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Tinnitus is the perception of an insistent, unpleasant ringing, buzzing or other consistent noise, located in or near the skull but without a definable external source.
Tinnitus is often perceived as a ringing or persistent high tone very close to or within the ear. Tinnitus is often regarded as a symptom of auditory conditions, such as damage to the tissues in the ear that control the perception of tones and frequencies.
An increasing number of researchers argue that tinnitus is a disorder of the connections between the inner ear and certain areas of the brain.
Some scientists had developed a theory that tinnitus was associated with deficiencies in vitamin B12.
Chronic inflammation of the middle ear (otitis media) may also be associated with some cases of tinnitus. Tinnitus related to otitis media may be improved by surgery to correct damage caused by this inflammation. The following statements have been disproved by certain studies - you may read these studies right here. If it is laymen who come up with such statements, it might be contributed to ignorance, but often enough it is physicians who make wrong statements despite being fully aware of their statements being incorrect. At this point we'd like to make it clear that the acoustic organ and the equilibrium organ is actually one and the same organ, which is the inner ear. The liquid systems located in the inner ear cause that too much of sound damages the equilibrium organ as well.
It is striking that scholastic medicine declares morbus meniere to be an inner ear disease. Tinnitus is not declared to be an inner ear disease, but a “symptom” or a “syndrom” (wikipedia) even though the tiny hair of the ear cells damaged by noise are actually verified as a cause.
As scholastic medicine denies achievements attributed to laser therapy, patients who achieve improvement or healing due to laser therapy are being monopolized by scholastic medicine and considered cases of spontaneous healing. We, the patients of LLLT, have to emphasize it explicitly that we are no cases of spontaneous healing as for that we have gone through too detailed experiences of the recovery process. When patients hint at the connection between the alteration of their ear noises and the time of their LLLT, this is led back to placebo effect. Activating such powers, however, also lies within the possibilities of every other physician.
Responding to the patient and explaining the intended therapy to him certainly is very important and builds up the patient's basic trust in the treatment that is going to be performed. However, patients experience their healing process on an acoustic level, and it most often extends over a longer period of time. The patients have been through a similar but nonetheless individual recovery process that is considered typical of laser therapy. Without laser therapy there are no such effects, which is also why even a highly empathetic doctor is unable to achieve the same effects as LLLT.
Over and over again in all kinds of fora and even by some physicians the story about the cut-through acoustic nerve is mentioned. The cutting through of the acoustic nerve and the unchanged tinnitus is not proved with evidence in medical literature.
That cutting through a nerve-line may phantom pain - which in the case of the acoustic nerve would be phantom pains - is explained by MD Wilden in his letter to the "Stern" that you can read on this website (german part) under "Die Medien". Amputation pain is not a phenomenon by which you could explain anything related to the ear, but rather a well-understood biological process. These are of course traumatized at the place of the amputation and may remain irritated for years and send nerval impulses that are received by the appropriate brain areas. We know that very well from surgery which treats amputation pains successfully by a so-called pre-amputation in which they make sure that a surgically perfect supply of the nerve-socks is guaranteed.
It seems as if the statement about the unalternated tinnitus is a core piece of the construct upon which the theory of the two places of tinnitus and its migration from the inner ear to diffuse brain regions is built upon. Thousands of patients whose inner ears have been successfully treated by low level laser therapy provide proof of the incorrectness of that theory, though.
In the “Apotheken Umschau” issued on September 15th 2009 they aim to suggest patients that tinnitus was a brain disease. A computer image of the brain shows activities in the acoustic center of a tinnitus-sufferer which are indicated by colourings of the activated brain regions. The brain does indeed create the impression of an acoustic experience whose sound and velocity can be measured by physicians.
By means of modern methods tinnitus in the acoustic cortex of the brain can be shown in a visual way (see above image). The study only had evidentiary value if at the same time it would be verified that no information of the affected inner ear reaches the brain via the acoustic nerve.
It goes without saying that those brain regions of a tinnitus patient are active that eventually need to process the false information coming from the acoustic nerve.
There is another discrepancy that derives from the comparison of tinnitus and morbus meniere definition and treatment as they start in the same organ.
The thousands of patients successfully treated by low level laser therapy in the inner ear prove the incorrectness of that way of thinking. Scholastic tinnitus research is thus evidentically on the wrong track and has arrived at a dead-end road. The American Surveillance Office FDA (Food and Drug Administration) jugded low level laser therapy to be a therapy free from side-effects. More than 30 years of clinical and experimental science have provided evidence that low level laser therapy has no unwanted side-effects. From time to time, patients treated with low level laser therapy report they perceived the noises in the ear to become louder upon laser treatment.
By irradiating the cochlea with low level laser, a cellular process in the inner ear is started. That process causes an alteration of the tinnitus which may be perceived as a tinnitus growing more vivid. At the latest after some time it soothes, though, and the noise in the ears settles at a lower level than before.
We three patients of the initiative for the LLLT, who have got much LLLT within the last years, don't feel any defect with our brain. This study gives evidence of the cochlea being penetrated by laser on the way to the auditory canal. In November 2006 Michael Zazzio at the Audio Laser-Kliniken in Sweden irradiated a pig's ear from the outside after dividing the skull of the pig. The tissue sample measured 36 millimeters from the tympanic membrane to the inner incision of the skull.
Through the results of the study, it is beyond doubt that LASER light in inner ear therapy gets into the inner ear cochlea through the ear canal, via the tympanic membrane, passing the hearing bones and getting through the shell of the cochlea if the LASER probe is placed correctly and in an optimal position, and if the LASER light is administrated in the right direction.
We deem those studies to be highly deplorable in which low level laser therapy is used at an energy level being too low or for a time period being too short.
The exact term of MD Wilden's therapy is not without good reason called: High-dosage Low Level Laser Therapy.
The following experiment set-up is planned: 68 spots of skin among 45 patients are selected.
By randomized principle those patients for the real sun exposure and those for placebo-exposure are determined. As the treaters who are not supposed to know whether they are applying sunlight or placebo, the experiment is set in such a manner that the treater can't see the light he is applying. As exposure time it is determined that once a week an exposure takes place for six minutes time. In the upcoming week there is another exposure of six minutes and in the following two weeks another six minutes each week.
In the end of the experiment, they come to the conclusion that there are no significant differences in exposure to sunlight and placebo light on the patients' skin.
Summing up, the investigator comes up with the conclusion that sunlight is not able to tan human skin.
The applied dosage was just too low and double-blind and randomization have not made the experiment any more realistic.
The following two studies, Nakashima and Mirz, are mentioned as supposed evidence of the ineffectiveness of low level laser therapy.
A 60 mw laser was used once a week, four times in four weeks for six minutes each, a wavelength is not indicated. A total of 24 minutes of laser in 4 weeks, that is to poor energy to fight against a tinnitus. Another study uses a weaker laser of 50 mw (wavelength 830 nm) and is applied for ten minutes per treatment. We are thinking that experts such as physicians should start thinking when confronted with these experimental descriptions. The case of the 29-year old Dietrich Hectors from Belgium, who wrote his last farewell in his "Facebook" profile, before he went out life. England, North-Wales, 2015:Deganwy man James Ivor Jones jumped to his death after being told there was no cure for his tinnitus.
The new AGXs3s Tinnitus, however, delivers two treatment solutions at once in a comfortable, nearly invisible hearing device: tinnitus therapy plus hearing aid. Our AudigyCertified™ hearing care experts have recently begun fitting this new technology and have seen promising results from patients who have reported achieving a new level of relief from their tinnitus. The purpose of this chapter is to provide background material on noise-induced hearing loss to facilitate understanding of the evidence on noise-induced hearing loss in military personnel presented in Chapter 3. In humans and other mammals, the auditory system consists of the external, middle, and inner ears (Figure 2-1), as well as the central auditory pathways in the brain. The mechanical activity of the basilar membrane leads to mechanical stimulation of the inner and outer hair cells. As noted in Chapter 1, various metrics have been used in the literature to quantify the sound levels associated with impulse and impact noise, including dBP and dB pe SPL. The relationship between noise-induced hearing loss and the peak amplitude of an impulse or impact noise is complicated.
Below the critical level, hearing loss grows by the rate of approximately 1–3 dB of hearing loss for each dB of increase in peak level.
Hearing loss that results from exposure to sound with energy spread across a wide range of frequencies, such as many broad-band noises and impulses common to most industrial and military settings, is typically characterized by a gradual increase in threshold as frequency increases. Although the group data from Cooper and Owen (1976) in Figure 2-3 reveal a clear decrease in hearing from 1000 Hz to 4000 Hz followed by a return toward better hearing at still higher frequencies (8000 Hz), a pattern that typifies a noise notch, this is not always readily apparent for individual data. In summary, there are four key acoustic parameters of a given noise exposure that determine the type and amount of the resulting hearing loss.
