**2. Current trends of thoughts concerning tinnitus pathophysiology**

Tinnitus is the perception of noise which is not generated by external stimulus [8]. It affects approximately 25% of the general population; one third on a frequent basis [9]. Tinnitus may be classified as auditory and para‐auditory tinnitus, with the former representing the major‐ ity of cases and the latter being subdivided into muscular and vascular tinnitus, sometimes referred as somatosounds [10].

According to the most recent trends of thought, tinnitus is not considered a disease, but a symptom, which may have multiple causes, sometimes even in a single patient [11, 12]. Noise exposure, metabolic and cardiovascular disease, presbycusis, ototoxicity and cranial and cer‐ vical trauma are the most frequently considered causes of tinnitus [12, 13]. Caffeine abuse, dietary factors, temporomandibular joint and cervical diseases have also been described as contributing factors [14–16].

Tinnitus is believed to be a central phenomenon that follows an initial peripheral dam‐ age [17–19]. The cochlear and/or auditory nerve damage may be permanent, temporary or even subclinical and central neuroplasticity, including decrease of efferent inhibition, tonotopical reorganization and activation of, or modulation by, non‐auditory areas have been demonstrated to account for many tinnitus features [17, 18]. Despite the general consensus regarding the role of peripheral damage on the onset of tinnitus, many other factors contribute to tinnitus distress [20]. The correlation of tinnitus improvement and hearing loss recovery in sudden sensorineural hearing loss exists, but is not robust [20]. Nevertheless, peripheral aspects of tinnitus may not be ruled out even in chronic tinnitus, considering that around 45% of the patients submitted to VIII pair neurectomy experi‐ mented tinnitus improvement [21]. Ménière disease, particularly, may be an important example of 'peripheral' tinnitus, considering that in the initial stages tinnitus (as well as the other symptoms) is intermittent and acute, with no sufficient time for the arousal of a fully manifested neuroplasticity.
