Paul W. Flint MD, FACS, in Cummings Otolaryngology: Head and Neck Surgery, 2021
Intensity
Sound pressure level measured in decibels (dB SPL), orintensity, is the primary acoustic correlate of loudness, although many factors influence the perception of loudness. Sound pressure level is influenced by frequency, vowel, speech sample, equipment, distance from the sound source, and ambient noise.77 The most common measures are average speaking and minimum and maximum sound pressure levels. On average, men and women speak at approximately 70 dB SPL (at a distance of 6 inches),40 although variability in conversational speech is significant. Minimum intensity is typically less than 60 dB, and maximum intensity is greater than 110 dB.39,78 Intensity measures are used to document patient symptoms of inadequate loudness, such as might occur with Parkinson disease or vocal fold motion impairment, or difficulty speaking quietly, which can occur with scarring or lesions.
Noise-induced TTS and its effects on loudness perception and speech discrimination were first studied in humans by Davis et al.3 as already described in Chapter 1. Recently, using confocal imaging of the inner ear in the mouse, Kujawa and Liberman11 showed that acoustic overexposure for 2 hours with an 8–16kHz band of noise at 100dB SPL caused a moderate, but completely reversible, threshold elevation as measured by ABR. The absence of permanent changes in the otoacoustic emissions indicated that the exposure left OHCs, and therefore likely the less susceptible IHCs as well, intact. They found that despite the normal appearance of the cochlea and normal hearing thresholds there was an acute loss of the ribbon synapses located on the medial side of the IHC connected to high-threshold low-SFR ANFs followed by a delayed progressive diffuse degeneration of the cochlear nerve (Figure 3.3). They concluded:
Figure 3.3. Noise trauma that only evokes temporary threshold shifts and temporary changes in otoacoustic emissions (top left) can still result in loss of synaptic ribbons (bottom left) and delayed loss of ganglion cells (right).
From Kujawa SG, Liberman MC. Adding insult to injury: cochlear nerve degeneration after “temporary” noise-induced hearing loss. Journal of Neuroscience 2009; 29: 14077–14085, copyright 2009, reproduced with permission of Society for Neuroscience.
“It is sobering to consider that normal threshold sensitivity can mask ongoing and dramatic neural degeneration in noise-exposed ears, yet threshold sensitivity represents the gold standard for quantifying noise damage in humans. Federal exposure guidelines (OSHA, 1974; NIOSH, 1998) aim to protect against permanent threshold shifts, an approach that assumes that reversible threshold shifts are associated with benign levels of exposure. Moreover, lack of delayed threshold shifts after noise has been taken as evidence that delayed effects of noise do not occur … The present results contradict these fundamental assumptions by showing that reversibility of noise-induced threshold shifts masks progressive underlying neuropathology that likely has profound long-term consequences on auditory processing. The clear conclusion is that noise exposure is more dangerous than has been assumed.”
The effects of the changes in the balance between excitation and inhibition following noise trauma (Section 3.1.2) were illustrated in several papers by Salvi and colleagues published in the 1990s. Salvi et al.27 measured local field potential (LFP) amplitude-level functions in the inferior colliculus of the chinchilla before and after a 5-day exposure to a 2kHz pure tone of 105dB SPL. After 25 days of recovery there was about 20–30dB hearing loss between 2 and 8kHz, with little or no hearing threshold shift at higher or lower frequencies. Generally less than 60% of the OHCs were missing in the region of hearing loss. The LFP amplitude-level functions measured at 4 and 8kHz showed a loss in sensitivity to low sound levels, a reduction in the maximum amplitude (commensurate with the above described loss of ribbon synapses in the IHC) and sometimes steeper than normal slopes. The amplitude-level functions measured at 2kHz also showed a loss in sensitivity; however, the maximum amplitude was often greater than normal. Even though there was no loss in sensitivity at 0.5kHz, the amplitude-level function was steeper than normal and the maximum amplitude of the LFP was almost always substantially larger than normal. The enhancement of the LFP amplitude from the inferior colliculus does not originate in the cochlea, but likely reflects an increased gain in the central auditory pathway, potentially as a result of loss of lateral inhibition from the less active neurons in the hearing loss region.
