Psychiatry. 2007 Nov;46(11):1425-36.
247. Gozal D, Kheirandish-Gozal L, Serpero LD, Sans Capdevila O, Dayyat E. Obstructive sleep apnea and endothelial function in school-aged
nonobese children: effect of adenotonsillectomy. Circulation. 2007 Nov 13;116(20):2307-14.
248. Guilleminault C, Huang YS, Chan A, Hagen CC. Cyanotic breath-holding spells in children respond to adenotonsillectomy for sleepdisordered breathing. J Sleep Res. 2007 Dec;16(4):406-13.
249. Gozal D, Capdevila OS, Kheirandish-Gozal L. Metabolic alterations and systemic inflammation in obstructive sleep apnea among nonobese
and obese prepubertal children. Am J Respir Crit Care Med. 2008 May 15;177(10):1142-9.
250. Walker P, Whitehead B, Gulliver T. Polysomnographic outcome of adenotonsillectomy for obstructive sleep apnea in children under 5 years
old. Otolaryngol Head Neck Surg. 2008 Jul;139(1):83-6.
251. Apostolidou MT, Alexopoulos EI, Chaidas K, Ntamagka G, Karathanasi A, Apostolidis TI, et al. Obesity and persisting sleep apnea after
adenotonsillectomy in Greek children. Chest. 2008 Dec;134(6):1149-55.
252. Guilleminault C, Quo S, Huynh NT, Li K. Orthodontic expansion treatment and adenotonsillectomy in the treatment of obstructive sleep
apnea in prepubertal children. Sleep. 2008 Jul 1;31(7):953-7.
253. Amin R, Anthony L, Somers V, Fenchel M, McConnell K, Jefferies J, et al. Growth velocity predicts recurrence of sleep-disordered
breathing 1 year after adenotonsillectomy. Am J Respir Crit Care Med. 2008 Mar 15;177(6):654-9.
254. de la Chaux R, Klemens C, Patscheider M, Reichel O, Dreher A. Tonsillotomy in the treatment of obstructive sleep apnea syndrome in
children: polysomnographic results. Int J Pediatr Otorhinolaryngol. 2008 Sep;72(9):1411-7.
255. Sullivan S, Li K, Guilleminault C. Nasal obstruction in children with sleep-disordered breathing. Ann Acad Med Singapore. 2008
Aug;37(8):645-8.
256. Tunkel DE, Hotchkiss KS, Carson KA, Sterni LM. Efficacy of powered intracapsular tonsillectomy and adenoidectomy. Laryngoscope.
2008 Jul;118(7):1295-302.
257. Friedman M, Wilson MN, Friedman J, Joseph NJ, Lin HC, Chang HW. Intracapsular coblation tonsillectomy and adenoidectomy for the
treatment of pediatric obstructive sleep apnea/hypopnea syndrome. Otolaryngol Head Neck Surg. 2009 Mar;140(3):358-62.
258. Kohler MJ, Lushington K, van den Heuvel CJ, Martin J, Pamula Y, Kennedy D. Adenotonsillectomy and neurocognitive deficits in children
with Sleep Disordered Breathing. PLoS One. 2009;4(10):e7343.
259. Nelson LM. Radiofrequency treatment for obstructive tonsillar hypertrophy. Arch Otolaryngol Head Neck Surg. 2000 Jun;126(6):736-40.
260. Nelson LM. Temperature-controlled radiofrequency tonsil reduction: extended follow-up. Otolaryngol Head Neck Surg. 2001a
Nov;125(5):456-61.
223
261. Friedman M, LoSavio P, Ibrahim H, Ramakrishnan V. Radiofrequency tonsil reduction: safety, morbidity, and efficacy. Laryngoscope.
2003a May;113(5):882-7.
262. Ericsson E, Ledin T, Hultcrantz E. Long-term improvement of quality of life as a result of tonsillotomy (with radiofrequency technique) and
tonsillectomy in youths. Laryngoscope. 2007a Jul;117(7):1272-9.
263. Berger G, Stein G, Ophir D, Finkelstein Y. Is there a better way to do laser-assisted uvulopalatoplasty? Arch Otolaryngol Head Neck Surg.
