Hearing loss induced tinnitus symptoms,noise cancelling headphones ear ache r?pido,hearing aids ringing in the ears - Plans On 2016

Tinnitus disturbs lives and negatively affects the quality of life of about 2% of the adult world population. AcknowledgmentsThis study was made possible by the Charite - Universitatsmedizin Berlin Research Funds.
Pure tone audiogram measured on the left and right ear of the male and female tinnitus patients with hearing loss in the upper frequency range.
Tinnitus frequency (A) and tinnitus loudness (B) measured in the right and left ear of the male and female tinnitus patients with hearing loss. Hearing loss measured in the right and left ears of patients with compensated and decompensated tinnitus.
Total TQ scores (A) and scores of the subscale “somatic complaints” (B) measured in patients with left-side, right-side or bilateral tinnitus. We have invented, optimized, and tested in animal experiments a magnetic injection system that can safely deliver therapeutics to the inner and middle ear. The inner ear is behind the blood-labyrinth barrier, thus drugs taken orally or injected systemically do not elute out of inner-ear blood vessels to reach inner ear tissue.
In this talk I will summarize how our magnetic system works, compare it to prior results (e.g. The aim of our study was to outline the prevalence of hyperlipidemia in patients who had high-frequency hearing loss and tinnitus due to noise exposure.
Cochlear hair cells and neural and central auditory pathways are involved in the generation of subjective tinnitus [1]. Decrease in internal diameter of the vascular bed resulting from hyperlipidemia compromises the oxygen transportation capability of the blood to the cochlea, and chronic hypoxia is likely to occur by the reduction in oxygen supply of the inner ear, which in turn would lead to insufficient adjustment of the cochlear metabolism.
This may result in the overproduction and accumulation of free radicals, which disturb the microcirculation of the cochlea and play an important role in ischemiainduced cochlear injury [7]. The reasons for the susceptibility to noise-induced hearing loss of patients who have been exposed to a noisy environment have been the subject of various studies.
Previous data indicate that the cochlea and the central auditory system age faster and earlier in patients with hyperlipidemia and that the risk of noise-induced hearing loss is much higher [5,11].
The aim of this study was to outline the prevalence of hyperlipidemia in patients who had high-frequency hearing loss and tinnitus due to chronic noise exposure and to evaluate the risk of developing sensory hearing loss in those patients as compared to risk in control subjects. We conducted this prospective study in 120 consecutive patients with complaints of chronic subjective tinnitus of varying degrees of severity and hearing loss due to noise exposure. The patients were examined otoscopically and were reviewed by an audiometric test battery including puretone audiometer (AC-30, IAC, Copenhagen, Denmark), stapes reflex, and tympanometry (Amplaid 775, Milan, Italy). Antilipid treatment with statin derivatives was planned once-daily oral dosing for up to 1-2 years (minimum, 12.4 months).
We then compared tinnitus scores and hearing levels in patients with no response to antihyperlipidemic therapy and in patients who had a normal blood cholesterol level after the treatment. The duration of tinnitus in patients with noise exposure varied from 2 months to 12 years (mean, 5.5 years). Of 22 patients in the unresponsive group, 6 had high cholesterol and triglyceride, 9 had high triglyceride, and 7 had high cholesterol only before the antilipidemic therapy. Of 20 patients in the responsive group, 7 had high cholesterol or triglyceride, 10 had high triglyceride, and 3 had high cholesterol only before the antilipidemic therapy. The difference between the pitch-match frequencies before and after therapy was not significant. Epidemiological investigations emphasizing the relationship between hearing loss and the risk factors for coronary artery disease date back to the 1960s [18]. Spencer [19] found that 42.3% of 300 patients with different symptoms of inner-ear pathology had clearly defined hyperlipoproteinemia.
The effect of hyperlipidemia on auditory perception has been studied clinically and experimentally.
The exact pathological mechanism for the hyperlipidemia-induced hearing loss remains obscure. In his study of 64 rats, Pillsbury [37] exposed half to loud noise and fed half of each subgroup a fat diet and found elevated auditory brainstem response thresholds in the hyperlipidemic animals. Studies investigating the restorative possibility of a low-cholesterol diet and antihyperlipidemic therapy on hearing loss and tinnitus are very few. LDL apheresis has been reported to be much more effective as compared with standard prednisolone, dextran, and pentoxifylline therapy in patients with sudden hearing loss [9]. In our study, changes in tinnitus scores before and after therapy in the responsive group were significant as compared with those in the unresponsive group.
