Sudden deafness in right ear,cute vintage jewellery uk,ear nose and throat orlando fl - You Shoud Know

Author: admin, 20.04.2014. Category: Severe Tinnitus Symptoms

Unter einem HA¶rsturz versteht man die plA¶tzliche, vollstA¤ndige oder teilweise HA¶rminderung auf einem Ohr, selten auf beiden Ohren. Es gibt eine Reihe mA¶glicher Ursachen von OhrgerA¤uschen (Tinnitus), die Ihrem Hals-Nasen-Ohren-Arzt bestens bekannt sind. Die grA¶AYten Heilungsaussichten haben Sie bei einem a€zfrischena€? Tinnitus a€“ also: Schnell zum Arzt! Wenn der chronische Tinnitus mit einem dauernden HA¶rverlust verbunden ist, sollte eine HA¶rgerA¤teversorgung erfolgen. Beim akuten Tinnitus wird meistens eine DurchblutungsstA¶rung vermutet, weshalb eine rasche Vorstellung beim Arzt wichtig ist.
In der NA¤hrflA?ssigkeit der Sinneszellen steigt der Sauerstoffgehalt um das 4- bis 6fache an und versorgt intensiv das gesamte Innenohr und damit auch Bereiche, die von einer Mangelversorgung betroffen sind.
Rechtzeitiger Behandlungsbeginn nach a€“ aber auch schon wA¤hrend a€“ einer erfolglosen Infusionsbehandlung. Parallele Infusionsbehandlung durch den mitbehandelnden Arzt oder durch das Druckkammerzentrum ist mA¶glich. One of the most confusing and contentious unsolved mysteries in otolaryngology, sudden deafness is a rapid loss of hearing. Most patients have reported onset of hearing loss within minutes to several hours and about one-third of patients will wake with the loss; others may find out the problem on trying to use the telephone, or describing a brief period of fluctuating hearing before the loss.
Auditory nerve damage due to certain drugs such as Gentamycin, streptomycin, chloroquin, etc. Identical experiences like loud noise can cause hearing loss in one person and leave another relatively unaffected. A sulfur-containing fatty acid, an alpha-lipoic acid helps to generate the energy that keeps us alive and working. The study has shown that the groups given the magnesium supplement were not as likely to experience permanent hearing damage as those given a placebo. Vitamin D deficiency has also been associated with otosclerosis (abnormal bone growth in the middle ear), presbycusis, unexplained and bilateral cochlear deafness, and sensorineural hearing loss. Always wear ear protection (disposable plugs or ear­phone-style headset) when using loud appliances for example power tools or lawn mowers; and when you know you will be exposed to sudden loud noises, such as when shooting a gun. Sudden deafness is a disorder characterized by an abrupt sensorineural hearing loss of unknown etiology.
Sudden deafness is defined by a high degree of abrupt sensorineural hearing loss without clear causes for the loss. Eighteen patients who had received MRI examinations were chosen from patients complaining of sudden deafness. Pure-tone audiometry and short-increment sensitivity index tests were conducted on all patients. To summarize, among the 18 subjects, 3 of the 5 patients (17%) with sudden deafness showing abnormal MRI findings had SBF of the VBS, 1 (5%) had an abnormal course of the VBS, and 1 (5%) had labyrinthine enhancement. Sudden deafness refers to abrupt sensorineural hearing loss of unknown etiology, often accompanied by tinnitus and vertigo.
Viral labyrinthitis causes sudden deafness owing to infections caused by such viruses as measles or mumps, and it may occur without any other general symptoms. In the past, MRI was mostly used for the diagnosis of lesions of the internal auditory canal and of the cerebellopontine angle, and particularly for acoustic neuroma in deaf patients [5]. Seltzer and Mark [4] also reported that the MRI results of all five patients experiencing sudden deafness showed Gd-DTPA enhancement of the cochlea and the vestibule.
Besides viral infections, circulation disorders of the inner ear are presumed to be a major cause of sudden deafness. Regarding the relationship between the abnormal findings on MRI and vertigo, our study found that all the cases showing abnormalities on MRI also showed canal paresis. No significant relationship was found between MRI results and the type of audiogram or degree of hearing loss.
Until now, the exact cause of sudden deafness has not been clarified, but abnormal blood flow of the inner ear is known as a cause of this disorder. IMPORTANT: By accessing and using this Website and any of its pages, you are agreeing to our Terms and Conditions of Use. Please read the said terms and conditions by clicking the link shown at the bottom of the screen before proceeding.