2003 Apr;129(4):447-53.
264. Shin SH, Ye MK, Kim CG. Modified uvulopalatopharyngoplasty for the treatment of obstructive sleep apnea-hypopnea syndrome: resection
of the musculus uvulae. Otolaryngol Head Neck Surg. 2009 Jun;140(6):924-9.
265. Pang KP, Woodson BT. Expansion sphincter pharyngoplasty: a new technique for the treatment of obstructive sleep apnea. Otolaryngol
Head Neck Surg. 2007 Jul;137(1):110-4.
266. Li HY, Wang PC, Lee LA, Chen NH, Fang TJ. Prediction of uvulopalatopharyngoplasty outcome: anatomy-based staging system versus
severity-based staging system. Sleep. 2006a Dec 1;29(12):1537-41.
267. Kinoshita H, Shibano A, Sakoda T, Ikeda H, Iranami H, Hatano Y, et al. Uvulopalatopharyngoplasty decreases levels of C-reactive protein
in patients with obstructive sleep apnea syndrome. Am Heart J. 2006 Oct;152(4):692 e1-5.
268. Lee MY, Lin CC, Lee KS, Wang YP, Liaw SF, Chiu CH, et al. Effect of uvulopalatopharyngoplasty on endothelial function in obstructive
sleep apnea. Otolaryngol Head Neck Surg. 2009 Mar;140(3):369-74.
269. Cahali MB, Formigoni GG, Gebrim EM, Miziara ID. Lateral pharyngoplasty versus uvulopalatopharyngoplasty: a clinical,
polysomnographic and computed tomography measurement comparison. Sleep. 2004 Aug 1;27(5):942-50.
270. Kezirian EJ, Goldberg AN. Hypopharyngeal surgery in obstructive sleep apnea: an evidence-based medicine review. Arch Otolaryngol Head
Neck Surg. 2006 Feb;132(2):206-13.
271. Ferguson KA, Heighway K, Ruby RR. A randomized trial of laser-assisted uvulopalatoplasty in the treatment of mild obstructive sleep
apnea. Am J Respir Crit Care Med. 2003 Jan 1;167(1):15-9.
272. Larrosa F, Hernandez L, Morello A, Ballester E, Quinto L, Montserrat JM. Laser-assisted uvulopalatoplasty for snoring: does it meet the
expectations? Eur Respir J. 2004 Jul;24(1):66-70.
273. Brown DJ, Kerr P, Kryger M. Radiofrequency tissue reduction of the palate in patients with moderate sleep-disordered breathing. J
Otolaryngol. 2001 Aug;30(4):193-8.
274. Blumen MB, Dahan S, Fleury B, Hausser-Hauw C, Chabolle F. Radiofrequency ablation for the treatment of mild to moderate obstructive
sleep apnea. Laryngoscope. 2002a Nov;112(11):2086-92.
275. Atef A, Mosleh M, Hesham M, Fathi A, Hassan M, Fawzy M. Radiofrequency vs laser in the management of mild to moderate obstructive
sleep apnoea: does the number of treatment sessions matter? J Laryngol Otol. 2005 Nov;119(11):888-93.
224
276. Bassiouny A, El Salamawy A, Abd El-Tawab M, Atef A. Bipolar radiofrequency treatment for snoring with mild to moderate sleep apnea: a
comparative study between the radiofrequency assisted uvulopalatoplasty technique and the channeling technique. Eur Arch Otorhinolaryngol. 2007
Jun;264(6):659-67.
277. Back LJ, Liukko T, Rantanen I, Peltola JS, Partinen M, Ylikoski J, et al. Radiofrequency surgery of the soft palate in the treatment of mild
obstructive sleep apnea is not effective as a single-stage procedure: A randomized single-blinded placebo-controlled trial. Laryngoscope. 2009
Aug;119(8):1621-7.
278. Hsieh TH, Fang TJ, Li HY, Lee SW. Simultaneous midline laser glossectomy with palatopharyngeal surgery for obstructive sleep apnoea
syndrome. Int J Clin Pract. 2005 Apr;59(4):501-3.
279. Li HY, Wang PC, Hsu CY, Lee SW, Chen NH, Liu SA. Combined nasal-palatopharyngeal surgery for obstructive sleep apnea: simultaneous
or staged? Acta Otolaryngol. 2005a Mar;125(3):298-303.