Acoustic trauma can occur following exposure to very intense noise, typically blasts > 150 dBA. Because sound levels in areas free from reflective surfaces, known as free fields, decay 6 dB per doubling of distance from the sound source, a key factor in such exposures may be the proximity of the individual to the blast. Individuals with mild or moderate permanent noise-induced hearing losses typically have some structural damage in their cochleas. The time course of cell degeneration and scar formation in the cochlea following a damaging noise exposure can be determined from animal studies only. Consider exposure to an intense sound for a specified duration, with the measurement of hearing thresholds performed at periodic intervals during the exposure and at several times following the exposure.
This less than perfect correlation has also been noted in the specific context of the study of recovery from noise exposure. We speculate that delayed recovery of thresholds in humans also signifies the occurrence of cochlear damage.
Limited data on PTS in humans appear to be consistent with these data from laboratory animals on recovery following noise exposure. Laboratory studies of TTS and PTS in humans and laboratory animals that have focused on recovery of hearing thresholds have typically been terminated soon after the thresholds have fully recovered (TTS) or appear to have stabilized for a period of days or weeks (PTS). It is noteworthy, however, that the modeling of noise-induced hearing loss and age-related hearing loss in ISO-1999 suggests that noise-induced hearing loss is almost asymptotic beginning at about 10–20 years of exposure and continuing through 40 years of exposure, especially for the milder amounts of hearing loss (ISO, 1990). Although an effort was made to focus on recent human studies, for some factors, the only studies have been in laboratory animals.
Although hearing loss in the industrial or military environment is most often attributed to noise exposure, there is increasing attention to whether co-exposure to chemical agents present in these environments may potentiate noise-induced hearing loss. Vapors from organic solvents, such as toluene, are often found in occupational environments involved in printing and painting, as well as in shipyards where paint spraying is common. Results of laboratory studies with animals showing increased risk for noise-induced hearing loss with exposure to solvents led to efforts to confirm these results in humans, given the widespread occupational exposures to these chemicals in noisy environments. 2011 NEW AUDIOLOGY TECHNILOGY Programmable 8 Channel Digital hearing aid price, View 8 CHANNEL hearring aid, Audiology Product Details from Saferlife Products Co., Ltd.
INTRODUCTION: The otoacoustic emission test is useful in monitoring hearing changes not yet detectable in pure-tone audiometry, as well as in monitoring cochlear damage caused by exposure to noise.
OBJECTIVE: To evaluate distortion product otoacoustic emissions in normal-hearing workers exposed to different occupational noise doses. CONCLUSION: The otoacoustic emissions are worse in the exposed groups compared to the unexposed group and the greater are the noise dose, worse are the results.
The complaint of subjective ear blockage (EB) is frequently associated with subjective idiopathic tinnitus.
In our evolving clinical tinnitus experience since 1979, at SUNY-Downstate Medical Center and the Martha Entenmann Tinnitus Research Center, in excess of 15,000 patients have been seen in neurotologic-audiologic consultation in whom different clinical types of tinnitus - predominantly a central-type severe disabling subjective idiopathic tinnitus (SIT) - have been identified with a medical audiologic tinnitus patient protocol (MATPP)4. In general, a significant associated complaint in SIT patients has been of ear blockage of fluctuant intensity located in the ear(s) with the SIT complaint. Our interest in the tympanic membrane displacement test (TMDT) and ICP and idiopathic intracranial hypertension (IIH) has paralleled, since 1979, an increasingly frequent clinical experience with SIT patients in whom the following conditions are present: (1) persistent complaint of ear blockage after control of eustachian tube obstruction or secondary EH (SEH) and (2) a reduced vestibular response with caloric, sinusoidal, harmonic rotary-chair testing or the Fukuda stepping test in the absence of subjective vertigo in the SIT ear. Our introduction to the TMD occurred in 2005, at the Fifth International Symposium: Meniere's Disease and Inner Ear Homeostasis Disorders, House Ear Institute, Los Angeles, CA. We have reported since 2006 our clinical experience with SIT in terms of the fluid dynamics between ear and brain, brain and inner ear fluid homeostasis, cochlear- or vestibular-type tinnitus, and SEH7. It has been hypothesized that persistence of the complaint of ear blockage in the SIT ear with maintenance and control of function in the external or middle and inner ear reflects an alteration in fluid dynamics between the ear and brain, a biologic marker being alteration or elevation of ICP, reflecting IIH, highlighted by the complaint of ear blockage. The experience with the TMDT for the diagnosis of IIH associated with tinnitus, also referred to as benign intracranial hypertension and pseudotumor cerebri, has been reported. Intracranial hypertension was reported in 1981 to become manifest with neurotologic symptoms: The most common presenting symptom was pulsatile tinnitus, followed by hearing loss, dizziness or vertigo, and aural fullness13. Historically, the clinical application of the TMD for measurement of ICP is supported by animal, human, basic science, and clinical investigations. Clinically, the publications cited in the next section support the hypothesis that an abnormal and fluctuating ICP is a factor related in the clinical course of a previously described subgroup of SIT patients. Of the two fluids within the cochlea, the endolymph and the perilymph, it is the perilymph that interfaces with the footplate, and it is the pressure of this fluid that is assessed by the Cerebral and Cochlear Fluid Pressure Analyser and the TMDT technique. In the guinea pig, Bohmer20 reported that "the endolymph indirectly communicates with the intracranial fluids via the endolymphatic sac and maintains homeostasis with the perilymphatic pressure across the Reissner's and other intralabyrinthine membranes. Perivascular or perineural routes between the intracranial and labyrinthine spaces may also provide a means of communication, but these may be significant only in cases of extremely elevated ICP or certain malformations. Clinical analysis of a trial of ICP measurement from the external auditory canal concluded that intra-aural pressure waves clearly reflect intracranial cardiovascular and respiratory pulsatility changes in cats23. In a guinea pig model, infrasound (0.1-10 Hz) within the perilymph induced longitudinal sinusoidal and gross displacement of the endolymph. Varying patency of the cochlear aqueduct and connectivity to the perilymphatic space of the cochlear labyrinth of the inner ear in human temporal bones was reported by Wlodyka27. Testing in normal subjects shows that stable TMDT results are obtained during the day and after exercise28. Noninvasive intracranial compliance monitoring by measurement of intra-aural pressure waves, performed on neurosurgical patients, has identified certain characteristics of the intra-aural pressure pulse that may allow for noninvasive measurement of ICP and compliance34,35. The Southampton Tympanic Membrane Displacement Analyzer, commercially available as the MMS-11 Cerebral and Cochlear Fluid Pressure (CCFP) Analyser, is able to measure extremely small displacements of the tympanic membrane pressure pulses at heartbeat and respiration frequencies that are transmitted from the intracranial pulse pressure to the tympanic membrane (Figure 1).
The tympanic membrane in humans is constantly in motion, principally of cerebral cardiovascular and respiratory origin. The ICP wave measurements can be obtained in two modes of operation: In the first, a TMD is evoked using the acoustic stapedial reflex. The mechanism of the TMD is hypothesized to be a reflection of increased ICP and perilymphatic pressure on the acoustic stapedial reflex and its action on the stapes footplate, ossicular chain, and tympanic membrane.
The TMDT is postulated to provide a "signature" of the underlying neurological disorder in terms of CSF hydrodynamics36. All patients selected according to the preceding protocol (n = 12) between July 2007 and March 2012 underwent a neurotologic examination of the head and neck, including microscopical examination of the ear canals and tympanic membrane for evidence of pulsation and auscultation of the ear canals, head, and neck. The 12 selected patients were further classified into two groups, the first group of 6 patients undergoing the TMDT on a single date and the second group of 6 undergoing TMD on sequential test dates.
Neurotologic and otologic physical examination identified integrity of the external ear canal and tympanic membrane with no spontaneous signs of labyrinthine irritation.
TMD recordings were obtained in the two groups of patients to observe the temporal course of the ICP in SIT. ICP is normally 7-15 mm Hg for a supine adult and becomes negative (averaging-10 mm Hg) in the vertical position. The subject of this case report is a 71-year-old white man with SIT, the quality of which was a high-pitched "ee" of constant duration located in the left ear. Associated complaints included hypertension, left-ear blockage that fluctuated with tinnitus intensity, nasal allergy, occasional unsteadiness, occasional frontal headache, head pressure, memory interference, and occasional delay in speech expression. The patient demonstrated a fluctuating ICP with sequential TMD testing between July 2007 and March 2012, prior to and after treatment with Diamox (Figures 4, 5). Significantly, objective improvement was noted in the TMD recording from abnormal IPPA ICP to normal, as noted in the elevated amplitude between July and September 2007 and in the normal IPPA amplitude and modulation by respiration between October 2007 and August 2008. Tinnitus treatment results targeting ICP as a manifestation of IIH with Diamox were positive in the short term (n = 2). In a preselected group of SIT patients (n = 12) resistant to attempts for tinnitus relief with instrumentation or medication, an abnormal ICP has been identified (n = 10). The fluctuations in the categories of the TMD recordings in the same patient at single or sequential recording dates are clinically considered to be a reflection of the dynamic state of the ICP and compliance in the presence of SIT and the influence of the environment and presence or absence of CNS disease. The results of a normal or abnormal ICP and reduced or normal compliance in this cohort of SIT patients supports clinical consideration of the presence of an IIH and indication for treatment. Spontaneous TMD recordings of intra-aural pressure waves were obtained in this cohort of SIT patients. The clinical significance of abnormal ICP and IIH as factors influencing the clinical course of SIT is suggested by the TMDT results we have obtained. The essential requirements of the TMDT are integrity and patency of the external ear canal, an intact tympanic membrane, and an intact ossicular chain. Clinical and basic science efforts at identifying the clinical significance of brain pulsatility have been ongoing for in excess of 60 years39. This report of using the TMD lends credence to the application of brain pulsatility to support the diagnosis of IIH in a particular cohort of SIT patients. The term congestive inner ear was first introduced in patients with increased ICP secondary to tumors40.
