Principles of tinnitology: tinnitus diagnosis and treatment a tinnitus-targeted therapy

OBJECTIVE: To provide to the tinnitus professional a rationale for establishing accuracy in tinnitus diagnosis and the selection of modalities of therapy (i.e., medication, instrumentation, and surgery) for attempting tinnitus relief for patients with tinnitus diagnosed by completion of a medical-audiological tinnitus protocol (MATPP) and clinical course and found to be subjective idiopathic tinnitus of the severe disabling type (SIT). BACKGROUND: The completion of a MATPP has been recommended since 1977 for each tinnitus patient in an attempt to establish an accurate diagnosis. A tinnitus-targeted therapy (TTT), a combined treatment of medication and instrumentation focusing on pharmacotherapy, has evolved from our ongoing clinical experience since 1977 (now in excess of 10,000 SIT patients) [1-4]. Principles for SIT treatment have evolved from the TTT experience that provides a rationale for attempting tinnitus relief. In this report, the term tinnitus refers to SIT. METHOD: The strategies of TTT are based on the clinical translation for SIT diagnosis and treatment of (1) fundamentals of neuro-otological diagnosis; (2) fundamentals of sensory physiology; (3) extrapolation for treatment of known underlying neurochemistries from nuclear medicine imaging results e.g. single-photon emission computed tomography and positron emission tomography; (4) hypothesis of mechanism of tinnitus production , Tinnitus Dysynchrony Synchrony Theory (TDST) [5] , and hypothesis of the transformation-transition of the sensation of an aberrant auditory sensation-tinnitus (i.e., sensory component)-to one of affect (i.e., the emotional-behavioral component), Final Common Pathway of Tinnitus (FCP)[8]; and (5) innovative application of drug therapies designed for indications other than tinnitus [2,3]. ResuLTS AND CONCLUSION: The ongoing clinical application of a rationale based on principles of diagnosis and treatment for SIT, which has evolved from our TTT clinical experience in SIT patients, continues to result in long-term tinnitus relief: in excess of 1 year in approximately 75% to 85% with medication and in 10% to 15% with instrumentation. SIT patients resistant to therapy persist at 10% to 15%.     

Tinnitology, Tinnitogenesis, Nuclear Medicine, and Tinnitus Patients

Since the 1970s, clinical interest in otolaryngology and audiology for both diagnosis and treatment of the symptom of tinnitus has witnessed the evolution of a new discipline: tinnitology. Tinnitology is an integrated discipline of basic sciences, neuroscience, and clinical medicine for the understanding of aberrant auditory phenomena unrelated to an external source of sound. To patients with subjective idiopathic tinnitus, nuclear medicine techniques of positron emission tomography and single-photon emission computed tomography provide correlation of structure and function, which improves the accuracy of the tinnitus diagnosis. Additionally, they provide a monitoring system to establish the efficacy of modalities of therapy attempting to provide tinnitus relief. Further, they provide information of neuroreceptors and neurochemistry in brain underlying or accompanying basic mechanism for production of specific clinical types and subtypes of tinnitus. This study reports the application of nuclear medicine techniques for a new clinical neuropharmacology protocol for tinnitus treatment highlighted by intratympanic drug therapy in predominantly cochlear-type tinnitus. We further report a neuroprotective drug therapy to control tinnitogenesis, an auditory epileptiform phenomenon. Additionally, we report the hypothesis of a benzodiazepine deficiency syndrome.     

Central nervous system neurodegeneration and tinnitus: a clinical experience. Part I: Diagnosis

In an evolving clinical experience since 1979, the medical significance of the symptom of tinnitus has been identified as a "soft" sign of neurodegeneration (ND) in the central nervous system (CNS) in a particular subset of tinnitus patients diagnosed with a predominantly central-type, severe, disabling, subjective idiopathic tinnitus. To highlight this experience, a retrospective review and analysis of consecutive tinnitus patients (N = 96) was conducted. Ninety-six tinnitus patients (ages 22-90 years) were seen in neurotological consultation from November 1, 2005, to June 30, 2007, all of whom had subjective idiopathic tinnitus of the severe disabling type (SIT). Of these 96 patients, 54 had SIT of the predominantly central type and of these, 18 (ages 39-75 years) were recommended for nuclear medicine imaging (single-photon emission computed tomography [SPECT] and fluorodeoxyglucose-positron emission tomography/computed tomography [FDG-PET/CT]). Patient selection for nuclear medicine imaging fulfilled the criteria of a medical-audiological ND tinnitus profile: completion of a patient protocol that diagnosed a predominantly central-type, severe, disabling, subjective, idiopathic tinnitus lasting in excess of 1 year, and failure of existing modalities of treatment attempting tinnitus relief. In 16 of the 18 patients, objective evidence of ND was reported in multiple neural substrates of brain obtained with SPECT or FDG-PET/CT of brain. Classification of CNS ND and tinnitus differentiated between (1) ND of nonspecific or unknown etiology; (2) ND manifested by perfusion asymmetries in brain associated with ischemia (n = 11/18); and (3) neurodegenerative CNS disease consistent with nuclear medicine criteria for senile dementia of the Alzheimer's type (n = 5/18). The diagnosis has been associated with cerebrovascular disease (n = 16/18). The identification of neurodegenerative CNS disease in a selected cohort of patients with subjective idiopathic tinnitus as a soft sign of such CNS disease has implications for diagnosis and treatment.     