Salvi et al.28 also compared some of the functional changes that occurred in the central auditory pathway after the cochlea was damaged by acoustic overstimulation or by carboplatin administration that selectively destroys IHCs in the chinchilla. Carboplatin is a chemotherapeutic drug used against some forms of cancer. It was introduced in the late 1980s and has fewer side effects compared to cisplatin. Cisplatin and carboplatin both interact with DNA. Acoustic trauma typically causes OHC loss and impairs the sensitivity and tuning of ANFs and reduces the neural output of the cochlea. Surprisingly, their noise-exposure results showed that restricted cochlear damage enhanced neural activity in the central auditory pathway. Despite a reduction in the auditory-nerve compound action potential (CAP), the LFP from the ICC increased at a faster than normal rate and its maximum amplitude was enhanced at frequencies below the region of hearing loss, confirming their results from a decade earlier (Figure 3.4). Following the exposure, some neurons showed substantial broadening of frequency tuning below CF, less inhibition, and a significant increase in discharge rate, consistent with a model involving loss of sideband inhibition.
Figure 3.4. LFP response amplitude-level functions recorded at the round window (CAP), the cochlear nucleus (CN) and inferior colliculus (IC) at 1000Hz pre- and 24 hour post-exposure with a 2.8-kHz tone presented at 105dB SPL for 2 hours. LFP amplitudes were normalized to maximum pre-exposure response. Arrows indicate the direction of amplitude change at moderate to high sound levels.
Reprinted from 29 Hearing Research, vol. 168, Wang J, Ding D, Salvi RJ, Functional reorganization in chinchilla inferior colliculus associated with chronic and acute cochlear damage, pages 238–249, copyright 2002, with permission from Elsevier.
Snyder et al.30 made mechanical lesions to 1-mm sectors of the spiral ganglion (SG). These lesions removed a restricted portion of the cochlear output to the brainstem, but left the organ of Corti and basilar membrane intact. Immediately after SG lesions, ICC neurons previously tuned to the lesion frequencies became less sensitive to those frequencies but more sensitive to lesion edge frequencies, resulting in a shift in their CFs. Notches in the excitatory response areas at frequencies corresponding to the lesion frequencies and expansion of spatial tuning curves were also observed. The CFs of neurons tuned to frequencies in the nonlesioned sectors remained unchanged. These “plastic” changes occur within minutes to hours following the lesion (cf. Figure 3.5 for primary auditory cortex). Snyder and Sinex32 subsequently recorded frequency-response areas of ICC multineuronal clusters to contralateral and ipsilateral tones after inserting and fixing-in-place tungsten microelectrodes. Response areas were recorded from most electrodes before, immediately after, and several hours after restricted mechanical lesions of the ganglion. Each ANF lesion produced a “notch” in the tone-evoked CAP audiogram corresponding to a narrow range of lesion frequencies with elevated thresholds. Responses of contralateral ICC neurons, which responded to these lesion frequencies, showed threshold elevations to the lesion frequencies with either no change in sensitivity to other frequencies or with dramatic decreases in threshold to lesion-edge frequencies. These changes in sensitivity produced shifts in CF that could be more than an octave. Thresholds for neurons with these new CFs matched the prelesion thresholds of neurons tuned to the lesion-edge frequencies. These results indicated that responses of ICC neurons were produced by convergence of auditory information across a wide range of ANFs and that the acute “plastic” changes occurred within 1 hour of an ANF lesion.
Figure 3.5. Effect of acoustic trauma on single-unit frequency tuning. After exposing to a 5-kHz tone for 1 hour at 120dB SPL, neurons with CFs above the TTF change their tuning and threshold. Here a neuron with a CF of 10kHz with threshold at 5dB SPL was recorded before and after the trauma; the threshold was initially high at about 50dB but after 3 hours 40 minutes was recovered to about 25dB SPL. As a result, the neuron was now tuned at 6kHz.
From 31 Noreña AJ, Tomita M, Eggermont JJ. Neural changes in cat auditory cortex after a transient pure-tone trauma. Journal of Neurophysiology, 2003; 90: 2387–2401.