Otologic and neurotologic experiences with the TMDT were reported for a series of patients whose diagnoses included pulsating tinnitus, IIH, Meniere's disease, perilymphatic fistula, perilymphatic hypertension, arterial stenosis, and Arnold-Chiari syndrome.
The cohort of SIT patients in this TMD study all had nonpulsatile, predominantly central-type, severe disabling subjective idiopathic tinnitus (SIT) resistant to attempts for tinnitus relief with instrumentation or medication, with associated neurotologic complaints highlighted by ear blockage and sensorineural hearing loss and CNS complaints highlighted by headache, head pressure, and cognitive interference in memory or speech expression or both. The associated complaint of ear blockage or aural fullness is clinically hypothesized to reflect fluctuation in the ICP of a persistent IIH.
Cerebral blood flow autoregulation (CBA) is the process by which cerebral blood flow is maintained at a constant level in normal brain. The pressure - volume relationship among ICP, volume of CSF, blood, and brain tissue and cerebral perfusion pressure is known as the Monro-Kellie doctrine or the Monro-Kellie hypothesis (1783). The issue of compliance has also been reported in experimental findings related to inner ear fluid pressure and to the effects of pressure changes on cochlear function in the guinea pig. The concept of compliance and its extrapolation from the ratio of the volume-pressure curve, obtainable with the TMD as a high amplitude of the cardiovascular pulse pressure, is significant for its clinical translation for evaluating the status of homeostatic function in both ear and brain.
EH is an enlargement of the endolymphatic space with a bulge of Reissner's membrane into the scala vestibuli of the cochlear labyrinth. The finding with TMDT of an elevated IPPA in the SIT ear, which supports the diagnosis of IIH in the present cohort of nonpulsatile SIT patients, is the basis of the following questions and hypothesis: Is the SEH that has been clinically identified in some SIT patients since 1981 with the MATPP and that is supported by vestibular testing in some SIT patients with and without vertigo a clinical manifestation of a IIH? We suggest that the volume-pressure relationships in a confined space be applied clinically to the ear as they have been for the brain. It is hypothesized for some, but not all, EH and SEH patients that the IPPA, reflecting alterations in volume - pressure relationships in brain, is transmitted to the ear predominantly by one or both of two routes - via the cochlear aqueduct or via pressure on the endolymphatic sac. The teaching from brain of compartmentalization of the effects of pressure and flow, which, although related physical phenomena, differ in the location for their measurement, are suggested to apply to the ear: That is, pressure pulses propagate at the speed of sound and the location for their measurement are not specific, but flow pulsations are site-specific39.
This is the first known report of the clinical application of inserting an external probe device into the external ear canal (Tympanic Membrane Pressure Analyser [Marchbanks] in a cohort of nonpulsatile, predominantly central-type severe disabling tinnitus patients (SIT) suspected to have an elevated ICP reflective of an associated IIH. In two groups of these preselected SIT patients, IPPA was demonstrated to be elevated and abnormal and to fluctuate in the clinical course of the SIT (overall abnormality in 10 of the12 patients). The patient preselection protocol used for identifying an elevated ICP and IIH in a particular cohort of SIT patients and the positive results reported for its identification with the TMDT in 10 of our 12 patients supports the continued use and modification of the TMDT reflective of an evolving clinical experience. The IPPA is reflective of the ICP and was identified with spontaneous single and serial recordings in 10 of 12 SIT patients with postural testing (supine, 30 degrees, and 45 degrees).
The IPPA abnormality, reflective of an increased ICP, is clinically considered to be a factor - not an etiology - for SIT, and is considered to influence the clinical course of SIT in a particular cohort of patients with a predominantly central-type tinnitus.
Extracranial identification of an IPPA and ICP with the TMDT in the clinical course of SIT has a dual function: identifying ICP as a factor influencing the tinnitus diagnosis, and objectively monitoring the efficacy of ICP-targeted therapy. The TMDT results of the identification and association of IIH, IPPA, and ICP in this observational report lends support to the clinical impression of an underlying ICP reflective of IIH and a basis for treatment in SIT patients such as those in our particular cohort. The principles of brain pulsatility are clinically considered to be applicable to the physiology of the inner ear and otologic and neurotologic complaints of hearing loss, tinnitus, vertigo, and ear blockage.
2011 new aberto se encaixam aparelho auditivo digital adaptacion abierta audifono, View auditivo digital, Saferlife Product Details from Saferlife Products Co., Ltd. It is not considered to be a condition in its own right, but a syndrome or symptom related to many forms of auditory damage or disorder.
Age-related hearing impairments, or disorders of the circulatory system around the ear, may also be related to this complaint. Some scientists conclude that tinnitus is in fact related to damage of the nervous tissue in or around the auditory cortex of the brain. A recent study including 100 patients with tinnitus found that 63 of these had low vitamin B12 levels.
As the natural molecule histamine is associated with the regulation of both inflammation and some auditory nervous tissue, drugs that block its receptors in the brain are currently proposed as treatments for tinnitus. Darius Kohan is renowned for his otology expertise and has been highlighted on several outlets such as a CBS spotlight on tinnitus and is often cited in WEB MD and other medical outlets. Wilden, the other medics and alternative practioners applying LLLT are attributed the gift to set free specific healing energies in their patients by responding to their patients in a special way.
My personal experience - as well as that of other patients such as Hansi Cross - confirms that. LASER light with a wavelength of just above 800 nm has better penetration ability in tissue than the 650 nm LASER, but the 800 nm LASER light is not as visible to the human eye as shorter wavelengths.
The conclusion that that low level laser therapy doesn't work for tinnitus is scientifically wrong. For our patients who struggle with tinnitus, we are excited to announce the arrival of a new treatment option from AGX Hearing that stands to not only help alleviate tinnitus symptoms but also address the hearing difficulties that often accompany the condition. The AGXs3s Tinnitus uses the patent-pending Multiflex Tinnitus Technology designed by Starkey® Hearing Technologies to help both conceal the symptoms of tinnitus with customizable, low-volume sound stimulus and compensate for any hearing loss that may contribute to the condition. We look forward to hearing more from our patients about the success they are experiencing with these new devices during their 75-day risk-free trial. Call today to make an appointment, and find out how our experienced hearing care providers and state-of-the-art tinnitus care can help improve your quality of life. The chapter begins with a general discussion of the structure and function of the auditory system, with particular emphasis on the periphery, and the impact of noise on the peripheral auditory system.


Sound waves enter the external ear through the pinna, travel through the external ear canal, and strike the eardrum.
Sound waves enter the pinna, travel through the external ear canal, and strike the eardrum, setting it in motion.
From the surface of each hair cell, thin hair-like processes (stereocilia) project into the overlying gelatinous tectorial membrane (Figure 2-2). The nerve fibers connected to the hair cells, primarily the inner hair cells, are excited by the neurotransmitter and transfer the auditory information to the brain.
The typical measures of impulse noise are the initial peak level and the duration of the first over-pressure.
First, the high peak levels associated with gunfire (140–190 dB pe SPL)1 may damage the cochlea by causing rapid mechanical failure and injury (Henderson and Hamernik, 1986). Sound levels for steady-state noise, on the other hand, are more commonly expressed as dBA.
Thus, intense explosions may result in large cochlear lesions and significant hearing losses. However, above the critical level, hearing loss grows 3–7 dB for each dB increase in the level of the impulse or impact noise.
Experimental studies with laboratory animals have shown that exposure to combinations of relatively benign impact and steady-state noise can lead to multiplicative interactions with hearing loss and cochlear damage, with the effects of the combined exposure being greater than the simple additive effects of impulse or continuous noise (Hamernik et al., 1981). A noise-induced temporary hearing loss, or temporary threshold shift (TTS), is characterized by an increase in the hearing thresholds at some frequencies immediately following exposure, depending on the frequencies comprising the noise and its intensity. Typically, the hearing loss abruptly reaches a maximum between 3000 and 6000 Hz, followed by a return toward normal hearing at still higher frequencies.
Discerning a noise notch in the pattern of hearing loss may be especially challenging in older adults for whom age-related hearing loss is super-imposed on a preexisting noise notch (see pp. One such approach to objectively define the presence or absence of a noise notch was advocated initially by Coles et al. For example, consider two individuals, A and B, such that A is located 1 meter from a blast and the sound level recorded at that location was 160 dBA.
