Genioglossus muscle activity and inspiratory timing in obstructive sleep apnea

Genioglossus muscle activity and inspiratomj timing in obstructive sleep apnea Satoshi Adachi, DDS, PhD," Alan A. Lowe, DMD, PhD, FRCD(C), b Masafumi Tsuchiya, DDS, PhD," C. Francis Ryan, MB, FRCP(C), c and John A. Fleetham, MD, FRCP(C) d

Vancouver, British Columbia, Canada Atypical tongue muscle activity during sleep may contribute to the development of obstructive sleep apnea (OSA). Inspiratory genioglossus (GG) muscle activity was investigated in 10 OSA adults and 4 symptom-free controls. On the basis of overnight monitoring during nonREM sleep, the duration of the inspiratory GG activity and the total GG activity cycle is shorter in patients with OSA. The duration of inspiration and the duration of one total respiratory cycle is also shorter in patients with OSA. The commencement time lag between inspiratory GG activity and the onset of inspiration is shorter in patients with OSA during nonapneic breathing which indicates that inspiratory GG activity is activated relatively later in these patients. Furthermore, the inspiratory GG activity occurs after inspiration during an apnea, but the timing of GG activity onset progressively advances during the apnea. Earlier GG reactivation occurs before inspiration during the first nonoccluded breath at the end of an apnea. During subsequent tidal breathing, the timing of the GG onset progressively decreases after the onset of inspiration until the next obstructive apnea occurs. This observation suggests that the timing relationship between GG inspiratory activity and inspiratory effort is of physiologic importance in the pathogenesis of OSA. Furthermore, it may explain why dental appliances, such as the tongue retaining device, are highly effective in the resolution of OSA in selected patients. (AMJ ORTHOD DENTOFAC ORTHOP 1993;104:138-45.) O b s t r u c t i v e sleep apnea (0SA) is characterized by recurrent upper airway occlusion during inspiration, t'7 The genioglossus (GG) muscle is believed to contribute to this occlusion. The role of the GG muscle in the resolution of OSA has been investigated at length. 8~~ Genioglossus muscle activity has been demonstrated in phase with inspiration during sleep, s Preferential activation of this muscle is correlated with pharyngeal opening and the resolution Of the apnea. 9:t~ A dynamic relationship between supraglottic pressure and GG muscle amplitude has been postulated to explain the upper airway occlusion in subjects with OSA. 9 However, the phasic time relationship between GG muscle activity and respiration during sleep has not been investigated in human subjects. The coordination of inspiratory GG muscle activity with inspira!ory effort

From the Faculty of Dentistry, The University of British Columbia. This project was supported by grant MA-3849 from the Medical Research Council of Canada and by grant 99 (87-1) from the British Columbia Health Care Research Foundation. 'Postdoctoral Fellow. Division of Orthodontics, Department of Clinical Dental Sciences. t'Professor and Head, Department of Clinical Dental Sciences. ':Assistant Professor, Department of Medicine. University ltospital. dAssociate Professor, Department of Medicine, University Hospital. Copyright 9 1993 by the American Association of Orthodontists. 0889-5406/93/SI.00 + 0.'10 8/1/34150

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has been proposed as an important factor during sleep since the patency of upper airway is in part maintained by the GG muscle. The onset of the GG activity has been shown to be earlier in response to increased negative pressure in the upper airway in dogs. 't It is not known whether the timing of GG muscle activity is abnormal in patients with OSA. The purpose of this study is to evaluate inspiratory GG muscle activity and its phasic interaction with inspiration in OSA patients and in control Subjects. METHODS Ten adult patients with moderate to severe OSA arid four symptom-free control subjects were evaluated. Demographic data for the OSA patients and control subjects are provided in Table I. All subjects Were men ranging in age from 32 to 71 years: The body mass index ranged between 25.61 to 45.17 kg/m2 for patients with OSA and between 22.44 to 32.18 kg/m~ for conirol subjects. Patients with OSA were selected on the basis of an initial diagnostic overnight polysomnogram. Apnea indices ringed from 17.50 to 52.00 apneas per hour, and the total apnea time varied from 13.11% to 45.03%. Intraoral bipolar surface electrodes for the GG muscle were fitted for each subject. The electrodes consisted of two silver balls (WI00 Unitek Ltd., USA) of 5 mm diameter separated by a 20 mm distance. They were positioned on the inner lower surface of a rubber base impression (Reprosil, Dentsply Ltd., Surrey, England) registered on the lingual surface of

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) :::::.:.::::::=z:::.~:~:~ '~

Fig. 1. Lateral and posterior diagrammatic representations of bipolar surface electrodes used to record from genioglossus muscle.