Tinnitus dyssynchrony-synchrony theory: a translational concept for diagnosis and treatment

The tinnitus dyssynchrony-synchrony theory (TDST) is a hypothesis that considers tinnitus to be an abnormal, conscious, auditory percept. It is believed to originate as an initial dyssynchrony in pre- or postsynaptic neuronal transmission within the peripheral or central nervous system (cortical or subcortical). It interferes in the excitatory and inhibitory process or processes involved in maintaining homeostasis for brain neurofunction, in multiple neural substrates, and acts as an aberrant auditory stimulus to express this dysfunction via the auditory system. The conscious auditory percept for tinnitus is hypothesized to reflect clinically a summation of synchronous activities of neuronal activity recordable from multiple neural substrates at the brain cortex. The transformation from the dyssynchrony of the aberrant auditory stimulus to one of synchrony and individual brain function of affect, somatosensory response, and consciousness is clinically considered to be a final common pathway for tinnitus. The clinical application of the TDST has increased the accuracy of tinnitus diagnosis and improved the efficacy of treatment modalities attempting tinnitus relief.     

Ultra-high-frequency ultrasonic external acoustic stimulation for tinnitus relief: a method for patient selection

We proposed a method for patient selection and application of criteria for predicting success with bone-conduction external acoustic stimulation using high-audio-frequency sound in the ranges of 10-20 kHz and 20-26 kHz for individuals with subjective idiopathic tinnitus (SIT) of the severe disabling type. Ultra-high-frequency (UHF) stimulation for tinnitus relief has been found to be most effective when residual neuronal function exists in the acoustic ranges of 10-14 kHz, with thresholds no greater than 40-50 dB sound pressure level (SPL). Ultrasonic (US) acoustic stimulation is recommended for patients with audiometric thresholds greater than 50-60 dB SPL for frequencies of 10-14 kHz. Fifty-two consecutive patients seen for the primary complaint of SIT of the severe disabling type received a trial of either UHF or US bone-conduction acoustic stimulation. Tinnitus relief was reported in 22 of the 52 patients. The application of criteria for patient selection predicted tinnitus relief in 20 of the 22.     

Brain and inner-ear fluid homeostasis, cochleovestibular-type tinnitus, and secondary endolymphatic hydrops

Secondary endolymphatic hydrops (SEH) has clinically been found to have a significant incidence of occurrence in patients with subjective idiopathic tinnitus (SIT) of a severe disabling type. The diagnosis is made clinically and has been established by integration in a medical audiological tinnitus patient protocol of the clinical history with results of electrodiagnostic cochleovestibular testing that fulfill the diagnostic criteria of inner-ear disease consistent with Ménière's disease. SEH is hypothesized to be a factor, not an etiology, influencing the clinical course of SIT. Alterations over time (i.e., delay in the homeostatic mechanisms in normnal function of the fluid compartments of the inner-ear perilymph, endolymph, or brain cerebrospinal fluid) result in endolymphatic hydrops and interference in normal function of the inner ear, with resultant inner-ear complaints that can be highlighted by tinnitus rather than by vertigo. The endolymphatic hydrops may be either localized or diffuse within the cochlear or vestibular labyrinth. The etiologies and mechanisms of cochleovestibular-type tinnitus are multiple and are influenced by the SEH. Classically, the tetrad of symptoms--episodic vertigo, fluctuating sensorineural hearing loss, tinnitus, and ear blockage--associated with the histopathological correlate endolymphatic hydrops has been diagnosed as Ménière's disease. Specifically, key etiological agents that have been identified as playing a role in the clinical course of tinnitus (e.g., noise exposure, stress) may serve as "triggers" or stressors (or both), resulting in interference in normal biochemical and physiological function of sensorineural structures in the inner ear or in neural structures in the brain. In both conditions, the alterations over time (i.e., delay) in the clinical manifestation of the tetrad of symptoms of inner-ear dysfunction, when highlighted by SIT rather than vertigo, otherwise fulfill the criteria for diagnosing SEH. The chief complaint of SIT, when presenting as one of the tetrad of inner-ear symptoms and otherwise diagnosed as Ménière's disease, has also been associated clinically with perfusion asymmetries in brain, identified by nuclear medicine brain imaging (single-photon emission computed tomography [SPECT] of brain), and reflects an interference in homeostasis in the blood-brain labyrinth or blood-brain barriers, with a resulting SEH. The medical significance of the SIT in some patients may be a gradual, progressive sensorineural hearing loss. The inclusion of SPECT of brain in SIT patients demonstrates a global approach for improving the accuracy of diagnosing the SIT symptom, for focusing on the contribution of central nervous system dysfunction to the development of SEH, and for understanding and influencing the clinical course of SIT.     