Jeanne Oiticica1, Roseli Saraiva Moreira Bittar2, Claudio Campi de Castro3, Signe Grasel4, Larissa Vilela Pereira5, Sandra Lira Bastos5, Alice Carolina Mataruco Ramos5, Roberto Beck5. Introduction: Sudden hearing loss (SHL) is an ENT emergency defined as sensorineural hearing loss (SNHL) > 30 dB HL affecting at least 3 consecutive tonal frequencies, showing a sudden onset, and occurring within 3 days. INTRODUCTIONSudden hearing loss (SHL) is an ENT emergency that was first described in 1944 (1), but remains poorly understood.
Falls der Tinnitus nach 1a€“2 Tagen noch besteht, ist ein Arztbesuch dringend erforderlich. A?ber Heilungsraten oder Besserungsraten existieren sehr unterschiedliche Expertenmeinungen. Es empfiehlt sich, im Wege einer Stufenbehandlung die verschiedenen BehandlungsmA¶glichkeiten einzusetzen. Der Betroffene empfindet manchmal sogar bei alltA¤glichen GerA¤uschen Schmerzen in den Ohren. Diese SchA¤digung kann man leider nicht operieren und TherapiemaAYnahmen sind nur begrenzt wirksam. Der chronische Tinnitus ist aber weder Vorbote eines Herzinfarktes noch eines Schlaganfalles. From the affected individuals, about 10% of have known causes which include infections, circulatory or neurological disorders, trauma, immune disorders or drugs toxic to the ears.
The most widely used treatment is high doses of steroids, and some people recover from SSHL, but not others. Lipoic acid has broad range of antioxidant action and thus giving defense against free radicals. A lower dosage of 20 to 50 mg daily is commonly recommended for use as a general antioxidant.
Magnesium can be taken in a supplement that includes magnesium, calcium and vitamin D for the most benefit, read below. Deficiency of vitamin D is probably one of the reasons and supplementation should be considered in persons with hearing loss as noted by researchers. Keep the volume low enough that you can easily hear the telephone and other sounds over the music. This is particularly important if you have repeated ear infections and have been treated with antibiotics. To determine whether establishing the pathogenesis of this disease is possible, this study analyzed the magnetic resonance imaging (MRI) of early stages of sudden deafness in combination with the clinical results of treatments. Many theories seek to explain the etiology of sudden deafness; however, its exact causes are not specified. If it is not cured at an early stage, deafness can be permanent; thus, an early and accurate diagnosis is essential. They were hospitalized at Pusan National University Hospital from November 2000 to May 2001. The vestibular function test consisted of air-caloric tests, and the results were measured with electronystagmography.
Figure 1 shows the Gd-DTPA-enhanced T1-weighted coronal image of patient 9, who had vertigo and sudden deafness in the left ear; the image reveals increased gadolinium enhancement in the left labyrinth. Gd-DTPA TI-weighted coronal image in left ear of subject with sudden deafness with vertigo.
The patient having an abnormal course of the VBS and the patient having labyrinthine enhancement also showed vertigo and canal paresis.
Schuknecht and Donovan [2] reported that the pathological findings of the temporal bones of patients having idiopathic sudden deafness showed an atrophy of the striae vascularis, the tectorial membrane, and the organ of Corti; these pathological findings are similar to those of a viral cochlear inflammation.
The inner ear artery, which supplies blood to the inner ear, is provided through the anterior inferior cerebellar artery, the basal artery, and the posteroinferior cerebellar artery with the rostral vertebral artery [6]. The response to treatment tended to be slow in patients with abnormal MRI findings, as compared with patients in whom MRI findings were normal.
In cases of SHL, a detailed investigation should be performed in order to determine the etiology and provide the best treatment. Je eher der Tinnitus, aber auch der HA¶rsturz behandelt werden, desto grA¶AYer sind die Heilungsaussichten. Die dB-Skala ist logarithmisch; jeweils 20 dB mehr entsprechen einer Verzehnfachung des Schalldrucks. Wenn Sie sich A?ber Ihre BedA?rfnisse und WA?nsche klar werden und diese rechtzeitig kommunizieren, vermeiden Sie manchen Stress. The root cause of sudden deafness lies in the vestibulocochlear nerve (Cranial nerve VIII), the inner ear, or central processing centers of the brain. Most people recover impulsively within a few weeks, but 15% experience progressively worsening symptoms. If the hearing loss is not severe, some doctors to not recommend any treatment but individuals who suffer from SSHL can be very fearful of the prospect of being permanently deaf in one ear, and this can set up a long treatment options that can be intimidating to the patient and the doctor.
