Neural correlates of the Heidelberg Music Therapy: indicators for the regeneration of auditory cortex in tinnitus patients? (original) (raw)
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Too Blind to See the Elephant? Why Neuroscientists Ought to Be Interested in Tinnitus
Journal of the Association for Research in Otolaryngology
A curative therapy for tinnitus currently does not exist. One may actually exist but cannot currently be causally linked to tinnitus due to the lack of consistency of concepts about the neural correlate of tinnitus. Depending on predictions, these concepts would require either a suppression or enhancement of brain activity or an increase in inhibition or disinhibition. Although procedures with a potential to silence tinnitus may exist, the lack of rationale for their curative success hampers an optimization of therapeutic protocols. We discuss here six candidate contributors to tinnitus that have been suggested by a variety of scientific experts in the field and that were addressed in a virtual panel discussion at the ARO round table in February 2021. In this discussion, several potential tinnitus contributors were considered: (i) inhibitory circuits, (ii) attention, (iii) stress, (iv) unidentified sub-entities, (v) maladaptive information transmission, and (vi) minor cochlear deaff...
Heidelberg Neuro-Music Therapy Enhances Task-Negative Activity in Tinnitus Patients
Frontiers in Neuroscience
Background: Suffering from tinnitus causes mental distress in most patients. Recent findings point toward a diminished activity of the brain's default-mode network (DMN) in subjects with mental disorders including depression or anxiety and also recently in subjects with tinnitus-related distress. We recently developed a therapeutic intervention, namely the Heidelberg Neuro-Music Therapy (HNMT), which shows an effective reduction of tinnitus-related distress following a 1-week short-term treatment. This approach offers the possibility to evaluate the neural changes associated with the improvements in tinnitus distress. We previously reported gray matter (GM) reorganization in DMN regions and in primary auditory areas following HNMT in cases of recent-onset tinnitus. Here we evaluate on the same patient group, using functional MRI (fMRI), the activity of the DMN following the improvements tinnitus-related distress related to the HNMT intervention. Methods: The DMN activity was estimated by the task-negative activation (TNA) during long inter-trial intervals in a word recognition task. The level of TNA was evaluated twice, before and after the 1-week study period, in 18 treated tinnitus patients ("treatment group," TG), 21 passive tinnitus controls (PTC), and 22 active healthy controls (AC). During the study, the participants in TG and AC groups were treated with HNMT, whereas PTC patients did not receive any tinnitus-specific treatment. Therapy-related effects on DMN activity were assessed by comparing the pairs of fMRI records from the TG and PTC groups. Results: Treatment of the TG group with HNMT resulted in an augmented DMN activity in the PCC by 2.5% whereas no change was found in AC and PTC groups. This enhancement of PCC activity correlated with a reduction in tinnitus distress (Spearman Rho: −0.5; p < 0.005). Conclusion: Our findings show that an increased DMN activity, especially in the PCC, underlies the improvements in tinnitus-related distress triggered by HNMT and identify the DMN as an important network involved in therapeutic improvements.
Cortical reorganization in recent-onset tinnitus patients by the Heidelberg Model of Music Therapy
Frontiers in neuroscience, 2015
Pathophysiology and treatment of tinnitus still are fields of intensive research. The neuroscientifically motivated Heidelberg Model of Music Therapy, previously developed by the German Center for Music Therapy Research, Heidelberg, Germany, was applied to explore its effects on individual distress and on brain structures. This therapy is a compact and fast application of nine consecutive 50-min sessions of individualized therapy implemented over 1 week. Clinical improvement and long-term effects over several years have previously been published. However, the underlying neural basis of the therapy's success has not yet been explored. In the current study, the therapy was applied to acute tinnitus patients (TG) and healthy active controls (AC). Non-treated patients were also included as passive controls (PTC). As predicted, the therapeutic intervention led to a significant decrease of tinnitus-related distress in TG compared to PTC. Before and after the study week, high-resolutio...
Hearing Research, 2013
Animal research has shown that loss of normal acoustic stimulation can increase spontaneous firing in the central auditory system and induce cortical map plasticity. Enriched acoustic environment after noise trauma prevents map plasticity and abolishes neural signs of tinnitus. In humans, the tinnitus spectrum overlaps with the area of hearing loss. Based on these findings it can be hypothesized that stimulating the auditory system by presenting music compensating specifically for the hearing loss might also suppress chronic tinnitus. To verify this hypothesis, a study was conducted in three groups of tinnitus patients. One group listened just to unmodified music (i.e. active control group), one group listened to music spectrally tailored to compensate for their hearing loss, and a third group received music tailored to overcompensate for their hearing loss, associated with one (in presbycusis) or two notches (in audiometric dip) at the edge of hearing loss. Our data indicate that applying overcompensation to the hearing loss worsens the patients' tinnitus loudness, the tinnitus annoyance and their depressive feelings. No significant effects were obtained for the control group or for the compensation group. These clinical findings were associated with an increase in current density within the left dorsal anterior cingulate cortex in the alpha2 frequency band and within the left pregenual anterior cingulate cortex in beta1 and beta2 frequency band. In addition, a region of interest analysis also demonstrated an associated increase in gamma band activity in the auditory cortex after overcompensation in comparison to baseline measurements. This was, however, not the case for the control or the compensation groups. In conclusion, music therapy compensating for hearing loss is not beneficial in suppressing tinnitus, and overcompensating hearing loss actually worsens tinnitus, both clinically and electrophysiologically.