Medical Significance of Tinnitus

The medical significance of a symptom or disease process in a patient is defined as a clinical manifestation of abnormal function of a living cell, tissue, organ or organ system(s). Tinnitus, an aberrant perception of sound unrelated to an external source of sound, has been identified to have a medical significance. The medical significance of tinnitus has been identified with a Medical Audiologic Tinnitus Patient Protocol since 1979. The highlights of this clinical experience include for diagnosis: tinnitus not to be a unitary symptom; the identification of clinical type and subtypes of tinnitus and a Final Common Pathway for Tinnitus of all clinical types particularly of the severe disabling type. For treatment a multidisciplinary approach has evolved including neurology, otology and psychiatry; a combined treatment protocol of drug therapy and instrumentation, based on differentiation between the components of the symptom of tinnitus i.e. sensory, affect, and psychomotor. Two diagnostic categories are identified: otologic/neurotologic and neurologic. The application of SPECT Imaging of Brain which has identified a Final Common Pathway for tinnitus and provides an increased diagnostic accuracy for tinnitus and a basis for selection of a neuropharmacology for tinnitus is discussed.     

Hyperinsulinemia: The Common Denominator of Subjective Idiopathic Tinnitus and Other Idiopathic Central and Peripheral Neurootologic Disorders

Hyperinsulinemia as determined by glucose/insulin tolerance identified an etiologic relationship to idiopathic Menière's disease. This was subsequently concurred with internationally by others. Proctor identified hyperinsulinemia in Subjective Idiopathic Tinnitus (SIT). Hyperinsulinemia and migraine with tinnitus and/or vertigo were also correlated.     

Central nervous system neurodegeneration and tinnitus: a clinical experience. Part II: translational neurovascular theory of neurodegenerative CNS disease and tinnitus

The translation of a neurovascular hypothesis for Alzheimer's disease to subjective idiopathic tinnitus (SIT) is presented as a challenge to the predominantly sensorineural view of SIT and its clinical application for tinnitus treatment. The concept of neurovascular dysfunction and neurodegeneration (ND) in SIT patients has been proposed and reported as an etiology in a particular subset of tinnitus patients with a diagnosis of medical-audiological tinnitus, through a medical-audiological tinnitus patient protocol, to be a predominantly central-type, severe, disabling SIT (n = 54 of 96). A medical-audiological ND tinnitus profile was the basis for selection of 18 SIT patients (n = 18 of 54) for nuclear medicine brain imaging (i.e., single-photon emission computed tomography or positron emission tomography, or both). Objective findings were reported in 16 of this cohort of 18 SIT patients selected for nuclear medicine imaging (88.9%). Classification of central nervous system (CNS) ND and tinnitus differentiated between (1) ND, nonspecific and of unknown etiology; (2) ND manifested by perfusion asymmetries in brain associated with ischemia (n = 11 of 18); and (3) ND CNS disease consistent with nuclear medicine criteria for senile dementia Alzheimer's-type disease (n = 5 of 18). The diagnosis was associated with cerebrovascular disease (n = 16 of 18). The identification of pathological processes of inflammation and ischemia, linked to ND, in a particular cohort of SIT patients may provide a basis for establishing the medical significance and treatment of SIT and influence the clinical course of the tinnitus.     