(Video) A Guide to Loudness Perception
Quite comparable studies had been done close to a decade earlier by Calford et al.,33 on the basis of frequency tuning curves (FTCs) of single neurons in primary auditory cortex of anesthetized cats before and after inducing a TTS by exposure to an intense pure tone. Peripheral TTS was monitored through the CAP threshold and in most cases involved a notch-like loss. Expansion of response areas was indicated by lower thresholds at some frequencies and by the emergence of sensitivity to previously ineffective frequencies. Contraction of both upper (high intensity) and lower boundaries of response areas was found; in the most extreme cases, neurons became totally unresponsive after the intense-tone exposure. The multitude of effects observed in this study was consistent with a differential effect of the TTS on the excitatory and inhibitory components of the response area of a given neuron.
Kimura and Eggermont34 also assessed the changes in frequency tuning by simultaneous recording of multi-units and LFPs in AI, anterior auditory field (AAF) and AII of cats before and immediately after 30-minute exposure to a loud (93–123dB SPL) pure tone. The average difference of the pure tone and the CF was less than one octave for 70% of the recordings. We found that the mean threshold at CF increased significantly in tonotopically organized AI and in AAF, but not in the nontonotopically organized AII. Multiunit response areas were usually similarly affected as LFP-based response areas (reflecting the output of the auditory thalamus) because the “damaged frequency area” was very similar. This suggested that the damage reflected peripheral activity changes. Enhancement of frequency response areas around CF, but at least one octave below the frequency of the traumatizing tone, suggests a reduction of inhibition likely as a result of the peripheral hearing loss.
The time course of the central changes leading to tonotopic reorganization is still a matter of debate. This question is important because it pertains to the understanding of cortical plasticity. That is, if cortical reorganization is induced immediately (or within a short period) after a peripheral damage, then the central changes may solely reflect the modification of the balance between excitatory and inhibitory inputs. In other words, an immediate reorganization after a hearing loss would suggest that no additional mechanisms are needed beyond the unmasking phenomena described above.28 On the other hand, if cortical reorganization occurs only several weeks or months after the peripheral damage, it suggests that reorganization involves, in addition to the passive unmasking phenomenon, use-dependent plasticity potentially leading to long-term synaptic potentiation or even axonal sprouting. A way to address this question is to study the immediate effect of a peripheral hearing loss on cortical tonotopic organization.
Changes in the neural activity in cat AI occurring within a few hours after a 1-hour exposure to a 120-dB SPL pure tone (5 or 6kHz) were assessed by recording, with two 8-microelectrode arrays, from the same multiunit clusters before and after the trauma.31,35Figure 3.5 illustrates what happens to the response at one particular recording site (the recording electrode array was kept in the same place) where the pretrauma CF of the neurons was ~10kHz and had a threshold of 5dB SPL. The FTC was relatively narrow and indicated sharp tuning. Because the trauma-tone frequency (TTF) was 5kHz, the CF in this case was 1 octave above the TTF and well in the frequency range where one expects a major effect of the exposure. Immediately after cessation of the trauma tone, the neural activity at that recording site was virtually absent in the frequency range covered by the pretrauma FTC. Instead most activity was at frequencies below the original FTC range, notably below 7.4kHz and with a threshold at CF of ~45dB SPL, i.e., a threshold increase of 40dB. About 1 hour 40 minutes after the trauma, the threshold of the neurons at this electrode had improved to ~40dB SPL and the major activity now occurred in the frequency range between 7.4 and 10kHz. Finally 3 hours 40 minutes after the exposure the CF had established itself at about 7kHz with a threshold of 25dB SPL, still an elevation of about 20dB compared to the pretrauma threshold. The average threshold elevation across 16 tone-exposed cats measured 6 hours after the trauma amounted to about 40dB for frequencies above 6kHz.
