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Arifov Sayfitdin Saidazimovich, Tashkent institute of advanced doctors Yunusova Gulnoza Yarkinovna, Tashkent institute of advanced doctors E-mail: bonusha-uz@list.ru
STUDYING THE CONDITION OF ACOUSTIC STEM POSSIBLE POTENTIALS IN PATIENTS WITH OTOSCLEROSIS
Abstract: The aim of this research was to study the characteristic changes in acoustic brainstem waves caused by potentials in patients suffering from otosclerosis in order to assess the functional state of the auditory analyzer pathways. 100 patients suffering from otosclerosis were studied. The age of patients ranged from 30 to 50 years. Depending on the side of the lesion involved in the otosclerotic process, the patients were divided into 2 groups: group 1 was 65 patients with bilateral otosclerosis, group 2 was 25 patients with unilateral otosclerosis. The study showed that the patients with otosclerosis have abnormalities in the conductive component of the auditory analyzer, which is confirmed by the results of the study of acoustic brainstem evoked potentials. In a two-sided process, changes are observed at the latency amplitude of all acoustic brainstem evoked potential waves. Whereas with a one-way process, changes in the latency and amplitude of the IV and V waves were not observed.
Key words: otosclerosis, acoustic brainstem evoked potentials, otoacoustic emission, auditory analyzer pathways.
The problems of complex diagnostics and treatment of the auditory path. Peak I and II come from the auditory nerve, patients with otosclerosis do not lose their relevance [2; 3; 4]. For many years, the state of various parts of the auditory analyzer in patients with otosclerosis has not lost its relevance. There are suggestions that otosclerosis is a degenerative process that affects the entire organ of hearing. But this question requires more detailed research and evidence. In the literature, science-based work in this direction is not enough.
In this regard, it was of interest to study the functional state of the auditory analyzer pathways in patients with otosclerosis.
The study of the functional state of the conducting pathways of the auditory analyzer in patients with otosclerosis will clarify its pathogenesis, which contributes to the improvement of diagnostic methods and complex treatment of this pathology.
To date, the existing arsenal of modern medical equipment, provides an opportunity to study the functional state of the auditory system throughout its length. Acoustic brain-stem evoked potentials [1, 6, 12] have proven themselves to objectively assess the functional state of the auditory analyzer pathways. The study of acoustic brainstem evoked potentials shows the state of the longest portion of the auditory analyzer. In particular, acoustic brainstem evoked potentials are far-field potentials and reflect the state of the auditory stem nuclei of different levels and the state of the auditory nerve [5].
Acoustic brainstem evoked potentials, being the earliest response potentials for the auditory stimulus, have a typical morphology. Peaks or waves appear in the responses. Each wave corresponds to an excited neuron in specific nuclei of
peak III comes from the cochlear nuclei. Peak IV is produced in the olive complex and V- in the lateral lemniske [10]. Waves appear at a certain latency of the corresponding stimulus intensity. The lower the intensity, the longer the latency. When high intensity neurons are excited faster, it means that synaptic transmission is faster. This leads to a shortening of latency. Thresholds of acoustic brainstem evoked potentials correlate well with subj ective tonal audiometry, which has been proven by many studies [13; 14].
Changes in acoustic brainstem evoked potentials are more specific than other modalities. Using the study of acoustic brainstem evoked potentials, it is possible to identify a lesion of the peripheral link of the auditory analyzer, the auditory nerve, stem structures, regardless of the age and degree of contact of the patient.
Thus, the study of the functional state of the auditory analyzer pathways in patients with otosclerosis will reveal new aspects of the pathogenesis of this disease.
Purpose of the study. To study the characteristic changes in acoustic brainstem waves caused by potentials in patients suffering from otosclerosis in order to assess the functional state of the auditory analyzer pathways.
Materials and methods. 100 patients suffering from otosclerosis were studied. The age of patients ranged from 30 to 50 years. The average age of 39.2 ± 8.6 years.
