Electromyogram


     and SAS
  a.1. Indications
         Oral Appliance
   a.3.1. AHI
   a.3.2. Sleep Quality 
             Variables
   a.3.3. 
Sleepiness
   a.3.4. Snoring
   a.3.5. Blood Pressure
   a.3.6. Upper Airway 
             Resistance Syndrome
   a.3.7. Side Effects
         Effect
   a.4.1. Anatomical Factors
   a.4.2. Functional Factors
   a.4.3. Sleep Position 
     Treatment
     SAS
         Periodontal Disease
         Heart Disease
         Metabolic Syndrome
     Appliances
    Studies
     Potentials
     Variation

To evaluate the efficiency of the oral appliance, the activity of masticatory and tongue muscles was investigated polysomnographically with and without the appliance. Fifteen patients (3 women and 12 men) with SAS, between the ages of 45 and 72 years (mean age 54.0 ± 8.4 years) were evaluated polysomnographically [59, 89].

Surface Ag/AgCl electrodes (EP12, Unique Medical, Tokyo, Japan) for the genioglossal muscle were placed midsagittally, midway between the mental protuberance and lower lip, and midway between the inner aspect of the mandible and hyoid bone (Figure 26) [59, 89]. Ag/AgCl electrodes were also used over the masseter muscle 15 mm apart in the direction of the main fibers. Two polyurethane coated fine wire electrodes (0.08 mm in diameter, Unique Medical, Japan) within a 60 mm long 23-gauge injection needle (0.65 mm in diameter, Terumo, Japan) were used through an intraoral route to record EMG activity from the inferior head of the lateral pterygoid muscle (Figure 26) [89]. The tips of these fine wire electrodes were exposed 1 mm and bent 3 mm and 5 mm into a hook from the tip. The wire electrodes were attached to the buccal face of the maxillary premolar with adhesive wax led out of the corner of the mouth to avoid movement artifacts [89]. The EMG signals were amplified with a band pass of 30 to 3000 Hz and with a 200 ms time constant. Polysomnographic recordings were performed.


Figure 26. Fine wire electrodes (a) in the needle for lateral pterygoid muscle EMG recording and intraoral appliance (b). Two polyurethane coated fine wire electrodes (0.08 mm in diameter) within a 60 mm long 23-gauge injection needle (0.65 mm in diameter) were inserted using the appliance (a) into the inferior head of the lateral pterygoid muscle. The tips of these fine wire electrodes were exposed 1 mm and bent 3 mm and 5 mm into a hook from the tip. After confirmation of correct placement of the fine wire electrodes, the appliance and needle were removed carefully.

During obstructive sleep apnea, airflow disappeared, but abdominal and chest movements remained partially (Figure 27). The genioglossal, masseter and lateral pterygoid muscles showed apparently reduced activity during obstructive sleep apnea (Figure 27). On the other hand, during central sleep apnea, both abdominal and chest movements disappeared completely, and the three muscles showed no obvious reductions (Figure 28).


Figure 27. Polysomnographic recording during obstructive sleep apnea. During obstructive sleep apnea, airflow disappeared, but abdominal and chest movements remained partially. The genioglossal, masseter and lateral pterygoid muscles showed apparently reduced activity during obstructive sleep apnea.


Figure 28. Polysomnographic recording during central sleep apnea. During central sleep apnea, both abdominal and chest movements disappeared completely, and the three muscles showed no obvious reductions.

The muscles demonstrated significantly lower EMG amplitudes (genioglossal muscle, p<0.0001; masseter muscle, p<0.005; lateral pterygoid muscle, p<0.005) during than before obstructive apneas, and significantly higher EMG amplitudes (genioglossal muscle, p<0.0001; masseter muscle, p<0.0001; lateral pterygoid muscle, p<0.0002 after the apnea) (Figure 29).



Figure 29. Relative muscle activity evaluated EMG activity before treatment as 100 %. The masseter muscle, the genioglossal muscle, and the inferior head of the lateral pterygoid muscle showed significantly lower electromyographic amplitudes during and higher amplitudes after obstructive apnea. The oral appliance helps maintain the tonus of the muscles by protracting the tongue and mandible even during sleep, which suggests that the activated muscles prevent the upper airway from collapsing (n=15).

The number of central apneic episodes per hour was low (1.7 ± 1.9). The central apnea index ranged from 0 to 6.4. No decrease in the mean EMG amplitude during central apneas was observed. The muscles showed significantly higher (genioglossal muscle, p<0.002; masseter muscle, p<0.003; lateral pterygoid muscle, p<0.003) EMG amplitudes after than during apneas.

