An integrative model of developing tinnitus – neurobiological tinnitus model

An integrative model of (subjective) tinnitus is presented, based on the most recent neurophysiological data in current discussion. We assume the involvement of altered brain functions in the development and maintenance of perceptions of tinnitus and outline various possibilities which could contribute to decompensation and chronic progression. Results to date suggest cortical plasticity as a likely mechanism to be involved in the chronic progression of tinnitus. In this sense, tonotopical maps in the auditory cortex are altered due either to a lack of afferent connections or to defective auditory perceptions resulting from pathological synaptic impulse transmission processes. The functional connectivity of various limbic, prefrontal, and temporal brain structures can be understood as the basis for particularly intense experiences of impairment and many secondary symptoms of decompensated tinnitus. Relationships between the processing of auditory signals and neural networks associated with somatosensory, attentional, cognitive and emotional processes are relevant for the genesis of the pathology. The discussions surrounding present models of the generation of tinnitus and its reinforcement to the point of decompensation make it clear that a uni-dimensional approach in clinical interventions is insufficient. Patients with decompensated tinnitus suffer from a complex somatic and psychological disorder. The interactive processes involving emotions, behaviour and symptoms, as well as the high comorbidity with affective and psychosomatic illnesses and the important influence of psychosocial factors (distress), make the use of stage-appropriate interdisciplinary treatments necessary.

Schlüsselwörter

brain imaging - fMRI-studies - neurophysiological models - tinnnitus