T a b l e I. D e m o g r a p h i c data for the 10 patients with obstructive sleep apnea and 4 s y m p t o m - f r e e controls

Patient 1 2 3 4 5 6 7 8 9 10 Mean SD

[

Age

l

BMl

I

AI

[TAT

46 40 49 32 41 40 68 51 50 71

32.78 26.28 25.61 41.64 33.30 27.70 45.17 30.78 25.73 29.76

46.72 34.81 52.00 51.38 25.79 41.13 29.19 28.42 17.50 20.44

35.82 45.03 43.00 42.28 20.98 36.39 19.70 19.93 13.11 22.95

48.8 12.4

31.88 6.72

34.68 12.53

29.92 11.76

Control 1 2 3 4

l

Age

[

BMI

38 37 32 38

29.62 22.44 24.11 32.18

36.3 2.9

27.09 4.58

Age is expressed in years, the body mass index (BMI) in kg/m'-, apnea indices (AI) in apneas/hour, and total apnea time (TAT) in percent of total sleep time.

lower teeth and attached gingiva. The electrodes were in contact with the dorsal surface of the inferior part of the GG muscle (see Fig. I). The GG electromyograph muscle activity was amplified, rectified, and integrated. Respiratory effort was monitored by respiratory inductive pneumography (Respitrace, Noninvasive Monitoring System Inc., Ardsley, N.Y.). Sleep and its various stages were documented by standard electrocncephalographic (EEG), electrooculographic, and electromyographic (EMG) criteria. The EEG was recorded with electrodes applied at C3-A2 and C4-AI (according to the international 10-20 system), and the EMG activity was obtained from the submental and GG muscles. Apnea was documented by an infrared CO., analyzer, which recorded from both the nose and the mouth. A single electrocardiogram was monitored to detect cardiac arrythmias. Arterial oxygen saturation (SaO~) was measured continuously with a digital oximeter. Transcutaneous carbon dioxide (TcCO~) was monitored with an infrared transducer (HP47210A) placed on the skin from

which the stratum comeum had been removed. An IBM PC microcomputer continuously monitored and stored airflow, SaO2, breathing pattern, TcCO,, and heart rate on a mass storage medium. The entire record was scored manually for sleep stage, apnea type, and duration, and merged with the rest of the data. Severity of the sleep apnea was assessed in terms of the apnea index (apneas per hour of total sleep time), the total apnea time (expressed as a percentage of the total sleep time), mean SaO2 and TcCO2. For apneic and nonapneic tidal breathing periods during nonrapid eye movement (nonREM) sleep, the onset and termination points of both inspiratory GG nmscle activity and inspiration were identified and digitized with a cross hair cursor on a tablet digitizer (HP9874A). Table II provides a description of the variables measured. The duration of inspiratory GG activity, total GG activity cycle, inspiration, and total respiratory cycle were calculated with a microcomputer system (model HP9816). The commencement and cessation time lag betv,'cen the inspiratory GG activity and the

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Table Ih Summary of the nine variables used to evaluate genioglossus inspiratory muscle activity and respiration Variable

[

Interpretation

a. GGi (seconds) b. GGtot (seconds) c. GGi/GGtot (%) d. e. f. g.

