Tinnitus pathogenesis is not yet clear, with further research, academia made a lot of possible mechanisms. Studies have shown that between neighboring excitatory neurons and hair cells synchronized discharge excess cations flow generating mechanism may be tinnitus, and neural plasticity changes lead to different forms of tinnitus is the structural basis for generating the mouth. 5 · serotonin (5-HT) as a neurotransmitter in the sensory nervous system neurotransmitters forming an important regulatory network that affect the auditory information filtering. Therefore, changes in 5-HT system function in the pathogenesis of tinnitus plays an important role. Another reported that Tinnitus is a hearing disorder phenomena, from the auditory pathway causes abnormal discharge any link. Generation mechanism which comprises two peripheral and central parts. Jastreboff other in neurophysiology and psychology based on the principle proposed neurophysiological model of tinnitus. The model suggests that, auditory pathways and some non-auditory system (particularly the limbic system) plane is different basic part tinnitus. Spontaneous electrical activity of nerve fibers can be detected subcortical center and uploaded to the auditory cortex is perceived as tinnitus. Subcortical center will detect the tinnitus signal is sent to the limbic system and the autonomic nervous system, the second system is activated, on the one hand makes it easier subcortical center tinnitus signal is detected, it also makes tinnitus is closely associated with negative emotions and the formation of conditioned reflex, long-term severe tinnitus makes this reflex can be strengthened, and ultimately the formation of tinnitus and the vicious circle between negative emotions; third aspect is that the activation of the limbic system memory processes initiated simultaneously, tinnitus signal is stored as it is central unpleasant signals, cochlear function recovered completely after the central may still have tinnitus and unpleasant feeling.
Generally, the cochlea is the primary lesion of tinnitus, but a lot of evidence that the central nervous system of the cerebral cortex involved in the generation and maintenance of tinnitus. Cochlear lesions completely restored, tinnitus is still sustainable existence, especially auditory nerve damage or lost after cutting, some patients still have tinnitus, or ringing in the ears actually worsened the original.
There are three important characteristics of the auditory system: auditory pathways at all levels, especially low-level presence of spontaneous neuronal electrical activity casual; auditory system according to the size of the external sound constantly adjust its sensitivity or gain; auditory system has central inhibition or feedback inhibition . Under normal circumstances, outside sound making activities between auditory nerve fibers synchronize spontaneous electrical activity of nerve fibers is not being felt as sound. When people are extremely quiet, soundproofed room or deafness, the auditory system automatically adjusts its gain increases, but also reduces the corresponding cortical olivocochlear efferent system central inhibition, therefore, nerve fibers can be self-generating activities subcortical central detected and uploaded to the auditory cortex is perceived as tinnitus. Subcortical center will detect the tinnitus signal is sent to the limbic system and the autonomic nervous system, the second system is activated, on the one hand makes it easier subcortical center tinnitus signal is detected, it also makes tinnitus is closely associated with negative emotions and the formation of conditioned reflex, long-term severe tinnitus makes this reflex can be strengthened, and ultimately the formation of tinnitus and the vicious circle between negative emotions; third aspect is that the activation of the limbic system memory processes initiated simultaneously, tinnitus signal is stored as it is central unpleasant signals, cochlear function recovered completely after the central may still have tinnitus and unpleasant feeling. Therefore, the central high sensitivity is an important mechanism for long-term severe tinnitus, we temporarily called "central high sensitivity theory." Clearly, early lesions in the cochlea can be, but the main pathological process or post-result is the hub, a recent functional brain imaging studies have confirmed that tinnitus patients with temporal lobe auditory cortex in the presence of high metabolic activity or an increase in regional cerebral blood flow, which may Tip of the brain responsible for tinnitus "tinnitus hub."
Systemic disease caused by tinnitus remains unclear. To be sure, systemic disease and tinnitus related, but the two are not one to one relationship. For example, some patients with hypertension have tinnitus and partly no tinnitus, high blood lipids in patients with tinnitus part of another part no tinnitus, other diseases as well. Central sensitivity correlated with innate and acquired qualities, but not with pain threshold is different, some people low threshold, manifested as pain or ringing in the ears intolerance.
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