280. Li HY, Li KK, Chen NH, Wang CJ, Liao YF, Wang PC. Three-dimensional computed tomography and polysomnography findings after
extended uvulopalatal flap surgery for obstructive sleep apnea. Am J Otolaryngol. 2005b Jan-Feb;26(1):7-11.
281. Li HY, Chen NH, Lee LA, Shu YH, Fang TJ, Wang PC. Use of morphological indicators to predict outcomes of palatopharyngeal surgery in
patients with obstructive sleep apnea. ORL J Otorhinolaryngol Relat Spec. 2004a;66(3):119-23.
282. Li HY, Chen NH, Shu YH, Wang PC. Changes in quality of life and respiratory disturbance after extended uvulopalatal flap surgery in
patients with obstructive sleep apnea. Arch Otolaryngol Head Neck Surg. 2004b Feb;130(2):195-200.
283. Li HY, Huang YS, Chen NH, Fang TJ, Liu CY, Wang PC. Mood improvement after surgery for obstructive sleep apnea. Laryngoscope.
2004c Jun;114(6):1098-102.
284. Li HY, Li KK, Chen NH, Wang PC. Modified uvulopalatopharyngoplasty: The extended uvulopalatal flap. Am J Otolaryngol. 2003 SepOct;24(5):311-6.
285. Neruntarat C. Genioglossus advancement and hyoid myotomy under local anesthesia. Otolaryngol Head Neck Surg. 2003a Jul;129(1):85-91.
286. Neruntarat C. Genioglossus advancement and hyoid myotomy: short-term and long-term results. J Laryngol Otol. 2003b Jun;117(6):482-6.
287. Neruntarat C. Hyoid myotomy with suspension under local anesthesia for obstructive sleep apnea syndrome. Eur Arch Otorhinolaryngol.
2003c May;260(5):286-90.
288. Powell N, Riley R, Guilleminault C, Troell R. A reversible uvulopalatal flap for snoring and sleep apnea syndrome. Sleep. 1996
Sep;19(7):593-9.
289. Nordgard S, Stene BK, Skjostad KW. Soft palate implants for the treatment of mild to moderate obstructive sleep apnea. Otolaryngol Head
Neck Surg. 2006b Apr;134(4):565-70.
290. Friedman M, Schalch P, Joseph NJ. Palatal stiffening after failed uvulopalatopharyngoplasty with the Pillar Implant System. Laryngoscope.
2006 Nov;116(11):1956-61.
291. Walker RP, Levine HL, Hopp ML, Greene D, Pang K. Palatal implants: a new approach for the treatment of obstructive sleep apnea.
Otolaryngol Head Neck Surg. 2006 Oct;135(4):549-54.
225
292. Goessler UR, Hein G, Verse T, Stuck BA, Hormann K, Maurer JT. Soft palate implants as a minimally invasive treatment for mild to
moderate obstructive sleep apnea. Acta Otolaryngol. 2007 May;127(5):527-31.
293. Nordgard S, Hein G, Stene BK, Skjostad KW, Maurer JT. One-year results: palatal implants for the treatment of obstructive sleep apnea.
Otolaryngol Head Neck Surg. 2007 May;136(5):818-22.
294. Walker RP, Levine HL, Hopp ML, Greene D. Extended follow-up of palatal implants for OSA treatment. Otolaryngol Head Neck Surg.
2007 Nov;137(5):822-7.
295. Friedman M, Schalch P, Lin HC, Kakodkar KA, Joseph NJ, Mazloom N. Palatal implants for the treatment of snoring and obstructive sleep
apnea/hypopnea syndrome. Otolaryngol Head Neck Surg. 2008 Feb;138(2):209-16.
296. Steward DL, Huntley TC, Woodson BT, Surdulescu V. Palate implants for obstructive sleep apnea: multi-institution, randomized, placebocontrolled study. Otolaryngol Head Neck Surg. 2008 Oct;139(4):506-10.
297. Powell NB, Riley RW, Guilleminault C. Radiofrequency tongue base reduction in sleep-disordered breathing: A pilot study. Otolaryngol
Head Neck Surg. 1999 May;120(5):656-64.