Tinnitus and hearing loss are frequently encountered after an acute acoustic and blast trauma or chronic noise exposure.
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International hearing experts at the XXXII World Congress of Audiology in Brisbane are discussing ways to offset a predicted increase in noise-induced hearing loss and tinnitus through increasing recreational and occupational noise exposure.
There are some who suggest that as a response to the prevalent noise, and with new gadgets, more and more people use music from personal players to escape from the environmental noise of the city.
Dr Morata believes the messages hearing health experts should be sending is for people to enjoy music or loud sports events in ways that are safe so their hearing abilities remains healthy. Outside what can be controlled through occupational health and safety regulations, finding ways to reduce the adverse health effects of increasing environmental noise exposure is a real challenge for hearing health experts, they explain.
Of the roughly 40 million Americans suffering from hearing loss, 10 million can be attributed to noise-induced hearing loss (NIHL). A bulldozer that is idling (note that this is idling, not actively bulldozing) is loud enough at 85 dB that it can cause permanent damage after only 1 work day (8 hours). When listening to a personal music system with stock earphones at a maximum volume, the sound generated can reach a level of over 100 dB, loud enough to begin causing permanent damage after just 15 minutes per day!
A clap of thunder from a nearby storm (120 dB) or a gunshot (140-190 dB, depending on weapon), can both cause immediate damage.
Because the damage from noise exposure is usually gradual, a person might not notice or might ignore signs of hearing loss until more pronounced symptoms of permanent hearing loss become evident.
Please review table the table below for more information on Sound, Sound Intensity, and Recommended Exposure Limits. Please refer to each suppressor type for specific barrel length minimums, based on your desired caliber.
The authors thank Nina Zirke and Theresa Morgenstern for collecting the data.ReferencesJastreboff, PJ. In contrast to prior magnetic systems, which can only pull-on (attract) magnetic nanoparticles and so would have to pull through the width of the human head in order to delivery nano-therapy into the middle or inner ear, our system can push (it can magnetically inject). It is thought that drugs delivered intra-tympanically into the middle ear also do not cross the oval window membranes sufficiently to effectively treat inner ear diseases.
Low-Cholesterol Diet and Antilipid Therapy in Managing Tinnitus and Hearing Loss in Patients with Noise-Induced Hearing Loss and Hyperlipidemia. We investigated the role of a low-cholesterol diet and antihyperlipidemic therapy to alleviate the severity of tinnitus and possibly promote hearing gain after therapy in patients with acoustic trauma. Analysis of the epidemiological data indicates that exposure to noise is widespread and is one of the most common causes of tinnitus, which leads to various somatic and psychological disorders and interferes with the quality of life [2]. Auditory perception in such cochleas is very sensitive to reduction of the oxygenation in the inner ear [6]. Platelet aggregation and blood viscosity due to high lipid levels will intensify inner-ear damage owing to slowing of microcirculation and will contribute to the development of both progressive and sudden hearing loss [8,9].
Gratton and Wright [10] demonstrated the accumulation of lipid in the stria vascularis and outer hair cells in chinchillas after experimentally induced hypercholesterolemia, which might intensify the detrimental effect of ototoxic drugs or noise. We instituted a low-cholesterol diet and antihyperlipidemic therapy to investigate whether any benefit accrued in terms of hearing gain and tinnitus relief. The project was approved by the local medical research ethical committee, and we obtained informed consent from each patient. Audiometric tests included air- and boneconduction thresholds for pure tones of 125-8,000 Hz, tests of speech reception and speech discrimination, contralateral and ipsilateral reflex measurements, and tympanometry.
Measurement of loudness of the tinnitus was based on subjective assessment by the patients.
Daily dosage ranged from 10 to 40 mg for simvastatin (Zocor) and from 10 to 80 mg for atorvastatin calcium (Lipitor). Average ages of patients in the unresponsive and the responsive groups were 39 and 42 years, respectively. Wilcoxon and Mann-Whitney U tests were used to compare the pretreatment data with the posttreatment results and to compare the results of responders and nonresponders.
None of these patients demonstrated any drop to normal ranges in cholesterol or triglyceride values after the treatment. When those patients were asked to qualify the severity of their tinnitus, seven rated their tinnitus as the same (35%), two rated it as increased (10%), seven rated it as decreased (35%), and four had no tinnitus (20%).