The damage may initially involve scattered loss of sensory cells, primarily outer hair cells, in the organ of Corti (undamaged sensory cells shown in Figures 2-2 and 2-4, part A). A number of studies have shown that outer hair cells often begin to degenerate during an exposure. For narrow-band stimuli, the maximum cochlear insult is often one-half to one octave higher in frequency than the exposure stimulus (Ward, 1973). Behavioral pure-tone thresholds, although not perfect indicators of the underlying cochlear pathology, represent the best available and most widely used measure of the underlying damage in humans. Thresholds measured in brief intervals during the exposure represent the growth or development of hearing loss, whereas those measured after the exposure is terminated represent the recovery at specific postexposure time intervals. Mills (1976) exposed four chinchillas to a 4-kHz octave-band noise at 80 dB SPL for 90 days and measured thresholds and threshold shifts behaviorally before, during, and for 150 days after the exposure. Given the reliability of clinical threshold measurements and the use of a severity classification scheme based on those measurements, these data provide evidence in humans of the stability of the postexposure hearing thresholds over an extended period of time. For at least 175 years, however, it has been known that one of the hallmarks of noise-induced hearing loss is the wide range of individual differences in hearing loss that can result from seemingly identical noise exposures (Temkin, 1933; Ward, 1965, 1968, 1995). In many of the animal studies, the exposures were exploratory and often not relevant to the occupational setting. Carbon disulfide, for example, is a chemical common in the clothing industry and is often neurotoxic; an interaction between noise exposure and exposure to carbon disulfide has been observed in some human studies (Franks and Morata, 1996).
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Site(s) of lesion include, but are not limited to, frequent obstruction in the external ear canal, interference in eustachian tube function and aeration of the middle ear(s), and endolymphatic hydrops (EH) of the inner ear. Additional significant ear complaints have included vertigo, high- and ultra-high-frequency sensorineural hearing loss greater than expected for the age of the patient, and hyperacusis. The MATPP identified the ear blockage to be obstruction in the external ear canal, interference in eustachian tube function and aeration of the middle ear(s), or SEH of the inner ear. Among the presentations were "Intracranial Pressure Waves and Inner Ear Homeostasis Disorders" by Robert J. This ongoing clinical experience has been the basis for the fluid dynamics vascular theory of brain and inner ear function in traumatic brain injury as a translational hypothesis for the diagnosis and treatment of SIT8. In addition, this article shares with the reader the evolution of a new science of brain pulsatility with application for otologic and neurotologic complaints of hearing loss, tinnitus, ear blockage, and vertigo, which complements conventional medical teaching focusing on brain pulsation, absolute ICP, and brain disease. Headache, chronic fatigue, "brain fog," tinnitus, visual obscurations, dizziness, and sometimes hearing loss are the principle symptoms of IIH.
The most common etiology was benign intracranial hypertension syndrome (pseudotumor cerebri).
The question of whether papilledema in the eye, and inner-ear complaints, including ear blockage, hearing loss, and vertigo, are analogous manifestations of an elevated ICP is not new. Identification and treatment of this abnormal ICP may improve diagnostic accuracy and treatment for this particular cohort of SIT patients. Positive endolymphatic-perilymphatic pressure gradients are secondary to and not the primary cause of hydrops formation. Experiments in the cat have demonstrated that labyrinthine pressure mirrors that of the cerebrospinal fluid (CSF) and that no change in labyrinthine pressure can be measured if the cochlear and vestibular aqueducts are sealed21,22. Though the displacements are very small, they cause a large endocochlear potential change (> 20 mV)24.
Reissner's membrane was visualized by confocal microscope in an isolated temporal bone of a guinea pig.
Cochlear aqueduct patency is known to be reduced with increasing age, falling to 50% in subjects older than 40 years and 30% in those older than 60. In brain, a pressure volume curve has been described based on the exponential pressure - volume relationship in the cranium. These normative data also demonstrate large intersubject differences; nevertheless, the correlation of test results within one individual is high. The TMD displacements are intra-aural waves of different morphologic types, measured in nanoliters and in milliseconds of time, reflective of the pulsatility in brain.
In most people, a fluid connection exists between the intracranial fluid and the fluids of the inner ear.
Increased ICP results in increased perilymphatic pressure, outward resting position of the stapes footplate, and inward movement of the tympanic membrane on reflex contraction of the stapedial muscle.
Exclusion patient criteria included all clinical types of tinnitus not classified as SIT, obstruction in the external ear canal, active middle-ear or inner-ear disease, and pregnancy.
The tinnitus evaluation included pure-tone air and bone conduction, 250- to 8000-Hz speech audiometry, tympanometry, and ultra-high-frequency audiometry. All patients were males aged 30-72 years who were resistant to conventional attempts for tinnitus relief with instrumentation or medication, and all were hypothesized to have a possible increased ICP based on associated clinical complaints and findings.
Immitance testing with the Grason Stadler Portable Handheld Tympanometer (Grason Stadler Eden Prairie, MN) revealed normal type A tympanograms. The tests were performed with the CCFP Analyser to obtain recordings of the waveforms of spontaneous displacement of the tympanic membrane accompanying testing in three positions - supine, 30-degree, and 45-degree - and reverse. Tinnitus summary, group 1: Tympanic membrane displacement (TMD) in a cohort of patients with nonpulsatile, predominantly central-type severe disabling subjective idiopathic tinnitus. Tinnitus summary, group 2: Tympanic membrane displacement (TMD) in a cohort of patients with nonpulsatile, predominantly central-type severe disabling subjective idiopathic tinnitus. Eight fell into the B and D waveform categories (abnormal IPPA and reduced CC), whereas two fell into the A and D waveform categories (normal IPPA and reduced CC).
This objective improvement correlated with a reported subjective reduction in SIT intensity, which continued with fluctuation until March 2012. The SIT relief is reflective of fluctuation in the ICP and the multifactorial conditions influencing brain pulsatility. This preliminary report of the clinical application of the TMDT for identifying an abnormal IPPA ICP in a particular cohort of SIT patients is considered to have accomplished the goals of the project. IPPA ICP with TMDT Spontaneous recordings of abnormal IPPA ICP were identified with the TMDT in groups 1 and 2 for a preselected SIT population suspected clinically of having an abnormal ICP.
Direct and or indirect measurements of the ICP are considered to be relative, not absolute, values. Both ICP and compliance may be factors influencing the clinical course of SIT in a preselected cohort of affected patients: Identification and treatment of these factors may influence the associated complaints cited previously and also may influence the clinical course in this particular cohort of SIT patients. The test-retest reliability of the TMD was positive, as demonstrated by the repeated TMD results recorded in both group 1 and 2 patients (see Figures 3,4).
The clinical significance to the patient of restoring the ICP from abnormal to normal for tinnitus relief was positive for the interval of TMDT testing reported at this time. A patent cochlear aqueduct or an alternative intracranial-labyrinthine fluid communication route is required for ICP and compliance assessment.
Introduction of the TMD is but one of a number of approaches for external identification of the ICP. Its clinical translation for tinnitus relief awaits larger clinical trials and outcome determinations that differentiate for SIT between control of the ICP and IIH and patients' report of tinnitus relief. Auditory function was studied in 25 patients with IIH and supratentorial tumors, the majority of whom had hearing loss. The conclusion was that TMDT was a valuable addition to the armamentarium of neurotologists and useful in identifying IIH in cases of pulsating tinnitus44. The etiology of the IIH is presumed to be cerebrovascular arterial hypertensive disease, not venous disease, based on the clinical history of this patient cohort.The pathophysiology is incomplete but we hypothesize that the disease features in this cohort reflect fluctuation in IIH, which is in turn reflective of alterations in the intracranial cardiovascular and respiratory wave pulsations. Transmission of the CSF increased intracranial cardiovascular and respiratory wave pulsations primarily via the cochlear aqueduct affects the perilymphatic compartment of the cochlear labyrinth24,25. Briefly, fluctuation in cardiac output has two effects on intracranial dynamics - temporal changes on pressure and flow.
Cerebral blood flow is determined by multiple factors including blood viscosity, degree of dilatation of blood vessels, and cerebral perfusion pressure. This hypothesis states that the cranial compartment is incompressible, and the volume inside the cranium is a fixed volume. Clinically, it can be considered to be the elasticity or rigidity of contents, fluid and solid, in a given space. A high compliance of Reissner's membrane seems to be the cause of this endolymphatic - perilymphatic pressure equalization. The significance of CC is demonstrated in the serial recordings of the TMD in the case report (see Figure 5). In our ongoing clinical neurotologic experience for SIT since 1972, and with a focus on SIT since 1979, the occurrence of SEH has been reported to be significant, and this diagnosis has been found to influence the clinical course of SIT and associated complaints of hearing5,47. Is what is diagnosed as SEH, a particular type of EH, a clinical reflection of increased IPPA and IIH? Specifically, the primary etiology for a particular type of EH may be cardiovascular and the clinical marker may be the increased IPPA and IIH. This view of pressure - volume alterations in brain, manifested by an increased IPPA and IIH, is considered to be supported by current thinking for hearing loss and Meniere's disease. The underlying endolymph volume change may result from a change in transport (such as if the endolymphatic sac switches from secreting fluid to resorbing fluid) so that endolymph volume declines with time without a membrane rupture taking place. A physical force, IPPA ICP, was correlated with the behavioral response to the SIT sensation with the TMDT. Abnormal IPPA was accompanied by reduced CC in 8 of the12 patients, whereas normal IPPA was accompanied by reduced CC in 2 patients, and results were incomplete for the other 2 patients.
