A Review of Inner Ear Barotrauma, Tinnitus, and Its Treatment

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UHM 2006, Vol. 33, No. 4 – Treatment of Tinnitus

Case Report

Tinnitus in an active duty navy diver: A review of inner ear barotrauma, tinnitus, and its treatment.

C. DUPLESSIS1, M. HOFFER2

1Naval Submarine Medical Research Laboratory, Groton, Connecticut 06349;2Department of Otolaryngology, Naval Medical Center San Diego, San Diego, CA 92134-2200

susbmitted 10/17/2005; ﬁnal copy accepted 1/23/2006

Duplessis C, Hoffer M. Tinnitus in an active duty navy diver: A review of inner ear barotrauma, tinnitus, and its treatment. Undersea Hyperb Med 2006; 33(4):223-230.This case elucidates subtle cues that must be appreciated by the examiner in diving related injuries, who may not have experience with barotrauma-mediated pathology. Inner-ear barotrauma (IEBT) does not mandate ostensible hearing loss or vertigo; tinnitus may be the sole manifestation. Symptoms may present hours or even days post-dive. A common misconception exists that there are no efﬁcacious treatment options for IEBT short of surgery for an overt perilymphatic ﬁstula (1). Treatment options are available including acute high dose steroid administration, as prescribed for acute noise- induced or idiopathic hearing loss, optimally administered within three weeks of the acute insult. Tinnitus does not necessarily constitute a chronic untreatable symptom, which the patient must learn “to live with” (6,7).

BACKGROUND treatments for tinnitus, with more novel treatments on the horizon. However, these are Tinnitus, derived from the Latin word not effectively promulgated in the literature. tinnire (“to ring”), is defined by the unwanted This case elucidates the subtle cues that auditory perception of internal origin (1,2). must be appreciated by the examiner in diving Tinnitus affects up to 30% of the adult related injuries, who may not have experience population, with incapacitating symptoms with barotrauma-mediated pathology. Inner-ear reported in 6% of those afflicted, and significant barotrauma (IEBT) does not mandate ostensible depression experienced in 40% (2,3). Given hearing loss or vertigo; tinnitus may be the sole similar psychoacoustic descriptions of tinnitus, manifestation. Symptoms may present hours or individuals differ radically in the perceived even days post-dive. A common misconception intrusiveness of symptoms. A sobering statistic exists that there are no efficacious treatment is that 94% of patients seeking medical care options for IEBT short of surgery for an overt are not offered treatment for their affliction, perilymphatic fistula. However, treatment exacerbating symptoms (3). Reassurance and options are available including acute high hope are as appropriate and the cognitive dose steroid administration, as prescribed for appraisal of tinnitus is an integral component acute noise-induced or idiopathic hearing loss, of the disease (4). There are efficacious optimally administered within three weeks of

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the acute insult (6,7). consultation rendered the diagnosis of IEBT. The patient was started on a course of high CASE dose steroids (60mg per day for 10 days).

A 20-year old white male, AD, US Navy Differential Diagnosis diver without significant prior medical history, Tinnitus is caused by ischemic (stroke), presented several days after the onset of tinnitus congenital, traumatic (otosclerosis, noise,barotr sustained after performing a no-decompression auma),inflammatory (autoimmune, mastoiditis), dive on air (20 feet for 40 minutes). The dive surgical,medicinal(chemotherapeutics), was uneventful, except for difficulty clearing malignant (acoustic neuroma) (1), neurologic, his ears, requiring a forceful Valsalva. Ringing metabolic (diabetes, hypothyroidism, vitamin

