Table 1.

Summary of etiology and probable pathogenesis of tinnitus.

Etiology of Tinnitus	Probable Pathogenesis
Vascular disorders (arterial bruits, arteriovenous shunts, paraganglioma, venous hums)	Tinnitus caused by vascular disorders (arterial bruits, arteriovenous shunts, paraganglioma, venous hums) is usually associated with blood flow or vascular abnormalities in the head or neck near the cochlea. When the blood vessels in the skull or neck are abnormal, they may stimulate hair cells in the cochlea (part of the inner ear) and transmit to the cochlea through the bony structure, so that tinnitus consistent with the heartbeat can be heard, causing pulsatile tinnitus [5].
Neurologic disorders	Tinnitus may be related to abnormalities in the central nervous system and problems in the limbic and autonomic nervous systems. The limbic system belongs to the non-auditory central part, mainly composed of the hippocampal formation, parahippocampal gyrus, cingulate, and amygdala. Some studies have shown that the limbic system is involved in the formation of tinnitus. Nervous system disorders (such as anxiety, depression) are closely related to parts of the limbic system such as the hippocampus and prefrontal lobe, resulting in tinnitus [6].
Eustachian tube dysfunction	The tension of the peripheral muscles of the eustachian tube produces asynchronous pulsatile tinnitus, while the incomplete closure of the eustachian tube reduces the effect of body sound masking, and the internal noise is abnormally transmitted to the ear, resulting in the self-sound of breathing and the perception of unusually loud sound, which makes it easier for patients to hear body voices [7].
Other somatic disorders (temporomandibular joint (TMJ) dysfunction)	Hypertonia of the masticatory muscles due to TMD and excessive tension of ligaments close to the ossicles of the middle ear may be associated with somatosensory tinnitus, and these abnormal signals may affect the auditory pathway through the cochlear nerve. However, somatosensory tinnitus persists after the auditory nerve is severed, so these peripheral system explanations cannot be the sole explanation for the source of somatosensory tinnitus. Furthermore, the trigeminal nucleus in the somatosensory system receives sensory inputs from the temporomandibular joint (TMJ) and projects them to the cochlear nucleus (CN) through different nerve fibers, which allows the somatosensory system to affect the auditory system by altering the spontaneous rate and the synchronized firing patterns among neurons in the hypothalamus or auditory cortex, resulting in tinnitus [8,9].
Originating from auditory system:
(1) ototoxic medications	Drug-induced deafness is mainly due to the imbalance of the ion concentration in the endolymph as a result of the toxicity of drugs, which damages hair cells, spiral ganglia, and vascular veins in cochlea, leading to tinnitus [10].
(2) presbycusis	With the increase in age, the inhibitory function of the auditory center on auditory afferent information is gradually weakened, which leads to further changes in the auditory system and produces tinnitus [11].
(3) otosclerosis	Conductive hearing loss, the loss of cochlear hair cells in the inner ear, and abnormalities in peripheral sensory pathways all lead to hearing deprivation. This deprivation activates neuroplasticity, ultimately resulting in the production of tinnitus. Furthermore, dysfunction of the middle ear muscles can result in alterations in the stimulation of the somatosensory system, ultimately leading to the development of tinnitus [12,13].
(4) vestibular schwannoma	The ephaptic coupling of nerve fibers through microvascular compression or other pathways can lead to the synchronous firing of many nerve cells, which may be associated with the development of tinnitus. Furthermore, aberrant vestibulocochlear nerve input signals and nerve damage can lead to auditory deprivation and trigger neuroplasticity, resulting in the development of tinnitus [14,15].
(5) Chiari malformations	Elevated intracranial pressure caused by hydrocephalus and obstructed cerebrospinal fluid outflow can lead to pulsatile tinnitus. Of course, it is not ruled out that the pressure of the cerebellar tonsil on the vestibulocochlear nerve causes non-pulsating tinnitus [12,15].
(6) noise-induced hearing loss	Noise deafness is mainly caused by noise changing the transmission of neurotransmitters in the auditory central nervous system, resulting in abnormal excitation of the auditory cortex to produce tinnitus [16].