Tinnitus, the phenomenon of ringing or buzzing in the ears without an external sound source is one of the most commonly reported symptoms in otorhinolaryngology and affects 10 - 15% of the general population. Models h...Tinnitus, the phenomenon of ringing or buzzing in the ears without an external sound source is one of the most commonly reported symptoms in otorhinolaryngology and affects 10 - 15% of the general population. Models have been developed to account for neural basis of tinnitus, its pathogenesis and its consequences on mental health （deRidder et al., 2013）. In most cases tinnitus onset follows a partial hearing impairment. Peripheral sensory deprivation due to cochlear damages may prompt increased neuronal activity in the central auditory system in order to adapt the neural sensitivity to the reduced sensory inputs. This central gain could over amplify the ＂neural noise＂ and thus trigger a homeostatic down-regulation of inhib- itory synapses in the auditory cortical map leading to specific reorganization of the cortical representation of the tinnitus percept. Dysfunctional feedback connections from limbic regions to auditory brain areas, interacting at the thalamic level, may account for the psychological impairment.展开更多
基金supported by KTS Klaus Tschira Stiftung g Gmb H.And many thanks to Dr.Carrie Ankerstein for stylistic and linguistic improvement of this paper
文摘Tinnitus, the phenomenon of ringing or buzzing in the ears without an external sound source is one of the most commonly reported symptoms in otorhinolaryngology and affects 10 - 15% of the general population. Models have been developed to account for neural basis of tinnitus, its pathogenesis and its consequences on mental health （deRidder et al., 2013）. In most cases tinnitus onset follows a partial hearing impairment. Peripheral sensory deprivation due to cochlear damages may prompt increased neuronal activity in the central auditory system in order to adapt the neural sensitivity to the reduced sensory inputs. This central gain could over amplify the ＂neural noise＂ and thus trigger a homeostatic down-regulation of inhib- itory synapses in the auditory cortical map leading to specific reorganization of the cortical representation of the tinnitus percept. Dysfunctional feedback connections from limbic regions to auditory brain areas, interacting at the thalamic level, may account for the psychological impairment.
