耳鸣中枢化机制与临床诊疗

耳鸣是耳科临床最常见的病症之一，其确切机制尚不明确，普遍认为耳鸣是由耳蜗病变的异常活动导致或触发的，然而，对慢性顽固性耳鸣耳蜗（外周）机制很难解释持续产生的耳鸣感觉。本文提出耳鸣中枢化机制：源于外周听觉系统损伤后导致异常神经活动对中枢的长期刺激（包括耳鸣的刺激），被中枢界定为不良刺激，由于听觉中枢可塑性的存在，因而，外周异常信号输入后，中枢首先要对外周输入信号进行适应，中枢为了适应这些不良刺激，在对不良刺激活动产生适应性变化过程中，可能导致相应的神经元的突触活动异常，最终逐渐引起大脑皮层某些区域（如听皮层）突触超微结构的改变并出现功能重组，这种可塑性变化可能使耳鸣持续存在，导致耳鸣源于耳蜗而存在于中枢，即耳鸣被逐渐中枢化。文中最后阐述并讨论了基于耳鸣中枢化机制的l临床耳鸣诊治。

Tinnitus.the mechanism of tinnitus centralization and clinical management

Tinnitus is the most common disease in Otology, and extremely difficult for treatment in clinic, the precise mechanism still remains unclear. There is universal agreement that tinnitus is induced or triggered by abnormal events in the cochlea （the abnormal events can result in abnormal neuronal activity in central auditory pathways that can then be finally perceived as tinnitus）. Neuroplastic events at the auditory cortex （AC） have been reported to include hyperactive of cortical neurons and an increase in neuronal synchronization. Our recent studies showed the changes markedly, in the expression of the excitatory glutamate receptor subtype NR2B in mR- NA and protein levels, and also some changes in synaptic ultrastructure of neurons in auditory cortex of tinnitus animal. We propose that the mechanisms of tinnitus centralization may arise from abnormal events in the cochlea, and result in abnormal neuronal activity at multiple levels which promote abnormal propagation of neural activity in the central auditory pathway. The plastic change may be positive and adaptive as with learning or memory, or in the compensation after abnormal events in the cochlea that results in new neuronal networks that restore normal function. Alternatively, the neuroplastic changes might be maladaptive leading perhaps to an imbalance in excitato- ry and inhibitory events in the brain. Indeed, tinnitus may be the consequence of such maladaptive neuroplastic brain alterations （synaptic structure） has even gone a step further and described tinnitus as the perceptual manifes- tation of plastic brain changes that result in abnormal neuronal activity. The neuroplastic changes may also make tinnitus persists, eventually leading to the existence of tinnitus cochlear-originated in the central pathway. They may also extend to non-sensory areas of the brain giving rise to the attentional and emotional aspects that often ac-company the disorder. New pathophysiological insights maybe prompt the development of management approaches to directly target the neuroplastic processes correlates of tinnitus.