These results indicate that the neural response properties, in terms of averaged peak driven firing rates, used to construct FTCs are changed after an exposure to a loud tone. In addition, as illustrated in Figure 3.6, the temporal pattern of the evoked discharges was also changed after an acoustic trauma. At higher intensities (>25dB SPL), the tone-evoked response was much shorter in duration after the trauma compared with that before the trauma. Indeed, before the trauma, a stimulus-locked response around CF is noted up to 60ms after the onset of the stimulus, whereas after the trauma, the response lasts up to only 35ms (with a minimum latency of 20ms, dotted vertical lines). In this example the changes in the temporal pattern of the firing rate were not accompanied by a CF shift (such as for the example shown in Figure 3.5). The shorter response duration after the trauma combines with a strong and long-lasting inhibition of the SFR that follows the response (post-activation suppression). This likely is the result of increased peak evoked unit firing rates following the trauma as a result of increased central gain.31
Figure 3.6. Effects of acoustic trauma on post-stimulus temporal response pattern. Two sets (before trauma, top row; after trauma, bottom row) of 7-dot displays showing spectral and temporal response properties of MU activity. Vertically: stimulus frequency is shown on a logarithmic scale; horizontally: time since stimulus onset is shown. Each dot display is obtained at fixed intensity level (indicated at top, in dB SPL). Note much shorter response duration after trauma compared with before, and inhibition of spontaneous firing rate after onset response after trauma over a relatively large frequency range (>1 octave).
From 31 Noreña AJ, Tomita M, Eggermont JJ. Neural changes in cat auditory cortex after a transient pure-tone trauma. Journal of Neurophysiology, 2003; 90: 2387–2401.
These unmasking phenomena suggested that the acoustic trauma-induced hearing loss caused a decrease in lateral inhibition. Rajan36 had earlier proposed a model in which surround and in-field inhibitions are differentiated. He hypothesized that a (moderate) hearing loss decreases the surround inhibition. He further suggested that a release from surround inhibition could unmask in-field inhibition (such as post-activation suppression as found in 31). The release from surround inhibition after cochlear damage (supposed to be tonic in this case) might then explain the unmasking of excitatory responses. Moreover, if the occurrence of in-field inhibition is delayed compared with the excitatory onset response,37 the sustained response should be shortened as observed in our study.
Tomita et al.38 investigated the effect of an acute hearing loss on temporal aspects of auditory processing reflected in the representation of a voice onset time (VOT; Figure 5.3) and gap-in-noise duration continuum in cat AI. Multiple single-unit activity related to the presentation of a /ba/–/pa/ continuum—in which VOT was varied in 5-ms steps from 0 to 70ms—was recorded from the same sites before and after an acoustic trauma using two 8-electrode arrays. They also obtained data for gaps, of duration equal to the VOT, embedded in noise 5ms after the onset to match the location of the VOT in the consonant–vowel stimuli. We specifically analyzed the maximum firing rate (FRmax), related to the onset of the vowel or trailing noise burst, as a function of VOT and gap duration. The changes in FRmax for /ba/–/pa/ continuum as a function of VOT matched the psychometric function for categorical perception of /ba/–/pa/ modeled by a sigmoid function (Figure 3.7). Acoustic trauma made the sigmoid fitting functions shallower, and shifted them toward higher values of VOT. The less steep fitting functions may be a neural correlate of an impaired psychoacoustic temporal resolution, because the ambiguity between /ba/ and /pa/ should consequently be increased.
Figure 3.7. A comparison of the responses to a /ba/–/pa/ continuum (a)–(b) and early gap (d)–(e) conditions from the same recording site. Dot displays (left column) and PSTH (middle column) are organized vertically according to VOT or gap duration and horizontally for time since the onset of the leading noise burst. Time windows for evaluation of the PSTHs to the trailing stimulus are selected (between dot lines) according to VOT or gap duration and the latency of peak response for the leading noise burst. The maximum firing rate in a 5-ms bin (FRmax) in these time windows is called the peak responses to the vowel or trailing noise burst, and plotted as a function of VOT or gap duration (right column) as follows: Average normalized maximum firing rate for the vowel (top right) and trailing noise burst after the early gap (bottom right) obtained before (filled circles) and after (open circles) the acoustic trauma (±SE). The sigmoid curves shown provide the best statistical fit to the data. Note that fitted curves for both the /ba/–/pa/ continuum and the early gap condition are shifted toward longer VOT or gap duration.
Reprinted from 38 Hearing Research, vol. 193, Tomita M, Noreña AJ, Eggermont JJ, Effects of pure tone exposure on voice onset time representation in cat auditory cortex, pages 39–50, copyright 2004, with permission from Elsevier.