After the placement of the appliance, EMG amplitude increased except for genioglossal muscle after obstructive and central apneas and during central apneas. The muscles exhibited significantly lower EMG amplitudes (genioglossal muscle, p<0.0001; masseter muscle, p<0.01; lateral pterygoid muscle, p<0.005) during obstructive apneas compared with before, and then significantly higher EMG amplitudes (genioglossal muscle, p<0.0001; masseter muscle, p<0.02; lateral pterygoid muscle, p<0.02) after the apneas (Figure 29). No decrease in the mean EMG amplitude during central apneas was observed. The muscles demonstrated significantly higher EMG amplitudes after than during the apneas (genioglossal muscle, p<0.02; masseter muscle, p<0.004; lateral pterygoid muscle, p<0.004). The EMG amplitude of the genioglossal muscle during obstructive apneas (16.9 ± 5.8μV) was significantly increased (p<0.03) by the appliance (27.6 ± 18.8μV). Similarly, the lateral pterygoid muscle showed significantly higher EMG amplitude (p<0.03) during obstructive apneas with (31.6 ± 17.8μV) than without (18.3 ± 11.5μV) the appliance.

The patency of the upper airway is maintained normally by muscle tone and elasticity of the upper airway muscle. Remmers et al. [98] reported that genioglossal EMG of patients with SAS consistently revealed periodicity: low level activity at the onset of obstruction and prominent discharge at the instant of pharyngeal opening. Hollowell and Suratt [136] found that the masseter muscle was activated in patients with SAS in a manner similar to the submental muscles. Similarly, in the current study, the masseter muscle, the genioglossal muscle, and the inferior head of the lateral pterygoid muscle showed relatively low EMG amplitudes during and high EMG amplitudes after obstructive apnea.

The coactivation of agonist (the genioglossal and the lateral pterygoid muscle) and antagonist (the masseter muscle) after the apnea was postulated to stabilize the mandible to prevent the upper airway from collapsing. Muscles under the surface electrodes for the genioglossal muscle in this study can include the genioglossus, geniohyoid, mylohyoid, anterior belly of the digastric, and platysma. However, Sauerland et al.[137] reported that muscle activities during respiration can be followed closely by this surface recording during respiration. Hollowell and Suratt [136] reported that the mouths of patients with SAS opened wider than those of normal subjects at the end of expiration and further still at the end of inspiration, particularly at the termination of apneas when the masseter and submental muscles contracted. Morikawa et al. [138] investigated anesthetized, curarized subjects who were supine with their necks extended and observed that closing their jaws increased the mean distance between their tongue and posterior pharyngeal wall from 11 to 17.5 mm. The mouth opening at the end of expiration could narrow the upper airway, whereas opening at the end of inspiration could reflect the effort to expand the airway through tracheal tug and submental muscle activation that results in an opening of the mouth to allow mouth breathing. The hypotonia of the masticatory and tongue muscles and the weight of mandible, particularly in the supine position, can lead to opening of the mouth and further dorsal displacement of the mandible and tongue, resulting in pharyngeal narrowing and airway resistance, and finally obstructive apnea. The coactivation of elevator and depressor muscles after an apnea could stabilize the mandible to prevent the oropharynx from obstruction.

The EMG amplitudes of muscles increased after insertion of the appliance in this study. The results indicated that the device activates the muscles. The EMG amplitude of the genioglossal muscle during obstructive apnea was significantly increased by the appliance. The lateral pterygoid muscle showed significantly higher EMG amplitude during obstructive apneas with the appliance than without it. The results suggest that, during obstructive apneas, the tonus of the muscles protracting the tongue and mandible were maintained at an increased vertical and protrusive position. So relaxation of muscle contraction did not occur, which resulted in a significant increase in mean EMG amplitude during obstructive apnea. The activated muscles that protract the tongue and mandible prevented the upper airway from collapsing.

No reduction in the mean EMG amplitude was seen during central apneas. Thus, central apneas are suggested to occur independent of masticatory and tongue muscle activity. In other words, a central apnea can occur in the case of a loss of neural chest and abdominal respiratory drive even if the muscles are active and the upper airway is patent. After placement of the device, the EMG amplitude of the genioglossal muscle decreased during and after central apneas. No significant changes were observed even after inserting the appliance. Central sleep apnea is a disorder characterized by repeated apneic episodes during sleep that result from temporary loss of respiratory effort [139]. Central apnea differs from obstructive or mixed apneas by the absence of upper airway collapse and subsequent ventilatory attempts against an occluded airway. In most patients with central apnea, no obvious cause or association can be detected. Önal et al. [140] postulated that central apneas result from an abnormality in inhibition of the expiratory “off-switch” or inspiratory “on-switch” mechanism. PCO2 is the primary stimulus to ventilation during sleep and loss of this drive, as occurs with hypocapnia, may produce dysrhythmic breathing. Patients with complete absence of ventilatory chemosensitivity such as occurs with Ondine’s curse (central alveolar hypoventilation) also have central apneas. Önal et al. [140] reported that, before the onset of a central apnea, the periodicity of diaphragmatic and genioglossal EMG disappeared for a few breaths, expiratory times gradually increased, and tracings of airflow and thoracoabdominal motion indicated that the apnea represents an extremely prolonged expiratory phase.

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