Dr. James C. Fleming, received his medical degree from the University of Tennessee Center for theHealth Sciences in June, 1974. He continued his medical training at the University of Tennessee in ophthalmologyand pursued fellowship training in ophthalmic plastic and reconstructive surgery at the Universityof Arizona. Returning to Memphis in 1980, he has served as Chief of Oculoplastics at the levelI trauma center for over twenty years. He joined the UT Department of Ophthalmology as a full-timephysician in January 1997 to head the Oculoplastic Service, and currently is honored to hold the PhilipM. Lewis Professor of Ophthalmology Chair. His service in the field of ophthalmology has been recognizedon a national level by the presentation of the Senior Achievement Award from the AmericanAcademy of Ophthalmology in 2005. He has held the office of president for the Tennessee Medical Association, andcontinues to serve as the chairman of the Tennessee Medical Association Delegation to the American Medical Association.Also, he was honored to serve as president of the American Society of Ophthalmic Plastic and ReconstructiveSurgery, his subspecialty organization.COL Gregory Risk is an Emergency Physician/Flight Surgeon currently assigned to USASOC. He completed SFQC asan 18D in 1982 and was assigned to 7th SFG. He graduated from the Indiana University School of Medicine in 1993and completed emergency medicine residency at Methodist Hospital in 1996. COL Risk was previously assigned as AsstDean, Joint <strong>Special</strong> <strong>Operations</strong> Medical Training Center.Aaron Noble Waite graduated from Brigham Young University with a BS in Zoology in 2001. He completedhis medical degree from the University of Utah School of Medicine in 2006 and an internal medicineinternship at the University Medical Center in Las Vegas Nevada in 2007. He is currently engagedin his final year of ophthalmology residency training at the University of Tennessee in Memphis.32Journal of <strong>Special</strong> <strong>Operations</strong> Medicine Volume 9, Edition 3 / <strong>Summer</strong> 09
Tinnitus, a Military Epidemic:Is Hyperbaric Oxygen Therapy the Answer?LCDR Thomas M. Baldwin, MD, MPTABSTRACTTinnitus is the phantom perception of sound in the absence of overt acoustic stimulation. Its impact on themilitary population is alarming. Annually, tinnitus is the most prevalent disability among new cases added to theVeterans Affairs numbers. Also, it is currently the most common disability from the War on Terror. Conventional medicaltreatments for tinnitus are well documented, but prove to be unsatisfying. Hyperbaric oxygen (HBO 2 ) therapymay improve tinnitus, but the significance of the level of improvement is not clear. There is a case for large randomizedtrials of high methodological rigor in order to define the true extent of the benefit with the administration ofHBO 2 therapy for tinnitus.THE PHYSIOLOGY OF HEARINGHearing is a series of events in which soundwaves in the air produce electrical signals and causenerve impulses to be sent to the brain where they are interpretedas sound. The auditory system consists of theexternal, middle, and inner ears, as well as the centralauditory pathways in the brain. Sound waves enter theexternal ear via the pinna and reach the middle earwhere they strike the eardrum and cause it to vibrate.The vibrations set the middle-ear bones (malleus,incus, stapes) in motion. Movement of the stapescauses pressure waves in the fluid contained within thecochlea, which contains the organ of Corti, the sensoryorgan for hearing. The primary sensory receptors forhearing, the inner hair cells, are found within the organof Corti as are the outer hair cells, which primarily facilitatethe sensory response of the inner hair cells. 1The fluid in the cochlea moves the top portion of thehair cells, called the hair bundle, which initiates thechanges that lead to the production of the nerve impulses.The nerve fibers connected to the hair cells, primarilythe inner hair cells, are excited and transfer theauditory information to the brain where they are interpretedas sound. 1, 2THE ETIOLOGY OF TINNITUSTinnitus, the perception of sound in the absenceof an external source, is a chronic and debilitatingcondition often described as ringing, hissing,buzzing, chirping, high-pitched squealing, or roaringin the ears or in proximity to the head. 2-4 According tothe National Research Council, tinnitus is considered asymptom rather than an illness. 2 The perceived noisecan be within one or both ears, within or around thehead, or perceived as an outside distant noise. It can bepulsatile or nonpulsatile and be continuous or occur intermittently.Tinnitus can be caused by or accompanymany conditions, including presbycusis, Meniere’s disease,otosclerosis, head injury, cerebellar-pontine angletumors, otitis media, meningitis, dental disorders, andcertain medications. However, most tinnitus is due tonoise induced sensorineural hearing loss with result-2, 5, 6ing dysfunction within the auditory system.The presence of tinnitus often is an early indicatorof cochlear hair cell dysfunction or loss, as in thecase of excessive noise exposure. 3 The pathogenesis isassumed to consist of micromechanical traumatic andbiochemical-metabolic damage to the outer hair cells. 3Studies have shown how hair cells of the inner earreact to damage caused by noise. 7,8 In acoustic trauma,defined as an acute impairment of hearing caused bysharp sounds, like that of a gun going off, the partialpressure of oxygen decreases significantly in the fluidspaces of the inner ear. 7 Morphological damage results,leading to intra and extracellular ion imbalancesand hearing damage. Histological findings areswelling and structural damage of the dendrites, alterationsof mitochondria and the cell-structure, separationof hair-cells from tectorial membrane, oedema ofthe endothelium, and oedematous closure of functionalendarteries with blocking of the microcirculation. 7 Ifthe swelling persists for a prolonged period, the haircells degenerate and are replaced by non-functioningendothelial cells. 7,9 PET scanning and functional MRIstudies indicate that the loss of cochlear input to neuronsin the central auditory pathways (such as occurswith cochlear hair cell damage due to noise trauma)can result in abnormal neural activity in the auditorycortex. 3 Such activity has been linked to tinnitus. It isimportant to note, that sounds of moderate intensity asencountered in everyday life usually do not affect theTinnitus, a Military Epidemic:Is Hyperbaric Oxygen Therapy the Answer?33
- Page 1 and 2: Volume 9, Edition 3 / Summer 09 Jou
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The Battle of Mogadishu:Firsthand A
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Task Force Ranger encountered enemy
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Peter J. Benson, MDCOL, USACommand
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Numerous military and civilian gove
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Anthony M. Griffay, MDCAPT, USNComm
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This is a great read that speaks di
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and twenty-eight. Rabies immune glo
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Rhett Wallace MD FAAFPLTC MC SFS DM
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LTC Craig A. Myatt, Ph.D., HQ USSOC
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LTC Bill Bosworth, DVM, USSOCOM Vet
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Europe, Mideast, Africa and SWAU.S.
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SOF and SOF Medicine Book ListWe ha
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TITLE AUTHOR ISBNCohesion, the Key
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TITLE AUTHOR ISBNI Acted from Princ
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TITLE AUTHOR ISBNRats, Lice, & Hist
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TITLE AUTHOR ISBNThe Healer’s Roa
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TITLE AUTHOR ISBNGuerilla warfare N
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TITLEAUTHORBlack Eagles(Fiction)Bla
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TITLE(Good section on Merrill’s M
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GENERAL REFERENCESALERTS & THREATSB
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Aviation Medicine Resources: http:/
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LABORATORYClinical Lab Science Reso
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A 11 year old boy whose tibia conti
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Meet Your JSOM StaffEXECUTIVE EDITO
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Special Forces Aidman's PledgeAs a