Duration of inspiratory genioglossus activity Duration of total genioglossusphasic cycle lnspiratory genioglossus activity time as a percentage of total genioglossus cycle time Duration of inspiration Duration of total respiratory cycle Inspiration time as a percentage of total respiratory cycle time Time lag of onset of inspiration after onset of genioglossus muscle activity Time lag of termination of inspiration after termination of gen!oglossus muscle activity Normalized amplitude of inspiratory genioglossus activity

Ti (seconds) Ttot (seconds) Ti/Ttot (%) Lil (seconds)

h. Li2 (seconds) i. GGa (%)

Table Ill. Mean and standard deviations (in seconds) of the time variables for patients with obstructive sleep apnea and for controls during nonapneic breathing Patients (n = 10) Variable

GGi GGtot GGi/GGtot Ti Ttot Ti/Ttot Lit Li2

"i Mean

1.48 3.09 49.90 1.33 3.06 43.80 0.03 -0.09

]

Controls (n = 4) SD

Mean

0.39 0.85 8.76 0.37 0.81 4.19 0.18 0.18

2.25 5.07 44.38 1.99 5.05 39.33 0.60 0.22

onset of inspiration were measured. In addition, the maximum amplitude of the inspiratory GG activity was determined (Fig. 2). Ten to 20 periods of three to nine breaths between apneas were selected during nonREM sleep for all OSA patients and control subjects. Alterations of the time lag in commencement and amplitude of the GG muscle activity were quantitated during two consecutive obstructive apneas and the intervening period of unobstructive breathing. The last three occluded breaths of an apnea, the first, middle, and last breaths, during the unobstructed period and the first three occluded breaths of the following apnea were evaluated. A comparison between patients and controls and a paired comparison between subsequent breaths were undertaken by means of the Wilcoxin t test.

RESULTS Data for the second experimental study with the GG electrode in place revealed mean apnea indices that ranged from 8.48 to 64.09 apneas per hour and total apnea times from 5.19% to 63.00%. These values did not differ significantly from those in the initial diagnostic study and confirmed that all the patients suffered

I

so

Probability

0.55 0.87 5.92 0.40 0.88 3.17 0.74 0.64

0.02* 0.01" 0.40 0.04* 0.01" 0.07 0.02" 0.40

from moderate tO severe OSA. Table III provides mean values and standard deviations for each of the variables measured during nonapneic breathing for the 10 patients with OSA and the 4 control subjects. The duration of inspiratory GG activity was significantly shorter in OSA patients (p = 0.02). The OSA patients also had shorter total cycle GG activity (p = 0.01), shorter durations of inspiration (p = 0.04), and shorter total respiratory cycles (p = 0.01). In addition, the time lag between the commencement of inspiratory GG muscle activity and inspiration was significantly shorter in OSA patients (p = 0.02). This latter finding indicates that during unobstructed breathing, inspiratory GG activity commences later in OSA patients than in control subjects. Table IV provides mean values for the commencement time lag (Lil) for each OSA patient during two obstructive apneas and the intervening nonoccluded tidal breathing. Asterisks in the table indicate statistically significant differences between corresponding phases. One patient (no. 4) did not reveal GG activity in phase with inspiration during the subsequent apnea,