The correlation between serum lipids and auditory dysfunction has been investigated before, and it has been reported that sensorineural hearing loss is more prominent in those with high levels of cholesterol, triglyceride, and lowLDL and in patients with low HDL concentration [18-23].


Increased blood viscosity and atherosclerosis of the cochlear vessels reduce the blood perfusion of the cochlea and promote hearing impairment [6,8,19,20,23,24]. When patients were required to qualify the severity of their tinnitus, 35% of the patients in the responsive group rated their tinnitus as decreased, and 20% of patients reported no tinnitus. Even though other factors making the patients susceptible to noise-induced hearing loss should be considered, on the basis of present results it can be concluded that the incidence of hyperlipidemia is high among patients with noise-induced hearing loss and that significant improvement in lowered intensity of tinnitus and in average hearing thresholds at higher frequencies can be achieved after lowering patients' serum lipid level [43]. People working before the mid1960s may have been exposed to higher levels of noise where there were no laws mandating use of devices to protect hearing. Le travail intellectuel est intense, la concentration est a son apogee, la memoire est quant a elle fortement sollicitee. A base d'imprimes palmiers, fleurs tropicales et autre toucans colores, la jungle fever fait rage chaque annee ! Morata, PhD (US National Institute for Occupational Safety and Health, from the Centers for Disease Control and Prevention) said our increase in noise exposure is caused by the world undergoing the fastest phase of growth and urbanization in human history. NIHL can be caused by a one-time exposure to loud sound as well as by repeated exposure to sounds at various loudness levels over an extended period of time. It is estimated that as many as 30 million Americans are exposed to potentially harmful sounds at work.
To analyze a possible association of the degree of hearing loss with the severity of tinnitus, we have performed a retrospective study using admission data on 531 patients suffering from chronic tinnitus.
This perception can be induced by various dysfunctions on several levels of the peripheral or central auditory pathway [1].
This allows us to use reasonable (safe, below FDA limits) magnetic fields over a short distance to delivery therapies into the middle or inner ear.
We have shown in preliminary rat experiments that our magnetic push forces can safely drive drug coated nanoparticles through the oval window membranes from the middle into the inner ear (without effecting hearing or causing other measurable side effects). Fortytwo hyperlipidemic patients with subjective tinnitus and hearing loss due to noise exposure were enrolled for the study. It has been reported that high-plasma cholesterol and triglyceride levels are one of the major risk factors for the development of occupational hearing loss [3-5]. It seems that noise and other metabolic disturbances have a synergistic effect on the development of tinnitus and hearing loss [5].
A diagnosis of acoustic trauma was verified by an ear, nose, and throat physician according to a clinical history of chronic noise exposure in patients who sought medical help for complaints of tinnitus and high-frequency hearing loss. Patients who had chronic otitis media or middle-ear effusion, those with an abnormal ear drum (perforation, retraction, etc.) or auditory canal, and those who had abnormal tympanometry (other than type A) were excluded.
In the study, from 120 patients we chose 42 male patients (35%) with elevated cholesterol or triglyceride or both (age range, 19-60 years; mean age, 45 years). The patients were separated into two groups: the "unresponsive" group, made up of 22 patients who had no response to either of the therapies and still had hyperlipidemia, and the "responsive" group, consisting of 20 patients who had lower cholesterol or triglyceride levels. The results of the blood lipid profiles were withheld from the individual to prevent a placebo effect with the tinnitus therapy. The significance of the difference in patient's comments on their tinnitus after the treatment ("same," "decreased," "increased," and "disappeared") was analyzed using McNemar and chi-square tests.
However, the incidence of hyperlipidemia among a selected group of patients with neurosensory hearing loss varies.
They selected a group of subjects aged between 20 and 50 years and compared auditory thresholds at high frequencies and serum lipid levels.
Noise and metabolic disturbances have a synergistic effect on the development of tinnitus and hearing loss. Effects of experimental cochlear thrombosis on oxygenation: Auditory function of the inner ear.
Direct effects of intraperilymphatic reactive oxygen species generation on cochlear function. Clinical utility of LDL-apheresis in the treatment of sudden hearing loss: A prospective, randomized study.
The relation of hearing in the elderly to the presence of cardiovascular disease and cardiovascular risk factors.
Appearance of free radicals in the guinea pig inner ear after noise-induced acoustic trauma. Progressive sensorineural hearing loss, subjective tinnitus and vertigo caused by elevated blood lipids.
