OBJECTIVE: To describe the current ideas about the manifestations of neural plasticity in generating tinnitus. DATA SOURCES: Recently published source articles were identified using MEDLINE, PubMed, and Cochrane Library according to the key words mentioned below. STUDY SELECTION: Review articles and controlled trials were particularly selected. DATA EXTRACTION: Data were selected systematically, scaled on validity and comparability. CONCLUSION: An altered afferent input to the auditory pathway may be the initiator of a complex sequence of events, finally resulting in the generation of tinnitus at the central level of the auditory nervous system. The effects of neural plasticity can generally be divided into early modifications and modifications with a later onset. The unmasking of dormant synapses, diminishing of (surround) inhibition and initiation of generation of new connections through axonal sprouting are early manifestations of neural plasticity, resulting in lateral spread of neural activity and development of hyperexcitability regions in the central nervous system. The remodeling process of tonotopic receptive fields within auditory pathway structures (dorsal cochlear nucleus, inferior colliculus, and the auditory cortex) are late manifestations of neural plasticity. The modulation of tinnitus by stimulating somatosensory or visual systems in some people with tinnitus might be explained via the generation of tinnitus following the nonclassical pathway. The similarities between the pathophysiological processes of phantom pain sensations and tinnitus have stimulated the theory that chronic tinnitus is an auditory phantom perception.
OBJECTIVE: To describe the current ideas about the manifestations of neural plasticity in generating tinnitus. DATA SOURCES: Recently published source articles were identified using MEDLINE, PubMed, and Cochrane Library according to the key words mentioned below. STUDY SELECTION: Review articles and controlled trials were particularly selected. DATA EXTRACTION: Data were selected systematically, scaled on validity and comparability. CONCLUSION: An altered afferent input to the auditory pathway may be the initiator of a complex sequence of events, finally resulting in the generation of tinnitus at the central level of the auditory nervous system. The effects of neural plasticity can generally be divided into early modifications and modifications with a later onset. The unmasking of dormant synapses, diminishing of (surround) inhibition and initiation of generation of new connections through axonal sprouting are early manifestations of neural plasticity, resulting in lateral spread of neural activity and development of hyperexcitability regions in the central nervous system. The remodeling process of tonotopic receptive fields within auditory pathway structures (dorsal cochlear nucleus, inferior colliculus, and the auditory cortex) are late manifestations of neural plasticity. The modulation of tinnitus by stimulating somatosensory or visual systems in some people with tinnitus might be explained via the generation of tinnitus following the nonclassical pathway. The similarities between the pathophysiological processes of phantom pain sensations and tinnitus have stimulated the theory that chronic tinnitus is an auditory phantom perception.