ISSN 1612-3352

Editors in Chief

Prof. Dr. Claus F. Claussen, Neurootological Research Institute of the Research Society for Smell, Taste, Hearing and Equilibrium Disorders at Bad Kissingen (4-G-F). Bad Kissingen, Germany.
Dr. med. Julia M. Bergmann,
Dr. med. Guillermo O. Bertora,
Otoneuroophthalmological Neurophysiology,
Buenos Aires, Argentina.

Production Managers

Dr. med. Julia M. Bergmann,
Dr. med. Guillermo O. Bertora,
Otoneuroophthalmological Neurophysiology,
Buenos Aires, Argentina.


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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., singlephoton
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.

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