Theta-gamma dysrhythmia and auditory phantom perception.

Tinnitus is considered an auditory phantom percept analogous to phantom pain. Thalamocortical dysrhythmia has been proposed as a possible pathophysiological mechanism for both tinnitus and pain. Thalamocortical dysrhythmia refers to a persistent pathological resting state theta-gamma coupling that is spatially localized at an area where normally alpha oscillations predominate. Auditory cortex stimulation via implanted electrodes has been developed to treat tinnitus, targeting an area of activation on functional MR imaging elicited by tinnitus-matched sound presentation. The authors describe a case in which clinical improvement was correlated with changes in intracranial recordings. Maximal tinnitus suppression was obtained by current delivery exactly at the blood oxygen level-dependent activation hotspot, which colocalizes with increased gamma and theta activity, in contrast to the other electrode poles, which demonstrated a normal alpha peak. These spectral changes normalized when stimulation induced tinnitus suppression, both on electrode and source-localized electroencephalography recordings. These data suggest that thetagamma coupling as proposed by the thalamocortical dysrhythmia model might be causally related to a conscious auditory phantom percept.

Burst spinal cord stimulation: toward paresthesia-free pain suppression.

INTRODUCTION: Spinal cord stimulation is commonly used for neuropathic pain modulation. The major side effect is the onset of paresthesia. The authors describe a new stimulation design that suppresses pain as well as, or even better than, the currently used stimulation, but without creating paresthesia. METHODS: A spinal cord electrode (Lamitrode) for neuropathic pain was implanted in 12 patients via laminectomy: 4 at the C2 level and 7 at the T8-T9 level for cervicobrachialgia and lumboischialgia, respectively (1 at T11 at another center). During external stimulation, the patients received the classic tonic stimulation (40 or 50 Hz) and the new burst stimulation (40-Hz burst with 5 spikes at 500 Hz per burst). RESULTS: Pain scores were measured using a visual analog scale and the McGill Short Form preoperatively and during tonic and burst stimulation. Paresthesia was scored as present or not present. Burst stimulation was significantly better for pain suppression, by both the visual analog scale score and the McGill Short Form score. Paresthesia was present in 92% of patients during tonic stimulation, and in only 17% during burst stimulation. Average follow-up was 20.5 months. CONCLUSION: The authors present a new method of spinal cord stimulation using bursts that suppress neuropathic pain without the mandatory paresthesia. Pain suppression seems as good as or potentially better than that achieved with the currently used stimulation. Average follow-up after nearly 2 years (20.5 months) suggests that this stimulation design is stable.

Bilateral dorsolateral prefrontal cortex modulation for tinnitus by transcranial direct current stimulation: a preliminary clinical study.

Tinnitus is considered as an auditory phantom percept. Preliminary evidence indicates that transcranial direct current stimulation (tDCS) of the temporo-parietal area might reduce tinnitus. tDCS studies of the prefrontal cortex have been successful in reducing depression, impulsiveness and pain. Recently, it was shown that the prefrontal cortex is important for the integration of sensory and emotional aspects of tinnitus. As such, frontal tDCS might suppress tinnitus as well. In an open label study, a total of 478 tinnitus patients received bilateral tDCS on dorsolateral prefrontal cortex (448 patients anode right, cathode left and 30 anode left, cathode right) for 20 min. Treatment effects were assessed with visual analogue scale for tinnitus intensity and distress. No tinnitus-suppressing effect was found for tDCS with left anode and right cathode. Analyses show that tDCS with right anode and left cathode modulates tinnitus perception in 29.9% of the tinnitus patients. For these responders a significant reduction was found for both tinnitus-related distress and tinnitus intensity. In addition, the amount of suppression for tinnitus-related distress is moderated by an interaction between tinnitus type and tinnitus laterality. This was, however, not the case for tinnitus intensity. Our study supports the involvement of the prefrontal cortex in the pathophysiology of tinnitus.

Tinnitus intensity dependent gamma oscillations of the contralateral auditory cortex.

BACKGROUND: Non-pulsatile tinnitus is considered a subjective auditory phantom phenomenon present in 10 to 15% of the population. Tinnitus as a phantom phenomenon is related to hyperactivity and reorganization of the auditory cortex. Magnetoencephalography studies demonstrate a correlation between gamma band activity in the contralateral auditory cortex and the presence of tinnitus. The present study aims to investigate the relation between objective gamma-band activity in the contralateral auditory cortex and subjective tinnitus loudness scores. METHODS AND FINDINGS: In unilateral tinnitus patients (N = 15; 10 right, 5 left) source analysis of resting state electroencephalographic gamma band oscillations shows a strong positive correlation with Visual Analogue Scale loudness scores in the contralateral auditory cortex (max r = 0.73, p<0.05). CONCLUSION: Auditory phantom percepts thus show similar sound level dependent activation of the contralateral auditory cortex as observed in normal audition. In view of recent consciousness models and tinnitus network models these results suggest tinnitus loudness is coded by gamma band activity in the contralateral auditory cortex but might not, by itself, be responsible for tinnitus perception.