They generally work to decrease inflammation, decrease swelling, and help the body to fight illness.
The researchers suggest that diabetes may lead to hearing loss by damaging the nerves and blood vessels of the inner ear.
Also, it has potential benefits for diabetic neuropathy, and it is proposed that it may help to prevent or repair nerve damage that causes hearing loss. You should be the only one able to hear your music if you are using a personal stereo unit with headphones.
The MRI findings of 18 patients with sudden deafness included three cases of slow blood flow of the vertebrobasilar system, one case of abnormal course of the vertebrobasilar system, and one case of labyrinthine enhancement. Recently, magnetic resonance imaging (MRI) has become an important method for evaluation of ear diseases.
Various suspected causes of sudden deafness include circulation disorder of the inner ear, viral infection, rupture of the cochlear membrane, syphilis, and allergy.
The 4-mm-thick axial and coronal MRI tests produced TI-weighted images, Gd-enhanced T1-weighted images, proton density images, and T2-weighted images.
Figure 2 shows the proton density axial image of patient 2, who had vertigo and sudden deafness in the right ear; this image displays increased signals in the basal artery, due to the SBF of the basal artery. In addition, the patients showing abnormal MRI findings did not respond well to treatment as compared to those with normal MRI findings (Table 2).

Generally, labyrinthitis caused by viral infection, blood circulation disorders, or rupture of the inner ear membrane are believed to cause sudden deafness [1]. The inflammation in the inner ear membrane can be found by conducting an antibody (Ab) test for viruses in the blood of affected patients. In many cases, the decrease in the blood supply to the inner ear artery is caused by a decrease in the blood supply to the VBS or by vascular obstruction of the inner ear artery itself [7,8]. However, the number of cases examined in this study was small; therefore, no statistical significance is claimed.
Therefore, we concluded that MRI is indispensable for examining patients with sudden deafness, especially those patients with accompanying vertigo.
Labyrinthine enhancement on gadolinium enhanced MRI in sudden deafness and vertigo:Correlation with audiologic and electronystagmographic studies. Contrast enhancement of labyrinth on MR scans in patients with sudden hearing loss and vertigo:Evidence of labyrinthine disease. Sudden sensorineural hearing loss associated with slow blood flow of the vertebrobasilar system. Otoacoustic emission (OAE) analysis, electronystagmography (ENG), bithermal caloric test (BCT), and vestibular evoked myogenic potential (VEMP) assessments may be used in addition to a number of auxiliary methods to determine the topographic diagnosis. Selten gibt es auch OhrgerA¤uschformen, bei denen die Schallquelle in Ihrem KA¶rper verborgen ist. SSHL is defined as an idiopathic hearing loss of sensorineural origin, greater than 30 dB in three connected frequencies that usually occurs in less than three days and in only one ear. Standard management of sudden deafness consists of removal of the known cause, antibiotics, steroids and inhalation of a mixture of carbon-dioxide and oxygen. Steroid treatment helps to some SSHL patients who also have conditions that affect the immune system, the body’s defense against disease. In the body, just one deficiency can have trickle down affect and makes it very hard to isolate the exact cause of sudden hearing loss, and many other disease process. MRI showed many abnormal findings in the temporal bone of sudden-deafness patients who also complained of vertigo.
To determine whether establishing the pathogenesis of sudden deafness is possible, we analyzed MRI scans of early stages of sudden deafness in combination with the clinical results of treatments. However, no theory has yet been established for the causes of this disease, so making a definite diagnosis is very difficult.
All patients were managed with same treatment protocol, which consists of high-dose steroid, low-molecular-weight dextran, and carbogen (95% O2 + 5% CO2) therapy.
Figure 3 depicts the proton density axial image of patient 6, who had vertigo and sudden deafness in the left ear; this image shows increased signals in the left vertebrobasilar artery, due to the SBF.