A comparison of auditory brainstem evoked potentials in hyperlipidemic and normolipidemic subjects. Exploration of the early auditory effects of hyperlipoproteinemia and diabetes mellitus using otoacoustic emissions.
Hypertension, hyperlipoproteinemia, chronic noise exposure: Is there a synergism in cochlear pathology? Effects of noise exposure and hypercholesterolemia on auditory function in the New Zealand white rabbit.
Hearing improvement after therapy for hyperlipidemia in patients with chronic-phase sudden deafness.
A prospective case-controlled study of 197 men, 50-60 years old, selected at random from a population at risk from hyperlipidemia to examine the relationship between hyperlipidemia and sensorineural hearing loss. Even outside of work, many people participate in recreational activities that can produce harmful noise (musical concerts, use of power tools, etc.). We have found that 83% of our tinnitus patients had a high frequency hearing loss corresponding to a noise-induced hearing loss (NIHL). Regardless of the original cause, all patients complain of hearing a tinnitus tone on either one (unilateral) or both sides (bilateral) of the head or ears. Using steroid-coated nano-particles we have shown therapeutic effect for treatment of acute tinnitus and noise-induced hearing loss.
All patients who were required to complete the questionnaire and who were subjected to clinical examination were military personnel.
A pure-tone signal was presented continuously at 50-Hz intervals at between 10- and 20-dB levels. We placed all these patients on a low-cholesterol diet or antihyperlipidemic therapy (Table 2).
When patients were asked to qualify the severity of their tinnitus, 10 rated their tinnitus as the same (47%), 9 rated it as increased (42%), 2 rated it as decreased (9%), and 1 patient had no tinnitus (2%). Lowry and Isaacson [12] reported 20% hyperlipoproteinemia among 100 patients with bilateral hearing loss. Lipidosis of the inner ear has been postulated by Nguyen and Brownell [33] as an alternate mechanism. Insufficient perfusion of the cochlea due to increased blood viscosity and microthrombosis related to hyperlipidemia has been claimed to cause susceptibility to noiseinduced hearing loss [35]. We found in our study that the incidence of hyperlipidemia among patients with noiseinduced tinnitus and hearing loss was 35%. Characteristics of tinnitus and etiology of associated hearing loss: A study of 123 patients. These cells respond to mechanical sound vibrations by sending an electrical signal to the auditory nerve. Sixty million Americans own firearms, and many people do not use appropriate hearing protection devices. Depending on the case, tinnitus tone may have low, medium or high frequency and be either relatively quiet (0–3 dB), going up to relatively loud (more than 16 dB). We have also demonstrated that magnetic pushing can drive nano-particles through the tympanic membrane, providing a non-invasive alternative to syringe or laser intra-tympanic injection. We excluded on the basis of their response to the questionnaire or clinical examination subjects who had a history of familial hearing loss, head trauma, collagen disease, neurological or hormonal disturbance, addiction to alcohol, or ototoxic drug therapy.
The main criteria for response to the antihyperlipidemic therapy was defined as a return to normal cholesterol or triglyceride levels after therapy or at least a 40% drop from either of the initial blood cholesterol or triglyceride levels if the values were slightly above the normal limits.
The latter authors showed that the lateral wall of outer hair cells from guinea pig cochlea incorporates water-soluble cholesterol. Axelsson and Lindgren [34] matched 78 men at age 50 years with high serum cholesterol levels to 75 randomly selected 50-year-old men and found significant correlation between noise exposure and high cholesterol level.
Different groups of hair cells are responsible for different frequencies (rate of vibrations). Warranty and policies are in the manuals: We suggest you read them to help you avoid costly and potentially fatal mistakes.
Interestingly, patients suffering from decompensated chronic tinnitus had a greater degree of hearing loss than the patients with compensated form of tinnitus.
Tinnitus may take acute (up to 3 months), sub-acute (4–12 months) or a chronic turn (longer than a year).
The difference between tinnitus scores in the unresponsive and responsive groups and the change in tinnitus scores before and after therapy in the responsive group were significant.
None of the patients had cerebrovascular disease, hypertension, electrolyte imbalance, cranial nerve deficit, or clinical signs of peripheral neuropathy. Then, the pitch-match frequency threshold of the tinnitus was measured as the tinnitus loudness match of the pure-tone stimulus presented with a 1-dB increase of tinnitus frequency. Morizono and Paparella [30], using cholesterolfed rabbits, showed increased auditory dysfunction with time at all frequencies. This uptake of cholesterol is accompanied by an increased stiffness of the cells, which may impair the cells' electromotile response.


