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.
FACT: Many people with tinnitus will also have a hearing loss. In fact, a recent French study showed that of 123 people with tinnitus surveyed only one did not have hearing loss. The British Tinnitus Association estimates that 90 percent of people with tinnitus also have a hearing loss. Moreover, research says that those who don’t may have a “hidden hearing loss.”
A large, 2014 study of almost 14,000 people found obstructive sleep apnea was linked to significantly higher rates of hearing impairment and hearing loss. Scientists think one reason for this is changes to blood flow to the ear that result in inflammation. (We know that sleep apnea causes changes to circulation and weakens blood flow to some areas of the body, including the brain.) A related factor? People with sleep apnea are at greater risk for high blood pressure, and high blood pressure can exacerbate hearing loss, according to research.
The majority of cases of tinnitus are subjective. Objective tinnitus is far less common. However, a diagnosis of objective tinnitus is tied to how hard and well the objective (outside) listener tries to hear the sound in question. Because of this problem, some clinicians now simply refer to tinnitus as either rhythmic or non-rhythmic. Generally, rhythmic tinnitus correlates with objective tinnitus and non-rhythmic tinnitus correlates with subjective tinnitus. Specific forms of tinnitus such as pulsatile tinnitus and muscular tinnitus, which are forms of rhythmic tinnitus, are relatively rare. Pulsatile tinnitus may also be known as pulse-synchronous tinnitus. Properly identifying and distinguishing these less common forms of tinnitus is important because the underlying cause of pulsatile or muscular tinnitus can often be identified and treated.
A common cause of tinnitus is inner ear hair cell damage. Tiny, delicate hairs in your inner ear move in relation to the pressure of sound waves. This triggers cells to release an electrical signal through a nerve from your ear (auditory nerve) to your brain. Your brain interprets these signals as sound. If the hairs inside your inner ear are bent or broken, they can "leak" random electrical impulses to your brain, causing tinnitus.