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but minimal activity in the second and third occluded breath was seen. The mean time lag between commencement of inspiratory GG activity and inspiration was - 0 . 3 1 - 0.27 seconds in the third respiratory cycle before unoccluded tidal breathing, which confirms the GG muscle activity commenced after the inspiratory effort began. The time lag increased during the next ( - 0 . 2 4 • 0.28 seconds) and the last inspiratory attempt (0.04 .4- 0.35 seconds) before resolution of the apnea. During unoccluded tidal breathing, the time lag at the first breath increased significantly to 0.21 • 0.20 seconds, which indicates the GG muscle was activated before inspiration. In the middle breath of the unoccluded tidal breathing period, the time lag dropped significantly (0.06 .4- 0.17 seconds), but the GG activity occurred before inspiratory effort. During the last unoccluded breath before the next apnea, it fell to - 0.11 • 0.21 seconds. The order of activation was reversed in that the GG activity commenced after the onset of inspiratory effort. In the first and third occluded breaths of the next apnea, the time lag became progressively more negative (from - 0 . 2 2 to - 0 . 3 3 seconds), which indicates a progressive delay of GG activation after the onset of apnea until the time lag reaches a value similar to that in the third last occluded breath of the previous apnea. The change in the commencement time lag during occluded and nonoccluded breaths is shown in Fig. 3. A progressive increase in the commencement time lag is demonstrated until the first nonapneic breath after which the time lag decreases during tidal breathing into the next apnea. Normalized GG amplitude data for identical phases during occluded and nonoccluded breathing are provided in Table V. The measured amplitudes were normalized as a percentage of the mean amplitude at the first unoccluded breath for each patient. The normalized GG activity was 22.09% • 10.28% (mean • SD) in the third occluded breath before tidal breathing. The GG activity progressively increased during the next (26.84% - 12.42%) and the last inspiratory effort (39.55% • 15.62%) before resolution of the apnea. There was a marked increase in GG muscle activity (100%) during the first unoccluded breath. It subsequently decreased (p < 0.05) in the middle (70.88% - 9.33%) and the last breath .(41.51% • 11.86%) during nonapneie breathing. During the subsequent apnea, the GG activity continued to decrease (p < 0.05) in the first occluded breath (24.90% • 7.32%). In the second and third occluded breaths, it decreased, but the differences were not statistically significant. The changes in GG activity are summarized in Fig. 4. A significant increase in GG amplitude at the time of pharyngeal opening is shown. A significant

141

-,--b

GG-

u

"-

g _..,,. Ven't

'Will

h r

Fig. 2. Diagrammatic representation of measurement variables. GG: Genioglossus muscle activity, Vent: respiratory efforts,

a:GGi, b:GGtot, c:GGi/GGtot, d:'ri, e:Ttot, t':Ti/Ttot, g:Lit, h:Li2, i:GGa. (See Table II for definitions).

decrease in GG activity during the nonapneic and the next apneic periods occurs. DISCUSSION Several types of electrodes have been developed to record GG muscle activity in human beings. Needle ~2 and fine wire electrodes8.9.t3.~4have been used. Insertion of such electrodes may be invasive and occasionally involves complications such as hematoma formation, fracture of electrodes, and pain. In some subjects, apprehension can result in atypical muscle activity. Genioglossus muscle surface electrodes are preferable since they are less invasive. Recently, two kinds of surface electrodes have been reported.~S-t7 One may record the EMG activity from the intrinsic muscles of the tongue together with the GG muscle since the electrodes are positioned on the dorsal surface of the tongue. ~s The other positions the electrodes against the ventral surface of the tongue where the bilateral GG muscles fuse. 16A7 The latter electrodes reveal similar frequency characteristics to traditional indwelling needle electrodes, and were confirmed to be valid for obtaining GG muscle activity, x6.~7Surface electrodes developed for the current experiment were modified to use 5 mm diameter silver balls rather than stainless steel wire. ~6 Our results demonstrate no change in apnea severity before and after insertion of such intraoral GG electrodes. The inspiratory activity in the human GG muscle has been identified during quiet awake breathing with the jaw closed or slightly open 8"~2'18 and during quiet

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American Journal of Orthodontics and Dentofacial Orthopedics August 1993

APNEA 0.6 0.5 0.4 0.3 0.2"

-3

-2

TIDAL BREATHING -1

First

Middle

Last

APNEA 1

2

3

0.1

0.0-m ~

" -0.2 -0.11 -0.3 -0.4 -0.5 -0.6 Airflow

Res,oiratory Effort

Fig. 3. Changes in the time lag (Lil) of initial inspiration after iniiial inspiratory genioglossus muscle activity in last three inspiratory attempts of apnea, first, middle, and last tidal breaths during tidal nonoccluded breathing, and first 3 inspiratory attempts in subsequent apnea. The vertical axis represent the time lag in seconds. Open squares denote the mean time lag, and vertical bars delineate standard error. The horizontal axis represents successive respiratory events9 Airflow is quantified by the infrared C02 analyzer and respiratory effort is a respitrace record of respiratory inductive plethysmography.