Enhancement of cochlear action potentials and auditory brainstem responses has been demonstrated after limited intake of cholesterol. However, patients were at the chronic phase, more than 1 month from the onset of the hearing loss. We're pretty easy to get along with but we claim no responsibility for misuse, abuse, or criminal intent of our products or the info on this site. In addition, we demonstrate that the degree of hearing loss positively correlates with the two subscales (“intrusiveness” and “auditory perceptional difficulties”) of the Tinnitus Questionnaire. Regarding the level of disturbance, tinnitus can be classified as compensated (low-level distress) or decompensated (high-level distress) [2]. A modified version of tinnitus retraining therapy: observing long-term outcome and predictors.
It seems that the order of destruction and the high-frequency nature of the auditory dysfunction are correlated not only with the frequency and severity of the noise exposure but with the presence of the secondary pathology, as the formation of vasoactive lipid peroxidation products after intense noise is similar to the condition seen in metabolic damage to the organ of Corti [7,14-17]. In a survey of 44 patients with cochlear-type hearing loss, Booth [26] found hyperlipidemia in 28% of the men and 10% of the women.
These authors observed hearing improvement of more than 10 dB in 9 of the 12 patients after antihyperlipidemic therapy. Our retrospective study provides indirect evidence supporting the hypothesis that the degree of noise-induced hearing loss influences the severity of tinnitus.
The major problem in patients with decompensated tinnitus is sleep interference, because the tinnitus tone keeps the patients awake. In this manner, preventive measures may provide restorative support to the injured cochlea.
We required all patients to rate their tinnitus from 1 to 10, with 10 being loudest (Table 1). If the sound is very quiet, it will not cause damage even if you listen to it for a very long time; however, exposure to some common sounds can cause permanent damage. Other diseases that follow include depression, a variety of phobias, anxiety disorders, problems with concentration and in extreme cases—suicide. Each level was defined by short explanations to simplify the patients' grading of their tinnitus.
With extended exposure, noises that reach a decibel level of 85 can cause permanent damage to the hair cells in the inner ear, leading to hearing loss. Approximately 30 per 100 adults experience tinnitus, whereas about 1–5 persons per 100 suffer from tinnitus and seek medical help [3,4]. In the Western world, tinnitus has a big economic impact [5].The onset of tinnitus can have various basis such as neurologic, traumatic, infectious or drug-related [6], however, the major cause of tinnitus is a hearing loss [5]. Hearing loss is usually caused by the aging process (presbycusis) or by the overexposure to noise (noise-induced hearing loss, NIHL). Occupational noise, together with environmental noise pollution, are two major factors contributing to the NIHL [7]. These, and a lot of other data, strongly indicate coexistence of both hearing dysfunctions.
Based on the above data we put forward a hypothesis that the degree of hearing loss could negatively influence the severity of tinnitus.To test our hypothesis we used a retrospective study using data acquired from 531 tinnitus patients.
This data were randomly collected on the admission of patients who reported to the day ward of Tinnitus Center at the Charite - Universitatsmedizin in Berlin between January 2008 and March 2010. ParticipantsWe have obtained the data from 531 tinnitus patients (sub-acute and chronic) admitted to a 7-day multimodal tinnitus therapy. In addition, tinnitus frequency (kHz) and tinnitus loudness (dB HL) were matched for each patient. Psychometry (Tinnitus Questionnaire)Tinnitus-related distress was assessed using validated standard German version of the tinnitus questionnaire (TQ). Influence of environmental factors on the evolution of industrial noise-induced hearing loss. The TQ is composed of 52 items allocated to six scales: emotional distress, cognitive distress, intrusiveness, auditory perceptual difficulties, sleep disturbances and somatic complaints [12].
The severity level of tinnitus was assigned as “compensated” (low-level distress) with TQ score ? 46 points and “decompensated” (high-level distress) with TQ score > 46 points. Spearman's rank correlation was used to test the statistical relationship between hearing loss and tinnitus parameters or tinnitus severity. Predominant Number of Patients with Chronic Tinnitus Has a Hearing LossOf all 531 tinnitus patients tested, 441 (83%; 220 men and 221 women) had a hearing loss in the upper frequencies (Figure 1), corresponding to a pattern found in the NIHL [13]. Assessing audiological, pathophysiological and psychological variables in tinnitus patients with or without hearing loss.