Paul W. Flint MD, FACS, in Cummings Otolaryngology: Head and Neck Surgery, 2021
Physical Examination
Physical examination includes careful otoscopy, often with the operating microscope. Pneumotoscopy is important to rule out middle ear effusions or a small perforation that could be the cause of CHL. A red blush due to a focus of otospongiotic bone may be seen over the promontory; this is known as theSchwartze sign. Tuning forks are essential for the evaluation of any patient with a hearing loss12 because they may confirm or rule out the finding of CHL on audiometry.
TheWeber test is performed by placing a 512-Hz fork on the center of the patient's forehead, bridge of the nose, or anterior incisors. The Weber test lateralizes to the ear with the conductive or greater conductive hearing loss (in the case of bilateral disease), and it lateralizes with 5 dB of conductive hearing loss. TheRinne test compares the patient's perception of the relative loudness of air conduction versus bone conduction. It is performed by placing the base of a 512- or 1024-Hz fork over the antrum behind the ear. The sound is compared with the loudness when the tines are placed 2 to 3 cm from the external ear canal; the tines of the fork should be parallel with the plane of the canal. The Rinne test is sensitive and can be used to predict the degree of the conductive component of the hearing loss. When the 512-Hz fork reveals bone conduction greater than air conduction, the patient has at least a 20- to 25-dB conductive hearing loss. If the patient reverses the 512- and 1024-Hz forks, the loss is at least 30 dB. Surgery should not be performed on a patient with a conductive hearing loss if the 512-Hz fork does not reverse, as in such cases there may be an increased risk of mobilizing the stapes at the time of surgery.
Audiometry
The audiometric evaluation includes air conduction, bone conduction, and speech audiometry performed by a trained audiologist. The typical audiogram demonstrates a unilateral or bilateral air-bone gap usually greater in the low frequencies. Bone conduction may show a distinct notch-like decrease at 2000 Hz, known as a Carhart notch, due to an impedance mismatch of the cochlea from stapes fixation.
(Video) Loudness perception in the field and laboratory
The immittance audiometry battery consists of tympanometry, static compliance, and acoustic reflex testing. Immittance audiometry can be helpful in cases of otosclerosis and can confirm lack of mobility of the stapes with absent acoustic reflexes. The middle ear pressure is not affected by otosclerosis and the tympanogram is normal, with a distinct peak that occurs within the normal range (type A) or with slightly increased stiffness (type As). Greater stiffness or a shallower type As tympanogram may point to tympanosclerosis or other ossicular fixation. Likewise, a type Ad tympanogram may suggest ossicular discontinuity as a cause of CHL.
Acoustic reflexes are a sensitive measure of the movement of the stapes. In the presence of otosclerosis, the reflex is absent. With early stapes fixation, the reflex may be abnormal, demonstrating a negative on-off effect, or diphasic reflex (Fig. 146.5). With more advanced disease, the reflex is absent when the probe is in the involved ear. As the disease and hearing loss worsen, the contralateral reflex is affected as a result of the degree of CHL in the otosclerotic ear.13
Kathryn Hopkins, in Handbook of Clinical Neurology, 2015
Loudness perception
Loudness is the perceptual attribute of sound related to intensity. Cochlear hearing loss is associated with abnormal loudness perception; detection thresholds are elevated, but the level of sound that is found uncomfortably loud is elevated by a smaller amount (Kamm et al., 1978). This means that the dynamic range of hearing is reduced, an effect known as loudness recruitment. Figure 27.5 shows mean loudness ratings for pure tones as a function of intensity for a group of normal-hearing listeners and three groups of listeners with cochlear hearing loss of 50, 55, and 60dB HL at the tone frequency. The slope of the loudness function is steeper for the hearing-impaired listeners, and the size of the slope increases with increasing hearing loss. Loudness recruitment is likely to arise directly as a result of outer hair cell damage. As discussed in the section on structures affected by sensorineural hearing loss, above, outer hair cells apply gain at low levels and result in a shallow, non-linear basilar membrane response. The slopes of the loudness functions plotted in Figure 27.5 correspond well with basilar membrane growth functions for animals with normal hearing and various degrees of outer hair cell loss.
Fig. 27.5. Relation between the slope of the loudness function and the degree of hearing loss for 78 listeners with noise-induced losses. The linear function was obtained by the least-squares method.