T a b l e IV. Individual data and the m e a n s and standard deviations (in seconds) for the time lag b e t w e e n initial inspiration and initial inspiratory genioglossus muscle activity

Apnea Patient

- 3

- 2

I 2 3 4 5 6 7 8 9 10

-0.86 -0.18 -0.36 -0.01 - 0.03 - O. 17 -0.22 -0.22 -0.45 -0.61

Mean SD

-0.31 0.27

Tidal breathing ]

Apnea

- I

First

[ Middle

-0.83 -0.13 -0.36 0.06 0.05 - O. l 0 -0.24 O.Ol -0.48 -0.41

-0.42 -0.07 -0.23 0.05 0.01 0.92 -0.17 0.13 0.09 0.07

0.31 0.10 -0.07 0. It O. 16 0.67 0.10 0.32 0.16 0.25

0.07 -0.03 -0.15 -0.01 0.05 0.46 0.06 0.21 0.06 -O.lO

-0.17 -0.23 -0.33 -0.03 0.00 0.41 -0.26 -0.08 -0.26 -0.18

-0.58 -0.26 -0.62 -0.03 - 0.09 0.33. -0.25 -0.17 -0.20 -0.38

-0.24 -0.14 -0.6l -- O,O! 0.50 -0.23 -0_31 -0.82 -0.28

0.02 0.43 -0.39 -0.15 -0.44 -0.57

-0.24 0.28

0.04 0.35

0.21 0.20

0.06 0_ 17

-0.11 0.21

-0.22 0.27

-0.24 0.37

-0.33 0.45

I .__11. 11. IL.

I

Last -0.62 -0.05 - 1.15

IL.JL...I

Asterisks indicate statistically significant differences at the 5% level between indicated phases.

sleep, g During inspiration, the tongue base advances w h e n the G G muscle contracts to enlarge the size of the oropharynx and reduce upper a i ~ v a y resistance. G e n i o g l o s s u s activity in phase with inspiration plays a definite role in the m a i n t e n a n c e o f upper airway patency. R e m m e r s - e t al. 9 demonstrated low level inspi-

ratory G G muscle activity w h e n the airway was occluded and suggested that a d y n a m i c relationship exists b e t w e e n supraglottic pressure and G G m u s c l e activity that could contribute to the pharyngeal occlusion in subjects with O S A . A p r o m i n e n t discharge at the termination o f an obstructive apnea suggests that the G G

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APNEA 120

-3

-2

TIDAL BREATHING First

-1

Middle

143

APNEA

Last

1

2

3

100"

6O

J

4O 20

0 Airflow Resoirato~ Effort

Fig. 4. Changes in amplitude of inspiratory genioglossus activity in last three inspiratory attempts of apnea followed by first, middle, and last tidal breaths during tidal nonoccluded breathing, and first three inspiratory attempts in next apnea. The vertical axis represents the normalized GG amplitude in percentage. The open squares denote the mean amplitude, and the vertical bars delineate the standard errors for each respiratory event. The horizontal axis representssuccessive respiratory events. Airflow is quantified by the infrared CO2 analyzer, and respiratory effort is a respitrace record.

Table V. Individual data and the means and standard deviations (in percent) for genioglossus maximum " inspiratory activity. All amplitudes were normalized as a percentage of the level at the first breath in the tidal breathing period Tir

Apnea Patient

-31

'l

'

First

breathing

JMiddle

Apnea I

I'

Last

I

1 2 3 4 5 6 7 8 9 10

16.77 20.47 10.64 21.89 33.20 6.02 38.13 31.63 26.44 15.73

20.54 23.98 11.87 24.16 48.54 9.79 40.50 36.35 32.18 20.45

27.33 34.03 14.24 42.56 52.47 17.66 60.61 48.02 46.46 52.10

100.00 100.00 100.130 100.00 100.00 100.00 100.00 100.00 100.00 100.00

61.13 81.05 61.81 74.46 71.76 84.38 79.88 58.34 62.88 73.08

27.29 55. I 1 32.78 31.51 58.24 57.50 47.01 37.22 36.85 31.64

27.39 16.23 15.61 26.66 39.22 32.60 21.59 25.27 25.63 18.88

23.48 13.18 l 1.85 I 1.71 29.10 16.73 39.58 17.36 35.25 15.21

21.80 12.63 11.02 13.58 28.80 6.64 38.66 24.69 26.03 12.06

Mean 9SD

22.09 10.28

26.84 12.42

39.55 15.62

100.00 0.00

70.88 9.33

4 i .51 11.86

24.90 7.32

21.34 ' 10.08

19.59 10.02

I ._J L . I I

.11

. I 1__. l J_.

