Hearing research
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Review
Implications and attitudes of audiologists towards smartphone integration in hearing healthcare.
In a relatively short period of time, modern societies have been transformed by the ubiquitous uptake of advanced and portable mobile communication, computation, and sensors available on smartphones. Looking forward, it is anticipated that smartphones will have an increasingly important role in health management including the delivery of hearing healthcare and operation of hearing instruments.
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The anatomy and physiology of olivocochlear (OC) efferents are reviewed. To help interpret these, recent advances in cochlear mechanics are also reviewed. Lateral OC (LOC) efferents innervate primary auditory-nerve (AN) fiber dendrites. ⋯ MOC-effect measuring methods and MOC-induced changes in human responses are also reviewed, including that ipsilateral and contralateral sound can produce MOC effects with different patterns across frequency. MOC efferents help to reduce damage due to acoustic trauma. Many, but not all, reports show that subjects with stronger contralaterally-evoked MOC effects have better ability to detect signals (e.g. speech) in noise, and that MOC effects can be modulated by attention.
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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.