commenced several hours post-dive, described B12 deficiency), idiopathic (presbycusis), as low level (rated as 1 on a scale of 10), high infectious (labyrinthitis), and psychologic pitched, unilateral (right ear), and constant since disorders. Diving related etiologies include inception. He denied other symptoms during or inner ear barotraumas (IEBT), inner ear post-dive; notably, vertigo, hearing loss, nausea, decompression sickness (DCS), and arterial vomiting, headache, visual changes, ataxia, or gas embolism (AGE). The dive profile, a no dizziness. He endorsed having a “cold” and decompression dive, maximum depth of twenty recent attendance at a rock concert. feet, without gas switching, is inconsistent with On examination, MMSE was without a diagnosis of inner ear DCS. AGE is ruled deficit. Exam findings were significant for out given the normal neurological exam and mobile tympanic membranes bilaterally, MMSE. Isolated tinnitus post-dive, without without evidence of middle ear effusions, associated symptoms, decreased the suspicion TM perforation, or hemotympanum. Nasal for IEBT. The presentation is most consistent and oral mucosa revealed mild congestion with viral labyrinthitis, and/or noise-induced consistent with the reported upper respiratory tinnitus. infection. There was no discernible evidence of nystagmus, and the rest of the neurological DISCUSSION exam was normal. The patient was educated on noise- Classification induced hearing loss, instructed to avoid loud Tinnitus may be broadly classified noise exposures, and to return for continued as either subjective or objective. Subjective or worsening symptoms. The patient was re- tinnitus is a phantom auditory perception evaluated six weeks later, prior to engaging without physical auditory or vibratory activity in further diving, and he reported continued in the cochlea, perceived only by the patient tinnitus. Subsequent audiological testing (3). Although most commonly associated revealed an isolated new right-sided 60-dB with hearing loss, it may occur with normal threshold shift at eight kilohertz with normal hearing. In objective tinnitus the examiner can speech reception testing, word recognition, appreciate the objectionable noise experienced acoustic reflex testing, and tympanometry by the patient, by placing a stethoscope over (type A tympanograms). Distortion Product the head and neck structures near the patient’s Otoacoustic Emission Testing (DPOAE) ear (1). Additional classification measures revealed emissions consistent with the include magnitude, quality, timing (progressive, audiogram and normal cochlear function. ENT fluctuating, intermittent, or constant), and pitch.

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Objective tinnitus is caused by sound The role of Central Nervous System emanating from the body either reaching the (CNS) Plasticity cochlea by bone conduction, or conducted The abnormal, novel or dearth of to the middle ear cavity without documented neural activity from the ear may induce CNS dysfunction of the auditory system. Sources neural plasticity (4)], including a redirection of include turbulent blood flow or muscle information to regions of the CNS that normally contractions (2). do not receive auditory input, including the Tinnitus quality may be tonal (ringing autonomic and limbic systems. This activation or whistling), or noise-like (roaring or hissing) yields many of the deleterious symptoms of (5). Tinnitus severity may be mild (audible tinnitus, including depression, hypertension, only when in a quiet place) or severe (disturbing anxiety, and insomnia, which correlate better symptoms degrading the quality of life) with reported severity, than psycho-acoustical (6). Pitch assessment may help differentiate measurement (8). etiologies. Low frequency tinnitus (< 250 Normally, the auditory system receives Hz) may reflect Menière’s disease. Higher and processes a large volume of acoustic pitch tinnitus is associated with noise induced information, transmitting a small fraction for hearing loss (7). conscious perception. Exposure to familiar and unimportant sound is blocked at the subconscious Pathophysiology level, “habituated”, without activation of the Tinnitus-related neuronal activity is not limbic and autonomic systems. However, in governed by mechanically-derived acoustics various types of inner ear injury, the abnormal, (8), but the brain’s perception and interpretation novel or even dearth of discharge activity may of novel or abnormal neural activity (1). The be incorrectly categorized as important, and thus altered perception inevitably stems from some processed for enhancement, amplification, and insult to the cochlear apparatus, the cochlea’s transmission. More importantly, the processed outer hair cells (OHC), and inner hair cells information may be transmitted erroneously to (IHC). Injury may lead to repetitive discharge the limbic and autonomic systems (via neural from the hair cells, spontaneous activity in plasticity), and the higher cortical auditory auditory nerve fibers, hyperactivity of cochlear centers for conscious perception (tinnitus). nuclei, or a reduction in normal suppressive Furthermore, when the CNS plastically activity of the central auditory cortex on activates a “conditioned reflex arc”(8) linking peripheral auditory nerve activity (1). the auditory with the limbic and autonomic A leading theory posits discordant nervous systems, “it establishes a detrimental, dysfunction of the OHC and IHC, postulating self-perpetuating, negative reinforcement, that tinnitus related neuronal activity is leading to tinnitus enhancement, and prevention generated in the dorsal cochlear nucleus from of habituation” (8). unbalanced activity transmitted by type I and type II auditory nerve fibers (derived from the Pathophysiology of Diving-Induced IHC and OHC respectively). This attractive Tinnitus theory reconciles various subcategories of Diving related inner ear pathology tinnitus; tinnitus experienced in the absence of includes DCS, AGE, and IEBT (9). IEBT is hearing impairment, and hearing impairment commonly ascribed to labyrinthine window unaccompanied by tinnitus (8). ruptures forming a perilymphatic fistula (5). Significantly, symptoms may not develop for

