Noise-induced Tinnitus
Dr. James Kaltenbach and associates at Wayne State University (Detroit, MI) have been trying to determine a neurophysiological mechanism of noise-induced tinnitus. For years now a lot of us have assumed that tinnitus is related to noise-induced mechanical damage of hair cells. Research now suggests the OHCs are damaged by working too hard to process hazardous noise (e.g., over metabolizing, overdosed with neurochemical transmitters). Dr. Kaltenback suggests intense sound exposure cause increases in spontaneous VIIIth nerve neural activity (hyperactivity) in the cochlear nucleus. It may be that the cause of tinnitus is due to over stimulation of auditory brainstem structures rather than damage just within the cochlea itself. Another theory proposes that OHC damage results in less input getting to the auditory cortex from the cochlea so that the cortex has trouble processing the more limited, “uneven” input. Hence, tinnitus is caused by the auditory cortex trying to “resolve” the fact that it is getting fewer signals coming in from the inner ear. I know, it sounds pretty incredible. Again, it reminds us of just how complex the auditory system is and the fact that damage or over-stimulation can affect any part of the neural auditory system (not just the cochlea).
Dr. Deepak Prasher at University College, London has been investigating objective evidence for tinnitus from spontaneous otoacoustic emission variability. Remember, spontaneous emissions are present without any acoustic stimulation. He measured spontaneous OAEs in Polish mill workers, exposed to 85-95 dB (A) for a mean of twelve and a half years, some of whom (104) reported the presence tinnitus and some of whom (94) did not. His results demonstrated that the incidence of spontaneous OAEs is higher in noise-exposed workers than in previous studies and that the stability of spontaneous emissions is significantly lower in those individuals with subjective tinnitus. The assumption here is that exposure to noise results in instability within the cochlea, which alters spontaneous otoacoustic emission activity.
Sound Conditioning: Protection Against Noise Trauma
Barbara Canlon and colleagues at the Karolinska Institutet, Stockholm, Sweden have studied the physiological process known as “preconditioning”. This is an active process found in many neuronal and non-neuronal systems that results in tolerance to subsequent detrimental forms of trauma or stress (i.e., noise). Preconditioning is typically induced by low level, non-damaging stimuli that could result in long-term protective effects. Preconditioning has been demonstrated to increase tolerance to light damage in the retina and ischemia, and noise damage in the cochlea. In animal studies, sound pre-conditioning appears effective in protecting against subsequent noise trauma for both low and high frequency stimuli. Although the basic mechanisms underlying this conditioning protection are not totally understood, Dr. Canlon believes it is related to the “conditioning sound” causing an increase in heat shock proteins, neurotrophins, antioxidants, and reduction of calcium flow. All of these things result in less OHC damage to noise trauma. Dr. Canlon also reported preliminary results indicate a sound conditioner can also be presented after a noise stimulus and still offer some protective effect. The Institutet recently performed a pilot study on young adults and the results demonstrate the feasibility of employing sound conditioning as a clinical therapy. There is still a lot of work that needs to be done in this area, but its encouraging that levels of noise close to, but not at the damage risk criteria of 85 dB (A) may actually protect the ear by stimulating the release of the “right” antioxidants and neurochemicals.
Novel Strategies in the Prevention and Reversal of Noise-induced Hearing Loss
Colonel Rick Kopke, MC, USA, staff neuro-otologist, Naval Medical Center, San Diego and co-director of the DOD Spatial Orientation Laboratory where I used to work part-time presented an overview of his work and that of others pertaining to hair cell rescue and restoration. Although the armed forces Audiology communities have made great strides in improving hearing conservation programs and reducing occupational hearing loss, hearing protection devices have their limitations. For example, the noise levels on aircraft carrier flightdecks and impulse noise produced by heavy and light artillery are so high that even double hearing protection cannot prevent PTS in all cases. Some data from the Army and the Marine Corps suggest earplugs may not sufficiently protect personnel from the impulse noise produced by M-16 rifles. And then you have the issue of real world hearing protector attenuation not being nearly as effective as fittings in a laboratory setting.
