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.
Available from: Alessandra Fioretti
- "The concept of neurovascular dysfunction and neurodegeneration in patients with subjective idiopathic tinnitus has been recently proposed and reported . "
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ABSTRACT: Tinnitus is a perception of sound in absence of sound stimulation. Tinnitus in many cases cannot be eliminated by conventional medical treatment with drugs or surgery. Some people who begin to notice tinnitus, whether spontaneous or induced by noise, trauma or other insult, will experience spontaneous resolution, but many patients will have persistent tinnitus. For some of them, tinnitus sensation will be joined by tinnitus suffering, with many adverse effects like anxiety, depression and sleep disorders. For these tinnitus sufferers the psychological and acoustic approach proposed by the Tinnitus Retraining Therapy and Acoustic Desensitization Protocol may be helpful. Periodically new treatments are suggested like low-frequency repetitive transcranial magnetic stimulation and sequential phase shift sound cancellation treatment based on the frequency and loudness matching of the tinnitus. The aim of this work is to review modern considerations for the treatment of tinnitus.
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ABSTRACT: 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]). The primary etiology-head trauma-results in an initial fluctuation, interference, or interaction in the normal fluid dynamics between brain and labyrinth of the inner ear, with a resultant clinical diversity of complaints varying in time of onset and severity. Normal function of the brain and ear is a reflection of a normal state of homeostasis between the fluid compartments in the brain of cerebrospinal fluid and perilymph-endolymph in the labyrinth of the ear. The normal homeostasis in the structures and contents between the two fluid compartment systems--intracerebral and intralabyrinthine--is controlled by mechanisms involved in the maintenance of normal pressures, water and electrolyte content, and neurotransmitter activities. The initial pathophysiology (a reflection of an alteration in the vascular supply to the brain-ear) is hypothesized to be an initial acute inflammatory response, persistence of which results in ischemia and an irreversible alteration in the involved neural substrates of brain-ear. Clinically, a chronic multisymptom complex becomes manifest. The multisymptom complex, individual for each TBI patient regardless of the diagnostic TBI category (i.e., mild, moderate, or severe), initially reflects processes of inflammation and ischemia which, in brain, result in brain volume loss identified as neurodegeneration and hydrocephalus ex vacuo or an alteration in cerebrospinal fluid production (i.e., pseudotumor cerebri) and, in ear, secondary endolymphatic hydrops with associated cochleovestibular complaints of hearing loss, tinnitus, vertigo, ear blockage, and hyperacusis. The FDVTBE integrates and translates a neurovascular hypothesis for Alzheimer's disease to TBI. This study presents an FDVTBE hypothesis of TBI to explain the clinical association of head trauma (TBI) and central nervous system neurodegeneration with multisensory complaints, highlighted by and focusing on cochleovestibular complaints. A clinical case report, previously published for demonstration of the cerebrovascular medical significance of a particular type of tinnitus, and evidence-based basic science and clinical medicine are cited to provide objective evidence in support and demonstration of the FDVTBE.
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ABSTRACT: 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., the sensory component)-to one of affect (i.e., the emotional-behavioral component) or, conversely, that an emotional-behavioral stimulus (affect) can result in the clinical manifestation of a sensation (a sensory stimulus). Understanding the pathophysiology of this transformation is fundamental for the diagnosis of tinnitus and the treatment of the patient, and it presents a dilemma to basic science, neuroscience, and clinical medicine. Clinically, tinnitus is not a unitary symptom; it constitutes many clinical types; can have its origin in the auditory or nonauditory systems and in the peripheral or central nervous system; and may be clinically manifest or subclinical. Accumulating evidence is presented to support the original hypothesis of an FCP. The resolution of this dilemma involves sensory processing (i.e., the integration, identification, and understanding of the ongoing, underlying, simultaneous, multiple associated brain function processes not only from one sensory modality but from multiple sensory modalities accompanying and associated with an FCP). In the FCP, the predominant brain function process is that of the sensory-affect transformation of a sensation and its conscious awareness by the affected patient. The neuroanatomical substrates identified in 1989 in tinnitus patients (reported originally in 1991 and published in 1995) are presented as a common framework for the hypothesis of an FCP. They further the understanding of the clinical heterogeneity of the tinnitus symptom, clinically manifest as multiple brain functions associated with the clinical course of tinnitus patients, particularly those with SIT. The FCP provides a model for tinnitus theory, diagnosis, and treatment. The FCP is not a tinnitus theory. Specifically, it is a hypothesis that attempts to explain how an aberrant auditory sensory stimulus becomes transformed into one of affect and somatomotor response. The neuroanatomical substrates of the FCP provide a basis for the identification of the involved neurocircuitries and neurochemistries. The physiology and biochemistry underlying the neuroanatomical substrates of the FCP provide a basis for translation for tinnitus diagnosis and treatment. The neuroanatomical substrates of the FCP are presented as algorithms of (1) components of a sensation (i.e., sensory, affect, and psychomotor), a translation from basic sensory physiology for tinnitus; (2) clinically manifest biophysiological brain functions and underlying processes associated with the tinnitus; (3) a model for investigation of metabolic-electrophysiological correlates for tinnitus; (4) the basis for an integrated theory of tinnitus and brain function (i.e., tinnitus dyssynchrony-synchrony theory; (5) a model for the identification of underlying neurocircuitries and neurochemistries involved in brain for the sensory-affect transformation of an aberrant auditory stimulus (tinnitus); (6) a model for the selection-introduction of innovative therapies attempting tinnitus relief; and (7) its clinical translation for objective monitoring systems for the determination of the efficacy of modalities of therapy attempting tinnitus relief. The hypothesis of the FCP for tinnitus and the identified neuroanatomical substrates, when viewed in terms of the physiology of sensory processing, is considered to be expanded and broader in its application for all sensations, normal or aberrant.
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