Descending auditory system/cerebellum/tinnitus

The cerebellum and the descending auditory system (DAS) are considered clinically significant for influencing the development of the clinical course of tinnitus of the severe disabling type. It is hypothesized that the SPECT of Brain perfusion asymmetries in cerebellum, demonstrated since 1993, reflect clinically the influence of an aberrant auditory stimulus i.e. tinnitus, on the activity and function of the descending auditory system highlighted by the cerebellum and the acousticomotor systems. SPECT of Brain perfusion asymmetries in the cerebellum have been demonstrated in 60-70% of tinnitus patients of the central type. Electrophysiologic support for this finding includes interference in ocular fixation suppression of the vestibulocular (VOR) with rotation and position testing. Abnormalities in cerebellar function are considered to reflect the psychomotor component of tinnitus. Support for the hypothesis is demonstrated with one patient with a predominantly central type tinnitus of the severe disabling type with cerebellar perfusion asymmetries and associated electrophysiologic evidence of interference in the VOR with rotation testing.     

Tinnitus treatment with customized sounds

Recent studies have indicated that the pathophysiological basis for tinnitus may be abnormal activity in the auditory areas of the brain rather than aberrant activity in the periphery. Tinnitus-related activity leads to changes in tonotopic representation in auditory cortex. However, such reorganization can be reversed through training-induced changes in the response pattern of cortical neurons. We address this problem by using customized sounds that reproduce the subjective experience to reduce overactive auditory circuits. The results of two preliminary studies indicate that customized sound therapy (CST*) aimed at this central dysfunction reduces tinnitus quickly and safely. Participants described immediate relief, showed changes on the Tinnitus Handicap Questionnaire, and reported changes in hearing threshold within 3 weeks. We also saw changes in the intensity dependence of the auditory N100 in tinnitus patients, supporting the idea that tinnitus reflects a reorganization of tonotopic maps in the auditory cortex. The main correlate of this reorganization was the enhanced contrast between responses to the perceived tinnitus pitch and tones approximately one octave lower. After 3 weeks of CST, the intensity dependence to the tinnitus pitch decreased, making these responses more similar to those from normal subjects responding to tones in the same frequency.     

Relief of idiopathic subjective tinnitus: is gabapentin effective?

OBJECTIVE: To assess the therapeutic benefit of gabapentin (Neurontin) for subjective idiopathic troublesome tinnitus. DESIGN: An 8-week, double-blind, randomized clinical trial. SETTING: Academic otolaryngology clinic in St Louis, Mo. SUBJECTS: One hundred thirty-five subjects with severe idiopathic subjective tinnitus of 6 months' duration or longer. INTERVENTION: Gabapentin, at a maintenance dosage of 900 to 3600 mg/d for 8 weeks, or lactose placebo. MAIN OUTCOME MEASURE: Change in the Tinnitus Handicap Inventory score from baseline to the study end point. RESULTS: The overall change in the Tinnitus Handicap Inventory score for the entire cohort from baseline to week 8 was 11.2; the change among the 59 subjects randomized to the gabapentin arm was 11.3 and the change among the 56 subjects in the placebo arm was 11.0. The difference was 0.03 (95% confidence interval, -5.5 to 6.2; P = .91). CONCLUSION: Gabapentin is no more effective than placebo for the relief of idiopathic subjective tinnitus. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00317850.     

Treatment of tinnitus with a customized, dynamic acoustic neural stimulus: underlying principles and clinical efficacy

Tinnitus has been challenging to treat with consistently positive results. The Neuromonics Tinnitus Treatment is a newly available approach to the treatment of clinically significant, problematic tinnitus (and reduced sound tolerance) that was developed with the intention of simultaneously addressing the auditory, attentional, and emotional processes underlying the condition. It uses a prescribed acoustic stimulus, customized for each patient's individual audiometric profile, which provides a broad frequency stimulus to address the effects of auditory deprivation, promotes relief and relaxation with the intention of reducing engagement of the limbic system/amygdala and autonomic nervous system, and applies the principles of systematic desensitization to address the attentional processes. This article describes the underlying principles behind this approach. It also summarizes evidence for clinical efficacy from controlled clinical studies and from a private practice clinical setting, where it has been shown to provide consistently positive outcomes for patients meeting suitability criteria.     