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hours or even days after the incident. The depth and duration of the dive, breathing gas, mechanism may be either implosive or explosive use of gas switching, decompression schedule, (10). These injuries may be compounded by work performed, phase of diving for symptom gas entry to the inner ear (11). onset and prior hyperbaric exposures. Perilymphatic fistulas may heal A complete head and neck and neurotologic spontaneously with conservative measures examination should be performed including an that mitigate middle and inner ear over- otoscopic and cranial nerve examination, and pressurization. If this fails, it may be amenable Weber, Rinne, Romberg’s, nystagmus, gait, to surgical correction, although the timing Dix-Hallpike, and dysmetria testing. remains controversial. What is perhaps not widely appreciated Diagnostic Studies is that IEBT may occur without window Middle ear studies include ruptures, and without overt otoscopic signs tympanometry, and stapedial reflex, reflex (10), manifest by inner ear hemorrhage, and decay and recruitment testing. Evaluate the intralabyrinthine injury, resulting in deficits cochlear-vestibular apparatus via audiologic to discrete tonal frequencies. Cochlear injury testing (pure tone and bone levels, speech may involve degeneration of IHC and OHC reception thresholds, speech discrimination, (typically more severely damaged) (11), and uncomfortable loudness levels). For severe suggesting a role for otoacoustic emissions cases, consider assessing pitch and loudness (OAE) testing in the diagnostic work-up. This matching (matching the frequency of the tinnitus mechanism of injury has been associated with a and estimating loudness with pure tones or more sudden onset of symptoms not amenable noise), minimum masking levels, and residual to treatment (10). inhibition (achieving resolution of symptoms The diving profile helps to differentiate for a defined period of time after exposure to inner ear DCS from IEBT. Inner ear DCS a masking tone in the pitch and intensity of the manifests itself during the ascent phase of the tinnitus (1), to identify those who may benefit dive, or shortly afterwards, and is associated from tinnitus masking therapy. Additional with deep diving, breathing gas changes, testing may include auditory brainstem response and other signs of DCS. This differentiation testing, otoacoustic emissions (OAE) testing, is important, as recompression treatment is MRI and CT imaging, tone-decay testing, and indicated for inner ear DCS, but not IEBT, electronystagmography (2). For unilateral although ongoing research may alter this tinnitus of unknown etiology, laboratory opinion (11). analysis may include CBC, lipid profile, glucose level, fluorescent treponema antibodies (FTA), MEDICAL EVALUATION OF TINNITUS Lyme titer, thyroid and autoimmune panel.

History and Physical Examination Treatment Pertinent history includes alcohol and Development of efﬁcacious treatment caffeine consumption, smoking, illicit drug has been handicapped by several issues, abuse, medications, and herbal use. Establish including the subjective nature of the disorder the tinnitus as objective or subjective. Identify and its multifaceted etiology impeding study its location, onset, timing, intensity, pitch, and targeted therapy (6). Fortunately, the quality, severity, and associated symptoms. A majority of patients with tinnitus require simple record of the dive proﬁle should include the reassurance and the possible recommendation

