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.
Although mitochondrial DNA variants are thought to predispose to hearing loss, a study of polish individuals by Lechowicz et al, reported that "there are no statistically significant differences in the prevalence of tinnitus and its characteristic features between HL patients with known HL mtDNA variants and the general Polish population." This would argue against mitochondrial DNA variants as a cause of tinnitus, but the situation might be different in other ethnic groups.
Atherosclerosis. With age and buildup of cholesterol and other deposits, major blood vessels close to your middle and inner ear lose some of their elasticity — the ability to flex or expand slightly with each heartbeat. That causes blood flow to become more forceful, making it easier for your ear to detect the beats. You can generally hear this type of tinnitus in both ears.
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