SSRI and Tinnitus

Anxiety/stress are common comorbid factors to chronic tinnitus. Thus, it common to see patients with tinnitus on selective serotonin reuptake inhibitors (SSRIs). SSRIs are believed to increase the extracellular level of the neurotransmitter serotonin by limiting its reuptake into the presynaptic cell, thereby increasing the level of serotonin available to bind to the post-sympatic receptor. SSRIs are commonly used to treat depression, anxiety, panic disorders, obsessive-compulsive disorder, chronic pain, etc. Common examples are sertraline (Zoloft), paroxetine (Paxil), and fluoxetine (Prozac). Previous research has suggested limited improvement in tinnitus with SSRIs and that use of these drugs with tinnitus patients should be limited to the application of treatment of the co-morbid anxiety/depression and not for tinnitus directly. There are also reports of tinnitus onset or exacerbation with SSRI.

Recently, Tang et al (2017) have provided some further insight into the role of serotonin on tinnitus and some additional support to not using SSRIs for tinnitus management. Using mice, Tang and colleagues examined changes induced by serotonin in the dorsal cochlear nucleus (DCN), the portion of the cochlear nucleus with inhibitory characteristics. Aberrant serotonin signaling has previously been implicated with hyperactivity in the DCN related to tinnitus. Tang identified that serotonin does not simply or globally increase activity in the DCN, but rather the neurotransmitter appears to suppress signaling through the auditory pathway while enhancing transmission through a multisensory pathway. This activation may have positive biological implications, such as integration of multisensory input for response to salient environmental events or negative implications, such as tinnitus and help explain modulation of tinnitus with head movement and changes in jaw position.

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Reference

Tang and Trussell. (2017) Serotonergic Modulation of Sensory Representation in a Central Multisensory Circuit is Pathway Specific. Cell Report 20(8):1844-1854.