Ultra-high-frequency acoustic stimulation and tinnitus control: a positron emission tomography study

Ultra-high-frequency (UHF) external acoustic stimulation with the UltraQuiet device (UQ) has been reported to provide significant relief of severe disabling-type tinnitus. The nuclear medicine imaging technique of positron emission tomography (PET) was selected as a monitoring system to compare objectively metabolic alterations in brain function before and after UHF/UQ and to correlate the PET data with the subjective behavioral response of patients reporting tinnitus relief. PET of brain was completed on 6 patients randomly selected from a cohort of 15 patients included in a protocol to establish long-term tinnitus relief with UHF/UQ. Twelve specific regions of interest (ROI) were selected for PET of brain examination on the basis of results obtained with single-photon emission computed tomography (SPECT) of brain examinations recommended for patients with severe disabling-type tinnitus and demonstrating significant perfusion asymmetries in the right and left brain ROI of the primary auditory cortex; frontal, temporal, parietal, and medial temporal lobes; and cerebellum. PET of brain results included ratios of post- and pre-UHF/UQ stimulation that demonstrated no random response in the selected PET of brain ROI and ratios of post- and pre-UHF/UQ stimulation that demonstrated three categories of response in the selected PET brain ROI for all six patients: hypermetabolism in three patients; hypometabolism in two; and a mixed response in one. Correlation was established for each patient among PET and electrophysiological responses of alteration in minimal masking levels, the residual UHF neuronal response as reflected in the UHF audiogram, and the subjective reported behavioral responses of patients (obtained from outcome questionnaires for tinnitus relief, which focused on tinnitus intensity, annoyance, severity index, and a subjective scale of value of the UHF/UQ device for tinnitus relief. The subjective behavioral response for tinnitus relief with UHF/UQ was found to reflect a dual effect: acoustic stimulation of the residual neuronal function in the UHF range (10-14 kHz) and audiometric thresholds of 40-50 dB sound pressure level (SPL), and the metabolic activity at brain cortex for neuronal reprogramming. The PET of brain categories of response suggested that the UHF/UQ "masking" is predominantly reflective of neuronal reprogramming at the brain cortex. Nuclear medicine PET of brain imaging has provided an objective monitoring system for attempting to establish the efficacy of UHF/UQ for tinnitus relief. No complication of the tinnitus was reported secondary to the PET of brain examination. This limited PET of brain study supports the clinical recommendation of the efficacy of UHF/UQ external acoustic stimulation for a selected population of patients with tinnitus of the severe disabling type.     

Idiopathic Subjective Tinnitus Treated by Amitriptyline Hydrochloride/Biofeedback

The efficiency of two treatment modalities for subjective/idiopathic tinnitus (SIT): biofeedback (BF) and amitriptyline hydrochloride (AT) was investigated in 225 randomly selected subjects. Findings show that after 10 weeks of treatment in the BF group, 43.5% of the patients reported an improvement of tinnitus during activity. In the AT group, 27.5% of patients reported subjective improvement of tinnitus at rest although only 15.8% of the AT patients reported improvement during activity. Biofeedback during rest had a significantly better effect on tinnitus disturbance than AT. No objective diminishment of tinnitus loudness was found as a result of any of the treatment modalities. We believe that BF can help tinnitus patients especially during periods of rest and we also suggest trying tricyclic antidepressant drugs such as AT for treatment of tinnitus patients, in small doses, however, to minimize the side effects of this drug. Subjective tinnitus (ST) is one of the most common and yet most unclear of otologic symptoms.(1-4) ST can accompany any type of hearing loss including both sensorineural as well as conductive hearing loss, and may originate from any part of the auditory pathway.(1,5) Treatment of ST must be primarily directed to the basic illness diagnosed after a thorough general ear-nose-throat and neurologic evaluation.(6) Severity of ST is evaluated both objectively, by determining the pitch and intensity of the tinnitus,(7) and subjectively as described by the patient. Because of the relatively high incidence of ST and in some patients, the severe personal reaction to it, many different treatments have been suggested, but generally only small to moderate success has been achieved in reducing tinnitus and its consequences, if any at all.(8) In this study we examined the effect of two treatment modalities: amitriptyline hydro-chloride and biofeedback.     

Tinnitus treatment with sound stimulation during sleep

A new strategy for idiopathic subjective tinnitus treatment - sound stimulation during sleep - has been applied. It was based on the acknowledgement that the auditory system also works during sleep, processing the incoming information. Eleven patients were stimulated every night during 6 months. The stimulus was a sound that mimetized the tinnitus and was fixed at the same tinnitus intensity, applied through an iPod. All patients decreased their tinnitus intensity in the first month of treatment (statistically significant), most of them in the first week. Tinnitus intensity continued decreasing in the following weeks; three patients presented periods of total silence.     

