title: Central nervous system neurodegeneration and tinnitus: a clinical experience. Part II: translational neurovascular theory of neurodegenerative CNS disease and tinnitus.
abstract: 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.
authors.affiliation: Department of Otolaryngology, State University of New York, Downstate Medical Center, Brooklyn, NY 11203, USA. metrc@inch.com
authors.forename: Abraham
authors.initials: A
authors.lastname: Shulman
authors.forename: Barbara
authors.initials: B
authors.lastname: Goldstein
authors.forename: Arnold M
authors.initials: AM
authors.lastname: Strashun
mesh_terms: D000367:Age Factors; D000544:Alzheimer Disease / Q000175:diagnosis* / Q000503:physiopathology / Q000628:therapy; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D002545:Brain Ischemia / Q000175:diagnosis* / Q000503:physiopathology / Q000628:therapy; D015897:Comorbidity; D015140:Dementia, Vascular / Q000175:diagnosis* / Q000503:physiopathology / Q000628:therapy; D004292:Dominance, Cerebral / Q000502:physiology; D015316:Genetic Therapy; D006801:Humans; D008279:Magnetic Resonance Imaging; D015213:Neuroimmunomodulation / Q000502:physiology; D018696:Neuroprotective Agents / Q000627:therapeutic use; D049268:Positron-Emission Tomography; D012039:Regional Blood Flow / Q000502:physiology; D024801:Tauopathies / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy; D014012:Tinnitus / Q000175:diagnosis* / Q000503:physiopathology / Q000628:therapy; D015899:Tomography, Emission-Computed, Single-Photon
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D018696:Neuroprotective Agents