Acoustic Injury Research Articles

Conditioning-related protection from acoustic injury: effects of chronic deefferentation and sham surgery.

The inner ear can be made less vulnerable to acoustic injury by a "conditioning" treatment involving exposure to a moderate-level acoustic stimulus before the acoustic overexposure. The present study was designed to explore the role of the olivocochlear (OC) system in this "protection." Guinea pigs were divided into a number of groups: some (trauma-only) were exposed to a traumatic noise for 4 h at 109 dB SPL; others (condition/trauma) were conditioned by daily exposure to the same noise at 85 dB SPL before the traumatic exposure. In OC-intact animals, the condition/trauma group showed significantly less permanent threshold shift (PTS) than the trauma-only group as measured via compound action potentials and distortion-product otoacoustic emissions (DPOAEs). Other animals with identical noise-exposure regimens underwent deefferentation surgery before the start of conditioning: the OC bundle (OCB) was cut in the brain stem, either at the midline (cutting the crossed OCB to both ears) or at the sulcus limitans (cutting all OC fibers to 1 side). Lesion success was quantified by measuring OC fascicles to the outer hair cell region in each ear. The results from the surgical groups showed that total loss of the OCB significantly increased the noise-induced PTS, whereas loss of the COCB only did not; that the conditioning exposure in deefferented animals increased, rather than decreased, the PTS from the traumatic exposure; and that animals undergoing sham surgery (brain stem cuts that failed to transect the OCB) appeared protected whether or not they received the conditioning noise exposure. The latter result suggests that conditioning-related protection may arise from a generalized stress response, which can be elicited by noise exposure, brain surgery, or a variety of other means. The former results make an OC role in the conditioning process, per se, difficult to assess, given the large effects of OC activity on general acoustic vulnerability.

Chronic cochlear de-efferentation and susceptibility to permanent acoustic injury

The question of whether olivocochlear (OC) efferent feedback can decrease permanent damage from acoustic overexposure was investigated by comparing the chronic threshold shifts and cochlear histopathology in guinea pigs either surgically de-efferented or sham-operated and then exposed (awake and unrestrained) to a 109- or 112-dB narrow-band noise centered at 10 kHz for 2 h. Threshold shifts were estimated using compound action potentials; hair cell loss and stereocilia condition were evaluated via light-microscopic examination of plastic-embedded surface preparations, and the degree of de-efferentation was assessed by measuring OC fascicles in the tunnel of Corti. Among animals exposed to 109-dB noise, the mean permanent threshold shift (PTS) was less than 25 dB, and there were no significant differences between normal and de-efferented animals with respect to either physiological or histological measures of acoustic injury. Among animals exposed to 112 dB, the mean peak PTS was roughly 50 dB. There was a small (but statistically significant) increase in PTS for de-efferented animals, especially at frequencies above the region of peak threshold shift; however, the patterns of hair cell loss and stereocilia damage were statistically indistinguishable. Thus, for these particular exposure conditions, sound-evoked activity in the OC system does not play a major protective role in the auditory periphery, except perhaps for the extreme basal regions of the cochlea.

Neurotransmitters and neuromodulators of the mammalian cochlea.

Major topics addressed in this review on neurotransmitters and neuromodulators of the mammalian cochlea are ; 2) neuronal circuity of the organ of Corti ; 2) hair cell neurotransmitter(s) ; efferent neurotransmitters and neuromodulators (acetylcholine, γ-aminobutyric acid, dopamine, enkephalins, dynorphins, calcitonin gene-related peptide, excitatory amino acids ; and 3) other neuroactive substances in the cochlea (adenosine, ATP, taurine, auditory nerve-activating substance, histamine)

The structural and functional consequences of acoustic injury in the cochlea and peripheral auditory system: A five year update

This presentation considers important developments and new trends related to acoustic injury in the peripheral auditory system reported during the past 5 years. The discussion begins with the effect overstimulation has on the "active" cochlear process, and the associated loss in receptive field (tuning curve) selectivity. Exposure to intense sound also changes the structure and function of the tectorial membrane, sensory hair bundles, tip links, and intracellular organelles. All of these injuries may change the way in which energy is delivered to the transduction channels of the hair cell. Important new evidence describing the quantitative relation between hair cell loss and permanent hearing loss is reviewed, and the possibility that specific exposure conditions cause unique lesions to the inner or outer hair cells is explored. Finally, the importance of hair cell regeneration in the chick cochlea, changes in the CNS following acoustic injury, and the cochlear vascular system are considered.

