To the Editor: We present, with interest, a case of a depressed gentleman, who suffered temporary hearing loss with subsequent auditory hallucinations:

Our patient is a 64-year-old White man, presenting with a Major Depressive Episode (MDE) of 1-month duration, with a Hamilton Rating Scale for Depression (Ham-D) score of 18 and auditory hallucinations (AH). He had no previous psychiatric, substance abuse, or medical history. His Mini-Mental State Exam score was 27/30.

Notably, he had hearing impairment, which had also begun 2 months before admission. His physical examination was remarkable only for bilateral cerumen impaction. Laboratory and radiological work-up were within normal limits, and both blood alcohol and urine drug screen were negative.

We began treating with olanzapine 5 mg bid and buproprion XR 150 mg qAM. Concurrently, he was treated with ceruminolytic drops and manual removal of cerumen until his external auditory canals were cleared. This resulted in marked improvement in his hearing. Five days later, the AH abated, despite a Ham-D of 16. Approximately 1 month later, his Ham-D was 4.

It has been reported that impacted cerumen does cause a significant degree of conductive hearing loss, with no significant correlation between the length of the cerumen plug and the severity of hearing loss.¹ Sensory (auditory) deprivation is followed by dramatic functional and structural changes in the auditory system. Notably, whereas cochlear injuries are accompanied by a reduced activity in the cochlear nerve, neural activity is increased at virtually all levels in the central auditory system in simple conductive hearing loss. This central hyperactivity could result from a central gain increase; the general purpose of this gain-modulation being to adapt neural sensitivity to the reduced sensory inputs, preserving a stable mean firing and neural coding efficiency.⁴ However, maintaining neural homeostasis at all costs, in the event of an auditory-system sensory deprivation, could be done at the price of amplifying “neural noise” due to the overall increase of gain (or sensitivity), ultimately resulting in the generation of AH.²

Alternatively, AH could result from an expanded cortical representation determined by an altered profile of input from the cochlea, which may pathologically enhance the functional importance of spurious neuronal activity.³

Other possible explanations for our patient's auditory hallucinations include a Major Depressive Episode with psychosis (MDEP). Although exact time to remission is impossible to predict, one review supports the hypothesis that a minimal of 3 weeks of treatment is necessary for MDEP to resolve.⁴ Thus, it would seem unlikely, that AH would respond to olanzapine after 5 days of treatment and removal of cerumen from auditory canals.

Auditory functional deafferentation has been experimentally induced within 24 hours of treatment and with removal of the offending agent, and returns to normal afferent activity by 5 days.⁵ Thus, the time course of “AH” remission in our patient, after treatment, seems to be supported by this result.