Dr. Kopke and others have noted that noise overexposure leads to the development of reactive oxygen species (ROS) in the cochlea. Think of the ROS as being “thieves” who steal from molecules in the outer hair cells that support healthy functioning. Superoxide, hydrogen peroxide, and hydroxyl radicals are examples of these villains. Noise overexposure makes the OHCs work harder and then the ROS activate and prevent the cells from replenishing their nourishment. Once a certain damage threshold is reached, cell apoptosis (death cycle) is initiated. New understanding has been obtained regarding the cell cycle and molecular mechanisms involved with OHC damage. Colonel Kopke and others have been using antioxidants (something we all have naturally in our bodies) and neurotrophins to combat ROS before the OHC death cycle reaches its threshold of no return. Dr. Kopke’s work with chinchillas has suggested that chemical intervention can significantly reduce TTS and PTS when the animals are exposed to hazardous noise levels. In other words, it may be possible to regenerate cochlear sensory cells after sensory cell loss and a PTS.
Josef Miller and Richard Altschuler of the Kresge Hearing Research Institute, University of Michigan and the Karolinska Institutet, Sweden have shown that the ROS prevent the natural antioxidants of the inner ear (glutathione) from doing its thing during noise overexposure, supporting the treatment theory that Dr. Kopke is pursuing. In addition, they have demonstrated that sound conditioning treatments appear to result in the increase of neurotrophins and antioxidant enzymes and direct administration of some neurotrophins can protect the inner ear from damage. Don Henderson, CDR Nanci Hight, MSC, USN, and their associates at State University of New York (SUNY) Buffalo’s Center for Hearing and Deafness have also done some great work in this area. They have shown sound conditioning does “toughen” the ear by increasing antioxidant enzymes and that treating the ear with glutathione doses also makes the ear more resistant to noise. Dr. Tom Taggart (Associate Professor, SUNY Buffalo), a geneticist I have been working with for the past year, has demonstrated that genes involved in protein synthesis, cytoskeletal proteins, and calcium binding are all significantly affected by noise exposure. Again, CDR Hight could explain all of this much better than I. I have been struggling to learn some basic concepts in microbiology and chemistry to better understand the “why” and “how” of chemical restoration of the inner ear.
So what does all this mean, anyway? It means we are beginning to understand just how hair cell damage occurs in the cochlea. By understanding the mechanisms underlying the damage, we may be able to develop chemical and/or acoustic treatments to prevent it from happening. The idea of chemical treatments for NIHL may seem threatening to some audiologists, e.g. is this going to limit our profession clinically? Are we threatened with losing our jobs? I don’t think so. I see this as an opportunity to extend our clinical profession. A professional is needed to perform auditory testing before and after administration of chemical agents to treat noise exposure and “sound conditioning” therapies are right up the audiologist’s alley in my opinion. I also do not believe that chemical or acoustical treatments will do away with the use of hearing protective devices. They will still be needed as additional insurance or protection against the harmful effects of high level continuous and impulse noises. The use of chemical agents may not totally prevent the occurrence of NIHL. Magnesium has already been used in clinical trials and we are on the verge of other agents being used as such. We are starting to make the transition from animal trials to human. I believe this line of research will continue to expand and develop and as hearing professionals we need to be a part of it.
Data was also presented by Sliwinska-Kowalska and colleagues (Institute of Occupational Medicine, Poland) showing that exposure to organic solvents (i.e., xylene and toluene, used in paint and lacquer manufacturing) increases NIHL significantly. In the rat, Dr. Campo (Institute of National Research, Vandoeuvre, France) has demonstrated that exposure to the solvent styrene can increase the risk of NIHL, but combined with ethanol its ototoxicity is much worse. I guess alcohol and solvents do not mix, so don’t drink when you are using paint thinner around the house! Seriously though, styrene appears to primarily target the OHCs and secondarily the spiral ganglions. Dr. Laurence Fechter (University of Oklahoma Health Sciences Center) showed that although the chemical asphyxiant carbon monoxide (CO) is not by itself ototoxic, in combination with noise releases those deadly reactive oxygen species (ROS) and can end up causing a great deal more NIHL than the noise alone. This is important considering the federal firefighter patients a lot of us evaluate. Firefighters are not exposed to constant noise throughout the week, their exposure is intermittent, but they are exposed to CO in the performance of their duties. For a long time now I have wondered why so many firefighters exhibit what appears to be more than the usual “notch” in the high frequencies.