298. Woodson BT, Nelson L, Mickelson S, Huntley T, Sher A. A multi-institutional study of radiofrequency volumetric tissue reduction for
OSAS. Otolaryngol Head Neck Surg. 2001a Oct;125(4):303-11.
299. Stuck BA, Maurer JT, Verse T, Hormann K. Tongue base reduction with temperature-controlled radiofrequency volumetric tissue reduction
for treatment of obstructive sleep apnea syndrome. Acta Otolaryngol. 2002 Jul;122(5):531-6.
300. Li KK, Powell NB, Riley RW, Guilleminault C. Temperature-controlled radiofrequency tongue base reduction for sleep-disordered
breathing: Long-term outcomes. Otolaryngol Head Neck Surg. 2002a Sep;127(3):230-4.
301. Riley RW, Powell NB, Li KK, Weaver EM, Guilleminault C. An adjunctive method of radiofrequency volumetric tissue reduction of the
tongue for OSAS. Otolaryngol Head Neck Surg. 2003 Jul;129(1):37-42.
302. Baisch A, Maurer JT, Hormann K. The effect of hyoid suspension in a multilevel surgery concept for obstructive sleep apnea. Otolaryngol
Head Neck Surg. 2006 May;134(5):856-61.
303. Bowden MT, Kezirian EJ, Utley D, Goode RL. Outcomes of hyoid suspension for the treatment of obstructive sleep apnea. Arch
Otolaryngol Head Neck Surg. 2005 May;131(5):440-5.
304. Dattilo DJ, Drooger SA. Outcome assessment of patients undergoing maxillofacial procedures for the treatment of sleep apnea: comparison
of subjective and objective results. J Oral Maxillofac Surg. 2004 Feb;62(2):164-8.
305. den Herder C, van Tinteren H, de Vries N. Hyoidthyroidpexia: a surgical treatment for sleep apnea syndrome. Laryngoscope. 2005
Apr;115(4):740-5.
306. Hsu PP, Brett RH. Multiple level pharyngeal surgery for obstructive sleep apnoea. Singapore Med J. 2001 Apr;42(4):160-4.
307. Jacobowitz O. Palatal and tongue base surgery for surgical treatment of obstructive sleep apnea: a prospective study. Otolaryngol Head Neck
Surg. 2006 Aug;135(2):258-64.
226
308. Ramirez SG, Loube DI. Inferior sagittal osteotomy with hyoid bone suspension for obese patients with sleep apnea. Arch Otolaryngol Head
Neck Surg. 1996 Sep;122(9):953-7.
309. Richard W, Kox D, den Herder C, van Tinteren H, de Vries N. One stage multilevel surgery (uvulopalatopharyngoplasty, hyoid suspension,
radiofrequent ablation of the tongue base with/without genioglossus advancement), in obstructive sleep apnea syndrome. Eur Arch
Otorhinolaryngol. 2007 Apr;264(4):439-44.
310. Riley RW, Powell NB, Guilleminault C. Obstructive sleep apnea and the hyoid: a revised surgical procedure. Otolaryngol Head Neck Surg.
1994 Dec;111(6):717-21.
311. Riley RW, Powell NB, Guilleminault C. Obstructive sleep apnea syndrome: a review of 306 consecutively treated surgical patients.
Otolaryngol Head Neck Surg. 1993a Feb;108(2):117-25.
312. Riley RW, Powell NB, Guilleminault C. Obstructive sleep apnea syndrome: a surgical protocol for dynamic upper airway reconstruction. J
Oral Maxillofac Surg. 1993b Jul;51(7):742-7; discussion 8-9.
313. Riley RW, Powell NB, Guilleminault C. Maxillofacial surgery and obstructive sleep apnea: a review of 80 patients. Otolaryngol Head Neck
Surg. 1989b Sep;101(3):353-61.
314. Riley RW, Powell NB, Guilleminault C. Inferior mandibular osteotomy and hyoid myotomy suspension for obstructive sleep apnea: a review
of 55 patients. J Oral Maxillofac Surg. 1989a Feb;47(2):159-64.