There were no significant differences in the hearing loss between the left and the right ear and between male and female patients in this group.
The mean age of tinnitus patients with NIHL-like audiogram was 50 years (SD = 13, min 16, max 79), with patients most frequently ranging between 40–60 years of age.
Tinnitus Characteristics in Patients with Hearing LossOf 441 tinnitus patients with NIHL-like audiogram, 319 patients had pure tone tinnitus whereas 122 patients had noise tinnitus. The values did not differ between female and male patients except for the subscale “somatic complaints” with woman having significantly greater scores than the male patients (Table 1).
Of the 441 patients, 335 patients suffered from compensated tinnitus (TQ ? 46 points) and 106 patients suffered from decompensated tinnitus (TQ > 46 points).
3.4 The Degree of Hearing Loss Correlates with Some of the Psychometric Parameters Measured by TQHearing loss was of significantly higher degree in patients with decompensated tinnitus than in patients with compensated tinnitus (Figure 3). This means that tinnitus patients with greater hearing loss experience higher tinnitus-related distress. We found no correlation between tinnitus frequency or loudness and distress caused by tinnitus. Influence of Age on the Psychometric ScoresOur recent study [14] revealed that the age of patients may influence their TQ values. Consequently, in the present study, we have subdivided the patients into three age groups and analyzed their TQ scores as a function of age.
Influence of Tinnitus Lateralization on the Psychometric ScoresWe compared the tinnitus-related distress between the patients with left-sided, right-sided and bilateral tinnitus.
DiscussionOur present work was aimed at analyzing the association between noise, the grade of the noise-induced hearing loss and the severity of tinnitus. Our results partially corroborate the findings of others by demonstrating a strong bond between the noise-induced hearing loss and tinnitus [10]. In fact, we have shown that 83% of patients with chronic and sub-acute forms of tinnitus have a high-frequency hearing loss, which is a substantially higher percentage than the 57% reported by Savastano or the 63% reported by Martines et al. The sample size in all studies was roughly similar, as were the age and gender distribution. However, there was a major difference in the duration of tinnitus between our and the other studies. In the Savastano study, 49% of tinnitus patients had suffered from tinnitus for a time shorter than one year – a group classified as acute and sub-acute tinnitus.
Based on the above evidence, one is tempted to cautiously speculate that the tinnitus associated with hearing loss has a greater chance of chronification than the tinnitus without hearing loss.
In the other study, Attias and colleagues have indentified a subgroup of patients with tinnitus, who were actively looking for a remedy. Our study gives a base for the explanation of how the degree of noise-induced hearing loss indirectly affects the severity of tinnitus by influencing negatively the loudness of tinnitus. In agreement with this, the degree of hearing loss correlated positively with two subscales (“intrusiveness” and “auditory perceptional difficulties”) of the Tinnitus Questionnaire. These particular items of TQ regard the ability to communicate, which is an integral part of the quality of life. With the increased distress of tinnitus, patients withdraw from their normal social life and avoid contacts with others, consistent with the decompensated form of tinnitus. Interestingly, we found that the patients suffering with decompensated tinnitus had a greater degree of hearing loss than the patients with compensated tinnitus.Noise pollution and occupational noise were demonstrated to induce asymmetric hearing loss, with the left side being affected more than the right one [13]. Although our analyses demonstrated no statistically significant differences in the hearing loss between the left and the right sides, we found that left-sided tinnitus is more distressing than the right-sided one.
Moreover, patients with the left-sided tinnitus had more complaints in the somatic subscale than the right-sided tinnitus patients. This could be attributed to neuroanatomic differences between the left and right parts of the auditory system.Noise—either occupational or environmental noise pollution—is a major preventable cause of the hearing loss and therefore of chronic tinnitus.
The consequences of noise exposure last for life, as the sensory auditory epithelium never regenerates. The price to pay for the noise exposure includes not only a limited ability to hear but also increased chance to develop chronic decompensated tinnitus, which separates the affected persons from normal social activities and significantly decreases the quality of life. ConclusionsOur study demonstrates that the chain of events started by overexposure to noise not only induces the hearing loss but also tinnitus with its co-morbidities, finally resulting in a decreased quality of life.



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