An integrative model of developing tinnitus based on recent neurobiological findings.
Brain imaging studies suggest that 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. Results to date suggest cortical plasticity as a likely mechanism to be involved in the chronic progression of 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. However, the neural bases of subjective impairment in tinnitus patients are unknown. An integrative model of developing tinnitus is presented here, 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. The discussions surrounding present models of the generation of tinnitus and its reinforcement to the point of decompensation make it clear that a unidimensional 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 co-morbidity with affective and psychosomatic illnesses and the important influence of psychosocial factors (distress), make the use of stage-appropriate interdisciplinary treatments necessary.
Georgiewa
Petra
P
Department of Medicine, Division of Psychosomatic Medicine and Psychotherapy, Charité-University Medicine Berlin, Campus Charité Mitte, Berlin, Germany.
Klapp
Burghard F
BF
Fischer
Franziska
F
Reisshauer
Annette
A
Juckel
Georg
G
Frommer
Joerg
J
Mazurek
Birgit
B
D001921:Brain / Q000378:metabolism / Q000473:pathology; D003056:Cochlear Nerve; D006801:Humans; D008954:Models, Biological; D008962:Models, Theoretical; D009415:Nerve Net / Q000378:metabolism; D009474:Neurons / Q000378:metabolism; D009482:Neurophysiology; D018377:Neurotransmitter Agents / Q000378:metabolism; D011584:Psychology; D014012:Tinnitus / Q000150:complications* / Q000453:epidemiology* / Q000378:metabolism / Q000473:pathology*
D018377:Neurotransmitter Agents