| pubmed-article:1330220 | pubmed:abstractText | Tinnitus is often related to a peripheral impairment which seems to trigger an abnormal autonomous functioning of the central auditory system. Moreover peripheral stimulations may diminish, and even suppress their perception, either through masking or through inhibition of an aberrant neuronal activity. Here we present an experimental model of peripheral deafferentation in which a decrease of neurochemical activity is observed in the brainstem auditory nuclei, followed by a progressive recovery after the peripheral destruction. This activity could represent a central morphofunctional correlate of tinnitus. Development of experimental models of tinnitus must be continued. Such models should allow the study of the basic physiological mechanisms behind tinnitus and suggest some therapeutic approaches which could be objectively evaluated. | lld:pubmed |
