Tinnitus is an auditory perceptual phenomenon that is defined as the conscious perception of internal noises without any outer auditory stimulation. Tinnitus may occur as a concomitant of practically all the dysfunctions that involve the human auditory system. Hence, damage to the middle ear, the cochlea, cranial nerve VIII (audiovestibular), and pathways in the brain from cochlear nucleus to primary auditory cortex all are likely candidates for explaining why tinnitus appears (Levine, 2001). A common distinction is between so-called objective tinnitus (somatosounds) and subjective tinnitus. In clinical settings, objective tinnitus represents a minority of cases. Examples of conditions related to objective tinnitus are spontaneous otoacoustic emissions, tensor tympani syndrome, and vascular lesions. Subjective tinnitus has been linked to sensorineural hearing loss caused by various deficits such as age-related hearing loss (presbyacusis), noise exposure, acoustic neuroma, and Ménière's disease (Levine, 2001), but also to other conditions such as temporomandibular joint dysfunction. Different neural mechanisms have been proposed, and tinnitus has been explained as the result of increased neural activity in the form of increased burst firing, or as a result of pathological synchronization of neural activity. Other suggested mechanisms are hypersensitivity and cortical reorganization (Rauschecker, 1999).