Depending on the side of the lesion involved in the oto-sclerotic process, the patients were divided into 2 groups: group 1 - patients with bilateral otosclerosis - 65 patients, group 2 - patients with unilateral otosclerosis - 25 patients. At
the same time, patients with a tympanic form of otosclerosis were selected to exclude the influence of the inner ear, which occurs when its form is mixed.
The control group consisted of 20 volunteers between the ages of 30-45 years old, with normal hearing (according to tonal threshold audiometry), who did not show any pathological changes during otoscopy, tympanometry - type "A" from two sides, delayed induced otoacoustic emission is recorded with both sides. An individual analysis of wave parameters of acoustic brainstem evoked potentials in patients was performed under the condition of counting the intensity of the stimulating signal from the hearing threshold of each patient (dB SL). In the control group, acoustic brainstem evoked potentials were estimated by sending tone bursts 40 dB SL above the threshold. For a given above-threshold volume of a stimulus, all waves of acoustic brainstem evoked potentials are distinguished.
The registration of the auditory evoked potentials was carried out on the Neuro-Audio apparatus (Neurosoft, Russia), in conditions of the patient's calm wakefulness. Patients in the study were in a reclining position.
The analysis of acoustic brainstem evoked potentials was performed at the end of the test using the function of marking the peaks of acoustic brainstem evoked potentials, measuring the amplitude of the selected peaks, fixing the FMP (Feature Modeling Plug-in) parameters, fixing the number of runs required to achieve 99% probability of signal reliability.
According to the results of the study, the smallest number of runs to obtain a reliable response is required when using the Chirp-stimulus with a frequency of 1000 Hz (Samkova).
Monaural acoustic stimulation was performed using 1000-Hz Cirp-stimulus headphones. The intensity of the stimulus was chosen individually at the rate of 40 dB above the subjective threshold and ranged from 100 to 120 dB. The frequency band is from 0.5 to 100 Hz, the number of averagings is 2000, the epoch of analysis is 10 ms. The response of acoustic brainstem evoked potentials was recorded during ipsilateral monaural stimulation. Allocation was carried out according to a single-channel scheme, with the location of the active electrodes at the ipsi-M1 point (mastoid of the side under study), the reference electrode - at the contra-M2 point (contralateral mastoid), grounding - Fpz. The study was carried out according to the parameters recommended by the manufacturer (N. Y. Shubina et al., 2013). The absolute latencies of peaks I, II, III, IV, V, peak intervals I - III, III - V, I - V, amplitudes of peaks I - Ia, III - IIIa, V - Va were analyzed.
Patients were enrolled after receiving informed consent for this procedure.
Results of research. The study revealed that in patients with otosclerosis, there is a general shift in the curve of acoustic brainstem evoked potentials to the right.
In the first group, an increase in the absolute latency of all the waves was observed, as well as an increase in the inter-peak intervals between all the waves of the acoustic brainstem evoked potentials. In the second group, the absolute latency of all waves was also increased compared with the control group. The peak interval, unlike the first group, increased in the interval I - II and II-III, and the peak interval III-IV and IV - V did not differ from the indicators of the control group (Table 1).
