Final common pathway for tinnitus: theoretical and clinical implications of neuroanatomical substrates.

A final common pathway (FCP) for tinnitus has been hypothesized since 1989 for all clinical types of tinnitus, particularly subjective idiopathic tinnitus (SIT) of the severe disabling type. This was intended to explain the transformation-transition of the sensation of an aberrant auditory sensation-tinnitus (i.e.

Fluid dynamics vascular theory of brain and inner-ear function in traumatic brain injury: a translational hypothesis for diagnosis and treatment.

It is hypothesized that in all traumatic brain injury (TBI) patients with a clinical history of closed or penetrating head injury, the initial head trauma is associated with a vibratory sensation and noise exposure, with resultant alteration in vascular supply to the structures and contents of the fluid compartments of brain and ear (i.e., the fluid dynamics vascular theory of brain-inner-ear function [FDVTBE]).

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.

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).

Congenital atresia of the external ear and tinnitus: a new syndrome.

Congenital atresia of the external ears and severe tinnitus has been reported by two patients to be contralateral to the atretic ear. The use of the nuclear medicine imaging technique of single-photon emission computed tomography (SPECT) of brain has demonstrated hypoperfusion in brain areas supplied by the middle cerebral artery on the side of the atretic ear. Ultrahigh-frequency audiometry (UHFA) has revealed a bilateral loss of hearing greater than expected for the age of affected patients.

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.

Benzodiazepine receptor distribution in severe intractable tinnitus.

Tinnitus affects nearly 50 million people in the United States, with a minority demonstrating marked functional impairment. Alterations of gamma aminobutyric acid (GABA) neuronal function and benzodiazepine receptor (BZR) function in particular have been implicated in the pathophysiology of severe, chronic tinnitus. The purpose of our study was to evaluate the distribution of BZR in the brain using 123I-iomazenil single-photon emission computed tomography (SPECT) imaging in patients with severe, intractable central tinnitus.

GABAA-benzodiazepine-chloride receptor-targeted therapy for tinnitus control: preliminary report.

Our goal was to attempt to establish neuropharmacological tinnitus control (i.e., relief) with medication directed to restoration of a deficiency in the gamma-aminobutyric acid-benzodiazepine-chloride receptor in tinnitus patients with a diagnosis of a predominantly central type tinnitus.