Tinnitus and underlying brain mechanisms
Current opinion in otolaryngology & head and neck surgery, 2012
Tinnitus is the sensation of hearing a sound when no external auditory stimulus is present. Most individuals experience tinnitus for brief, unobtrusive periods. However, chronic sensation of tinnitus affects approximately 17% (44 million people) of the general US population. Tinnitus, usually a benign symptom, can be constant, loud and annoying to the point that it causes significant emotional distress, poor sleep, less efficient activities of daily living, anxiety, depression and suicidal ideation/attempts. Tinnitus remains a major challenge to physicians because its pathophysiology is poorly understood and there are few management options to offer to patients. The purpose of this article is to describe the current understanding of central neural mechanisms in tinnitus and to summarize recent developments in clinical approaches to tinnitus patients. Recently developed animal models of tinnitus provide the possibility to determine neuronal mechanisms of tinnitus generation and to te...
Tinnitus: causes and clinical management
The Lancet Neurology, 2013
Tinnitus is the perception of sound in the absence of a corresponding external acoustic stimulus. With prevalence ranging from 10% to 15%, tinnitus is a common disorder. Many people habituate to the phantom sound, but tinnitus severely impairs quality of life of about 1-2% of all people. Tinnitus has traditionally been regarded as an otological disorder, but advances in neuroimaging methods and development of animal models have increasingly shifted the perspective towards its neuronal correlates. Increased neuronal fi ring rate, enhanced neuronal synchrony, and changes in the tonotopic organisation are recorded in central auditory pathways in reaction to deprived auditory input and represent-together with changes in non-auditory brain areas-the neuronal correlate of tinnitus. Assessment of patients includes a detailed case history, measurement of hearing function, quantifi cation of tinnitus severity, and identifi cation of causal factors, associated symptoms, and comorbidities. Most widely used treatments for tinnitus involve counselling, and best evidence is available for cognitive behavioural therapy. New pathophysiological insights have prompted the development of innovative brain-based treatment approaches to directly target the neuronal correlates of tinnitus. Lancet Neurol 2013; 12: 920-30 Department of Psychiatry and Psychotherapy (B Langguth MD, P M Kreuzer MD) and Interdisciplinary Tinnitus Center (B Langguth, P M Kreuzer, References 1 Krog NH, Engdahl B, Tambs K. The association between tinnitus and mental health in a general population sample: results from the HUNT Study. J Psychosom Res 2010; 69: 289-98. 2 Axelsson A, Ringdahl A. Tinnitus-a study of its prevalence and characteristics. Br J Audiol 1989; 23: 53-62. 3 Pilgram R. Tinnitus in der BRD. HNO aktuell 1999; 7: 261-65. 4 Shargorodsky J, Curhan GC, Farwell WR. Prevalence and characteristics of tinnitus among US adults. Am J Med 2010;
Considerations on tinnitus retraining therapy and transcranial magnetic stimulation
Revista Neurociências, 2021
Introduction. Tinnitus is a subjective perception of sound in the absence of an external acoustic stimulus. It has negative behavioral feelings associated, e.g., depression, insomnia, difficulty of concentration, anxiety, irritability, and panic. The feelings impact negatively on the social and economic life of individuals. Empirical data suggest that disorders in the auditory cortex and its neural pathways give rise to abnormal spontaneous activations associated with tinnitus. Understanding the causes remains challenging. However, the current hypothesis suggests that clusters of neural networks and subnetworks are involved in tinnitus generation. Central dynamic neuroplasticity induced by a peripheral loss of auditory input can cause tinnitus noise. To date, there is no widespread consensus about the most effective therapy for treating tinnitus. Objective. To reflect on two tinnitus therapies: Tinnitus Retraining Therapy (TRT) and Transcranial Magnetic Stimulation (TMS). Method. A narrative review. Explicit and systematic criteria were not adopted in searching for the theoretical framework. Results. TMS is promising compared to TRT because TMS acts on tinnitus neural mechanisms. TRT is effective on a behavioral level since it relieves mild and moderate tinnitus' negative feelings. Conclusion. TRT does not advance on the neural source, but only on the tinnitus perception. TMS acts directly on the neural causes. Both therapies have limitations and can work for some patients. However, the effect of TMS seems more efficient, although transient.
2012
Tinnitus is an auditory phantom sensation (ringing of the ears) experienced when no external sound is present. Most but not all cases are associated with hearing loss induced by noise exposure or aging. Neuroscience research has begun to reveal how tinnitus is generated by the brain when hearing loss occurs, and to suggest new avenues for management and prevention of tinnitus following hearing injuries. Downregulation of intracortical inhibition induced by damage to the cochlea or to auditory projection pathways highlights neural processes that underlie the sensation of phantom sound.
Nordic Journal of Music Therapy
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