In vitro Alexandrite laser angioplasty: A study on fibre conduction and tissue effects

Pulsed ultra-violet excimer laser radiation is capable of tissue ablation with only minimal thermal injury of adjacent tissue structures. Since difficult fibre optic coupling of energy was observed, alternative Q-switched laser sources capable of ablation of atherosclerotic plaque are under current investigation. To evaluate tissue effects of Alexandrite laser radiation, 160 arterial segments with macroscopic evidence of atherosclerotic disease were treated. The laser light was transmitted via silica based quartz fibres with different diameters. Using the Q-switched Alexandrite laser at the fundamental wavelength (748 nm) with a pulse duration of 300 ns the energy density threshold for tissue ablation was found to be in the range of 63 to 126 J cm−2 using a 300μm fibre. On macroscopic examination only limited thermal and acoustic injury was found in crater adjacent tissue structures. Crater edges were even and did not reveal signs of crater charring or debris in the crater lumen. However, the histological cross-sections revealed thermal injury extending from 100 up to 200μm lateral into adjacent tissue. The crater margins revealed fissuring as a result of shock wave injury. Thermal damage was most evident if irradiation of atherosclerotic tissue was performed in blood.

The olivocochlear efferent bundle and susceptibility of the inner ear to acoustic injury

1. The role of the efferent olivocochlear bundle (OCB) in protecting the inner ear from acoustic injury was studied in the anesthetized cat. Middle-ear muscles (MEM) were cut to eliminate possible effects of this feedback system on the auditory periphery. In each of a series of animals, the OCB was unilaterally transected. The animal was then exposed binaurally to an intense pure tone, and the resultant damage to the two sides compared by measuring threshold shifts in the compound action potential from each ear. Data from each animal provide one control measurement (threshold shift with an intact OCB) and one experimental measurement (threshold shift without a functional OCB). 2. Two experimental series were analyzed. In one the OCB was electrically stimulated, providing maximal firing rates in the efferents projecting to the control ear. In another series the OCB was not electrically stimulated: thus any OCB activity to the control ear was only that evoked by the acoustic stimulation itself. 3. In neither experimental series was there evidence that activity in the OCB provides protection from acoustic injury. These results are in disagreement with conclusions drawn from experiments with acoustic overstimulation of guinea pigs. 4. Interpretations for the discrepancy between the present study and those on guinea pigs include interspecies differences and the possible contribution of the MEM reflex or cochlear blood-flow changes to previously observed effects.

Recanalization of arterial occlusions with a lensed fiber and a holmium:YAG laser.

Laser recanalization of totally occluded swine iliac arteries was performed to assess the safety and efficacy of a lensed fiber laser angioplasty system with a holmium:YAG (2.1 microns) laser. Silica lenses of 1.0 mm, 1.3 mm, and 1.5 mm in diameter attached to the distal end of a 300-microns diameter silica fiber delivered fluences of 79.5 J/cm2, 31.4 J/cm2, and 25.5 J/cm2, respectively. The pulse duration of the laser was 250 microseconds and the repetition rate was 4 Hz. The mean length of the total occlusions was 5.3 +/- 2.0 cm (range 0.5 cm to 8.0 cm). Successful recanalization was obtained in 16/16 lesions without angiographic vessel perforation. Angiographically significant residual stenoses (greater than 50%) remained in every case following successful laser recanalization. Histologically there was minimal evidence of thermal or acoustic tissue injury; however, in 4 of 16 arteries there was evidence of deep arterial dissection following laser recanalization. We conclude that this lensed fiber coupled with a holmium:YAG laser is a safe and effective method for crossing total occlusions in the relatively straight iliac arteries of this animal model.

Laser‐induced photoacoustic injury of skin: Effect of inertial confinement

Argon-fluoride (ArF) excimer laser-induced acoustic injury was confirmed by ablating the stratum corneum (s.c.) inertially confined by water in vivo. Hairless rats were irradiated through a quartz chamber with flowing distilled water or air and a 2.5 mm aperture. The laser was adjusted to deliver 150 mJ/cm2 at the skin surface for both conditions. Partial and complete ablation of the s.c. was achieved with 12 and 24 pulses, respectively. Immediate damage was assessed by the transmission electron microscopy. Partial ablation of the s.c. through air produced no damage, whereas partial ablation through water damaged skin to a mean depth of 114.5 +/- 8.8 microns (+/- SD). Full thickness ablation of the s.c. through air and water produced damage zones measuring 192.2 +/- 16.2 and 293.0 +/- 71.6 microns, respectively (P less than 0.05). The increased depth of damage in the presence of inertial confinement provided by the layer of water strongly supports a photoacoustic mechanism of damage. The damage induced by partial ablation of the s.c. provides evidence that photochemical injury is not a significant factor in the damage at a depth because the retained s.c. acts as a partial barrier to diffusion of photochemical products. Combined with our previous studies, these experiments demonstrate that pressure transients are responsible for the deep damage seen with 193 nm ablation and that photoacoustic effects must be considered when using short-pulse, high-peak power lasers.

