[Abstract] OBJECTIVE: To observe the performance of aberration product otoacoustic emission (DPOAE) examination in patients with severe sleep apnea hypoventilation syndrome (SAHS) and analyze its significance. METHODS: Twenty-four patients diagnosed with severe SAHS by sleep apnea monitoring were selected as the experimental group, and 10 cases of normal population with age and sex matching the experimental group were used as the control group. DPOAE examination and pure tone audiometry were applied to both groups, and the results of sleep monitoring and DPOAE examination were analyzed. RESULTS: There was no decrease in subjective hearing in patients with severe SAHS, but the DPOAE response amplitude at each frequency from 0.75 to 8 kHz was significantly lower than that of the normal control group, and the results were significantly different compared with the normal group; the DPOAE response amplitude was significantly correlated with the decrease in blood oxygen saturation. Conclusion: Decreased oxygen saturation in patients with severe SAHS can lead to decreased otoacoustic response amplitude of the aberrant product, and this index is highly sensitive and can be used as an indicator to determine early cochlear damage in patients with SAHS.
[Keywords]
Aberrant product otoacoustic emissions; Sleep apnea hypoventilation syndrome
Sleep apnea hypoventilation syndrome (SAHS) is apnea or sleep hypoventilation with decreased oxygen saturation due to factors such as upper airway obstruction during sleep or central. Whereas hypoxemia can produce damage to the function of end organs, the supply vessels of the cochlea are peripheral vessels, and at the same time the cochlea is very sensitive to hypoxia, so we applied aberration product otoacoustic emission (DPOAE) to examine the function of the cochlea in patients with severe SAHS and evaluate the relationship between severe SAHS and early auditory damage.
1. Materials and methods
1.1 Clinical data: Patients diagnosed with severe SAHS by sleep respiratory monitoring and clinical examination in our sleep center between January 2008 and February 2009 (refer to OSAHS diagnostic criteria [1]) were selected, and patients with respiratory disorder index (AHI) index >40 times/h were enrolled as the experimental group. There were 18 male cases and 6 female cases with medical history of 6 months to 10 years, AHI index in the range of 40 to 78 times/h, mean oxygen saturation from 82% to 92.5%, and the lowest oxygen saturation of 60%; among them, 18 cases were obstructive type, 3 cases were mixed type, and 3 cases were hypoventilation; the control group were healthy volunteers without sleep snoring and pauses in the same period, 8 male cases and 2 female cases, with age and gender matching the experimental group. The average age of the two groups was 25~60 years old, the average age of the experimental group was 44.2±5.2, and the average age of the control group was 42±4.5. All patients underwent acoustic conduction resistance and pure tone audiometry, the conduction resistance tympanogram was type A, the ipsilateral stapedius muscle reflex was positive, there was no previous history of hearing loss or ear disease, and there was no history of noise exposure or ototoxic drug use.
1.2 Examination instruments and methods
1.2.1 Polysomnography (PSG) (Beijing Oriental Wantai): monitoring and recording indexes including AHI index, mean oxygen saturation, minimum oxygen saturation, etc.
1.2.2 Aberration product otoacoustic emission (Bio-logic, USA, 580-OAEAX5) test: The otoacoustic emission of the aberration product was detected and recorded with an otoacoustic emission meter in a soundproof shielded room, technical parameters: ambient background noise <30dB, two pure tone signals with an intensity of 70 dBSPL were taken as the initial stimulation sound, and the ratio of the two frequencies was f2/f1= 1.3, the range of geometric mean of f1 and f2 was 0.5~8.0 kHz, and the intensity of 2F1~F2 was read, and a total of 0.75, 1.0, 2.0, 4.0, 8.0
kHz5 frequency points for measurement.
1.2.3 Acoustic conductance (Madsen, Denmark, ZODIAC901) and pure tone audiometry (Madsen, Denmark, MIDIMATE622) testing: The 24 patients and controls enrolled were given routine acoustic conductance and pure tone audiometry examinations, except for hearing threshold changes due to middle ear factors.
1.2.4 Statistical processing: All test results requiring statistical analysis were analyzed using CHISS Chinese Koji statistical software: t-test for comparison of means and correlation analysis.
2 Results
2.1 Pure tone audiometry and acoustic conductance examination: all patients did not complain of subjective hearing loss, acoustic conductance examination of the tympanogram were A-shaped, pure tone audiometry examination of the experimental group in 2 cases of 3 ears high frequency hearing threshold at 35dB, the rest of the hearing threshold threshold threshold <25dB.