315. Riley RW, Powell NB, Guilleminault C. Inferior sagittal osteotomy of the mandible with hyoid myotomy-suspension: a new procedure for
obstructive sleep apnea. Otolaryngol Head Neck Surg. 1986 Jun;94(5):589-93.
316. Sorrenti G, Piccin O, Scaramuzzino G, Mondini S, Cirignotta F, Ceroni AR. Tongue base reduction with hyoepiglottoplasty for the treatment
of severe OSA. Acta Otorhinolaryngol Ital. 2004 Aug;24(4):204-10.
317. Stuck BA, Neff W, Hormann K, Verse T, Bran G, Baisch A, et al. Anatomic changes after hyoid suspension for obstructive sleep apnea: an
MRI study. Otolaryngol Head Neck Surg. 2005a Sep;133(3):397-402.
318. Verse T, Baisch A, Maurer JT, Stuck BA, Hormann K. Multilevel surgery for obstructive sleep apnea: short-term results. Otolaryngol Head
Neck Surg. 2006 Apr;134(4):571-7.
319. Yin SK, Yi HL, Lu WY, Guan J, Wu HM, Cao ZY. Genioglossus advancement and hyoid suspension plus uvulopalatopharyngoplasty for
severe OSAHS. Otolaryngol Head Neck Surg. 2007 Apr;136(4):626-31.
320. Fujita S, Woodson BT, Clark JL, Wittig R. Laser midline glossectomy as a treatment for obstructive sleep apnea. Laryngoscope. 1991
Aug;101(8):805-9.
321. Mickelson SA, Rosenthal L. Midline glossectomy and epiglottidectomy for obstructive sleep apnea syndrome. Laryngoscope. 1997
May;107(5):614-9.
322. Andsberg U, Jessen M. Eight years of follow-up--uvulopalatopharyngoplasty combined with midline glossectomy as a treatment for
obstructive sleep apnoea syndrome. Acta Otolaryngol Suppl. 2000;543:175-8.
227
323. Chabolle F, Wagner I, Blumen MB, Sequert C, Fleury B, De Dieuleveult T. Tongue base reduction with hyoepiglottoplasty: a treatment for
severe obstructive sleep apnea. Laryngoscope. 1999 Aug;109(8):1273-80.
324. Sorrenti G, Piccin O, Mondini S, Ceroni AR. One-phase management of severe obstructive sleep apnea: tongue base reduction with
hyoepiglottoplasty plus uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg. 2006 Dec;135(6):906-10.
325. Woodson BT, Fujita S. Clinical experience with lingualplasty as part of the treatment of severe obstructive sleep apnea. Otolaryngol Head
Neck Surg. 1992 Jul;107(1):40-8.
326. Li HY, Wang PC, Hsu CY, Chen NH, Lee LA, Fang TJ. Same-stage palatopharyngeal and hypopharyngeal surgery for severe obstructive
sleep apnea. Acta Otolaryngol. 2004d Sep;124(7):820-6.
327. Djupesland G, Schrader H, Lyberg T, Refsum H, Lilleas F, Godtlibsen OB. Palatopharyngoglossoplasty in the treatment of patients with
obstructive sleep apnea syndrome. Acta Otolaryngol Suppl. 1992;492:50-4.
328. Miljeteig H, Tvinnereim M. Uvulopalatopharyngoglossoplasty (UPPGP) in the treatment of the obstructive sleep apnea syndrome. Acta
Otolaryngol Suppl. 1992;492:86-9.
329. Faye-Lund H, Djupesland G, Lyberg T. Glossopexia--evaluation of a new surgical method for treating obstructive sleep apnea syndrome.
Acta Otolaryngol Suppl. 1992;492:46-9.
330. Woodson BT. A tongue suspension suture for obstructive sleep apnea and snorers. Otolaryngol Head Neck Surg. 2001b Mar;124(3):297303.
331. Woodson BT, Derowe A, Hawke M, Wenig B, Ross EB, Jr., Katsantonis GP, et al. Pharyngeal suspension suture with repose bone screw for
obstructive sleep apnea. Otolaryngol Head Neck Surg. 2000 Mar;122(3):395-401.
332. DeRowe A, Gunther E, Fibbi A, Lehtimaki K, Vahatalo K, Maurer J, et al. Tongue-base suspension with a soft tissue-to-bone anchor for
obstructive sleep apnea: preliminary clinical results of a new minimally invasive technique. Otolaryngol Head Neck Surg. 2000a Jan;122(1):100-3.