Quantitative Assessment of Inner Ear Pathology Following Ototoxic Drugs or Acoustic Trauma

Techniques currently used in the assessment of structural and/or functional damage to the peripheral auditory system are summarized. Two histological approaches are described: one which allows light microscopic evaluation of all structures of the auditory periphery, and a second which concentrates on the sensory cells and their innervation. The latter technique allows electron microscopic analysis of selected regions after a thorough light microscopic survey. Two electrophysiological methods are described as well: a single-fiber approach which provides detailed information about cochlear condition at all frequency locations and a simpler and faster evoked-potential approach which is well suited to screening for cochlear changes. The correlations between structural and functional changes are described using examples from studies of acoustic injury of the inner ear.

Acoustic injury of the inner ear: Morphological and physiological perspectives

Of the many approaches to the study of acoustic injury, one of the most fruitful has been to view the functional changes in the response properties of single auditory‐nerve fibers. Since each cochlear afferent contacts only one inner hair cell, single‐fiber responses provide a functional window onto a restricted portion of the cochlear duct. Through the use of intracellular labeling, which allows the cochlear origin of selected afferents to be precisely specified, correlations between structural and functional changes have been made on the single‐cell level. Correlations so obtained have revealed the functionally important structural changes underlying acoustic injury of the inner ear. Morphological data from both the light‐ and electron‐microscopic levels suggest that most sound‐induced permanent threshold shifts can be accounted for quantitatively based on the loss of sensory cells and/or the damage to their stereocilia. Of all the structures in the inner ear, the stereocilia, and especially the “rootlets” that anchor them to the tops of the hair cells, appear to be the most vulnerable to permanent damage from acoustic overstimulation. The structural changes underlying reversible threshold shifts are clearly different from those underlying permanent loss, but exactly which structural changes underly the temporary losses are much less clear. Structure‐function correlations in damaged ears have also helped define the contributions of inner versus outer hair cells to the response properties of auditory‐nerve fibers. Damage to inner versus outer hair cells results in strikingly different abnormalities in neural tuning, spontaneous activity, and maximal discharge rates. The nature of these differences suggests that auditory perceptual abilities would be very different given threshold shifts of identical severity but differing balance of damage to the two classes of sensory cells.

Toy weapons and firecrackers: a source of hearing loss.

Although acoustic injury as a result of exposure to noisy toys and firecrackers has been reported previously, most of these studies have been conducted on adults. The purpose of this prospective study, conducted at the time of Deepawali, an Indian festival of fireworks, was two-fold: 1. to measure the acoustic output of representative samples of toy weapons and firecrackers and the intensity level at critical spectator points from the site of emission; and 2. to determine the auditory status of a cross section of the target population, involving 600 participants from various age groups, before and after exposure to firecracker noise at Deepawali. The average sound level at a distance of 3 m was 150 dB, thus exceeding the damage risk criterion for adults (i.e., 130 dB peak level). An average 30 dB persistent sensorineural hearing loss was found in 2.5% of the target population as a result of toy weapon/firecracker noise during Deepawali. The 9- to 15-year-old age group was most affected. A judicious approach in the manufacture and use of toy weapons and firecrackers, in addition to legal restraints, is advocated.

Recoveries of whole-nerve AP thresholds, amplitudes and tuning curves in gerbils following noise exposure

The recoveries of whole-nerve action potential (AP) thresholds, AP amplitudes and AP tuning curves in gerbils were monitored following two weeks of exposure to band-pass noise at 85 dBA. Recordings were made by means of electrodes chronically implanted in the subjects' bullas. The noise exposure caused threshold elevations in all of our subjects, with the greatest shifts occurring an octave or more above the 2 kHz upper cutoff frequency of the noise. The magnitudes of the shifts varied greatly (up to 26 dB) across subjects. Thresholds of animals with the smallest initial loss of sensitivity returned to pre-exposure values within 16 days, while those of animals with greater initial losses remained elevated beyond 16 days. AP amplitudes and AP tuning curves (APTCs) were most affected at frequencies where the initial threshold shifts were greatest. At these frequencies AP amplitudes were reduced, and APTCs showed broadened tips, reduced tip-to-tail ratios, and in some cases a shift in the frequency of the tip. These effects did not necessarily reverse with threshold recovery, suggesting that AP amplitudes and AP tuning curves are more sensitive indices of acoustic injury than are AP thresholds.

学校教師の音響外傷と思われるＣ｀５´‐ｄｉｐについて

学校教師の音響外傷と思われるＣ｀５´‐ｄｉｐについて

Hair cell loss and regeneration after exposure to intense sound in neonatal chicks.

