Abstract
Studies carried out by Brainstem Evoked Auditory Potentials (BEAP) in Noise-Induced Hearing Loss (NIHL) workers show different results in relation to neuronal involvement, not involving bus drivers as study object. AIM: to use BEAP in a prospective case/control clinical study to check whether or not there is neural auditory pathway involvement in bus drivers with NIHL. MATERIALS AND METHODS: we selected 50 bus drivers between 27 and 40 years with mild to moderate NIHL, and 20 individuals between 29 and 40 years with normal hearing and without prior history of noise exposure. BEAP tests were carried out and the traces were analyzed. RESULTS: in the NIHL group, the auditory thresholds in 3, 4 and 6 kHz were significantly higher in the left ear. In the NIHL group, potentials PI, PIII and/or PV were not present in a small number of the individuals; we observed a statistically significant increase in PI, PIII and PV absolute latencies, (LIP) LIP I-III interpeak latencies, bilaterally and LIP I-V in the left ear. CONCLUSION: in the NIHL group, besides sensorial injury, changes in BEAP latencies suggest an early functional injury of the first auditory pathway afferent neuron.
Highlights
Noise is one of the most prevalent noxious physical agents present in the work environment today, and one of the major problems found in factories, means of transportation and in the very getting together of people.Prolonged exposure to high intensity sounds produces successive changes to inner ear structures, initially transitional and later permanent
In the noise-induced hearing loss (NIHL) group, the ear laterality by the Wilcoxon test of the tonal thresholds of the audiometric frequencies of 3, 4 and 6 kHz, showed that they were significantly higher in the left ear (Table 1)
In the NIHL group, PI was not seen in 18% (N=9) of the ears, of which 10% (5/50) represented the right ear and 08% (4/50) the left
Summary
Noise is one of the most prevalent noxious physical agents present in the work environment today, and one of the major problems found in factories, means of transportation and in the very getting together of people.Prolonged exposure to high intensity sounds produces successive changes to inner ear structures, initially transitional and later permanent. The final result is damage to the sensorial hair cells and its highest expression is the destruction of most of the organ of Corti, causing noise-induced hearing loss (NIHL). Experimental studies showed the involvement of neural structures in NIHL1-3. Such studies have shown, besides degenerative alterations caused to the outer and inner hair cells, the involvement of neuronal synapses near sensorial cells and the degeneration of afferent fibers of the cochlear nerve. These authors suggest two hypotheses which could explain the neuronal damage: neural hyperactivity by the excessive acoustic stimulation and/or neuronal response to the hair cells degeneration
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