|Figure 1: The outer ear consists of the auricle (unlabelled), the external auditory canal, and the lateral surface of the tympanic membrane (TM). The middle ear includes the medial surface of the eardrum, the ossicular chain, the eustachian tube, and the tympanic segment of the facial nerve. The inner ear includes the auditory-vestibular nerve, the cochlea and the vestibular system (semicircular canals). The auditory nerve, also called the cochlear nerve, transmits sound to the brain.|
Carbon monoxide (CO) poisoning can cause hearing loss in addition to anoxic brain damage. The type of hearing loss is "sensorineural", which means that it is due to damage to the cochlea or 8th nerve (see figure 1 above). The literature largely consists of single case reports, as of course, there are few situations where there are groups of individuals exposed to CO. (Pillon, 2012; Skrzypczak et al, 2007; Michalska-Piechowiak, T., M. Miarzynska, et al. (2004).)
According to Baker and Lilly (1977), hearing loss is uncommon, but when present may often display a U-shaped audiometric curve. In other words, a "cookie bite" as is seen in persons with congenital hearing loss.
One would think that damage would be maximum in the most metabolically active cells -- the outer hair cells (causing loss of OAE's), and at high frequencies.
According to most sources, CO causes hair cell death, and also potentiates noise induced hearing loss (Chen et al, 1999; Fechter et al, 2000; Young et al, 1987).
Makishima et al (1977) suggested that instead, CO causes damage to central auditory pathways. We think although there is no doubt that diffuce anoxic brain damage would likely be associated with damage to auditory pathways, it seems unlikely to us that this is the mechanism for CO toxicity which has been noted in rats to be due to hair cell loss.
At the present writing, we have no method of bring dead inner ear hair cells back to life. Accordingly, treatment is "assistive", usually in the form of hearing aids if hearing loss is severe. CO poisoning may be reversible with time (Lee et al, 2002). Free radical scavengers and glutamate blockers have been reported to protect against CO toxicity, but of course, these are rarely in place prior to the exposure.