I

Asterisks represent statistically significant differences at the 5% level between indicated phases.

muscle participates in the establishment of a patent upper ai~vay.9'~~ 9 In this study, preferential activity in the GG muscle was observed at the resolution of upper airway occlusion, and it decreased during subsequent tidal breathing. Reduced GG activity was again seen during the next apnea. Sttch findings support the con-

cept that varying amounts of GG mnscle activity could influence the onset and the termination of obstructive apnea. The diaphragm demonstrates similar inspiratory activity as the GG muscle. -'~ Many of the same factors that stimulate activity of the thoracic inspiratory mus-

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Adachi el al.

cles appear to stimulate activity of the upper airway dilating muscles. The GG muscle activity is greater than that seen in the diaphragm at the termination of obstructive apnea. ~~The two sets of muscles may differ in their sensitivity to various stimuli. In animal studies, the respiratory drive to the upper airway muscles increases disproportionately to the thoracic musclesfl ~ A recent report2z suggests possible fatigue in the GG muscle in OSA patients. In the present study, the onset of the inspiratory GG activity preceded inspiration in control subjects. Such results suggest that the GG musculature advances the base of the tongue to reduce upper airway resistance before negative subatmospherie pressure is generated by the inspiratory effort of the intrathoracic muscles. In OSA patients, the mean commencement time lag was also positive, but significantly less than that seen in control subjects. This suggests that the onset of inspiratory GG activity in OSA patients is delayed during inspiration when compared with control subjects. A detailed examination o.f the changes in the timing of GG activity in apneic and nonapneic breathing periods adds to our understanding of the contribution of the GG muscle to the pathogenesis of OSA. The negative time lag in the third last occluded breath during an apnea reveals that inspiratory GG activity follows the onset of inspiration. However, toward the end of an apnea, the timing of the onset of the GG muscle activity progressively increases. The GG muscle activity precedes the onset of inspiration at the termination of an obstructive apnea. This timing in conjunction with the increased amplitude seen in the GG muscle, may contribute to the relief of the upper airway occlusion by moving the base of the tongue forward and by reducing the collapsibility of the anterior pharyngeal wall before the generation of the negative upper airway pressure. A large decrease in the time lag was demonstrated during the middle and last breaths in nonapneic breathing before the next obstructive apnea. Conversely, a progressive delay in GG activity would predispose to upper airway occlusion and obstructive apnea. The patients with OSA fail to stabilize their upper airway during progressive asphyxia. 23 In normal awake human beings, GG muscle activity increases progressively in responseto hypoxia and hypercapnia in a direct linear response with the diaphragm. 24 Upper airway occlusion is relieved by increased upper airway muscle activity in response to increased subatmospheric pressure in the larynx, tension receptor inputs in the chest wall, and metabolic changes in the muscle. '9 Mathew et al. ~ found that increases in the negative pressure in the larynx in cats augmented GG muscle activity and proposed that this response was mediated by the su-

American Journal of Orthodontics and Dentofacial Orthopedics /lugu.s.t 1993

perior laryngeal nerve and mucosal receptors. Van Lauteren et al." reported that increased negative pressure in the larynx in dogs advances the onset of GG activity in relation to diaphragmatic muscle activity. Such an observation may be related to our results in human OSA patients. A progressive increase in negative upper airway pressure during an obstructive apnea may advance the onset of GG activity and lead to a termination of the apnea. However, why the increased amplitude and advanced timing of the onset of GG inspiratory activity cannot be maintained in OSA subjects to facilitate unobstructed breathing is unclear. In a recent report, 26 we demonstrated that tongue volume is larger in patients with OSA when compared with symptom-free subjects. It may be that patients with OSA have an altered reflex response complicated by an enlarged tongue related to tissue edema during sleep and/or adipose tissue deposits. CLINICAL IMPLICATIONS

