Transient tinnitus, which is experienced by almost every adult, is an auditory hallucination caused by auditory dysfunction and becomes a symptom when it exceeds the physiological limit. If the tinnitus becomes persistent and severe (some patients have a central source of tinnitus and complain of tinnitus in the brain, which is a special form of tinnitus), it not only interferes with normal life and sleep, but can also lead to cardiovascular disease, digestive disorders, anxiety and depression. Understanding the issues related to tinnitus classification, pathogenesis and mechanism of occurrence is crucial to the recognition and treatment of tinnitus. Tinnitus caused by cochlear lesions can be classified as organic tinnitus, while those not caused by cochlear lesions should be classified as functional tinnitus. According to the characteristics of tinnitus, it can be divided into two categories: subjective tinnitus (tinnitus for short) and other-perceived tinnitus. The former is felt by the patient and cannot be heard by others, and is very common clinically; the latter can be heard by others and is rare clinically, and its basis of occurrence is related to myoclonus or vascular malformation. In patients with conductive deafness, the tinnitus is mostly low-pitched, such as machine roar, blowing wind, or running water, while in patients with sensorineural deafness, the tinnitus is mostly high-pitched, such as cicada. Tinnitus can be caused by adjacent tissue lesions in the ear or by systemic lesions. Anxiety, fatigue or emotional stress can easily trigger tinnitus, but patients with such tinnitus may have completely normal hearing at the time of consultation, and no substantial local or systemic lesions can be detected. Tinnitus can be unilateral or bilateral, and the tone can be high or low, such as cicada, machine roar or siren sound, etc. Most or most of the patients with persistent tinnitus have hearing impairment. The author’s statistics on tinnitus patients in the past 10 years show that there is a significant and continuous increase in the number of patients with persistent severe tinnitus who have completely normal hearing, and this type of tinnitus is also called primary tinnitus. The prevalence of varying degrees of pathological tinnitus is about 20%, and tinnitus patients who significantly affect their quality of life account for about 2-3% of the adult population. A large sample of the general population aged 55-99 years showed that the prevalence of tinnitus was 30.3%, and half of them had tinnitus lasting more than 6 years. The prevalence of tinnitus is high in patients with sensorineural deafness and 83% in patients with autoimmune inner ear disease. A survey of patients with iron deficiency anemia by the authors of this article suggests that the incidence of intermittent or persistent tinnitus in this population is about 35%. It is generally believed that abnormalities of the auditory nerve sensation due to various causes and the displacement of the relative relationship between the capsule and the auditory hair cells are associated with the occurrence of tinnitus. Tinnitus associated with sensorineural deafness may be due to loss or alteration of normal spontaneous activity of cells in the damaged part of the cochlea, or to a diminished ability of the auditory nerve to filter afferent signals. The triad of tinnitus, hypoacusis, and hypoacusis (especially after cranial trauma and acute acoustic injury) is a common pathophysiological condition that occurs based on abnormalities in the function of cochlear hair cells, firstly causing a malfunction in the conduction of acoustic signals to the auditory center, and secondly, hypoacusis, in which the auditory center receives and possibly reshapes the malfunctioning acoustic signals. neuroplasticity) can increase the amount of acoustic signals received by the auditory center, causing auditory hypersensitivity, and the reception of phantom acoustic signals, causing tinnitus. In turn, the reception of phantom acoustic signals by the auditory center induces a reorganization of the acoustic signals received by the auditory center itself, aggravating the hearing impairment. Temporomandibular joint dysfunction can stimulate the auriculotemporal nerve, open the somatosensory bypass, and induce increased excitability of the dorsal nucleus of the cochlea, thereby altering auditory nerve plasticity and causing tinnitus. Therefore, according to the current understanding of 5-hydroxytryptamine regulation of nerve excitability and plasticity, decreasing the tone of 5-hydroxytryptaminergic nerves can worsen tinnitus, while improving temporomandibular joint function or/and enhancing the excitability of 5-hydroxytryptaminergic nerves can help prevent the formation of tinnitus memory loops. Therefore, for persistent severe tinnitus of more than 1 month duration, clinical signs should be examined first, and audiological examinations (generally including electrical audiometry, acoustic conductance, brainstem potential, and otoacoustic emissions) should be selected based on the signs to analyze the site of origin of the tinnitus, and then targeted treatment should be taken based on the results of local and systemic etiology.