The clinical significance of these preliminary TMDT results for overall tinnitus treatment is to be established over the long term. The correlation of treatment efficacy for ICP control and reported subjective tinnitus relief is considered to be separate and individual for each SIT patient. Assistant Clinical Professor, Department of Otolaryngology, SUNY - Downstate Medical Center, and Director of Audiology, Martha Entenmann Tinnitus Research Center, Inc., Brooklyn, NY. Consultant Clinical Scientist, Neurological Physics Group, Medical Physics, University Hospital Southampton, NHS Foundation Trust, UK. PhD, is managing director of Marchbanks Measurement Systems Ltd., a spinoff company from Southampton University that supports research with the Tympanic Membrane Displacement Analyzer. People with tinnitus hear a sound that is not related to any sound source outside the body. Psychoacoustic characterization of the tinnitus spectrum: Implications for the underlying mechanisms of tinnitus.
Residual inhibition functions in relation to tinnitus spectra and auditory threshold shift. Residual inhibition functions overlap tinnitus spectra and the region of auditory threshold shift.
Other cases may be related to exposure to very loud or destructive levels of noise, such as from an explosion, industrial equipment or farming equipment. Others have found associations between increased activity in further brain regions, age of tinnitus onset and distress caused by the syndrome. However, treating this deficiency had no significant effects on the complaint in these patients. Other new and emerging treatments for tinnitus focus on the potential indicated by the studies into its links with abnormal brain activity, as mentioned earlier. Due to the irreperability of morbus meniere even here the brain is considered to be responsible. Because this laser was a pulsed laser in a frequenz from 10 to 1500 hertz there was the real applied energy very small.
Instead of six minutes per week MD Wilden applies 30 minutes five times a week, which adds up to 150 minutes for each ear, which is 25 times as much as in the study. If hearing loss is experienced in the same frequency range as the tinnitus, the logic goes, often restoring hearing within that range of sound can help to mask the tinnitus. As an introductory offer, we are offering $500 off a pair of these revolutionary new devices through the month of February! The effects of noise on hearing thresholds are reviewed next, followed by a review of the time course for the development of hearing loss from noise exposure. Movement of the basilar membrane and organ of Corti relative to the tectorial membrane deflects the stereocilia and opens ion channels in the hair cells. This is the A-duration and is less than 1 millisecond (msec) for handguns and several msec for large cannons.
Since simple conversions among these various metrics are not possible, the committee chose to report sound levels using the specific metric employed in the studies reviewed. However, above these peak sound pressure levels, the auditory system is damaged primarily by the large displacements caused by high peak levels.
This accelerated growth of hearing loss with increase in peak sound pressure level above the critical level is one of the factors that make high-level impulse and impact noise particularly dangerous (Henderson and Hamernik, 1986).
Error bars at 250 and 8000 Hz represent ±1 standard deviation and were the only standard deviations reported by the authors of this study for the average pure-tone thresholds at individual frequencies. Knowledge of values for each of these four parameters is necessary, but not sufficient, to fully assess the hazard of a given exposure to hearing. When a portion of the organ of Corti ruptures, it does not reattach to the basilar membrane. Permanent noise-induced hearing loss may also result in damage to or destruction of other important structures in the cochlea, including fibrocytes in the spiral ligament and limbus and cells of the stria vascularis (Liberman and Mulroy, 1982; Hirose and Liberman, 2003) (Figure 2-2). Additional outer hair cells, as well as inner hair cells and various supporting cells, may degenerate for days to a few weeks following termination of the exposure. For humans, the research conducted on the growth and recovery of hearing loss associated with noise exposure has primarily used changes in behavioral measures of hearing threshold, either TTS or PTS. Rather, the emphasis in this section is placed on their conclusions and recent findings (since 1990) that serve to supplement these earlier reviews.
In addition, in the human studies, details of the exposures to noise and other agents were not always available, especially for an individual subject. Styrene, which is widely used in manufacturing and in the chemical and petroleum industries, is another organic solvent whose effects have been shown in animal studies to combine synergistically with noise (Morata and Campo, 2001).
For the subjective idiopathic tinnitus patient, the evaluation of a persistent subjective complaint of EB, in the absence of a site of lesion in these frequent locations, has been hypothesized since 1979 to reflect a fluctuation or elevation of intracranial pressure (ICP)1-3. The blockage persisted in the SIT ear following control of the clinically identified site of lesion of the blockage.
Marchbanks and "Meniere's Disease, Secondary Endolymphatic Hydrops, and Tinnitus" by Abraham Shulman. Identification and treatment or control of ICP may be a factor influencing the clinical course, in general, of all clinical types of tinnitus and, in particular, of this cohort of SIT patients. A case report will demonstrate the result of translation of an elevated ICP for tinnitus treatment on the clinical course of the SIT patient. Animal and human results of identification of ICP with an external probe device in the ear canal, recording tympanic membrane displacement, reflective of the IPPA and its modulation by respiration, may be translated for this subgroup of SIT patients.
Sismanis14,15 noted that "pulsations of the cerebrospinal fluid, mainly originating from the circle of Willis, are transmitted to the exposed medial aspect of the venous sinuses (transverse and sigmoid), resulting in periodic compression to their walls. An excellent summary of past efforts since 1924 both in animal and humans concluded that alterations in ICP can explain some inner-ear complaints including hearing loss, tinnitus, and vertigo. The cochlear aqueduct is the main fluid communication route between the intracranial and perilymphatic fluids; it runs from the subarachnoid space and enters the cochlea in a niche just near the round window17-19. In experimental EH, deterioration of auditory thresholds was partially correlated to the presence of positive endolymphatic-perilymphatic pressure gradients. Acute EH was generated by exposure of the guinea pig ear to nontraumatic low-frequency tone25.
The function of the organ was followed by measuring its physiologic response after applying static pressure and repeated tone bursts of more than 80 dB26. From this, it is concluded that the TMDT gives the optimum results when testing for pressure changes within the same individual, such as changes that may occur with symptoms or treatment30,31. A trial of ICP measurement from the external auditory canal concluded that intra-aural pressure waves clearly reflect intracranial changes in humans, thus proving Marchbanks's hypothesis33.
The cardiovascular component is the predominant waveform, modulated by the respiratory component.
The MMS-11 CCFP Analyser is used to provide an indirect measure of baseline (static) cerebral and cochlear pressures by the detection of low-frequency pressure waves that are emitted from the ear, a component of which is of intracranial origin. Clinically, increased ICP reflects intracranial hypertension, whereas low pressure reflects intracranial hypotension. Reduced ICP results in an inward resting position of the stapes footplate and outward displacement of the tympanic membrane on muscle contraction.17 Measurements appear to reflect cerebral autoregulation in some cases. Vestibular caloric and sinusoidal harmonic rotary-chair testing was performed on all SIT patients.
Magnetic resonance imaging of brain with contrast reported no significant CNS pathology, with only occasional white matter changes, in 10 of the 12 subjects in this study.
The tinnitus evaluation identified SIT, masking curve type 4; and an abnormal result on QEEG.
The TMDT at that time demonstrated an abnormal ICP as measured by an increased IPPA amplitude and normal modulation by respiration, with a reduction in compliance, which correlated with a reduction in the subjective SIT relief reported in March 2012. The addition of the clinically associated complaints reported by this special cohort of SIT patients into the MATPP may be the basis for a clinical protocol for identifying abnormal ICP and the diagnosis of IIH.
Specifically, the concept of compliance and the TMDT results in SIT patients with abnormal ICP and reduced compliance, normal ICP with reduced compliance and, possibly, abnormal ICP with normal compliance may supplement classical clinical thinking about the medical significance of a CNS complaint, to be based not only on the absolute value of the ICP but on the relative value of ICP and compliance, a mathematical approximation based on observed data, for brain disease diagnosis and treatment.
These claims are supported by a recent article that concluded that the pulsatility of the ICP may be more relevant than static ICP in the diagnostic setting for patients with IIH38. The spontaneous, not the evoked, mode of elicitation of intraaural pressure waves is recommended for TMD testing in SIT patients, specifically to avoid a potential increase in tinnitus intensity that may accompany the audiological threshold recommended for eliciting the acoustic reflex in the evoked mode of the TMD.
