Effets de l'intoxication au monoxyde de carbone et de l'exposition au bruit sur les systèmes auditifs périphérique et central
Some studies have shown that acute poisoning with carbon monoxide (CO) may cause a hearing loss in humans. However, those studies failed to document and take into account the history of noise exposure in their participants. Moreover, in many of those studies, evaluation methods were used that today are not considered valid. The interpretation of the most affected test frequencies and of the potential severity of hearing loss are thus limited. The first study is a synthesis of case studies from literature (n=11) aiming to document which test frequencies are the most susceptible to demonstrate a hearing loss, and how auditory thresholds recover over time. Despite the important variability in the information available regarding the participant’s noise exposure, past medical history and treatments provided for carbon monoxide poisoning, our synthesis showed evidence for high frequencies hearing loss after acute carbon monoxide poisoning, with potential for recovery over time. However, most subjects included in the synthesis were not treated with hyperbaric oxygen therapy, the gold standard treatment for CO poisoning. Moreover, aggravation of the hearing loss by age or noise exposure may have occurred. Auditory thresholds were the only means for assessment of hearing in these subjects. Effects of the CO poisoning on several other hearing functions remain unknown. The participants of the second study were treated with hyperbaric oxygen therapy following acute CO poisoning (n=12). Since CO poisoning is known to cause memory and concentration effects and animal data suggest an auditory central effect of CO poisoning, the test battery included peripheral tests, such as hearing thresholds up to 16 000 Hz, as well as auditory processing tests. As in the first study, some of the participants presented a hearing loss in the high frequencies, sometimes followed by recovery. The second study shows a notch configuration in participant’s audiogram despite the absence of a history of noise exposure. No evidence of auditory processing changes attributed to carbon monoxide poisoning was found. When abnormal results were found, noise exposure, age or hearing loss effects seem the most plausible cause, except possibly for a correlation between CO poisoning severity and dichotic digit test results in the left ear. Outer hair cells damage has been long considered as an early sign of noise exposure. However, recent animal studies have found an even greater sensibility to noise in inner hair cells synapses with auditory nerve fibers. This synaptopathy is believed to lead to delayed auditory nerve fiber deterioration in the central auditory system. In humans, the effects of these changes are not well documented because of the available measurement tools (non-invasive measurements). The third and final study focussed on chronic noise exposure effects on auditory processing in middle-aged participants (n=25). Poorer performances for the tests using speech stimuli were found compared to normative data for young adults found in the literature. When compared to a middle-aged group taken from the literature, poorer low frequency gap detection scores were also found. Rank correlations between auditory brainstem responses to clicks and auditory processing performances also suggest that neural synchrony impacts auditory processing capacities. Those correlations were independent (rho < 0.4) from age and hearing loss effects. These results suggest that noise-induced cochlear synaptopathy may lead, after many years, to auditory processing alterations. If this is true, it may be necessary to review the interpretation of some existing studies that participants with chronic exposure to noise had a strictly cochlear hearing damage.
Voies auditives centrales Carbon monoxide Noise Hearing loss Hearing system Auditory processing Central hearing pathways Electrophysiology Auditory brainstem response Humans