Altered GG muscle activity in OSA subjects as documented in this report may be significantly improved by the use of a tongue retaining device (TRD). 27Dental appliances offer several advantages over other therapy choices for OSA since they are inexpensive, noninvasive, easy to fabricate, reversible, quiet, and well accepted by patients. 2s The TRD is a custom-made appliance with an anterior bulb that, by means of negative pressure, holds the tongue forward during sleep. For those patients with blocked nasal passages, a modified TRD with lateral airway tubes is also available. In a recent study, :9 a sample of 60 men with respiratory disturbance index (RDI) values > 12.5 who had two or more times the apnea rate during supine sleep in comparison with their lateral sleep rate were assigned to four treatment groups: TRD only, posture alarm, TRD plus posture alarm, and health habit instruction. When the traditional 50% reduction in RDI was'used as the index of successful treatment, 73% of the TRD group and 80% of the TRD plus posture alarm group were successful. The 15 subjects treated with the TRD alone had a reduction in mean RDI from 27.4 to 11.4. Patency of thenasal airway and an initially low side index were the two factors significantly related to successful control of OSA with the TRD. For the 15 subjects in the TRD plus posture alarm group, lower initial obesity and higher weight loss during treatment were the factors associated with best success. A mean RDI reduction from 30.7 to 7.9 was seen for the latter group. The effectiveness of the TRD in these OSA subjects may be partially related to the forward tongue posture that compensates for the altered GG muscle activity. Since there appears to be a change in the timing relationship

American Journal of Orthodontics and Dentofacial Orthopedics Volume 104, No. 2

b e t w e e n G G inspiratory activity and inspiratory effort in O S A subjects, the T R D m a y prevent the o b s e r v e d airway o c c l u s i o n by a d v a n c i n g the base o f the tongue .28 We are indebted 1o Mrs. M. Wong for her software expertise, Geoffrey Edgell for his technical assistance, and I. Ellis for transcribing the manuscript to its final form. REFERENCES 1. Guilleminault C, Dement WC. Sleep apnea syndromes. KROC Foundation series, vol 11. New York: Alan R Liss, 1978. 2. Haponik EF, Smith PL, Bohlman ME, Allen RP, Goldman SM, Bleecker ER. Computerized tomography in obstructive sleep apnea. Am Rev Respir Dis 1983;127:221-6. 3. Suratt PM, Dee P, Atkinson RL, Armstrong P, Wilhoi TSC. Fluoroscopic and computed tomographic features of pharyngeal airway in obstructive sleep apnea. Am Rev Respir Dis 1983;127:487-92. 4. Bohlman ME, tlaponik EF, Smith PL, Allen RP, Bleecker ER, Goldman SM. CT demonstration of pharyngeal narrowing in adult obstructive sleep apnea. Am J Roentgenol 1983;140: 543-8. 5. Lowe AA, Santamaria J, Fleetham J, Price C. Facial morphology and obstructive sleep apnea. A.,,t J ORTttOD DEN'I'OFACORTtIOP 1986;90:484-91. ": 6. Lowe AA, Gionhaku N, Takeuchi K, Fleeflaam JA. Three-dimensional CT reconstructions of tongue and airway in adult subjects with obstructive sleep apnea. Ar,t J OR'roODDErrrOFAC ORrHOP 1986;90:364-74. 7. Wei J, Cherniack N, Dempsey J, Edelman N, Phillipson E, Remmers J. Respiratory disorders of sleep: pathophysiology, clinical implications and therapeutic approaches. Am Rev Respir Dis 1987;136:755-61. 8. Sauerland EK, Harper RM. Electromyographie activity of the genioglossus muscle. Exp Neurol 1976;51:160-70. 9. Returners JE, DeGroot WJ, Sauerland EK, Anch AM. Pathogenesis of upper airway occlusion during sleep. J Appl Physiol 1978;44:931-8. 10. Onal E, Lopata M, O'Connor TD. Pathogenesis of apneas in hypersomnia sleep apnea syndrome. Am Rev Respir Dis 1982;125:167-74. 1I. Van Lauteren E, Van der Graft W, Parker D, Strohl K, Cherniack N. Nasal and laryngeal reflex responses to negative upper airways pressure. J Appl Physiol 1984;56:746-52. 12. Sauerland EK, Mitchell SP. Electromyographic activity of the human genioglossus muscle in response to respiration and to positional changes of the head. Bull LA Neurol Soc 1970;35:6973. 13. Lowe AA, Johnston W. Tongue and jaw muscle activity in response to mandibular rotations in a sample of normal and anterior open-bite subjects. AM J ORTHOD1979;76:565-76. 14. Lowe AA. Correlations between orofacial muscle activity and craniofacial morphology in a sample of control and ;interior openbite subjects. AM J OR'ntOD 1980;78:89-98.