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of white noise masking; very few patients have In patients with hearing loss at symptoms severe enough to require extensive frequencies < 4 kHz, a hearing aid may intervention. Treatment modalities should improve both hearing and tinnitus by raising incorporate education, counseling, reassurance the background sound level (3). and support. Conservative treatment includes lifestyle and dietary modification. Avoid loud Biofeedback noise, and potentially ototoxic medications. In biofeedback, surface electrodes are Dietary modifications include abstinence from placed on muscles in the upper quadrant, neck nicotine, caffeine and alcohol. and face. Patients are instructed in methods to Other treatments include transcutaneous relax muscle tension identified on a computer electrical nerve stimulation (TENS), sound output, visualizing real-time success through therapy (tinnitus maskers), biofeedback, computer screen monitoring (12). cognitive-behavioral therapy, tinnitus retraining therapy (TRT), medications (oral Tinnitus Retraining Therapy (TRT) and transtympanic), alternative therapies, and Although repair of a damaged cochlea surgery. A brief synopsis of each follows: is not yet possible, the brain’s detection and interpretation of signals can be modified, TENS Therapy exploiting its inherent plasticity (8). TRT is TENS utilizing continuous or modulated a method based on the neurophysiological alternating current applied to various points model of tinnitus, predicated upon the model on the external pinna and tragus has proven of neuroplasticity. The method attempts to to be a safe and effective modality in certain induce sustained habituation of reactions populations, with efficacy ranging from 33- and perceptions to intrusive tinnitus and 82% (12). The physiological mechanism external sounds (8). It eliminates neuroplastic remains elusive, but has been theorized to connections linking the auditory with the limbic involve increased cochlear blood flow, direct and autonomic nervous systems. Specifically, cochlear stimulation, and an adaptation of the the brain is trained to filter abnormal signals, pain gate theory. Electric current may restore preventing them from activating the limbic the deprivation of neural activity in the auditory and autonomic nervous systems. This leads to nerve, which engenders the phantom sensation habituation of tinnitus-evoked reactions, and of tinnitus(7). reductions in signals reaching higher cortical levels involved in perception (habituation Sound Therapy of tinnitus perception) (8). TRT has been Sound therapy, via tinnitus maskers, has reported to produce significant and sustained been efficacious in almost 90% of patients (13). improvement in symptoms in over 80% of Devices can be designed on an individual basis, patients. providing frequency selective masking. Future masking devices may utilize high frequency bone Surgical Options conduction, circumventing the need for ear For the special case associated with occlusion (13). Evidence suggests that some traumatic induced perilymphatic fistula patient’s achieve an accumulation of residual formation, surgical correction, performed early inhibition with chronic usage (5). There are is a viable option. Timing remains controversial also bedside maskers, which may be utilized (10). for symptoms interfering with sleep (13).

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Alternative Therapies associated with Menière’s Disease (19,20). Alternative therapies of anecdotal Transtympanic steroidal administration efﬁcacy include early institution of hyperbaric has proven efﬁcacious for the treatment of

oxygen therapy (HBO2), and low level laser sudden sensorineural hearing loss (SSNHL), therapy (14). Both may increase oxygen autoimmune inner ear disease (AIED), and delivery and ATP synthesis in stressed or Menière’s disease (18). Transtympanic injured cochlear tissues (14). steroidal delivery has successfully improved hearing in patients with SSNHL unresponsive Medications to oral steroid administration (17), or in Medications of anecdotal efficacy whom oral steroids are contraindicated include vitamins, herbs, antioxidants, carbogen (18). Transtympanic steroid therapy has also inhalation (14,15), alprazolam (in patients proved effective for primary tinnitus. Sakata’s with insomnia and anxiety)(13), and lidocaine. group utilized intratympanic steroids on 1214 Recent evidence suggests that anti-oxidants patients with cochlear tinnitus and reported may have some impact on tinnitus (19). a 71% response rate (21). Shulman’s group Perhaps not promulgated in the medical reported a similar success rate of 70% when literature is that steroids (6) may be a highly using transtympanic steroids for tinnitus (22). efficacious treatment for barotraumatically There are still a number of questions with mediated tinnitus-when administered early. regards to the use of transtympanic medicines, Furthermore, transtympanic medicinal in general, and steroids in particular for the administration is increasing in prevalence, treatment of inner ear disorders. The best route and transtympanic steroidal administration of administration, best total dose, best dosing has proven efficacious for the treatment of frequency, and the best end point of therapy sudden sensorineural hearing loss (SSNHL), still need to be determined. Nevertheless, autoimmune inner ear disease (AIED), and transtympanic steroids are now a common Menière’s disease (20). treatment for tinnitus (23). Oral steroids are proven to improve the symptoms of sudden sensorineural Treatment for Diving-Induced hearing loss (SSNHL) (16,17). Standard Tinnitus practice increasingly incorporates the acute The diving literature supports initial administration of high dose oral steroids for a conservative treatment of suspected IEBT, variety of cochlear maladies including acute endorsing caution against CSF/intracranial noise and barotraumatically induced hearing pressure elevation, which may propagate to loss. the inner ear. ENT referral is suggested for Transtympanic Therapy persistent suspicion of perilymphatic fistulas. Transtympanic (intratympanic) Not publicized in the literature, diving or perfusion therapies are emerging for targeted otherwise, is the potential role of steroid diffusion of medications across the round administration (oral and intratympanic) for window membrane into the inner ear fluids, acute IEBT, as touted for acute noise induced reducing systemic side effects, and achieving hearing loss. higher localized concentrations (16, 18). The crux of treatment is early Transtympanic medical therapy (using intervention. Tinnitus, whether isolated, or gentamycin) has become standard and accepted associated with other symptoms, temporally therapy for vertigo, hearing loss, and dizziness related to diving, suggests the possibility of

