Neurophysiological correlates of residual inhibition in tinnitus: Hints for trait-like EEG power spectra.

OBJECTIVE: To investigate oscillatory brain activity changes following acoustic stimulation in tinnitus and whether these changes are associated with behavioral measures of tinnitus loudness. Moreover, differences in ongoing brain activity between individuals with and without residual inhibition (RI) are examined (responders vs. non-responders). METHODS: Three different types of noise stimuli were administered for acoustic stimulation in 45 tinnitus patients. Subjects resting state brain activity was recorded before and after stimulation via EEG alongside with subjective measurements of tinnitus loudness. RESULTS: Delta, theta and gamma band power increased, whereas alpha and beta power decreased from pre to post stimulation. Acoustic stimulation responders exhibited reduced gamma and a trend for enhanced alpha activity with the latter localized in the right inferior temporal gyrus. Post stimulation, individuals experiencing RI showed higher theta, alpha and beta power with a peak power difference in the alpha band localized in the right superior temporal gyrus. Neither correlations with behavioral tinnitus measures nor stimulus-specific changes in EEG activity were present. CONCLUSIONS: Our observations might be indicative of trait-specific forms of oscillatory signatures in different subsets of the tinnitus population related to acoustic tinnitus suppression. SIGNIFICANCE: Results and insights are not only useful to understand basic neural mechanisms behind RI but are also valuable for general neural models of tinnitus.

[On the interdisciplinary S3 guidelines for the treatment of chronic idiopathic tinnitus]. / Zur interdisziplinären S3-Leitlinie für die Therapie des chronisch-idiopathischen Tinnitus.

INTRODUCTION: Tinnitus is a frequent symptom, which, particularly in combination with comorbidities, can result in a severe disease-related burden. Chronic idiopathic tinnitus (CIT) is the most frequent type of tinnitus. A considerable number of treatment strategies are used to treat CIT-for many of which there is no evidence of efficacy. In order to enable scientific evidence-based treatment of CIT, German interdisciplinary S3 guidelines have recently been constructed for the first time. Here we present a short form of these S3 guidelines. MATERIALS AND METHODS: The guidelines were constructed based on a meta-analysis of the treatment of chronic tinnitus performed by the authors. Additionally, a systematic literature search was performed in the PubMed and Cochrane Library databases. Furthermore, a systematic search for international guidelines was performed in Google, as well as in the Guidelines International Network and National Guideline Clearinghouse (USA) database. Evidence was classified according to the Oxford Centre for Evidence-Based Medicine system. RESULTS: According to the guidelines, alongside counselling, manualized structured tinnitus-specific cognitive behavioral therapy (tCBT) with a validated treatment manual is available as evidence-based therapy. In addition, the guidelines recommend concurrent treatment of comorbidities, including drug-based treatment, where appropriate. Particularly important is treatment of anxiety and depression. Where a psychic or psychiatric comorbidity is suspected, further diagnosis and treatment should be performed by an appropriately qualified specialist (psychiatrist, neurologist, psychosomatic medicine consultant) or psychological psychotherapist. In cases accompanied by deafness or hearing loss bordering on deafness, cochlear implants may be indicated. CONCLUSION: No recommendations can be made for drug-based treatment of CIT, audiotherapy, transcranial magnetic or electrical stimulation, specific forms of acoustic stimulation or music therapy; or such recommendations must remain open due to the lack of available evidence. Polypragmatic tinnitus treatment with therapeutic strategies for which there is no evidence of efficacy from controlled studies is to be refused.

Surgical brain modulation for tinnitus: the past, present and future.

Tinnitus treatment has traditionally been restricted to ENT surgeons, audiologists, psychologists and psychiatrists. Recently, both basic and clinical research has focused on the brain's involvement in the generation of tinnitus, opening the tinnitus field up to neurologists and neurosurgeons specialized in the field of tinnitus. Non-pulsatile tinnitus can be considered an auditory phantom phenomenon, analogous to phantom pain, both with regards to pathophysiological mechanisms, clinical characteristics, and treatment approaches. Thus the understanding of tinnitus has benefited a lot from translating available knowledge of the somatosensory (pain) system to the auditory system. A literature review of neuromodulatory approaches to tinnitus is integrated in a single center's experience with invasive neuromodulation treatments for tinnitus. This is compared to findings from neuromodulatory treatment of chronic pain syndromes. The past, present and future options for functional neurosurgical approaches are outlined. In the past only destructive approaches were used, consisting of nerve lesions and frontal lobotomies. Presently neurostimulation trials are ongoing evaluating the effect of auditory cortex stimulation, frontal cortex stimulation, thalamic (VIM) and caudate stimulation as well as amygdalohippocampal stimulation, yielding suppression rates between 10 and 70%. Further potentially promising targets include the anterior cingulate, the medial geniculate bodies (MGB), the periaqueductal gray/ tectal longitudinal column (PAG/TLC), the dorsal cochlear nucleus, as well as the C2 and trigeminal nerve. Understanding tinnitus and its potential neuromodulation treatments is relatively simple for a neurosurgeon specialized in pain or a pain physician, based on the pathophysiological and clinical analogies. Similarly to pain a multidisciplinary approach can be advocated, and in view of the epidemiology and amount of suffering associated with this enigmatic symptom further investment in possible neuromodulation treatments is warranted.

Modulating cerebello-thalamocortical pathways by neuronavigated cerebellar repetitive transcranial stimulation (rTMS).

OBJECTIVES: Increasing evidence suggests that dysfunctions of the cortico-cerebello-thalamocortical circuit are involved in the pathophysiology of neuropsychiatric disorders. This study explores the effects of cerebellar repetitive transcranial magnetic stimulation (rTMS) on cerebello-thalamocortical pathways. METHODS: Ten healthy volunteers received MRI-guided rTMS in four separate sessions (120% motor threshold, 1000 stimuli) over either the medial or the right lateral cerebellum using frequencies of 1 and 10 Hz. Motor cortex excitability was assessed before and after the intervention by paired-pulse transcranial magnetic stimulation. RESULTS: Depending on stimulation frequency, cerebellar rTMS differentially modified intracortical inhibition. Low frequency rTMS increased short intracortical inhibition (SICI), whereas high frequency rTMS had no significant effect on SICI. CONCLUSIONS: These results suggest that rTMS over the cerebellum can modulate cerebello-thalamocortical pathways in a frequency-specific manner.

TMS for treatment of chronic tinnitus: neurobiological effects.

Results of neurophysiological and neuroimaging studies suggest that some forms of chronic tinnitus can be regarded to be "hyperexcitability syndromes", caused by abnormal focal brain activity. Low frequency repetitive magnetic stimulation (rTMS) is an efficient method to selectively reduce the abnormally increased activity in distinct cortical areas. An increasing amount of clinical data suggest that low frequency rTMS might be an effective therapy that is directed at the cause of some forms of chronic tinnitus. To further explore the underlying neurobiological mechanisms we investigated the effect of rTMS on cortical excitability in healthy human subjects using the protocol, which has been successfully used for the treatment of tinnitus. We determined different parameters of motor cortex excitability (resting motor threshold, RMT; active motor threshold, AMT; short intracortical inhibition, ICI; short intracortical facilitation, ICF; and the duration of the cortical silent period, CSP) before and after 5 days of low frequency rTMS (2000 stimuli/day at 110% of RMT) over the left auditory cortex. Five sessions of low frequency rTMS resulted in a significant prolongation of the CSP. All other signs of cortical excitability that we studied remained unchanged. These findings suggest, that low frequency rTMS may evoke long-term depression (LTD)-like effects resulting in enhancement of subcortical inhibition.