Review of Opioid-Associated Hearing Loss and Possible Mechanism of Opioid-Mediated Endothelin-1-Dependent Cochlear Vasoconstriction

Review of Opioid-Associated Hearing Loss and Possible Mechanism of Opioid-Mediated Endothelin-1-Dependent Cochlear Vasoconstriction

Within the past several decades, there have been multiple reports of profound sensorineural hearing loss attributed to opioid use. Among the implicated opioids are both prescription analgesics used within their recommended dosages such as codeine, hydrocodone/ acetaminophen, and oxycodone/acetaminophen, as well as illicit substances such as heroin. Opioid-associated hearing loss has lead to both reversible and irreversible profound bilateral hearing loss, and the mechanism by which this occurs is currently unknown. Audiometry, otoacoustic emission, and auditory brainstem responses suggest that the lesion is cochlear in origin, as does the finding that patients with irreversible loss respond well to cochlear implantation. A plausible mechanism for this loss is opioid-induced vasoconstriction causing cochlear ischemia and subsequent hearing loss. Opioid receptors have been found in the inner ear in various animal models, and opioids are well-known to promote diminished blood flow, ischemia, and infarction. Opioids are also known to increase the production of and stimulate the release of endothelin-1, which is a potent endogenous vasoconstrictor that is found throughout the body as well as in the inner ear. In this review, we summarize the reports of opioid-associated hearing loss and propose that this hearing loss is mediated by vasoconstriction and cochlear ischemia via opioid-mediated stimulation of the vasoconstrictor endothelin-1.