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IEBT. Symptoms may present many hours or CONCLUSION days post-dive. A perilymphatic fistula is not a pre-requisite to diagnose IEBT, which we The patient in this report had some now realize may be occult, and which may improvement in symptoms after therapy be treatable with high dose oral steroids, or despite its administration some six weeks intratympanic steroid administration. after the insult. The audiogram improved in the threshold shift at 8k from 60 to 40 Prevention of Diving Related Inner dB after treatment, with a commensurate Ear Barotrauma decrease in symptoms, remaining stable on The best treatment for diving-related serial testing twelve weeks later. Whether this barotrauma is prevention. This includes improvement is related to the steroid treatment, ensuring patency of the Eustachian tubes prior to or the natural evolution of tinnitus resolution, diving, and early and frequent autoinflations to is debatable. Earlier recognition of IEBT, with equilibrate middle ear pressures during diving. steroid administration, may have garnered The diving candidate should be instructed in the a better outcome. Fortunately, this diver did maneuvers, which may be attempted to open not experience any decrement in pure-tone the Eustachian tubes including, the Valsalva, audiometric thresholds in the frequency ranges the Toynbee, the Frenzel, the Lowry, and the of 500-2000 Hz, or speech discrimination scores Edmonds techniques. Additional preventive that may have undermined future diving. strategies include descending in the vertical Divers experience significant high- head up position, avoiding diving when unable frequency sensorineural hearing loss, to equilibrate the middle ear (due to upper exceeding matched controls (10). Divers may respiratory tract infections, allergies, irritant be vulnerable to insidious sub-clinical inner- exposures, and medications), and avoidance ear damage from exposures to hyperoxia, of alcohol, and allergic triggers prior to diving IEBT, and noise predisposing synergistically (such as dairy products). to permanent sensorineural hearing loss, which is not apparent on contemporary pure- PROGNOSIS tone audiometry, and which may be otherwise mitigated or circumvented with timely steroid Without treatment, cochlear low treatment. frequency hearing may improve for a few Otoacoustic emission (OAE) testing weeks, but the remaining high-frequency is a more sensitive measure than pure tone hearing loss is usually permanent (10). conventional audiometry in assessing inner- In permanent vestibular injury, central ear injury (particularly high frequency injury), compensation may, after some time, render from myriad insults including impulse noise the patient asymptomatic. Unfortunately, exposure from firearms affording more lead time similar mechanisms do not exist for permanent to administer interventions (steroids)(24,25). cochlear injury (11). Tinnitus often improves The author is currently investigating the utility over six to twelve months, presumably as of OAE testing in identifying sub-clinical inner damaged sensory endings are repaired or die ear injury after repetitive diving exposures. (10). A residual high pitch tone accompanied This case elucidates the subtle cues, by a residual high frequency hearing loss often which must be appreciated by the examiner in remains (11). diving related injuries. It is prudent to engage ENT consultation early in the evaluation of