The history is the mainstay of the diagnosis of most parasomnias. Key features include age of onset, time of night of the events, memory for the events, and family history (Table 377-8). Because NREM parasomnias are a mixture of deep NREM sleep with the awake state, these events are more common in the first third of the night, are associated with no or little memory for the event, and are not stereotypical. Events are more likely to occur with sleep deprivation, alcohol ingestion, sleeping in strange environments, and coincidental conditions that predispose to arousals, such as sleep apnea. Patients are neurologically and psychiatrically normal during wakefulness.
REM sleep behavior disorder usually begins in late adulthood, but it can occur in children. In this disorder, patients lose the muscle atonia of REM sleep and thus act out during their dreams, sometimes injuring themselves or bed partners.15 This nonstereotypical motor activity is often associated with vivid recall of a dream that correlates with the witnessed behavior. Patients can have multiple events typically in the latter half of the night. This behavior disorder can be provoked by medications such as tricyclic antidepressants, monoamine oxidase inhibitors, and serotonin reuptake inhibitors.
The diagnosis is based on the documented excessive electromyographic activity during REM sleep and the history of dream enactment. If the patient demonstrates stereotypic sleep motor behavior, rather than the characteristic nonstereotypical behavior of REM sleep behavior disorder, the possibility of epilepsy (Chapter 375) should be considered. Because chronic REM sleep behavior disorder has been linked to the subsequent development of Parkinson disease (Chapter 381), multiple system atrophy (Chapter 381), and Lewybody dementia (Chapter 374), patients should have a detailed neurologic examination to look for subclinical features.
Other nocturnal events can present as sensory phenomena or sleep-related movements. Nightmares are emotionally disturbing dreams associated with fear, anxiety, anger, or sadness. Nightmares most commonly occur after a psychologically disturbing event, but may also occur as a result of antihypertensive medications, antidepressants, or dopamine agonists. Exploding head syndrome is the painless perception of a loud sound or sense of an explosion, typically in light sleep. Bruxism is a disorder of jaw clenching or grinding that can cause tooth damage and headaches. Rhythmic movement disorder is associated with body rocking or head banging in the transition from wake to sleep.
Patients who have nocturnal events with atypical features, a risk of harm, signs or symptoms of other sleep disorders, or excessive daytime sleepiness should undergo in-laboratory video polysomnography, with extended EEG recording if seizures are being considered.
Treatment
Therapy first should focus on ensuring safety for individuals who may injure themselves or others (e.g., placing the bed on the floor, blocking windows, or moving the patient’s bedroom to the ground floor), decreasing factors that may provoke events such as NREM parasomnia by causing arousals, and avoiding inciting factors such as sleep deprivation, alcohol, and short-acting hypnotic agents. Pharmacologic treatment with clonazepam (0.5 to 2) mg and tricyclic antidepressants (Chapter 369,Table 369-5) has been tried for NREM parasomnias with varying success. Treatment of sleep apnea reduces both NREM and REM events. For REM sleep behavior disorder, most patients respond well to clonazepam (0.25 to 3 mg) or melatonin (3 to 20 mg). Rhythmic movement disorder is typically refractory to medication therapy. Nightmares may respond to removal of the provocative substance or may require prazosin (5 to 15 mg) or imagery rehearsal therapy.
(Video) Staying Safe While Getting Loud: SPL, Sound Exposure, and Loudness Perception in Concert Sound
The Perception of Musical Tones
Andrew J. Oxenham, in The Psychology of Music (Third Edition), 2013
5 Models of Loudness
Despite the inherent difficulties in measuring loudness, a model that can predict the loudness of arbitrary sounds is still a useful tool. The development of models of loudness perception has a long history (Fletcher & Munson, 1937; Moore & Glasberg, 1996, 1997; Moore et al., 1997; Moore, Glasberg, & Vickers, 1999; Zwicker, 1960; Zwicker, Fastl, & Dallmayr, 1984). Essentially all are based on the idea that the loudness of a sound reflects the amount of excitation it produces within the auditory system. Although a direct physiological test, comparing the total amount of auditory nerve activity in an animal model with the predicted loudness based on human studies, did not find a good correspondence between the two (Relkin & Doucet, 1997), the psychophysical models that relate predicted excitation patterns, based on auditory filtering and cochlear nonlinearity, to loudness generally provide accurate predictions of loudness in a wide variety of conditions (e.g., Chen, Hu, Glasberg, & Moore, 2011).
