Hey all, Apologies if this has been discussed before; my browsing through these forums has not turned up this particular approach as of yet so I thought I would post it -- even though it is a bit old. Has anybody heard of this type of treatment or experienced it? It seems like an interesting approach that gets to the root of tinnitus in cases of sensorineural hearing loss. _________________________________________ http://journals.lww.com/otology-neu...uppression_of_Tinnitus_with_High_Rate.21.aspx Electrical Suppression of Tinnitus with High-Rate Pulse Trains Rubinstein, Jay T.*†; Tyler, Richard S.*‡; Johnson, Abigail*; Brown, Carolyn J.*‡ Otology & Neurotology: May 2003 - Volume 24 - Issue 3 - pp 478-485 Tinnitus Abstract Hypothesis: Application of high-rate pulse trains (e.g., 4800 pps) to the cochlea may represent an effective treatment of tinnitus. Background: Tinnitus is a widespread clinical problem with multiple treatments but no cure. A cure for tinnitus would restore the perception of silence. One plausible hypothesis for the origin of tinnitus associated with sensorineural hearing loss is that it is due to loss or alteration of the normal spontaneous activity in the deafferented regions of the cochlea. Electrical stimulation of the cochlea with 5000-pps pulse trains can produce spontaneous-like patterns of spike activity in the auditory nerve. Methods: Eleven volunteer human subjects with bothersome tinnitus and high-frequency sensorineural hearing loss underwent myringotomy and temporary placement of a round window electrode. High-rate pulse train stimuli were presented at various stimulus intensities and tinnitus, and stimulus perception were scaled by the subject. Three cochlear implant recipients with tinnitus in the implanted ear underwent similar stimulation. Results: Five of 11 (45%) of transtympanic subjects showed substantial or complete tinnitus suppression with either no perception or only a transient perception of the stimulus. Three showed tinnitus suppression only in association with the perception of the stimulus. Three showed no effects on tinnitus. A similar pattern of responses was seen in the cochlear implant subjects. Conclusions: Although the study lacked an ideal placebo control, the results are promising and support further research to develop a clinically useful intervention for this troubling disorder. Tinnitus affects between 10% and 30% of the population. Of those affected, 20% have tinnitus sufficiently bothersome to seek medical attention (1). For many of these patients, tinnitus is a handicap that interferes significantly with their quality of life. Arguably more than any other otologic disorder, tinnitus remains refractory to current therapy. Masking is an effective management strategy for some patients (2), and unblinded, uncontrolled clinical experience suggests that “tinnitus retraining therapy” may benefit others (3). Antidepressants are effective if depression coexists with the tinnitus (4). Likewise, with comorbid anxiety, anxiolytics may be of benefit. Yet, none of the above therapeutic strategies actually decreases the loudness of tinnitus in the absence of a masking stimulus. Substantial literature exists to establish the psychoacoustic properties of tinnitus (5). Recent studies demonstrate, in addition, that a physiologic correlate of tinnitus may be visualized using a variety of functional imaging techniques (6,7). Thus, whereas it is clear that emotional responses to tinnitus vary widely across subjects and are clearly pathologic in some, there is no question that the underlying perception of tinnitus can by itself be a disabling handicap deserving of significant intervention efforts (8). There is a long history of attempts to suppress tinnitus with electrical stimulation. Beginning in 1801 and continuing throughout the 19th century, several authors described the effects of electrical stimulation on the ear (9). These early attempts concluded that anodal direct current applied to the ipsilateral mastoid or zygoma could suppress or eliminate tinnitus in some patients, whereas cathodal stimulation caused auditory percepts and an increased intensity of tinnitus. These findings were subsequently verified in this century by Hatton (10) and in multiple publications from Bordeaux (11–14). The latter group applied electrical stimuli via a transtympanic electrode to the round window and promontory. Subsequently, it was reported that tinnitus suppression is a common beneficial side effect of cochlear implantation (15–22), although the reported efficacy rate varied from 28% to 79% of patients. These effects may be mediated either peripherally or centrally. Peripheral electrical