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15. Yoshida K, Takada K, Adachi S, Sakuda M. Approach to tongue activity by means of miniature surface electrodes. J Dent Res 1982;61:1148-52. 16. Doble EA, Leiter JC, Knuth SL, Daubenspeck JA, Bartlett D Jr. A noninvasive intraoral electromyographic electrode for genioglossus muscle. J Appl Physiol 1985;58:1378-82. 17. Milidonis MK, Widmer CG, Segal RL, Kraus SL. Surface intraoral genioglossus EMG recording technique for kinesiologic studies. AM J ORTIIODDENTOFACORTIIOP1988;94:240-4. " 18. Lowe AA, Sessle BJ, Gurza S. Regulation of genioglossus and masseter muscle activity in man. Arch Oral Biol 1977;22:57984. 19. Vincken W, Guilleminault C, Silvestri L, Cosio M, Grassini A. lnspiratory muscle activity as a trigger causing the airways to open in obstructive sleep apnea. Am Rev Respir Dis 1987;135:372-7. 20. Onal E, Lopata M, O'Connor TD. Diaphragmatic and genioglossal electromyogram responses to CO2 rebreathing in humans. J Appl Physiol 1981;50:1052-5. 21. Weiner D, Mitra J, Salamone J, Cherniack N. Effect of chemical stimuli on nerves supplying upper airway muscles. J Appl Physiol 1982;52:530-6. 22. Hollowell DE, Suratt PM. Fatigue of the genioglossus produced by inspimtory loading in normal subjects. Am Rev Respir Dis 1988;138:75. 23. Issa F, Sullivan C. Upper airway closing pressures in obstructive sleep apnea. J Appl Physiol 1984;57:520-7. 24. Patrick G, Strohl K, Rubin S, Altose M. Upper airway and diaphragm muscle responses to chemical stimulation and loading. J AppI Physiol 1982;53:1133-7. 25. Mathew O, Abu-osba K, Thach B. Influence of upper airway pressure changes on genioglossus muscle respiratory activity. J Appl Physiol 1982;52:438-44. 26. Lowe AA, Fleetham JA, Adachi S, Ryan CF. Cephalometric and CT predictors of apnea index severity. AM J ORTIIOD DENTo~^c OR~OP [in press]. 27. Cartwright R' Samels~ C" The effects ~ a n~ treatment for obstructive sleep apnea--the tongue-retaining device. J Am Med Assoc 1982;248:705-9. 28. Lowe AA. Dental appliances for the treatment of snoring and/or obstructive sleep apnea. In: Kryger M, Roth T, and Dement W, eds., Principles and practice of sleep medicine 2nd ed., Philadelphia: WB Saunders, [in press]. 29. Cartwright R, Ristanovic R, Diaz F, Caldarelli D, Alder G. A comparative study of treatments for positional sleep apnea. Sleep 1991;14:546-52. Reprint requests to:

Dr. Alan A. Lowe Professor and ttead Department of Clinical Dental Sciences Faculty of Dentistry University of British Columbia 2199 Weshrook Mall Vancouver, B.C., Canada V6T IZ3