The International Tinnitus Journal

The International Tinnitus Journal

Official Journal of the Neurootological and Equilibriometric Society
Official Journal of the Brazil Federal District Otorhinolaryngologist Society

ISSN: 0946-5448

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Brain and Inner-Ear Fluid Homeostasis, Cochleovestibular-Type Tinnitus, and Secondary Endolymphatic Hydrops

Author(s): Abraham Shulman and Barbara Goldstein

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 normal 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 (singlephoton 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.