However, our clinical experience with SIT is the basis for recommending interval examination, including repeat TMD testing, to establish the clinical significance of ICP identification and treatment for long-term tinnitus relief and the diagnosis of IIH. Long-term follow-up is recommended in a large specific cohort of SIT patients to establish the incidence of abnormal ICP and IIH and the medical significance of such findings for long-term tinnitus relief.
Transmission of CSF to perilymph was hypothesized to be via the cochlear aqueduct and was the etiology of the hearing loss41. Intracranial subarachnoid CSF pressure transmission onto the endolymphatic sac results in an initial increased pressure into the endolymphatic duct, which, over time, results in EH and SEH.
Specifically, pressure pulses are not dependent on location and can be measured anywhere within the cranium, whereas flow pulsations are highly dependent on location of measurement. The cerebral blood flow is equal to the cerebral perfusion pressure divided by the cerebrovascular resistance45.
The cranium and its constituents (blood, CSF, and brain tissue) create a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another44.
Graphically, the compliance of a system is inverse to the slope of the pressure - volume curve. In experimental EH, endolymphatic pressure is higher (> 100 Pa) than perilymphatic pressure. Specifically, a reduction in CC with a normal IPPA ICP preceded an increase in IPPA ICP and a reported subjective reduction in tinnitus relief. Is the primary origin and pathophysiology of the otologic histopathophysiologic correlate of EH the brain and not the ear? The result via pressure on the endolymphatic sac influences volume, pressure, and compliance changes in the endolymphatic duct, which, over time, results in extension and distention of Reissner's membrane into the scala vestibuli. Specifically, "endolymphatic hydrops may initially not be pathologic, and the symptoms arising from hydrops may be mild or negligible, but . In the normal cochlea, the rate of longitudinal endolymph flow is extremely low, so that flow does not make a significant contribution to the homeostasis of ions in endolymph.
This application involved recording and demonstrating with single and serial spontaneous recordings an abnormality of the intraaural pulse pressure waves and fluctuation in the ICP, supportive for the presumption of IIH.
Fluid dynamics vascular theory of brain and inner-ear function in traumatic brain injury: A translational hypothesis for diagnosis and treatment. Inflammatory disease and trauma involving middle ear and inner ear: Central nervous system disease and cerebrovascular disease. The search for idiopathic intracranial hypertension: An investigation of cerebral to cochlear pressure transfer as a direct cause of reversible and irreversible audiological disorders. Otologic manifestations of benign intracranial hypertension syndrome: Diagnosis and management. Cochlear and cerebrospinal fluid pressure: Their interrelationships and control mechanisms. Hydrostatic pressure in the inner ear fluid compartments and its effects on inner ear pressure. A trial of intracranial pressure measurement from external auditory canalexperimental analysis. Longitudinal endolymph movements and endocochlear potential changes induced by stimulation at infrasonic frequencies. Acute endolymphatic hydrops generated by exposure of the ear to non-traumatic low frequency tone. Compartmental analysis of compliance and outflow resistance of the cerebrospinal fluid system. Tympanic membrane displacement test in regular assessment in eight children with shunted hydrocephalus. Non-invasive perilymphatic pressure measurement in normal hearing subjects using the MMS- 10 Tympanic Membrane Displacement Analyser. A trial of intracranial pressure measurement from external auditory canal - clinical analysis. Applications of the Marchbanks transcranial-cerebral sonography technique in neurootology: Preliminary report. Brain and inner-ear fluid homeostasis, cochleovestibular-type tinnitus, and secondary endolymphatic hydrops. Tinnitus may have a significant negative impact on the life quality of those affected by it. Different research groups have concluded that chronic tinnitus may be associated with an impaired connection between the cerebral cortex, which controls advanced functions such as memory, perception of the environment and cognition, and the thalamus, which supplies the cortex with sensory information.
A recent study, including 974 patients, indicated that hearing aids were preferable and more effective in treating blast-related tinnitus compared to noise generators.


Presuming further research confirms the findings of these studies, deep brain stimulation (a form of implant placed in the brain to correct this activity) may be a viable option for severe treatment-resistant tinnitus. There is a question that remains unanswered by scholastic medicine: What happens to the inner ear when the brain starts to take over the creation of sounds. In this case, though, the equilibrium organ in the inner ear is accepted so be the signaler of the error impulse and in severe cases destroyed by antibiotics.
Alternatively, some patients have found a measure of relief in sound-masking devices that attempt to conceal the tinnitus with low-volume background noise. Next, exogenous and endogenous risk factors that may alter an individual’s susceptibility to noise-induced hearing loss are reviewed. The nerve fibers that terminate on the hair cell bases are extensions of the auditory neurons. Channel opening depolarizes the hair cells so they release a neurotransmitter from their bases.
For impact noise, the two principal descriptors are the highest peak in a series of successive peaks (reverberations) and the so-called B-duration, the duration from the highest peak level to a point in time when the reverberations have decayed either 10 or 20 dB. It is a clinical hallmark often used to distinguish noise-related high-frequency hearing loss from that associated with other etiologies, such as ototoxic medications or aging. The dashed line connecting thresholds at 1000 and 8000 Hz provides a visual representation of the Notch Index (NI) metric. A graphic demonstration is provided by drawing a line to connect the hearing thresholds at 1000 and 8000 Hz, as illustrated by the dashed line in Figure 2-3.
Although there can be some variation in the audiometric pattern of hearing loss for pure-tone thresholds following exposure to noise, the hallmark of noise-induced hearing loss is a characteristic noise notch in the audiogram that typically occurs between 3000 and 6000 Hz. Assuming that the blast can be modeled as a point source in a free field, the sound level at the location occupied by B will be 130 dBA.
In humans and other mammals, outer hair cells are usually the first type of sensory cell to be damaged or destroyed by excessive noise (Bredberg, 1968; McGill and Schuknecht, 1976) (Figure 2-4, part B). Furthermore, these differences in location of the greatest cochlear damage are accurately reflected in the pattern of hearing loss.
Threshold shifts of about 30 dB may require 3–6 days for the temporary component of the threshold shift to disappear.
After termination of the exposure, thresholds recovered to a 30-dB shift over 8 days, reached a plateau, and then recovered another 10 dB between 60 and 150 days. Similar findings (4 percent classified as having worse hearing at follow-up) were reported by Melinek et al. Although the definitive studies to address this issue have not been performed, based on the anatomical and physiological data available on the recovery process following noise exposure, it is unlikely that such delayed effects occur.
When noise, diuretics, or aminoglycosides (common antibiotics, such as gentamicin) are used in combination, for example, synergistic interactions occur such that the hearing loss from the combination of agents is greater than the hearing loss from either agent alone. Overall, results from animal studies generally suggest that although exposure to noise and solvents individually may be at safe levels, simultaneous or successive exposures to both may increase susceptibility to noise-induced hearing loss. An increased risk of hearing loss was also observed for aircraft maintenance personnel exposed to jet fuel and noise on an Air Force base (Kaufman et al., 2005). Discussions after our presentations allowed us to share our evolving experiences with SIT and TMDT and to consider the potential role of TMD and brain pulsatility for SIT in general and for SEH specifically.
The result may be increased efficacy for tinnitus relief with existing modalities of instrumentation or medication9-11. The identification and translation for treatment and control of ICP as a manifestation of IIH may influence the clinical course of this patient subgroup.
These periodic compressions convert the laminar blood flow into turbulent flow, resulting in vibrations of the vessel walls and production of pulsatile tinnitus". This same report supported the existence of an "obligatory" interrelationship between ear and ICP16. A change in pressure, however, occurred later than the first deterioration in auditory function. A 3-minute, 200-Hz tone at 115 dB was sufficient to generate an acute EH condition in 29 guinea pigs25. An ear probe inserted into the ear canal of the ear to be tested is connected to the analyzer. In the second operational mode, TMD is spontaneous: That is, baseline ICP is extrapolated based on measurement of the ongoing spontaneous displacement of the tympanic membrane, hypothesized to be reflective of ICP waves principally of cerebral cardiovascular and respiratory origin. These two incomplete TMD recordings were associated with an inability to maintain an adequate seal of the probe in the ear canal.
Abnormal amplitude and modulation were reported in July and September 2007, November 2008, and March 2012, concurrent with subjective reports of elevated intensity of the patient's SIT. The initial manifestation of benign intracranial hypertension syndrome as perilymphatic fistula was presented in three cases40. It is hypothesized that fluctuation in the degree of the abnormal ICP and compartmentalization of the increased pressure effect within the cochlear and vestibular labyrinths of this transmitted pulsation on the underlying sensorineural tissue become clinically manifest in gradually increasing complaints of ear blockage, tinnitus, vertigo, and hearing loss in some SIT patients.
Pressure measurement is usually restricted to the lateral ventricle, cisternum magnum, or brain parenchyma.
The serial recordings with the TMD speculatively provide a monitor for recording of CBA (see Figure 4). With an increase in ICP, the concurrent reduction in intracranial compliance results in an increase in the pulse wave amplitude. These pressure gradients occur only in late stages of hydrops, probably when Reissner's membrane has lost its high compliance after long-standing distension20.
