Participants
The EEG data from the two experimental subjects from a previous study (EB Bae, 2019) were included in this study. We compared the EEG data between the experimental group (N=2) and the control group (N=15). Of the two experimental subjects, one had tinnitus and the other had hyperacusis; thus, we selected patients with the same disorders as a positive control group from the previous researches database. EEG data of 17 subjects in total were used from completed clinical trials which introduced in the previous studies.
Because the two subjects had normal hearing, we selected EEG data from patients who had the same normal hearing from these approved research databases. In the first study, 7 out of 80 subjects had normal hearing; the mean score for right ear hearing was 8 (±4) dB and 8.9 (±4.9) dB for left ear hearing. In the second study, the control EEG data were from 8 out of 9 subjects who had normal hearing; the mean score for right ear hearing was 5 (±3.6) dB and 6.1 (±3.9) dB for left ear hearing (Table S1). Thus, the EEG data from a total of 17 subjects, 2 in the test group and 15 in the control group, all with an otologic disorder, were used in this study. In total, the EEG data from eight tinnitus cases were used. One case was for the test group and seven cases were for the control group. From the hyperacusis database, one case was used for the test group, and eight cases were used for the disorder control group (Table 1).
Experimental subjects
The experimental subject with tinnitus has been working at a noisy construction site with an extremely loud booming sound that could cause hearing loss in healthy people, such as a metal banging sound or sound from heavy equipment. Even if his bilateral hearing thresholds were within normal range, see Table 1, tinnitus was developed because of chronic exposure to an extremely noisy working environment during working hours for a long duration 16,43.
Although the noise level of the working environment was not enough to cause hearing loss in this subject, it is thought that tinnitus, which is commonly found in hearing loss patients, is caused by chronic exposure to loud noises 12. The tinnitus sound got louder on the day he worked, and he also complained that his tinnitus remained even on his off-day. During much of his working hours, he was exposed to high random frequencies and high intensity noise; thus, he was defenseless exposed to the sound and had to listen to the noise throughout his working hours. As a result, he experienced auditory trauma from the occupational noise in his working environment 3,26,44-46.
Another otologic disorder is chronic hyperacusis. Hyperacusis has different symptoms than those of tinnitus in that the condition cannot be recognized without an external noise 8. Tinnitus is a ringing sound usually in the hearing damaged ear that occurs all the time without any external noise 1,9,47. However, hyperacusis symptoms in normal hearing usually occur only when patient heard a sound in a noisy environment. Sound or noise is a necessary condition to provoke symptom of hyperacusis. In the second experimental case, the female patient was aware of her physical symptoms herself when she was exposed to only a noise louder than her uncomfortable level (UCL).
She was a teacher in a girl’s high school. Most of her unpleasant sounds came from the working environment. The sounds that provoked her symptoms were piano, food plate scraping, stereo sound, and speaker sound in the playground, and she also got symptoms when teenage girls would suddenly shout loudly. These sounds are unpredictable, high frequency, loud and can cause hyperacusis symptoms. The UCL was measured by pure-tone audiometry, and the mean threshold was 84.3 (±5.0) dB. She had the same UCL on the right and left ear. This UCL was a higher intensity than that of the other hyperacusis controls whose average thresholds were 76.3 (±19.5) dB (Table S1.). Each patient’s noise condition is described in the supplementary data (SI 1.).
Electroencephalography test
The same procedure was used as in a previous study (prev. ref). EEG data were recorded from the two experimental subjects and 15 controls. Two reference electrodes were located each on the right and left ear, and we used the average reference montage. EEG was recorded in a sound- and electrically-shielded booth. While recording the EEG for 5 minutes, no sound was induced except for case 2 with hyperacusis. Post-processing of the EEG data included baseline correction, eye movement and other artifact rejection, interpolation of bad channels, and averaging using Independent Component Analysis methods.
Analysis
Comparisons were done among the two noise conditions in the experimental subjects and the control group. A total of three groups were used: the no sound exposed state (NS) group, the after noise induced condition (aNI) group, and the positive control group (see figure 2).
The neuronal power density of each group was represented by brain topography. The color scale bar of the gamma band was normalized to 20% of the maximum thresholds, and the gamma-theta ratio was normalized to 300%.
Neuronal activity was evaluated by the amplitude and frequency rates. Brain areas were grouped by bilateral auditory and non-auditory cortex; statistically, a minimum of four channels were used for auditory cortex (see, figure 1, 2). Non-parametric analysis was done by two-independent test. Moreover, Kruskal Wallis test was done among the three groups. All the statistically results presented in this study were obtained by SPSS v.23, IBM.
Using Low-Resolution Brain Electromagnetic Tomography (LORETA) program, we compared the activity of the whole brain area among the noise induced states of the two experimental subjects, the no sound exposed state, and the positive control group.