Table 1.- The latency parameters of acoustic brainstem evoked potentials in patients with otosclerosis (M±o)
Parameters Control group 1-group 2 - group
Peak latency, ms I 1.83 ± 0.14 2.48 ± 0.15* 2.38 ± 0.14*
II 2.81 ± 0.1 3.63 ± 0.19* 3.56 ± 0.17*
III 3.97 ± 0.16 4.91 ± 0.13* 4.9 ± 0.13*
IV 5.12 ± 0.12 6.26 ± 0.21* 6.02 ± 0.18*.**
V 5.83 ± 0.17 7.39 ± 0.17* 6.76 ± 0.16*.**
Inter-peak interval, ms I-II 0.98 ± 0.12 1.15 ± 0.06* 1.18 ± 0.06*
II-III 1.16 1.28* 1.34*
III-IV 1.15 1.35* 1.12**
IV-V 0.71 1.13* 0.74**
I-V 4.0 4.91* 4.38*.**
I-III 2.14 ± 0.13 2.43 ± 0.11* 2.52 ± 0.11*
III-V 1.86 ± 0.17 2.48 ± 0.11* 1.79 ± 0.13**
*- statistically significant changes compared with the control group (p < 0.05); ** - statistically significant changes compared with the 1 - group (p < 0.05)
So, if in the control group the latency of the I, III and V 4.91 ± 0.19 and 7.39 ± 0.13 ms, and among patients of the waves was 1.83 ± 0.14, 3.97 ± 0.1 and 5.83 ± 0.16 ms, among 2nd group 2.38 ± 0.14, 4.9 ± 0.17 and 6.76 ± 0.13, respectively. patients of the 1st group, these figures were 2.48 ± 0.15,
In this case, the peak intervals I-II and II-III, in the control group were 0.98 ms and 1.16 ms. In the first group, these figures significantly increased to 1.15 ms and 1.28 ms, while in the second group, a significant increase was also observed to 1.18 ms and 1.34 ms, respectively. Inter-peak intervals III-IV 8
and IV-V differed in the two examined groups. So, if in the control group these figures were 1.15 and 0.71 ms, in the first group there was an increase to 1.35 and 1.13 ms, whereas in the second group these figures did not differ from the control group, amounting to 1.12 and 0.74 ms, respectively.
Control
2-side otosclerosis 1-side otosclerosis
Figure 1.
Wave latency curves of acoustic brainstem evoked potentials in the control group and patients with otosclerosis.
Figure 1 shows how there is a shift in the curve of the acoustic brainstem evoked potentials to the right, and the differences in its IV and V waves.
Thus, the peak interval I-II and II-III were equally extended in both groups compared to the control, whereas intervals III-IV and IV-V were significantly increased compared to the control only in patients of the first group, and in the second group these indicators did not differ from control. Intervals III-IV and IV-V in the first and second groups differed significantly among themselves.
When assessing the amplitude of the waves, we paid attention to the detection threshold of the V wave in the control group and in the examination groups. It was revealed that in the control group the threshold of detection of the V wave corresponded to the threshold of hearing, which was detected during a tone audiogram. In patients with otosclerosis, the threshold for detection of the V wave acoustic brainstem evoked potentials was increased by 20-25 dB, i.e. All waves
of acoustic brainstem evoked potentials in the control group were distinguished when the threshold was increased by 20 dB above the threshold of the audiogram, and in patients with otosclerosis only with an increase of 40 dB above the patient's hearing threshold. This indicates a sharp decrease in wave amplitude. A comparative analysis of wave amplitudes was carried out with an increase in the stimulus of 40 dB above the patient's hearing threshold.
In the first group, a statistically significant decrease in the amplitude of all waves was observed. Thus, the amplitude of waves I-Ia and III-IIIa in the control group was 0.13 ^V and 0.36 ^V, in the first and second groups these figures were reduced, and in the first group they were 0.056 and 0.18 ^V and in the second group 0.059 and 0.18 ^V, respectively. The amplitude of the V-Va wave in the control group was 0.47 ^V, while there was a difference in the groups, i. e. if in the first group the amplitude of the V-Va wave was 0.34 ^V and was significantly different from the control group, in the second group this indicator was 0.45 ^V and did not differ from the control group (table 2).
Table 2.- Wave amplitude parameters of acoustic brainstem evoked potentials in patients with otosclerosis (M ± o)
Parameters Control group 1-group 2-group
Peak amplitude, ^V I-Ia 0.13 ± 0.02 0.056 ± 0.02* 0.059 ± 0.01*
III-IIIa 0.36 ± 0.05 0.18 ± 0.04* 0.18 ± 0.04*
V-Va 0.47 ± 0.03 0.34 ± 0.05* 0.45 ± 0.05**
* - statistically significant changes compared with the control group (p < 0.05); ** - statistically significant changes compared with the 1-group (p < 0.05)
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Discussion. The main changes identified in the study of acoustic brainstem evoked potentials in otosclerosis was to increase the latency and decrease the amplitude of the peaks.