These researchers further reported that when the enhancement was confined to certain segments of the cochlea, deafness existed at the frequency of the region predicted by the enhancement. Although the exact mechanism and significance of SBF in sudden deafness are unknown, a temporary decrease in blood flow occurred at the onset of sudden deafness [11]. In particular, 5 of the 11 (45%) patients with sudden deafness and accompanying vertigo showed abnormalities on MRI, and 3 of the 11 patients (27%) showed SBF. In CW Cummings, JM Fredrickson, LA Harker (eds), Otolaryngology Head and Neck Surgery, 3rd ed. Objective: To evaluate the contribution of OAE analysis, BCT, VEMP assessment, and magnetic resonance imaging (MRI) to the topographic diagnosis of SHL. Mit der HBO bestehen zusA¤tzliche Behandlungschancen, um spA¤tere chronische Beschwerden Ihres Sinnesorgans Ohr zu verhindern. By taking less processed sugar in diet, you can low your blood sugar and thus reverse some of the debilitating effects. As compared with normal cases, the cases showing abnormal findings on MRI did not respond well to treatment. To discover the exact causes of sudden deafness, the authors examined the relationships between patients' symptoms and the results of acoustic and vestibular function tests by analyzing abnormal findings on MRI, in particular the slow blood flow (SBF) of the vertebrobasilar system (VBS) and labyrinthine enhancement on MRI augmented by gadolinium (Gd-DTPA). Figure 4 shows the proton density axial image of patient 5, who had vertigo and sudden deafness in the right ear; the image exhibits an abnormal course of the right vertebrobasilar artery. Therefore, gadolinium enhancement of the labyrinth is characteristic of labyrinthine diseases [3,4,6].
Additionally, they reported that viral labyrinthitis was diagnosed in nine patients and leutic labyrinthitis was diagnosed in two. Method: Cross-sectional and retrospective studies of 21 patients with SHL, as defined above, were performed. About half of the patients undergoing treatment recover hearing within the first few days and the other half within 3 months, but a small percentage show delayed recovery (9).Despite its sudden onset, which is often associated with symptoms such as dizziness and tinnitus, the pathophysiology of this condition remains undefined. Allerdings sollte der gesamte Behandlungsprozess nicht zu sehr in die LA¤nge gezogen werden. As it is a medical emergency, a person who experiences SSHL should visit a doctor immediately.
We concluded that MRI is indispensable for examining patients with sudden deafness, especially those who have accompanying vertigo. The patients underwent the following exams: audiometry, tympanometry, OAE analysis, BCT, VEMP assessment, and MRI. Routine tests for diagnostic evaluation fail to detect the etiology in up to 88% of the cases (10).
Sex, affected side, degree of hearing loss, and cochleovestibular test results were described and correlated with MRI findings. The list of potentially causative or associated agents is long; many of these are etiologic factors such as vestibular nerve schwannoma, infections, stroke, and neoplastic lesions, whereas others are only associated factors for which a causal relationship remains to be established (viral, autoimmune, vascular mechanisms) (11-13). Early diagnosis and therapeutic management improve the patients' quality of life.Tinnitus and aural fullness are reported in 95% of the patients with SHL, whereas dizziness is present in 55% of the cases showing the involvement of the posterior labyrinth and suggesting a worse prognosis (14). A detailed investigation of patients with SHL should be performed in all cases, the main objective of which should be to determine the etiology of the event in an effort to provide the best treatment for that patient.
The latter group also reported that the SBF of the VBS demonstrated high-signal proton density images [12-14]. When the audiovestibular test results were added to the MRI findings, the topographic SHL diagnosis rate increased from 20% to 45%. OAEs are low-intensity acoustic signals generated by nonlinear mechanical activity of the OHCs of the organ of Corti (18). Conclusion: Only combined analysis via several examinations provides a precise topographic diagnosis.
OAEs can occur spontaneously (spontaneous OAEs) or in response to acoustic stimuli (evoked OAEs), which, once amplified, can be detected in the external auditory canal (EAC) (19).
Isolated data do not provide sufficient evidence to establish the extent of involvement and, hence, a possible etiology.
