Antidepressants are occasionally associated with tinnitus (Robinson, 2007). For example, Tandon (1987) reported that 1% of those taking imiprimine complained of tinnitus. In a double-blind trial of paroxetine for tinnitus, 3% discontinued due to a perceived worsening of tinnitus (Robinson, 2007). There are case reports concerning tinnitus as a withdrawal symptom from Venlafaxine and sertraline (Robinson, 2007). In our clinical practice, we have occasionally encountered patients reporting worsening of tinnitus with an antidepressant, generally in the SSRI family.
Demographic variables (age, sex, type of tinnitus) and baseline THI scores of placebo (n = 16) and treatment (n = 11) groups did not significantly differ from one another at the start of the study. At 3 months, participants in the treatment group reported significantly lower scores on the THI when compared to the placebo group (p < .05). The treatment group also showed an 11-point drop in THI scores when comparing baseline and 3 months (p < .05; please see Figure 2). THI scores for the placebo group comparing both time points were non-significant. Past studies have indicated that the minimum change in the THI score to be considered clinically significant is a drop of 6 to 7 points.9 As such, the results of our clinical study suggest that tinnitus and its related symptoms can produce a clinically significant reduction in tinnitus within the first 3 months using the personalized music-based therapy.
Supporting the idea that central reorganization is overestimated as "the" cause of tinnitus, a recent study by Wineland et al showed no changes in central connectivity of auditory cortex or other key cortical regions (Wineland et al, 2012). Considering other parts of the brain, Ueyama et al (2013) reported that there was increased fMRI activity in the bilateral rectus gyri, as well as cingulate gyri correlating with distress. Loudness was correlated with values in the thalamus, bilateral hippocampus and left caudate. In other words, the changes in the brain associated with tinnitus seem to be associated with emotional reaction (e.g. cingulate), and input systems (e.g. thalamus). There are a few areas whose role is not so obvious (e.g. caudate). This makes a more sense than the Wineland result, but of course, they were measuring different things. MRI studies related to audition or dizziness must be interpreted with great caution as the magnetic field of the MRI stimulates the inner ear, and because MRI scanners are noisy.
Another thing that tinnitus and sleep problems share? A tendency among people to brush them off, and try to “tough it out,” rather than addressing their conditions. It’s not worth it, to your health or your quality of life. If you’re having trouble sleeping and you have symptoms that sound like tinnitus, talk with your doctor about both, so you can sleep better—and feel better— soon.
A diagnosis of tinnitus is based upon identification of characteristic symptoms, a detailed patient history, a thorough clinical evaluation and complete audiologic testing. These steps will help to differentiate rhythmic tinnitus from non-rhythmic tinnitus. It cannot be overemphasized that tinnitus is a symptom of another underlying condition and not a diagnosis in and of itself. Because of the high number of underlying causes of tinnitus, a variety of specialized tests to detect the specific cause may be necessary. Attempting to identify the underlying cause of tinnitus is the first step in evaluating a person with tinnitus.
When tinnitus is unexpected and unwelcomed, it can lead to a negative reaction to the tinnitus. This can create a vicious cycle. When tinnitus is perceived, it can prompt emotions, including frustration, fear, unhappiness, etc. These can, in turn, cause physical reactions such as anxiety and stress. This reinforces the tinnitus and perpetuates the cycle.
Some persons with severe TMJ (temporomandibular joint) arthritis have severe tinnitus. Generally these persons say that there is a "screeching" sound. This is another somatic tinnitus. TMJ is extremely common -- about 25% of the population. The exact prevalence of TMJ associated tinnitus is not established, but presumably it is rather high too. Having TMJ increases the odds that you have tinnitus too, by about a factor of 1.6-3.22 (Park and Moon, 2014; Lee et al, 2016). This is the a large risk factor for tinnitus, similar to the risk from hearing loss (see table above).
An assessment of hyperacusis, a frequent accompaniment of tinnitus, may also be made. The measured parameter is Loudness Discomfort Level (LDL) in dB, the subjective level of acute discomfort at specified frequencies over the frequency range of hearing. This defines a dynamic range between the hearing threshold at that frequency and the loudnes discomfort level. A compressed dynamic range over a particular frequency range is associated with subjectve hyperacusis. Normal hearing threshold is generally defined as 0–20 decibels (dB). Normal loudness discomfort levels are 85–90+ dB, with some authorities citing 100 dB. A dynamic range of 55 dB or less is indicative of hyperacusis.
Avoid a too-quiet bedroom. People with tinnitus may find it easier to sleep in a less quiet bedroom, and may benefit from white noise or other sleep-friendly sounds that help mask and minimize their tinnitus. To my patients who are looking to introduce soothing sounds to their sleep environment, I recommend the iHome Zenergy Sleep System, which combines relaxing sounds with aromatherapy and sleep-promoting light therapy.
Meniere’s disease isn’t directly connected to tinnitus, but people with Meniere’s often experience it, at least temporarily. Meniere's disease is an inner ear disease that typically only affects one ear. This disease can cause pressure or pain in the ear, severe cases of dizziness or vertigo and a ringing or roaring tinnitus. While Meniere’s isn’t fully understood, it appears that several relief options for tinnitus can also help with this disease. Patients are often advised to reduce stress and lower their consumption of caffeine and sodium.