Some models incorporate partial loudness predictions (Chen et al., 2011; Moore et al., 1997), others predict the effects of cochlear hearing loss on loudness (Moore & Glasberg, 1997), and others have been extended to explain the loudness of sounds that fluctuate over time (Chalupper & Fastl, 2002; Glasberg & Moore, 2002). However, none has yet attempted to incorporate context effects, such as loudness recalibration or loudness enhancement.
Tinnitus - An Interdisciplinary Approach Towards Individualized Treatment: Towards understanding the complexity of tinnitus
Dirk De Ridder, ... Sven Vanneste, in Progress in Brain Research, 2021
3 Conclusion
Vagus nerve stimulation is a promising new tool for the treatment of chronic tinnitus. Current protocols produce a clinically significant but moderate improvement in tinnitus distress and a modest benefit in tinnitus loudness perception. Although the potential to use neural plasticity to reduce or eliminate the neural drivers of ongoing tinnitus is exciting, much work is needed to more completely understand the neural basis of tinnitus and to develop tailored therapies to address the suffering caused by this heterogeneous condition. Whether pairing of the vagus stimulation with non-tinnitus or tinnitus-matched sounds is essential is still to be determined. Current evidence for paired or unpaired vagus nerve stimulation in the setting of tinnitus is insufficient for FDA approval.
G. Rider, ... D. Stool, in Encyclopedia of Toxicology (Third Edition), 2014
Sound Measurement
From the standpoint of sound toxicity, the most important properties of sound are power (or loudness) and frequency (or pitch). Sound power is usually expressed using the logarithmic decibel (dB) scale chosen to accommodate human loudness perception. Increasing sound intensity by 10dB is perceived as an approximate doubling in loudness but represents a tenfold increase in sound power.
Sound frequency is usually expressed in units of cycles per second or Hz. Humans have a useful hearing range of approximately 20–20000Hz, but are most sensitive to frequencies between about 1000 and 6000Hz (for reference, the lowest and highest notes on the piano are 27.5 and 4186Hz, respectively.) This increased sensitivity is due in part to the shape of the external portion of the ear and the ear canal, which serve to amplify frequencies in this range.
Human loudness perception depends in a complex manner on both frequency and the overall loudness of sound. (Forexample, bass is more difficult to hear in music played at low volume than in the same music played at high volume.) Tocapture this behavior, two weighting scales have been developed for use in sound hazard analysis. The most common of these is the A weighting scale, which is used to assess occupational and environmental noise. The A scale weights sounds in the 1000–6000Hz range much more heavily than low-frequency sounds. The A-weighted intensities (dBA) of some common sounds are listed in Table 3. By contrast, the C weighting scale is used for very loud sounds and is a much flatter function of frequency.
Table 3. Intensity and response for some common sounds
Ruth Litovsky, in Handbook of Clinical Neurology, 2015
Loudness
Another aspect of auditory perception that relates to sound level or intensity is that of perceived loudness of a stimulus. Whereas discrimination, whereby we measure whether a listener was correct when s/he reported whether a stimulus changed or did not change, is objective, loudness perception is subjective. Any subjective perception is difficult to measure in listeners, including not only infants and children, but adults as well. Loudness is an attribute for a sound that places perception on a scale ranging from inaudible/quiet to loud/uncomfortable, in response to change in sound pressure level (intensity). Because there is no correct answer, there is some challenge in knowing when and how to reinforce a child and how to train the child to respond. Nonetheless, it appears that, while some children have difficulty learning the task, others can perform similarly to adults (Serpanos and Gravel, 2000). Because loudness growth is abnormal in people with hearing loss, such that loudness grows rapidly over a small range of intensities, emphasis on understanding the importance of loudness perception maturation may come from the audiologic literature, with hearing-impaired children. Evaluations of hearing-aid fittings and perceived loudness of speech signals after amplification become clinically crucial, so that the speech signal is heard, understood, and comfortably presented (e.g., Scollie et al., 2010; Ching and Dillon, 2013). Future work on basic psychophysics may be important in order to capture the perception of young infants and children with typical hearing, and benchmark their abilities, so that expectations are appropriate for children who are fitted with hearing aids.