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diving related inner-ear injury. IEBT does not 2003;36(2):337-44. mandate ostensible hearing loss or vertigo; 13. Vernon, J., & Meikle, MB. Masking devices and alprazolam treatment for tinnitus. Otolaryngologic tinnitus may be the sole manifestation. Clinics of North America, 2003;36(2):307-320. Symptoms may present hours or even 14. Seidman, M., & Babu, S. Alternative medications days post-dive. Treatment options may be and other treatments for tinnitus: facts from ﬁction. Otolaryngologic Clinics of North America, 2003; available including acute high dose steroid 36(2):359-81. administration, as prescribed for acute noise- 15. Joachims, H. Antioxidants in treatment of induced or idiopathic hearing loss, optimally idiopathic sudden hearing loss. Otol Neurotol, 2003;24(4):572-5. administered within three weeks of the acute 16. Light, J.S., H. Transtympanic perfusion: indications insult. The effectiveness of steroid treatment and limitations. Curr Opin Otolaryngol Head Neck in diving related injuries has not been studied, Surg, 2004;12:378-83. 17. Lefebvre, P. Steroid perfusion of the inner ear for and should be subject to future clinical trials. sudden sensorineural hearing loss after failure Tinnitus does not inexorably dictate a chronic of conventional therapy: a pilot study. Acta untreatable symptom, which the patient must Otolaryngol, 2002; 122(7):698-702. learn “to live with” (6,7). 18. Jackson, L., & Silverstein, H. Chemical perfusion of the inner ear. Otolaryngologic Clinics of North America, 2002;35(3):639-53. REFERENCES 19. Hoffer, ME, Allen KA, Kopke RD, Weisskopf R, Gottshall KR, Moore R, & Wester, DC. Transtympanic 1. Crummer, RH Diagnostic Approach to Tinnitus. vs. Sustained Release Administration of Gentamicin: American Family Physician, 2004; 69(1):120-6. Kinetics, Morphology, and Function. Laryngoscope, 2. Heller, A. Classiﬁcation and epidemiology of 2001; 111:1343-1357 tinnitus. Otolaryngologic Clinics of North America, 20. Hoffer ME, Kopke RD, Weisskopf R, Gottshall 2003;36(2):239-48. KR, Moore R, Allen KA, Wester DC, & Balaban 3. Schwaber, M. Medical Evaluation of Tinnitus. C. Use of the Round Window Microcatheter in the Otolaryngologic Clinics of North America, Treatment of Menière’s Disease. Laryngoscope, 2003;36(2):287-92. 2001; 111:2046-2049 4. Sismanis, A. Tinnitus: Advances in evaluation and 21. SakataE, Itoh A, ItohY. Treatment of cochlear management. Otolaryngologic Clinics of North tinnitus with dexamethasone infusion into the America, 2003; 36(2):xi-xii. tympanic cavity. Int Tinnitus J, 1996;2:129-35 5. Vernon, J., & Meikle, MB. Tinnitus: Clinical 22. Shulman A, Goldstein B. Intratympanic drug Measurement. Otolaryngologic Clinics of North therapy with steroids for tinnitus control:a America, 2003; 36(2):293-305. preliminary report. Int Tinnitus J, 2000;6:10-21 6. Hoffer, M., Wester, D., Kopke, RD., Weisskopf, 23. Hoffer ME, Wester D, Kopke RD, Weisskopf P, P., & Gottshall, K. Transtympanic management of Gottshall KR. Transtympanic tinnitus. Otolaryngologic Clinics of North America, Management of Tinnitus. Otolaryngol Clin of N 2003;36(2):353-8. Am, 2003;36(2):353-58 7. Moller, A. Pathophysiology of Tinnitus. 24. Pawlaczyk-Luszczynska, M., Bak, M., Fiszer, Otolaryngologic Clinics of North America, M., Kotylo, P., & Sliwinska-Kowalska, M. 2003;36(2):249-66. Temporary changes in hearing after exposure to 8. Jastreboff, P., Jastreboff, MM. Tinnitus Retraining shooting noise, Int J Occup Med Environ Health, Therapy for patients with tinnitus and decreased 2004;17:285-94. sound tolerance. Otolaryngologic Clinics of North 25. Lapsley-Miller, J.A., Boege, P., Marshall, L., America, 2003;36(2):321-6. Shera, C.A., and Jeng, P.S. Stimulus-Frequency 9. Bove, A., Bove and Davis’ Diving Medicine. 2004, Otoacoustic Emissions Validity & Reliability of Philadelphia: Saunders. SFOAEs Implemented on MIMOSA Acoustics 10. Edmonds, C., Lowry, C., Pennefather, J., & Walker, SFOAE Measurement System V2.1.18 Groton, R., Diving and Subaquatic Medicine. 4th ed. 2002, CT: Naval Submarine Medical Research New York: Arnold. Laboratory; 2004 Feb. Report No.: 1231. 11. Bennett, P.E., DH, Physiology and Medicine of Diving. 2003, Great Britain: Saunders. 12. Steenerson, R.C. Tinnitus reduction using transcutaneous electrical stimulation. Otolaryngologic Clinics of North America,

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