The sound stimulus reaches the cochlea and induces vibration of the basilar membrane, which in turn causes deflection of OHC stereocilia, ion flow, a voltage difference, and subsequent contraction of these cells to generate electromotility, which is thought to be responsible for the phenomenon of OAEs. The presence of OAEs indicates that the conductive mechanisms of the ear (external ear canal, tympanic membrane, and ossicular chain) and the OHCs are functioning properly, and therefore, in any kind of hearing loss (HL), OAE assessment is a valuable step. However, we must remember that OAEs do not provide information about the inner hair cells (IHC), the eighth cranial nerve, or the ascending auditory pathways. Spontaneous OAEs reveal narrow band acoustic energy from the cochlea regardless of the presence of a sound stimulus. They are of little clinical importance because they are present in only 40-60% of subjects with normal hearing (20). Evoked OAEs can be classified as transient-evoked otoacoustic emissions (TEOAEs) and distortion-product otoacoustic emissions (DPOAEs).
TEOAE responses are caused by acoustic stimuli, usually clicks, but frequency-specific stimuli such as tone bursts and tone pips can also induce these responses. Although a click is a broadband stimulus that activates the whole cochlea, TEOAEs can provide the "frequency-specific" pattern of the cochlea. They can be divided into frequency bands representing responses from different segments of the cochlea (21). DPOAEs are generated in the cochlea in response to the simultaneous presentation of 2 pure tones (f1 and f2 stimuli).
The cochlea has nonlinear properties that produce changes in the output signal that are not directly related to the input signal, creating responses at frequencies other than those provided by the 2 input signals. These responses are called distortion products and indicate normal activity of the inner ear.
The 2f1-f2 ratio is the most commonly used as it results in the most robust and reliable responses. As they arise from OHCs (peripheral auditory system), responses are supposed to be compatible with auditory thresholds in the case of sensory HL.
In the case of retrocochlear pathology, DPOAE responses may be present even with thresholds worse than 45 dB HL and abnormal ABR since DPOAEs reflect pre-neural sensory activity from the cochlea. Studies indicate that about 20% of patients with a retrocochlear pathology have normal DPOAEs.
Expanding lesions in the internal auditory canal (IAC) or posterior fossa may decrease the cochlea blood flow and affect the presence of OAEs. In SHL, the OAE test is a fast and elegant method for confirming HL, excluding any psychogenic deafness, and monitoring treatment outcome (17).The ENG permits electrical recording of eye movements and is the most common method used for the diagnosis of peripheral vestibular disorders. The caloric test allows for independent assessment of the right and left labyrinths (horizontal semicircular canals) in response to bithermal irrigation of the external auditory canal. Thus, the caloric test provides a functional assessment of the horizontal semicircular canal and superior vestibular nerve, contributing to the topographic study of the peripheral organ and ascending vestibular pathways.The VEMP assessment is a newly developed vestibular test that is used clinically to analyze otolith function and is the only specific test for the inferior vestibular nerve. In primitive vertebrates, the saccule is not part of the vestibular system but is a structure of the auditory system.
In most vertebrates and humans, the saccule is sensitive to acoustic stimuli but is involved with vestibular function.
Furthermore, as a noninvasive and low-risk test, the VEMP assessment does not depend on cochlear integrity and may be present in patients with profound deafness. In this way, VEMP analysis assesses the integrity of the sacculocollic reflex, which depends on the functional integrity of the macula of the saccule, inferior vestibular nerve, lateral vestibular nucleus, descending vestibulospinal tract, and the accessory nerve to the sternocleidomastoid muscle (SCM) and its neuromuscular junction.
Therefore, unlike other exams, VEMP assessment enables the study of structures not commonly assessed by traditional vestibular tests (the saccule and inferior vestibular nerve) as well as the descending and ascending vestibular pathways. Some authors describe a positive correlation between the presence of normal VEMP and a good prognosis for hearing recovery in patients with SHL (22, 23).
Other authors have noted normal VEMP results in all patients with SHL (24), or did not relate these to hearing outcome. However, VEMP assessment can contribute to the diagnosis of different neurotologic diseases, including Meniere's disease, superior semicircular canal dehiscence, benign paroxysmal positional vertigo (BPPV), vestibular neuritis, and vestibular schwannoma, and it is a great method for topographic diagnosis.

It evaluates not only the neural structures, but also the sensory structures of the saccule, which are sensitive and responsive to acoustic stimuli, although they do not contribute to hearing. For example, in a case of SHL of vascular origin, the lesion is expected to be large and involve not only the cochlea, but also the vestibule, damaging a greater number of sensory-neural structures. In such cases, combined analysis of audiological and electrophysiological test results and imaging studies may contribute directly to the topographic diagnosis of the lesion and to the subsequent prognosis of the patient's SHL.