Effects of “Nondamaging Sound” on the Adult Auditory Brain
Jos J. Eggermont, in Noise and the Brain, 2014
Adult auditory plasticity is represented in learning and training effects on the brain. Adult auditory plasticity is also reflected in the acclimatization time course to full usefulness of new hearing aids and cochlear implants. Even simple manipulations, such as long-term plugging the ears or exposing them to relatively soft sound, profoundly affect the loudness perception measured afterwards and also produces changing neural activity in auditory cortex, thalamus and midbrain. Most of these changes have been demonstrated in animals following long-term exposure to behaviorally irrelevant sound and appear to be very long lasting. The induced changes, in tonotopic maps, in spontaneous and stimulus-driven firing rates and in neural synchrony, take several weeks of exposure to fully develop and then recover in quiet over a period that extends over at least three months. The findings illustrate potentially destructive effects of moderate long-term sound exposure on speech understanding in children and adults in the absence of audiometric hearing loss.
The amplitude, or height of the sound wave, determines how much energy it contains and is perceived as loudness (the degree of sound volume). Larger waves are perceived as louder.
Loudness is a measurement of sound. It essentially means how strong or intense an auditory noise is to an individual. Loudness is a subjective measure- it differs between individuals. The noise level will seem too loud for some while too low for others.
Humans use two important cues to help determine where a sound is coming from. These cues are: (1) which ear the sound hits first (known as interaural time differences), and (2) how loud the sound is when it reaches each ear (known as interaural intensity differences).
Each frequency of a complex sound maximally vibrates the membrane at one location. Because of this mechanism, we hear different pitches within the sound. A louder sound increases the amplitude of the vibration, so we hear loudness. Signals sent to the brain from auditory nerve are then interpreted as sounds.
Sound occurs when energy causes air particles to move closer together and further apart. The closer the particles get or the further apart they get, the greater the sound's amplitude. Sound amplitude causes a sound's loudness and intensity. The bigger the amplitude is, the louder and more intense the sound.
Some common synonyms of loud are earsplitting, raucous, stentorian, and strident. While all these words mean "marked by intensity or volume of sound," loud applies to any volume above normal and may suggest undue vehemence or obtrusiveness.
The amplitude of the sound waves and their distance from the sound source. It is determined by the quantity of energy that initiated the waves. Waves with a higher amplitude have much more energy or intensity, thus they sound louder.
The answer to this question is clearly no. You might suspect, that the higher the frequency, the louder we perceive a noise, but frequency does not tell us how loud a sound is. Intensity or loudness is the amount of energy of a vibration and is measured in decibels (dB). If a sound is loud, it has a high intensity.
It is defined from the receiver's end, which means loudness for a person is the amount of sound that person hears. It is related to the sound wave's amplitude. Higher the amplitude, the higher the sound energy, and hence, the higher the intensity.
Sensation occurs when sensory receptors detect sensory stimuli.Perception involves the organization, interpretation, and conscious experience of those sensations.
The pitch of a sound is our ear's response to the frequency of sound. Whereas loudness depends on the energy of the wave. In general, the pitch is the reason behind the difference in voice quality of different individuals.
The answer to this question is clearly no. You might suspect, that the higher the frequency, the louder we perceive a noise, but frequency does not tell us how loud a sound is. Intensity or loudness is the amount of energy of a vibration and is measured in decibels (dB). If a sound is loud, it has a high intensity.
Amplitude can describe two different concepts. In psychology, it can describe the magnitude or strength of a reaction or of a stimulus. For example, results from a study could be described as having a strong amplitude. In physics, amplitude is the measure of the magnitude of a wave's oscillations during a wave cycle.
It is defined from the receiver's end, which means loudness for a person is the amount of sound that person hears. It is related to the sound wave's amplitude. Higher the amplitude, the higher the sound energy, and hence, the higher the intensity.
Introduction: My name is Dan Stracke, I am a homely, gleaming, glamorous, inquisitive, homely, gorgeous, light person who loves writing and wants to share my knowledge and understanding with you.
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