333. Thomas AJ, Chavoya M, Terris DJ. Preliminary findings from a prospective, randomized trial of two tongue-base surgeries for sleepdisordered breathing. Otolaryngol Head Neck Surg. 2003 Nov;129(5):539-46.
334. Miller FR, Watson D, Malis D. Role of the tongue base suspension suture with The Repose System bone screw in the multilevel surgical
management of obstructive sleep apnea. Otolaryngol Head Neck Surg. 2002 Apr;126(4):392-8.
335. Terris DJ, Kunda LD, Gonella MC. Minimally invasive tongue base surgery for obstructive sleep apnoea. J Laryngol Otol. 2002b
Sep;116(9):716-21.
336. Sorrenti G, Piccin O, Latini G, Scaramuzzino G, Mondini S, Rinaldi Ceroni A. Tongue base suspension technique in obstructive sleep apnea:
personal experience. Acta Otorhinolaryngol Ital. 2003 Aug;23(4):274-80.
337. Vicente E, Marin JM, Carrizo S, Naya MJ. Tongue-base suspension in conjunction with uvulopalatopharyngoplasty for treatment of severe
obstructive sleep apnea: long-term follow-up results. Laryngoscope. 2006 Jul;116(7):1223-7.
338. Kühnel TS, Schurr C, Wagner B, Geisler P. Morphological changes of the posterior airway space after tongue base suspension.
Laryngoscope. 2005a Mar;115(3):475-80.
228
339. Omur M, Ozturan D, Elez F, Unver C, Derman S. Tongue base suspension combined with UPPP in severe OSA patients. Otolaryngol Head
Neck Surg. 2005 Aug;133(2):218-23.
340. Santos Junior JF, Abrahao M, Gregorio LC, Zonato AI, Gumieiro EH. Genioplasty for genioglossus muscle advancement in patients with
obstructive sleep apnea-hypopnea syndrome and mandibular retrognathia. Braz J Otorhinolaryngol. 2007 Jul-Aug;73(4):480-6.
341. Foltan R, Hoffmannova J, Pretl M, Donev F, Vlk M. Genioglossus advancement and hyoid myotomy in treating obstructive sleep apnoea
syndrome - A follow-up study. J Craniomaxillofac Surg. 2007 Jun-Jul;35(4-5):246-51.
342. Liu SA, Li HY, Tsai WC, Chang KM. Associated factors to predict outcomes of uvulopharyngopalatoplasty plus genioglossal advancement
for obstructive sleep apnea. Laryngoscope. 2005 Nov;115(11):2046-50.
343. Miller FR, Watson D, Boseley M. The role of the Genial Bone Advancement Trephine system in conjunction with
uvulopalatopharyngoplasty in the multilevel management of obstructive sleep apnea. Otolaryngol Head Neck Surg. 2004 Jan;130(1):73-9.
344. Neruntarat C. Genioglossus advancement and hyoid myotomy: short-term and long-term results. J Laryngol Otol. 2003 Jun;117(6):482-6.
345. Hendler BH, Costello BJ, Silverstein K, Yen D, Goldberg A. A protocol for uvulopalatopharyngoplasty, mortised genioplasty, and
maxillomandibular advancement in patients with obstructive sleep apnea: an analysis of 40 cases. J Oral Maxillofac Surg. 2001 Aug;59(8):892-7;
discussion 8-9.
346. Waite PD, Wooten V, Lachner J, Guyette RF. Maxillomandibular advancement surgery in 23 patients with obstructive sleep apnea
syndrome. J Oral Maxillofac Surg. 1989 Dec;47(12):1256-61; discussion 62.
347. Hochban W, Brandenburg U, Peter JH. Surgical treatment of obstructive sleep apnea by maxillomandibular advancement. Sleep. 1994
Oct;17(7):624-9.
348. Prinsell JR. Maxillomandibular advancement surgery in a site-specific treatment approach for obstructive sleep apnea in 50 consecutive
patients. Chest. 1999 Dec;116(6):1519-29.