All patients followed the outpatient care protocol for SHL, including providing a detailed history, and undergoing an ENT physical examination as well as the following exams: pure tone and speech audiometry, tympanometry, DPOAE analysis, ENG, VEMP assessment, laboratory tests, and MRI. When the patient showed no speech discrimination at the highest intensity permitted by the equipment, we tested the speech detection threshold (SDT).
Immitance measurements included tympanometry and contralateral acoustic reflex thresholds at 500 to 4000Hz.
The reflex was considered present when detected for at least 1 of 4 frequencies and absent when no response was detected for any frequency.
To ensure proper acquisition of OAEs, the test was performed in a quiet environment with a noise level 6dB. When significant responses were obtained for 5 or more frequencies, DPOAEs were considered to be present. In this case, further analysis was undertaken to determine whether DPOAEs were consistent with auditory thresholds. We used SCOUT software (Natus Medical Incorporated, Mundelein, Il, USA) for these analyses.Bithermal Caloric Test - BCTBefore the BCT analysis, the patient underwent a standard ENG test battery with the aim of excluding other functional findings that could influence the post-caloric response.
The test sequence consisted of recordings of eye movements in response to stimuli: (1) saccade test, (2) spontaneous nystagmus with open eyes (SNEO), (3) smooth pursuit (SP), (4) optokinetic test (OPK), (5) static position tests - supine, right ear down, left ear down, Rose, sitting, body right and body left, (6) BCT. In the BCT analysis, we considered nystagmus of both labyrinths, measured through the angular velocity of the slow-phase velocities (SPV). We observed the nystagmus direction, rhythm, amplitude, and frequency, and compared the functioning of the labyrinths. To evaluate the response symmetry between the vestibules, 2 values were calculated: (a) Unilateral Weakness (UW) and (b) Directional Preponderance (DP).
UW shows the relative difference between the right and left ear responses, and DP shows the relative difference of right beating vs. UW has a high clinical value and indicates a vestibular asymmetry of peripheral or central origin; it always points to the weaker ear. During the test, the patient remained comfortably seated with neck rotation contralateral to the sound stimulation. The sound stimuli were presented through insert earphones (ER-3) calibrated according to ANSI S1.40-1984 (American National Standard Institute, 2001). The surface electrodes were placed on the forehead (ground), the upper part of the sternum (negative), and the upper third of the contracted SCM muscle (positive electrode). The impedance was 40% (with the lowest amplitude from the SHL side) or the absence of a response on the affected side, suggesting saccule and inferior vestibular nerve involvement.Magnetic resonance imaging (MRI) of the inner ear and brain stemMRI of the inner ear was carried out by spin-echo and fast spin-echo sequences in T1 and T2, with multiplanar acquisition before and after intravenous administration of the paramagnetic contrast agent (gadolinium). MRI was considered abnormal only when findings were obviously related to SHL, such as schwannoma of the eighth cranial nerve (intracanalicular or cerebellopontine angle), internal carotid artery obstruction, stroke, and cochleovestibular lesions (inflammation or vascular), as previously described (26). The level of statistical significance was set at 5% (p RESULTSBetween January 2011 and January 2012, 40 patients diagnosed with SHL were treated at the Department of Neurotology, Hospital das Clinicas, University of Sao Paulo School of Medicine.
No patient refused to participate in the study, had contraindications to any of the exams, or missed their follow-up visits. Figure 1 shows the distribution of the degree of NSHL observed in 20 patients at the beginning of the analysis.
Although DPOAE were requested at the time of initial evaluation, in view of the test schedules and the demand of the institution, some of these tests were eventually completed during follow-up of SHL after partial or complete recovery of NSHL, and the results were consistent with the audiometric thresholds obtained at the same time as the DPOAE tests. Analyzing the 4 abnormal tests, we found that in 2 cases the lesion arose from the eighth cranial nerve (schwannoma) ipsilateral to the SHL. In case 9, MRI revealed an expansive lesion inside the right IAC, protruding into the ipsilateral cerebellopontine angle (CPA) (Figure 5). In case 11, MRI showed an expansive lesion located in the right CPA and IAC, with enlargement and partial obliteration of the ipsilateral cistern (Figure 6). Among the 2 patients with eighth cranial nerve schwannomas, DPOAEs were absent in 1 (case 9) but present in the other (case 11). In this case, the test was performed later, during follow-up of SHL, and after complete recovery of audiometric hearing thresholds.