An increase in acoustic brainstem evoked thresholds indicates that the number of functioning axons and neurons is decreasing. When comparing the amplitudes of the waves, a significantly smaller amplitude of all the waves of acoustic brainstem evoked potentials in patients with otosclerosis was also revealed.
The decrease in activation of the auditory nuclei caused by otosclerosis can be interpreted as a reduced stimulation of the activation of neurons.
There was interest in changes in acoustic brainstem evoked potentials in a one-way process, since it is known that the auditory pathway has a cross. Most of the axons II of the neuron, which, on the curve of acoustic brainstem evoked potentials, constitutes the third wave, switches to the opposite side, switching in the upper olive and the nuclei of the trapezoid body. Another, smaller part of the fibers ends on its own side. The axons of the nucleus of the upper olive and trapezoid body (III neuron) are involved in the formation of the lateral loop, in which there are fibers of the II and III neurons.
The main differences in the two groups were observed on the latency of the IV and V waves, as well as on the inter-peak intervals I-V and III-V.
With conductive hearing loss, the time required to transmit sound along the middle ear and activate the cochlea increases. The total amount of sound energy reaching the cochlea decreases. Consequently, the latency of wave I is inhibited, and the curve of the intensity of the latency of wave V shifts to the right by an amount equivalent to hearing loss, without any change in the slope of the curve. Since the latency of wave I is extended longer than the latency of wave V, the interval between intervals V-I is reduced [9]. But according to the results of our study in patients with bilateral otosclerosis, we observed an increase in both absolute and relative latency of all waves.
The data from the study show that a decrease in peripheral auditory stimulation in itself is detrimental to the efferent and afferent innervation of the hair cells in ways similar to that
observed with age-related and noise-induced hearing loss. The mechanisms underlying cochlear deefferentation, according to the authors, indicate a decrease in cholinergic stimulation in the auditory nerve to the level of the olycochlear complex, which is confirmed by experimental studies [8].
The reasons for these changes can be explained by experimental studies. In the study of the metabolic activity of the auditory nuclei through the measurement of the absorption of 2-deoxyglucose, experimental conductive hearing loss led to a marked decrease in its absorption [15]. In another study, there was a significant decrease in the activity of cytochrome oxidase in conductive hearing loss in the ipsilateral antero-ventral cochlear nuclei [16].
In addition, according to other authors, with experimentally induced conductive hearing loss, a decrease in vGluT1 expression in the presynaptic terminal, a decrease in the size of synaptic vesicles, and an increase in the thickness of the post-synaptic membrane in the cochlear nucleus were found [7]. Conductive hearing loss also led to a decrease in the number of synchses of the cochlear nerve in the cochlear nuclei [11].
Thus, the resulting changes in the waves of acoustic brainstem evoked potentials in our study indicate the presence of functional changes in the conductive segment of the auditory system in patients with otosclerosis.
All these changes result from a lower rate of activation of distribution in afferent pathways and a delayed reaction to cortical and subcortical levels. It is possible that the decrease in the amplitude of the acoustic stem waves evoked potentials is a consequence of prolonged deafferentation, which leads to a decrease in the nuclei in the stem structures of the auditory tract [12].
Findings:
1. Patients with otosclerosis have abnormalities in the conductive component of the auditory analyzer, which is confirmed by the results of the study of acoustic brainstem evoked potentials.
2. In a two-sided process, changes are observed at the latency amplitude of all acoustic brainstem evoked potential waves. Whereas with a one-way process, changes in the latency and amplitude of the IV and V waves were not observed.
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