Efficacy of gabapentin on subjective idiopathic tinnitus: a randomized, double-blind, placebo-controlled trial

Tinnitus can cause extreme morbidity. Despite many attempts to find a treatment for idiopathic cases, they remain difficult to manage. Because nerve injury is one of the suspected etiologies of tinnitus and because gabapentin has been found to be effective in treating nerve injuries, some authors have attempted to determine if gabapentin has a role in treating tinnitus. Although gabapentin was found to be ineffective for tinnitus in these previous studies, to the best of our knowledge no studies have been performed that took into consideration the presence of various accompanying factors and concomitant diseases that might influence its effect. We conducted a prospective, randomized, double-blind, placebo-controlled clinical trial of gabapentin for idiopathic tinnitus. We treated 40 patients with gabapentin and measured its effectiveness by comparing differences between pre- and post-treatment Tinnitus Severity Index (TSI) values and tinnitus loudness scores. We also compared these outcomes with those of a group of 40 matched placebo controls. At study's end, we found no significant differences between the gabapentin and control groups in mean decreases in TSI value and loudness score (p=0.85 and p=0.12, respectively). However, we did find that patients with hypertension, diabetes, and/or dyslipidemia showed a better response to gabapentin than did those with tinnitus alone (p=0.01). We conclude that although there was no statistically significant difference between gabapentin and placebo in treating isolated tinnitus or tinnitus overall, patients with concomitant hypertension, diabetes, and/or dyslipidemia may benefit from gabapentin.     

Organization of tinnitus management in Poland

Spontaneous idiopathic tinnitus is a significant interdisciplinary therapeutic problem. Based on different programs of tinnitus treatment, we organized a team of physicians, psychologists and engineers in order to establish the needs for the first Tinnitus Clinic in Poland. At the same time, together with number of clinical centres, scientific societies and non-governmental organizations, we carried out training and an information campaign throughout the country and initiated the first epidemiological studies survey about tinnitus in Poland. Over a period of 2 years we have provided care for almost 1000 patients, including them in a IS 24-month therapeutic program at the clinic. As a method of choice, Tinnitus Retraining Therapy (TRT) based on a neurophysiological model of tinnitus origin is used. We present here epidemiological data on tinnitus and hyperacusis in Poland.     

Organization of Tinnitus Management in Poland

Spontaneous idiopathic tinnitus is a significant interdisciplinary therapeutic problem. Based on different programs of tinnitus treatment, we organized a team of physicians, psychologists and engineers in order to establish the needs for the first Tinnitus Clinic in Poland. At the same time, together with number of clinical centres, scientific societies and non-governmental organizations, we carried out training and an information campaign throughout the country and initiated the first epidemiological studies/survey about tinnitus in Poland. Over a period of 2 years we have provided care for almost 1000 patients, including them in a 18-24-month therapeutic program at the clinic. As a method of choice, Tinnitus Retraining Therapy (TRT) based on a neurophysiological model of tinnitus origin is used. We present here epidemiological data on tinnitus and hyperacusis in Poland.     

A Final Common Pathway for Tinnitus - The Medial Temporal Lobe System

A final common pathway for tinnitus is hypothesized to exist for all patients with tinnitus. Its function is the transition of the sensory to the affect component of the symptom of tinnitus. Single Photon Emission Computerized Tomography (SPECT) with the radio isotope TC99-HMPAO has identified side to side perfusion asymmetries highlighted by that of the amygdala - hippocampal complex. Adjacent perfusion asymmetries involving the frontal, temporal and parietal lobes suggest a interneuronal network resulting in the transition of the sensory to the affect components of the symptom of tinnitus. It is hypothesized that a fundamental function of the amygdala - hippocampal structures is the establishment of a paradoxical auditory memory for tinnitus. It is a result of alteration in auditory masking found in all tinnitus patients. A paradoxical memory for an aberrant auditory signal i.e., tinnitus, is considered to be the initial process in the transition of the sensory to the affect component. Underlying mechanisms are hypothesized to exist and to be highlighted by a diminution of inhibition mediated by gamma aminobutyric acid (GABA) due to disconnection from excitatory (glutamate) inputs. Blockage of GABA mediated inhibition results in Tinnitogenesis, a epileptiform auditory phenomena. The overall hypothesis of a final common pathway for tinnitus; the role of the MTLS; and clinical support for this hypothesis is presented.