Hearing research
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Since 1992, the Speech Recognition in Noise Test, or SPRINT, has been the standard speech-in-noise test for assessing auditory fitness-for-duty of US Army Soldiers with hearing loss. The original SPRINT test consisted of 200 monosyllabic words presented at a Signal-to-Noise Ratio (SNR) of +9 dB in the presence of a six-talker babble noise. ⋯ In 2013, a new 100-word version of the test was developed that eliminated words that were either too easy or too hard to make meaningful distinctions among hearing impaired listeners. This paper describes the development of the original 200-word SPRINT test, along with a description of the procedure used to reduce the 200-word test to 100 words and the results of a validation study conducted to evaluate how well the shortened 100-word test is able to capture the results from the full 200-word version of the SPRINT.
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The US Navy, through an Office of Naval Research (ONR) lead effort on Noise Induced Hearing Loss (NIHL), is investigating methods and techniques to mitigate hearing loss for the crews and warfighters. Hearing protection is a viable and increasingly popular method of reducing hearing exposure for many ship crew members; however, it has limitations on comfort and low frequency effectiveness. Furthermore, Personal Hearing Protection (PHP) is often used improperly. ⋯ Such approaches also can be made to work in the lower frequency range where hearing protection is not as effective. This paper describes non-hearing protection methods being implemented to mitigate and control noise within the US Navy and US Marine Corps. These approaches reflect the latest changes to Mil-Std 1474E, Appendix F.
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Noise exposure and the subsequent hearing loss are well documented aspects of military life. Numerous studies have indicated high rates of noise-induced hearing injury (NIHI) in active-duty service men and women, and recent statistics from the U. S. ⋯ Army, Navy, and Marine Corps. Details related to hardware, signal processing, and testing efforts are provided, along with example tactical military noise data and lessons learned from early fieldings. Finally, we discuss the continued need to prioritize personalized dosimetry in order to improve models that predict or characterize the risk of auditory damage, to integrate dosimeters with hearing-protection devices, and to inform strategies and metrics for reducing NIHI.
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Common causes of hearing loss in humans - exposure to loud noise or ototoxic drugs and aging - often damage sensory hair cells, reflected as elevated thresholds on the clinical audiogram. Recent studies in animal models suggest, however, that well before this overt hearing loss can be seen, a more insidious, but likely more common, process is taking place that permanently interrupts synaptic communication between sensory inner hair cells and subsets of cochlear nerve fibers. The silencing of affected neurons alters auditory information processing, whether accompanied by threshold elevations or not, and is a likely contributor to a variety of perceptual abnormalities, including speech-in-noise difficulties, tinnitus and hyperacusis. Work described here will review structural and functional manifestations of this cochlear synaptopathy and will consider possible mechanisms underlying its appearance and progression in ears with and without traditional 'hearing loss' arising from several common causes in humans.
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For decades, we have presumed the death of hair cells and spiral ganglion neurons are the main cause of hearing loss and difficulties understanding speech in noise, but new findings suggest synapse loss may be the key contributor. Specifically, recent preclinical studies suggest that the synapses between inner hair cells and spiral ganglion neurons with low spontaneous rates and high thresholds are the most vulnerable subcellular structures, with respect to insults during aging and noise exposure. This cochlear synaptopathy can be "hidden" because this synaptic loss can occur without permanent hearing threshold shifts. ⋯ Second, in human studies, the data supporting cochlear synaptopathy are indirect although rapid progress has been made. To fully identify changes in function that are directly related this hidden synaptic damage, we argue that a battery of tests including both electrophysiological and behavior tests should be combined for diagnosis of "hidden hearing loss" in clinical studies. This new approach may provide a direct link between cochlear synaptopathy and perceptual difficulties.