stimulation may have a direct electrical influence on a peripheral tinnitus, or it may have an indirect influence by creating activity that is passed to a central mechanism where the tinnitus reduction occurs. In addition, it is important to consider whether auditory perception of the electrical stimulation occurs during electrical suppression of tinnitus. The promising early results with direct current anodic stimuli, the knowledge that direct current cannot be applied continuously without causing tissue injury, and the success with cochlear implants has led to numerous studies of alternating current stimulation for suppression of tinnitus (23–28). These studies have used external and middle ear electrodes and a variety of stimulus waveforms. Again, they suggest that in some patients, tinnitus can be suppressed and occasionally eliminated. None of these studies was placebo controlled, however, and this is of significant concern. A tinnitus suppression device, the Theraband, initially produced considerable enthusiasm (29) but was relegated to historic interest after a carefully designed, double-blind placebo-controlled trial (30). This device did, however, produce a verifiable, repeatable, and clinically relevant tinnitus suppression in one subject. Such a rigorous study is feasible only if tinnitus can be suppressed without producing an auditory or somatosensory percept. In our efforts to better understand the physiology of cochlear implants and to improve signal processing strategies for them, we have uncovered certain properties of auditory nerve responses to electrical stimulation that may be of benefit to some tinnitus patients (31). Ideally, electrical stimulation would suppress tinnitus without producing any new auditory percepts. Patients with tinnitus who successfully make therapeutic use of acoustic masking still find the sound of the masker intrusive, although less so than the tinnitus. Preliminary work indicates that electrical stimulation of the cochlea can decrease tinnitus in some patients, but this is best documented in people with cochlear implants. In this setting, tinnitus is suppressed along with the production of an auditory percept, and it is unclear whether the tinnitus suppression is due to a nonspecific increase in neural activity (masking) or specifically affects tinnitus-related activity. If tinnitus originates from abnormal firing patterns of the auditory periphery, restoration of normal patterns should alleviate it. Current cochlear implants provide high levels of speech perception in some patients but do not restore “normal” activity to the auditory nerve. Normally, the peripheral auditory nerve fibers are spontaneously active in quiet (32). This spontaneous firing of the auditory nerve is due to continuous, undriven release of neurotransmitter by the inner hair cell synapse (33). This release process and the resulting firing patterns of the spiral ganglion have been extensively observed, modeled, and analyzed in multiple species. For durations on the order of seconds, transmitter release reflects a Poisson process (34). Refractory properties of the auditory neurons modify the transmitter release process, resulting in spike times reflecting a renewal process; i.e., a Poisson process with dead time. Early theories about the peripheral origin of tinnitus suggest that loss of this normal pattern of spontaneous activity can lead to abnormal central auditory activity perceived as sound (35,36). In this light, spontaneous activity may be viewed as the “code for silence.” This theory is consistent with the fact that most tinnitus is associated with hearing loss and most hearing loss is associated with loss or alteration of spontaneous activity (37). It also explains why cochlear nerve section is usually ineffective and not uncommonly makes tinnitus worse (15). The efficacy of acoustic masking with white noise can then be explained through the effect of such noise on the periphery, evoking spike intervals similar to spontaneous activity. The primary difference between spontaneous activity and noise-evoked responses is the across-fiber correlation that acoustic noise produces in the neurons that innervate adjacent locations on the basilar membrane. We have demonstrated with a computational model that an appropriate electrical stimulus may produce a spontaneous-like renewal process in the auditory nerve, which is uncorrelated across fibers (31). Much of the underlying theory has been confirmed in animal studies (38,39). The purpose of this study was to test the hypothesis that such a high-rate pulsatile electrical stimulus can suppress tinnitus in humans without producing an audible percept.