Is the finding with the TMDT at this time in a preselected cohort of SIT patients of an increased IPPA ICP support for consideration that the IPPA and cardiovascular disease may be an etiology for a subgroup of EH, SEH, and Meniere's disease patients? The net effect of both routes of IPPA transmission, in ear as in brain, is a reduction in compliance as the pressure within each compartment is increased, with interference in underlying structure and function and clinical manifestations of hearing loss, tinnitus, vertigo, and ear blockage. However, recent studies in our lab suggest that when endolymph volume is disturbed, longitudinal flows may be induced that play a part in the recovery of normal volume. In: Proceedings of the Fifth International Symposium on Meniere's Disease and Inner Ear Homeostasis Disorders. A typical approach is to have subjects match the percept of an external stimulus to that of the tinnitus. The applied energy in some cases equals even less than one percent of the energy used in a treatment by MD Wilden. This is followed by a discussion of national and international standards that have been developed to estimate the amount of noise-induced hearing loss to be expected from a given noise exposure and to separate the effects of noise from age-related changes in hearing. When the fibers of the cochlear nerve are stimulated by the sensory cells, auditory information is transmitted to the brain. The nerve fibers conduct auditory information to the brain when the hair cells release neurotransmitter. The actual critical level is dependent on the specific waveform of the impulse and impact noise (Henderson and Hamernik, 1986). In these cases, postexposure improvement of thresholds may continue for 30 days or longer, but in general, thresholds will not return to preexposure values.
Having thresholds between 1000 and 8000 Hz (especially those at 2000, 3000, and 4000 Hz) that fall at or below the dashed line is thought to indicate the presence of a high-frequency notch in the hearing loss. As noted, the hearing loss associated with acoustic trauma often is severe and spans a wide range of frequencies, much broader than that represented by the high-frequency, noise-notch pattern of hearing loss associated with other types of noise exposures. Whereas A may experience acoustic trauma from such a blast, including the development of a severe hearing loss affecting a wide range of frequencies, this will be much less likely for B, who might, through repeated such exposures over time, develop the more common noise-notch pattern of hearing loss.
Phalangeal scars, formed from supporting-cell processes, replace missing hair cells, and squamous epithelial scars, formed from supporting cells on the basilar membrane, replace degenerated portions of the organ of Corti. For example, the noise-notch pattern of hearing loss (Figure 2-3) is associated with underlying damage to the sensory cells in the basal portion of the cochlea; that is, the portion of the cochlea tuned to those frequencies.
On this basis, it was assumed that if an individual completely recovered from a TTS, the inner ear had not sustained permanent structural damage. The animals were no longer exposed to noise and thresholds were assessed again at age 36 months, which is near the end of the gerbil’s life. In some cases, such as exposures to solvents or use of aminoglycoside antibiotics, the exogenous factors not only interact with noise exposure but also produce hearing loss themselves. However, inconsistencies in results of animal studies have been observed, and the extent of the interaction is highly species-specific.
However, taken together, results of human studies are equivocal, and the design of these occupational studies is often confounded by a lack of control groups and poor quantification of the exposures. In this cohort of SIT patients, the ear blockage persisted after treatment of SEH in the SIT ear. Therefore, positive endoperilymphatic pressure gradients may contribute to, but are not the only cause of, hearing impairment".
Diaphragm movements in the sensor attached to the probe track tympanic membrane movements to record the tympanic membrane displacement, which is recorded as a volume displacement and is reflective of the ICP. Raw-data analysis of the intracranial waveforms has been supplemented by systems analysis, all of which is providing clinical markers of disease in brain and fluid dynamic relationships with eye and ear, thereby improving the accuracy of diagnosis of the complaint and its site of lesion. An update of this initial experience and its translation for treatment of both perilymphatic fistula and EH was reported in ten cases43. This hypothesis is supported by the evidence of animal and human studies previously cited in this article. Flow measurement varies with magnitude and pulsatility of the flow, the type of fluid, and the location. The measurement of the compliance is not direct but rather indirect extrapolation of the ratio of volume change to pressure change. These flows may be directed toward the cochlear apex (when endolymph volume is reduced) or toward the cochlear base (when endolymph volume is increased). For example, the amplitude and frequency of a tone can be varied such that its percept matches the tinnitus.
This syndrome may also have deleterious effects on the emotional, psychological and functional status of the patient.
The distinction between impulse and impact noise becomes blurred in many real-life situations because impulse noise can reflect off the ground, or other surfaces, and the reflections add to the initial impulse noise, creating a large, more complicated waveform that is best described using the B-duration (Hamernik and Hsueh, 1991).
Exposure to impulse noise can result in acoustic trauma from a limited number of exposures, including a single exposure, but can also result in conventional noise-induced hearing loss from extended periods of exposure to impulse noise over many weeks, months, or years. Based on across-species comparisons from chinchillas to humans, the critical levels for humans are likely to be approximately 10 dB higher than those observed in chinchillas.
Dobie and Rabinowitz (2002) describe a corresponding metric, referred to as the notch index (NI), that is simply the mean of the hearing thresholds at 1000 and 8000 Hz subtracted from the mean of the hearing thresholds at 2000, 3000, and 4000 Hz. Importantly, individuals A and B may each subsequently report having heard a loud blast in a case history, but the hazard to hearing will be much greater for individual A, who is closer to the blast.
However, because the inner ears of these individuals were not examined microscopically, the occurrence of permanent structural damage could not be ruled out. During the period from 18 to 36 months of age, hearing losses of 0–50 dB can occur in gerbils that are non-noise exposed at a young age and reared entirely in a quiet environment. With these caveats in mind, we proceed to a review of evidence on the effects of certain exogenous and endogenous factors on the amount of noise-induced hearing loss measured following noise exposure. Some of the inconsistencies may relate to differences in the sites of damage of the ototoxins and their mode of transmission. Typically, the hearing of a group of unexposed workers is compared to the hearing of groups of workers exposed to noise only, to solvent only, and to both noise and solvent. Notable additional associated complaints are head pressure, headache, and cognitive complaint(s) of interference in memory and speech expression - in short, a combination of ear and brain function complaints. In agreement with accepted CSF mechanics, these pressure waves are seen to increase in amplitude as the mechanical compliance of the CSF system declines with increasing ICP. The 2007 to 2012 TMDT recordings demonstrated (1) normal amplitude of the cardiovascular pressure wave (IPPA) with abnormal modulation by respiration and reduced CC in October 2007 and (2) fluctuation of CC (reduced and abnormal in October 2007 and August 2008, normal in November 2007, and abnormal in March 2012). The TMD measurement of the cardiovascular and respiratory intracranial pulsations is predominantly that of the subarachnoid compartment of the intracranial CSF system37. The conditions under which flows can be induced and the role they play in volume regulation are presently being studied. However, because of the high risk of hearing loss from high-level impulses and the variability in subsequent noise-induced hearing loss, a more conservative criterion of 140 dB SPL has been adopted for humans. Values of NI greater than 0 dB are thought to indicate the presence of a notch, whereas those less than 0 dB do not. Observations from Operation Iraqi Freedom suggest that even when personnel are close enough to suffer a blast injury that results in medical evacuation, four out of ten such individuals escape without permanent hearing loss, although many do experience acoustic trauma resulting in a severe or profound hearing loss (Chandler, 2005). The pattern of hearing loss measured following noise exposure provides valuable information about the extent and severity of the underlying damage, especially in the middle and high frequencies following exposures to broad-band sounds. For example, the damaging effects of noise affect primarily the inner ear and occur via acoustic transmission, whereas chemical exposures may reach the inner ear and the central nervous system by being inhaled or absorbed through the skin and circulated through the bloodstream. In this cohort of SIT patients, in whom the complaint of ear blockage is marked, experience has been limited with, or patients have proven resistant to, attempts at tinnitus relief with medication and instrumentation targeting conditions in ear or brain identified with the MATPP to influence the clinical course of SIT.
Types 2 and 3 are intra-aural pressure waves that are associated with respiration; in type 3, the amplitude of the cardiovascular pulse varies with the phase of the respiration. Significant is the compartmentalization already in place in the anatomic distribution of the fluid systems of the inner ear. A concept has been proposed that a disturbance of the resorption system in the endolymphatic sac would cause a "backing-up and an accumulation of endolymph, resulting in the development of hydrops""49.
For the hearing thresholds displayed in Figure 2-3, the notch index is 12 dB and is consistent with poorer hearing thresholds at 2000–4000 Hz than at 1000 and 8000 Hz. Although it is likely that the same phenomenon is true for humans, there is insufficient evidence to support this generalization.
Moreover, noise and chemical exposure records for individual study participants often are not available. The type 4 intra-aural pressure wave has been named the M wave, is of unknown origin, and was not demonstrated at this time. Using chinchillas, administration of cisplatin during noise exposure resulted in greater hearing loss and hair cell loss than occurred for either agent alone, but the interaction was dependent on the noise level. Therefore, exposures must be estimated from area surveys rather than from dosimetry or biological monitoring. Measurement of the IPPA of the cardiovascular component is the objective measurement of the ICP and perilymphatic cochlear pressure. The simplicity of the notch index and similar metrics is appealing, although additional research is needed to establish its reliability, as well as sensitivity and specificity in the identification of noise-induced hearing loss in the general population. Clearly, the noise exposed animals in this study did not have unusual changes in hearing levels that were manifested long after the noise exposure was terminated.