349. Li KK, Powell NB, Riley RW, Troell RJ, Guilleminault C. Long-Term Results of Maxillomandibular Advancement Surgery. Sleep Breath.
2000;4(3):137-40.
350. Wagner I, Coiffier T, Sequert C, Lachiver X, Fleury B, Chabolle F. [Surgical treatment of severe sleep apnea syndrome by
maxillomandibular advancing or mental tranposition]. Ann Otolaryngol Chir Cervicofac. 2000 Jun;117(3):137-46.
351. Bettega G, Pepin JL, Veale D, Deschaux C, Raphael B, Levy P. Obstructive sleep apnea syndrome. fifty-one consecutive patients treated by
maxillofacial surgery. Am J Respir Crit Care Med. 2000 Aug;162(2 Pt 1):641-9.
352. Goh YH, Lim KA. Modified maxillomandibular advancement for the treatment of obstructive sleep apnea: a preliminary report.
Laryngoscope. 2003 Sep;113(9):1577-82.
353. Smatt Y, Ferri J. Retrospective study of 18 patients treated by maxillomandibular advancement with adjunctive procedures for obstructive
sleep apnea syndrome. J Craniofac Surg. 2005 Sep;16(5):770-7.
229
354. Dekeister C, Lacassagne L, Tiberge M, Montemayor T, Migueres M, Paoli JR. [Mandibular advancement surgery in patients with severe
obstructive sleep apnea uncontrolled by continuous positive airway pressure. A retrospective review of 25 patients between 1998 and 2004]. Rev
Mal Respir. 2006 Nov;23(5 Pt 1):430-7.
355. Hochban W, Conradt R, Brandenburg U, Heitmann J, Peter JH. Surgical maxillofacial treatment of obstructive sleep apnea. Plast Reconstr
Surg. 1997 Mar;99(3):619-26; discussion 27-8.
356. Cohen SR, Simms C, Burstein FD. Mandibular distraction osteogenesis in the treatment of upper airway obstruction in children with
craniofacial deformities. Plast Reconstr Surg. 1998b Feb;101(2):312-8.
357. Li KK, Powell NB, Riley RW, Guilleminault C. Distraction osteogenesis in adult obstructive sleep apnea surgery: a preliminary report. J
Oral Maxillofac Surg. 2002b Jan;60(1):6-10.
358. Wang X, Wang XX, Liang C, Yi B, Lin Y, Li ZL. Distraction osteogenesis in correction of micrognathia accompanying obstructive sleep
apnea syndrome. Plast Reconstr Surg. 2003 Nov;112(6):1549-57; discussion 58-9.
359. Monasterio FO, Drucker M, Molina F, Ysunza A. Distraction osteogenesis in Pierre Robin sequence and related respiratory problems in
children. J Craniofac Surg. 2002 Jan;13(1):79-83; discussion 4.
360. Wittenborn W, Panchal J, Marsh JL, Sekar KC, Gurley J. Neonatal distraction surgery for micrognathia reduces obstructive apnea and the
need for tracheotomy. J Craniofac Surg. 2004 Jul;15(4):623-30.
361. Steinbacher DM, Kaban LB, Troulis MJ. Mandibular advancement by distraction osteogenesis for tracheostomy-dependent children with
severe micrognathia. J Oral Maxillofac Surg. 2005 Aug;63(8):1072-9.
362. Denny AD, Talisman R, Hanson PR, Recinos RF. Mandibular distraction osteogenesis in very young patients to correct airway obstruction.
Plast Reconstr Surg. 2001 Aug;108(2):302-11.
363. Rachmiel A, Aizenbud D, Pillar G, Srouji S, Peled M. Bilateral mandibular distraction for patients with compromised airway analyzed by
three-dimensional CT. Int J Oral Maxillofac Surg. 2005 Jan;34(1):9-18.
364. Mitsukawa N, Satoh K, Suse T, Hosaka Y. Clinical success of mandibular distraction for obstructive sleep apnea resulting from
micrognathia in 10 consecutive Japanese young children. J Craniofac Surg. 2007 Jul;18(4):948-53.
365. Shen W, Jie C, Chen J, Zou J, Ji Y. Mandibular distraction osteogenesis to relieve pierre robin severe airway obstruction in neonates:
indication and operation. J Craniofac Surg. 2009 Sep;20 Suppl 2:1812-6.