Neonatal chicks (between 1 and 3 days of age) were exposed to an intense pure tone for 48 hours, then killed immediately after removal from the sound, or 14 days later. Nonexposed age-matched animals served as controls. The inner ear was removed and the auditory receptor organ (the basilar papilla) was prepared for evaluation by scanning electron microscopy. The site of injury on the papilla was described in terms of hair-cell loss and location. The ears with no recovery showed a discrete lesion area, within which there was complete disruption of the hair-cell field and a 35% loss in hair cells. After 14 days' recovery, no hair cell loss could be detected, though the lesion could still be recognized by the disorganization of hair cells in the previously injured area. These data demonstrate hair-cell restoration after severe acoustic injury from intense sound exposure in the neonatal ear.

Ionic changes in cochlear endolymph of the guinea pig induced by acoustic injury.

The effects of acoustic overstimulation on the endocochlear potential (EP) and on concentrations of ions (K+, Na+, Cl-, H+, HCO3-, and Ca2+) in endolymph were investigated using ion-selective microelectrodes. A slight but significant elevation of the EP and alkalinization of the endolymph were induced by acoustic overstimulation, whereas there was little change in the K+, Na+, Cl-, and HCO3- concentrations. The changes in H+ and HCO3- concentrations implied a depression of PCO2, suggesting an increase in blood flow to the cochlea. On the other hand, the Ca2+ concentration increased abruptly to 48 times the pre-exposure value. In contrast, no significant change in the Ca2+ concentration was observed in cochleae with damaged hair cells. We discuss the mechanism of the tone-induced Ca2+ elevation in endolymph and its effect on hearing acuity.

Electrophysiology of the auditory system.

This review has attempted to summarise the properties of electro physiological responses in the auditory system. The treatment was broad and consequently somewhat sketchy. For a more detailed recent treatment of the physiology of the auditory system the reader is referred to Pickles (1982), Møller (1983), or Altschuller et al (1986). The data on acoustic injury have been reviewed recently by Schmiedt (1984). Discussions of a number of topics such as development, hair cell function and speech encoding are found in Berlin (1984).

The Ionic Changes in the Cochlea Endolymph of the Guinea Pig Induced by Acoustic Injury

The Ionic Changes in the Cochlea Endolymph of the Guinea Pig Induced by Acoustic Injury

Pulsed excimer laser angioplasty of human cadaveric arteries

Laser angioplasty has been limited by the lack of precise control of thermal and acoustic vascular injury. Pulsed excimer lasers, by contrast, have a capacity to affect target tissue without heat dispersion or damage to surrounding structures. The ablative properties of three excimer wavelengths, krypton fluoride (249 nm), xenon chloride (308 nm), and xenon fluoride (351 nm), were investigated with the use of fresh human cadaveric normal and atherosclerotic femoral arteries. Light and electron microscopy demonstrated clean cuts with histologically normal edges. There was no evidence of either thermal or acoustic damage with any of the wavelengths studied. The depth of ablation varied directly with the number of pulses and inversely with tissue density while the incision width remained constant. The excimer laser appears to offer significant advantages over its conventional counterparts for the ablation of atherosclerotic plaque.

The anatomical consequences of acoustic injury: A review and tutorial.

The anatomic consequences of acoustic overstimulation are explored in this presentation, and attention is directed toward issues where improvements in technology and empirical observation are needed before further advances in our understanding can be achieved. Gains have been made in the last decade in appreciating sound-induced cochlear injury, but there is now a need to evaluate not only cochlear pathology but also the functional state of the surviving structures. There is a wealth of information about the susceptibility of inner or outer hair cells to acoustic injury; however, the etiology of this injury is not yet fully understood. In addition, current ideas concerning the effects of noise on hair-cell stereocilia, hair-cell synapses, the cochlear vascular supply, and the central auditory pathways are in a state of flux and are either undergoing revision or emerging. Other issues, such as the basis of temporary or permanent threshold shift at the cellular level, and the individual differences in susceptibility to injury are in need of a fresh approach. It would seem that the time is now ripe to review our knowledge, recognize its gaps, and develop testable hypotheses concerning the mechanisms of acoustic injury to the ear.

Acoustic injury and the physiology of hearing.

A critical bibliography of published articles concerning the effects of noise exposure on hearing has been compiled for the NIH. The review concentrated on articles published over the last 14 years; however, historical highlights of the past 50 years or so were included for continuity. This paper attempts to summarize in tutorial fashion the results of that review with regard to auditory physiology in general and explores some of the current issues with specific reference to acoustic injury. To date, most of the effort toward understanding acoustic injury has been focused on the auditory periphery; the emphasis is clear simply from the number of papers published in that area. On the other hand, the response of the central nervous system to noise exposure or to any type of damage in the periphery is essentially unknown. It would seem that it is now time to assume a more balanced approach and recognize the importance of the CNS with regard to understanding the overall consequences of acoustic injury.