It is possible that the most common cause of pulsatile tinnitus is sigmoid sinus diverticulum and dehiscence, which can be collectively referred to as sinus wall abnormalities or SSWA. The sigmoid sinus is a blood carrying channel on the side of the brain that receives blood from veins within the brain. The blood eventually exits through the internal jugular vein. Sigmoid sinus diverticulum refers to the formation of small sac-like pouches (diverticula) that protrude through the wall of the sigmoid sinus into the mastoid bone behind the ear. Dehiscence refers to absence of part of the bone that surrounds the sigmoid sinus in the mastoid. It is unknown whether these conditions represent different parts of one disease process or spectrum, or whether they are two distinct conditions. These abnormalities cause pressure, blood flow, and noise changes within the sigmoid sinus, which ultimately results in pulsatile tinnitus. Narrowing of the blood vessel that leads into the sigmoid sinus, known as the transverse sinus, has also been associated with pulsatile tinnitus.
Being exposed to loud noise on a regular basis from heavy equipment, chain saws or firearms are common causes of hearing loss and tinnitus. Noise-induced hearing loss and tinnitus can also be caused by listening to loud music through headphones or attending loud concerts frequently. It is possible to experience short-term tinnitus after seeing a concert, but long-term exposure will cause permanent damage.
About 25-30 million Americans have tinnitus as a condition, and they experience these noises on a regular, most often daily, basis. About 40 percent of people with tinnitus hear tinnitus noise through 80 percent of their day. And for a smaller group of people—about 1 in 5, tinnitus is disruptive enough to significantly interfere with daily functioning, becoming disabling or nearly disabling.
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.
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.
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