366. Looby JF, Schendel SA, Lorenz HP, Hopkins EM, Aizenbud D. Airway analysis: with bilateral distraction of the infant mandible. J
Craniofac Surg. 2009 Sep;20(5):1341-6.
367. Genecov DG, Barcelo CR, Steinberg D, Trone T, Sperry E. Clinical experience with the application of distraction osteogenesis for airway
obstruction. J Craniofac Surg. 2009 Sep;20 Suppl 2:1817-21.
368. Mathijssen I, Arnaud E, Marchac D, Mireau E, Morisseau-Durand MP, Guerin P, et al. Respiratory outcome of mid-face advancement with
distraction: a comparison between Le Fort III and frontofacial monobloc. J Craniofac Surg. 2006 Sep;17(5):880-2.
230
369. Flores RL, Shetye PR, Zeitler D, Bernstein J, Wang E, Grayson BH, et al. Airway changes following Le Fort III distraction osteogenesis for
syndromic craniosynostosis: a clinical and cephalometric study. Plast Reconstr Surg. 2009 Aug;124(2):590-601.
370. Xu H, Yu Z, Mu X. The assessment of midface distraction osteogenesis in treatment of upper airway obstruction. J Craniofac Surg. 2009
Sep;20 Suppl 2:1876-81.
371. Eun YG, Kim SW, Kwon KH, Byun JY, Lee KH. Single-session radiofrequency tongue base reduction combined with
uvulopalatopharyngoplasty for obstructive sleep apnea syndrome. Eur Arch Otorhinolaryngol. 2008 Dec;265(12):1495-500.
372. Benazzo M, Pagella F, Matti E, Zorzi S, Campanini A, Frassineti S, et al. Hyoidthyroidpexia as a treatment in multilevel surgery for
obstructive sleep apnea. Acta Otolaryngol. 2008 Jun;128(6):680-4.
373. Verse T, Baisch A, Hormann K. [Multi-level surgery for obstructive sleep apnea. Preliminary objective results]. Laryngorhinootologie. 2004
Aug;83(8):516-22.
374. Kao YH, Shnayder Y, Lee KC. The efficacy of anatomically based multilevel surgery for obstructive sleep apnea. Otolaryngol Head Neck
Surg. 2003 Oct;129(4):327-35.
375. Friedman M, Ibrahim H, Lee G, Joseph NJ. Combined uvulopalatopharyngoplasty and radiofrequency tongue base reduction for treatment of
obstructive sleep apnea/hypopnea syndrome. Otolaryngol Head Neck Surg. 2003b Dec;129(6):611-21.
376. Vilaseca I, Morello A, Montserrat JM, Santamaria J, Iranzo A. Usefulness of uvulopalatopharyngoplasty with genioglossus and hyoid
advancement in the treatment of obstructive sleep apnea. Arch Otolaryngol Head Neck Surg. 2002 Apr;128(4):435-40.
377. Lee NR, Givens CD, Jr., Wilson J, Robins RB. Staged surgical treatment of obstructive sleep apnea syndrome: a review of 35 patients. J
Oral Maxillofac Surg. 1999 Apr;57(4):382-5.
378. Elasfour A, Miyazaki S, Itasaka Y, Yamakawa K, Ishikawa K, Togawa K. Evaluation of uvulopalatopharyngoplasty in treatment of
obstructive sleep apnea syndrome. Acta Otolaryngol Suppl. 1998;537:52-6.
379. Johnson NT, Chinn J. Uvulopalatopharyngoplasty and inferior sagittal mandibular osteotomy with genioglossus advancement for treatment
of obstructive sleep apnea. Chest. 1994 Jan;105(1):278-83.
380. Eun YG, Kwon KH, Shin SY, Lee KH, Byun JY, Kim SW. Multilevel surgery in patients with rapid eye movement-related obstructive sleep
apnea. Otolaryngol Head Neck Surg. 2009 Apr;140(4):536-41.
381. Nelson LM. Combined temperature-controlled radiofrequency tongue reduction and UPPP in apnea surgery. Ear Nose Throat J. 2001b
Sep;80(9):640-4.
231
Fly UP