Nonoccupational noise exposures are also difficult to estimate and control for in analyses. Other than this study, however, there are no other data from studies of laboratory animals in which hearing thresholds were measured throughout the animals’ life spans after recovery appeared to be complete. Thus, the percept of a particular matched tone may be quite different to the subject with tinnitus from that of a normal hearing investigator wanting to interpret the pitch and loudness of the matched tone.A relatively new method to identify the characteristics of tinnitus is the tinnitus spectrum test.
This procedure results in a plot of likeliness versus frequency, which is termed the tinnitus spectrum.
The shape of the tinnitus spectrum displays a remarkable resemblance to the tone audiogram: Stimuli with frequencies for which a hearing loss exists display a larger likeliness than stimuli for which the hearing threshold is (near) normal.
This suggests that the spectral content of the tinnitus resembles that of the hearing loss.Although the similarity of the tinnitus spectrum and the tone audiogram is of great interest, it appears to limit the clinical applicability of the tinnitus spectrum measurement. If the spectrum and the audiogram are similar in shape, it could be argued that the spectrum can be predicted from the audiogram or vice versa. This prompted us to make a detailed study of the correspondence between spectrum and audiogram.
If the correspondence is very tight, it must be concluded that the spectrum has no additional value for diagnostic purposes.
However, if in a subclass of patients, the spectrum and audiogram are dissimilar, the spectrum appears to provide additional information that could not have been revealed with the audiogram alone.
Then, the spectrum has an added value.In this paper, we confirm that the tinnitus spectrum has a shape that is similar to the tone audiogram.
However, in an initial evaluation of our data, we noted a remarkable subdivision in cases of high-frequency hearing loss: In some patients, the stimuli with the highest frequency were judged to be less similar to the tinnitus than lower-frequency stimuli.
This suggests that the tinnitus spectrum contains information that is not present in the tone audiogram. We decided to group our patients based on characteristics of the tinnitus spectrum, to evaluate whether the differences between the spectra reflected any other patient characteristics. The tinnitus lateralization was right-sided in 32 subjects, left-sided in 22 subjects and bilateral or central in 26 subjects. All subjects underwent standard tone-audiometry at the octave frequencies from 250 Hz to 8000 Hz and an assessment of the tinnitus spectrum as part of a clinical protocol.
The protocol also included the Tinnitus Handicap Inventory (THI) [5] and the Hospital Anxiety and Depression Scale (HADS) questionnaires. All acoustic stimuli were generated on a Tucker-Davis 3 system and presented via Telephonics THD49 headphones. The computer screen displayed a user interface that contained instructions and sliders, as relevant during the cause of the test session.
Subjects used a turning knob (Powermate USB multimedia controller, Griffin Technology) to control the sliders on the screen. The measurements were controlled by a custom-built Matlab computer program.During an initial phase of the test, subjects learned to use the turning knob. They were shown that they could control sliders on the computer screen by turning the knob. Furthermore, the knob was used to control the loudness of an acoustic stimulus, in order to familiarize them with the perceptual loudness concept.After the initial training phase, all subsequent stimuli were presented at the tinnitus ear in the case of lateralized tinnitus and at the right ear for non-lateralized tinnitus.
Subjects were first presented with three narrowband stimuli, centered at 3 kHz, and were asked which of the three mostly resembled their tinnitus. The second stimulus was referred to as "ringing," and was similar to "hissing," except that the bandwidth was only 3% of the center frequency.
Subjects could match the loudness of the external stimulus by turning the control knob, and confirmed their choice by pushing the knob. For each frequency, the matching procedure was performed 3 times.Finally, stimuli were presented at the nine frequencies, respectively. At each stimulus frequency, the stimulus was presented three times at the average tinnitus-matched intensity (obtained in the previous step). They could control the position of a slider along the scale by turning the knob, and confirmed their response by pushing the knob.
The boxes have lines at the lower quartile, median, and upper quartile values, whiskers are at the extreme data values (within 1.5 times the interquartile range), outliers are denoted by a "+". We defined a 20-point downward drop between the peak of the tinnitus spectrum and the likeliness at 8 kHz to be a relevant decrease in likeliness.
Group 1 consisted of the individuals where the tinnitus spectrum was a monotonously increasing function of the test frequency. In some cases, there was a small likeliness drop at the higher frequencies, but this drop was smaller than the 20 points threshold value.
In group 2, the tinnitus increased monotonously up to a certain frequency, beyond which there was a drop of at least 20 points in likeliness. These subjects typically had a tinnitus spectrum that decreased with increasing test frequency. Group 1 shows increasing spectra, group 2 has spectra with a distinct peak, group 3 consists of the remaining subjects, often displaying low - frequency tinnitus spectra.
Furthermore, the distribution of tinnitus qualities (tonal, ringing, and hissing) and tinnitus lateralization was not significantly different between the groups. Thus, despite the fact that the tinnitus spectra differed, all these other characteristics were similar across the three groups.[Figure 3] displays the median tinnitus spectra of the three groups. Consistent with the definition of the groups, the spectrum in group 1 is a monotonously increasing function, and in group 2 the spectrum slopes down at higher frequencies. The remaining group 3 displayed a median spectrum that slopes down with increasing frequencies.
In all three groups, the largest median hearing loss was present at high frequencies (>2 kHz). The two groups with a predominantly high-frequency tinnitus spectrum (Groups 1 and 2) had remarkably similar audiograms.
There is a large spread in correlation values, although most subjects show a positive correlation, typically indicating a patient where increasing likeliness corresponds with increasing hearing loss.
Outliers are denoted by a "+"Click here to viewThe relation between the peak of the tinnitus spectrum (the frequency at which the likeliness was largest) and the peak in the audiogram (the frequency of the maximum hearing loss) is shown in [Figure 6]. A negative value indicates that a stimulus at a frequency below that of the largest hearing loss resembled the tinnitus most.
The three subject groups are shown by separate colorsClick here to viewWhen comparing subjects with an absolute peak difference larger than one octave with subjects with a smaller peak difference, the first group had worse hearing thresholds. So, subjects with worse low frequency hearing showed a larger deviation between threshold and tinnitus spectrum. In subjects with a high-frequency tinnitus spectrum (group 1 and 2), the audiogram indicated a high-frequency hearing loss.
This confirms the previous findings by Norena et al, [2] König et al, [7] and Roberts et al. In one group (group 1), the tinnitus likeliness increased with frequency over the entire frequency range. In another group (group 2), there was an optimum frequency (at 5 kHz in the group median tinnitus spectrum, [Figure 3]b), and the likeliness decreased towards higher frequencies. At this point, it is unclear whether group 1 and 2 correspond to two separate tinnitus classes.
The criterion to define group 1 and 2 (a 20-point drop in likeliness) was rather arbitrarily chosen.
However, our analysis emphasizes that in a number of tinnitus patients (group 2) the likeliness clearly decreases toward higher frequencies.These results seem consistent with a recent study by Sereda et al, [8] who showed that in a subgroup of tinnitus patients, the tinnitus pitch is on the edge of the audiogram. Our group 2, with tinnitus at the slope of the audiogram, may correspond to their edge group. One neurophysiological theory of tinnitus [9] predicts that tinnitus will be at the edge of the audiogram. Our results suggest that this neurophysiological model can be applied to a subgroup of tinnitus subjects.
However, the largest group of tinnitus patients [8] (group 1 in this paper) are not consistent with the edge theory. A candidate mechanism to explain the results in this group would be homeostatic plasticity, which has been hypothesized to result in tinnitus within the hearing loss frequency range. In this theory, tinnitus is generated by an increase in spontaneous activity in the auditory centers in the frequency range of the hearing loss, consistent with the finding in group 1 of our study population.Group 3 consisted of patients in which the lower frequencies were primarily present in the tinnitus percept. Interestingly, this group also had a high-frequency hearing loss, although they had an additional loss for the lower frequencies. This group demonstrates that the tinnitus does not always occur near the frequency of maximum hearing loss.
The comparison of the peak values of the spectrum and the audiogram [Figure 6], showed that on average the tinnitus pitch was 2.6 octaves below the maximum hearing loss.
The fact that we found a rather large number of patients (20%) that could not be attributed to group 1 or 2, may reflect the fact that patients were selected from a specialized out-patient tinnitus clinic in a tertiary referral center (in our department).
We speculate that this may have biased our patient population.The partial dissociation between the audiogram and the tinnitus spectrum (in groups 2 and 3) shows that the spectrum technique provides information that could not have been obtained by tone audiometry alone. Therefore, the spectrum measurement may develop into a technique that can differentiate between classes of tinnitus. This may eventually contribute to an effective management of tinnitus, as various classes of tinnitus may require different therapeutic interventions.



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