title: Fluid dynamics vascular theory of brain and inner-ear function in traumatic brain injury: a translational hypothesis for diagnosis and treatment.
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.
authors.affiliation: Department of Otolaryngology, Health Science Center at Brooklyn, State University of New York, Downstate Medical Center, Brooklyn, USA. metrc@inch.com
authors.forename: Abraham
authors.initials: A
authors.lastname: Shulman
authors.forename: Arnold M
authors.initials: AM
authors.lastname: Strashun
mesh_terms: D001812:Blood-Brain Barrier / Q000502:physiology; D001930:Brain Injuries / Q000175:diagnosis* / Q000503:physiopathology* / Q000628:therapy; D002545:Brain Ischemia / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy; D015170:Cerebrospinal Fluid Pressure / Q000502:physiology; D003051:Cochlea / Q000503:physiopathology; D007758:Ear, Inner / Q000098:blood supply* / Q000503:physiopathology*; D004710:Endolymph / Q000502:physiology; D018159:Endolymphatic Hydrops / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy; D018495:Fluid Shifts / Q000502:physiology*; D019788:Fluorodeoxyglucose F18; D006311:Hearing Disorders / Q000175:diagnosis* / Q000503:physiopathology* / Q000628:therapy; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D008575:Meniere Disease / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy; D019636:Neurodegenerative Diseases / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy; D018377:Neurotransmitter Agents / Q000502:physiology; D010498:Perilymph / Q000502:physiology; D049268:Positron-Emission Tomography; D011559:Pseudotumor Cerebri / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy; D015899:Tomography, Emission-Computed, Single-Photon; D014722:Vestibule, Labyrinth / Q000503:physiopathology
chemical_list: D018836:Inflammation Mediators; D018377:Neurotransmitter Agents; D019788:Fluorodeoxyglucose F18