2.2 Sleep breathing monitoring and DPOAE response amplitude results
Subjects in both groups had disturbed respiratory index, mean oxygen saturation (SO2) and 1 kHz , 2
As shown in Table 1, the DPOAE response amplitude and blood oxygen saturation were statistically significantly different between the experimental and control groups (p<0.05), and the correlation between blood oxygen saturation and DPOAE response amplitude in the experimental group was analyzed by linear regression method, which showed that the DPOAE response amplitude and blood oxygen saturation were statistically different from each other. response amplitude and oxygen saturation had a negative linear correlation (r= -0.167); DPOAE response amplitude and AHI index showed a negative linear correlation (r= -0.123).
Table 1 AHI index, oxygen saturation (SO2) and DPOAE response amplitude in subjects of both groups (X±s)
Group AHI SO2 DPOAE response amplitude
Experimental group 59.8±12.5* (88.5±3.5)% ＊ 6.41±3.25*
Control group 4.2±2.2 (94.5±1.2)% 14.26±4.26
Note: Compared with the control group,* p<0.05
2.3 Results of response amplitude for each frequency of DPOAE
Table 2 Amplitude of each frequency response amplitude and statistical results of subjects in both groups (X±s)
Group Number of ears Stimulation frequency (kHz)
0.75
1.0 2.0
4.0
8.0
Experimental group 48 4.56±6.88*
7.46±7.66
8.67±4.84
7.97±5.38
2.73±6.55
Control group 20 9.98±2.99 13.05±5.85 14.98±5.79 15.29±3.95 14.91±5.03
t-value
3.196 2.508 3.619 4.800 6.466
p-value
0.0029 0.0154 0.0009 0.0000 0.0000
3 Discussion
Otoacoustic emission is an active mechanism that originates in the cochlea and is an audio energy produced by the outer hair cells of the cochlea and released into the external auditory canal through the conduction of the auditory chain and the tympanic membrane, which is an important part of normal human auditory physiology. DPOAE is a monitoring method for early reflection of cochlear function, with normal pure tone audiometry results in 8% to 47% of those with early cochlear damage. DPOAE is triggered by different frequency evoked sources, and it reflects the function of outer hair cells in cochlear segments at various frequencies from 0.5 to 8 kHz, and the specificity and stability of each frequency can indicate the basilar membrane segments involved [2]. telischi et al [3] found that otoacoustic emissions showed earlier impairment of cochlear function by ischemia than ABR through animal tests, and also that DPOAE was more sensitive than pure tone audiometry. Severe sleep apnea hypoventilation syndrome (SAHS) is an apnea or sleep hypoventilation caused by factors such as upper airway obstruction or central during sleep, accompanied by a decrease in oxygen saturation. SAHS can cause functional keying damage to systemic organs (including the cochlea), and thus the application of DPOAE to detect cochlear function in patients with SAHS can lead to early detection of cochlear damage.
In our study, we found that although patients with severe SAHS did not have any conscious hearing loss, and there was no significant hearing loss in the primary auditory examination, the response amplitude of DPOAE at all frequencies was significantly decreased, and the difference was significant compared with that of normal control group. The reason for the impairment of cochlear function in patients with severe SAHS is that frequent apnea or hypoventilation during sleep puts the body in a long-term hypoxic state, causing hypoxemia, hypercarbia, and metabolic disorders [4]; long-term hypoxia can also lead to an increase in compensatory erythropoietin, increased red blood cells, altered blood rheology, and viscous blood; the cochlear supply vessels are terminal vessels without collateral circulation, and this anatomical feature also makes the cochlea a vulnerable This anatomical feature also makes the cochlea a vulnerable organ. These combined factors can affect the oxygen and energy supply to the cochlea, resulting in delayed excitation transmission to the auditory system and decreased inner ear function. In addition, the noise generated by snoring in patients with severe SAHS may also cause noise-related damage to the cochlea.
This study suggests that severe SAHS can affect cochlear function early, as evidenced by a decrease in the response amplitude of each frequency of the DPOAE, which is altered earlier than subjective pure-tone audiometry. Since cochlear function is susceptible to damage, and this damage may precede functional changes in other important organs, otoacoustic emissions can be an important method to evaluate the condition of SAHS and provide a theoretical basis and guidance for early intervention in SAHS.
The study also found that the magnitude of the reduction in DPOAE was not uniform in patients with severe SAHS, with the magnitude of the reduction being greater in the middle and high frequencies, and the difference was more pronounced when compared to the normal population. Whether this difference is due to the anatomy of the cochlea or to other factors needs to be further investigated.
What is the cause of this difference?