Abstract
BackgroundTinnitus is an auditory phantom phenomenon characterized by the sensation of sounds without objectively identifiable sound sources. To date, its causes are not well understood. Previous research found altered patterns of spontaneous brain activity in chronic tinnitus sufferers compared to healthy controls, yet it is unknown whether these abnormal oscillatory patterns are causally related to the tinnitus sensation. Partial support for this notion comes from a neurofeedback approach developed by our group, in which significant reductions in tinnitus loudness could be achieved in patients who successfully normalized their patterns of spontaneous brain activity. The current work attempts to complement these studies by scrutinizing how modulations of tinnitus intensity alter ongoing oscillatory activity.ResultsIn the present study the relation between tinnitus sensation and spontaneous brain activity was investigated using residual inhibition (RI) to reduce tinnitus intensity and source-space projected magnetencephalographic (MEG) data to index brain activity. RI is the sustained reduction (criteria: 50% for at least 30 s) in tinnitus loudness after cessation of a tonal tinnitus masker. A pilot study (n = 38) identified 10 patients who showed RI. A significant reduction of power in the delta (1.3–4.0 Hz) frequency band was observed in temporal regions during RI (p ≤ 0.001).ConclusionThe current results suggest that changes of tinnitus intensity induced by RI are mediated by alterations in the pathological patterns of spontaneous brain activity, specifically a reduction of delta activity. Delta activity is a characteristic oscillatory activity generated by deafferented/deprived neuronal networks. This implies that RI effects might reflect the transient reestablishment of balance between excitatory and inhibitory neuronal assemblies, via reafferentation, that have been perturbed (in most tinnitus individuals) by hearing damage. As enhancements have been reported in the delta frequency band for tinnitus at rest, this result conforms to our assumption that a normalization of oscillatory properties of cortical networks is a prerequisite for attenuating the tinnitus sensation. For RI to have therapeutic significance however, this normalization would have to be stabilized.
Highlights
Tinnitus is an auditory phantom phenomenon characterized by the sensation of sounds without objectively identifiable sound sources
A condition (RI vs control; referred to as CO ) × time interaction was found to approach significance (F (1, 8) = 4.663, p = 0.063). With this interaction being in accordance with our hypotheses, post-hoc analyses were conducted. These analyses revealed that even though intensity was significantly reduced under both conditions, this reduction was slightly more pronounced for residual inhibition (RI) (RI: t (7) = 4.366, p = 0.003, CO: t (7) = 3.657, p = 0.008; see Figure 2 depicting single subject data)
Please note that the mean pre-tinnitus loudness is not 10 for every subject. This limitation is due to a decrease in tinnitus loudness over the course of the experiment in some subjects)
Summary
Tinnitus is an auditory phantom phenomenon characterized by the sensation of sounds without objectively identifiable sound sources. Previous research found altered patterns of spontaneous brain activity in chronic tinnitus sufferers compared to healthy controls, yet it is unknown whether these abnormal oscillatory patterns are causally related to the tinnitus sensation. Weisz et al [12,13] found an altered spontaneous brain activity pattern in human chronic tinnitus subjects compared to normal hearing controls This pathological pattern comprised a marked reduction in alpha power (8–12 Hz) and enhancement in delta (1.5–4 Hz) and gamma power (>30 Hz) at rest. Changes in other brain areas and frequency bands are explored
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