In the other 2 cases with abnormal MRIs, the lesion was located in the cochlea on the same side as the SHL. The lesion was described by the radiologist as a focus of post-contrast enhancement in the cochlea, vestibule, and ipsilateral semicircular canals suggestive of inflammation (viral labyrinthitis, fibrotic tissue) in 1 (case 6), and as enhancement of the ipsilateral cochlea (possible inflammation) in the other (case 18).
In the 2 latter cases, DPOAEs were absent, which was in agreement with the MRI findings showing cochlear enhancement, and helped to prove that the auditory lesion was peripheral, involving the OHCs, and not neural. Thus, ENG showed no vestibular function ipsilateral to the lesion in both cases, even without any sign on MRI of a lesion extending into the posterior labyrinth in case 18.We also evaluated the mean difference between the initial and final PTA to compare the average hearing recovery among patients whose topographic diagnosis showed smaller, more restricted lesions (absent or Cn or SVn lesions) or more extensive lesions (Cn + VSn or Cn + VSn + IVn). Case 4 was excluded from the analysis because only the initial audiometry results were available and no differences between the initial and final PTA could be calculated. Distribution of DPOAE results in patients with SHL.DISCUSSIONIn this cross-sectional study of 21 patients with SHL, abnormal MRI findings were seen in 20% of cases, which is similar to the results of a previous report on SHL at our institution that showed abnormal MRI findings in 25% of those studied (28).
The small difference in abnormal MRI findings may be due to the smaller sample size used in this study. We chose to use DPOAE as an inclusion criterion because the test permits the evaluation of each frequency separately and responses may be present with hearing thresholds up to 45 dB HL, whereas TEOAEs are usually absent when the thresholds exceed 20-30 dB HL (29). Therefore, this test is not only important for the differential diagnosis of peripheral and central lesions, but also because absent responses in the initial SHL evaluation exclude the possibility of psychogenic deafness (PD) or simulation.Psychogenic deafness (PD) is a type of conversion disorder and can be defined as HL that cannot be explained by organic lesions or anatomical or physiological changes. In such cases, the patient's clinical history reveals psychological factors that could act as a trigger at the beginning of the event. It is possible to establish the diagnosis by comparing behavioral (pure tone audiometry) and objective tests (ABR and DPOAE), as these usually show divergent results: patients typically exhibit elevated pure tone thresholds but normal ABR and DPOAE responses. This patient presented with initial severe HL although tests failed to show any evidence of a structural lesion and follow-up showed a full recovery. Malingering may also lead to divergent results between behavioral and objective tests, but in contrast to PD, it is usually is associated with an inconsistent history, personal advantages associated with deafness, and differences between pure tone audiometry and SRT >15 dB, which can be detected by an experienced audiologist. Therefore, in routine clinical evaluation of patients with SHL, DPOAE is a valid tool and contributes to diagnostic accuracy. If an unexpected response is present during the initial evaluation, the possibility of a retrocochlear lesion should be considered and investigated.In our study, DPOAEs were eventually performed late during follow-up of SHL and not as part of the initial test as planned. This can happen even if the cause of SHL is an expansive lesion of the IAC or PCA, provided cochlear blood flow is preserved and cochlear integrity is ensured.
In case 11, normal VEMP and DPOAE test results suggested normal saccular, inferior vestibular nerve, and cochlear (OHC) function.
Pure tone and speech audiometry results were normal at the time the DPOAE was performed, indicating complete hearing recovery after initial moderate HL.
We speculate that the initial hearing impairment caused by the expansive lesion extending from the IAC to CPA may have improved as a result of decreased edema resulting in a favorable treatment outcome. In the same case, the absence of a right vestibular response, as shown by BCT, suggests that only the superior vestibular nerve was affected.In case 9, the lesion was primarily located in the right IAC (although protruding into the CPA), and the test results (complete deafness on PTA, absent DPOAEs, abnormal VEMP, hypoactivity in BCT) confirmed that the whole cochleo-vestibular system was affected on this side. Therefore, in our view, DPOAE analysis is an important test for SHL evaluation since it is the only one that assesses cochlear function.Patients underwent a complete ENG evaluation in order to rule out other changes to vestibular-ocular function suggestive of central involvement.
The importance of vestibular evaluation in SHL becomes clear when we look at the cases with abnormal MRIs. Cases 6, 9, 11, and 18 were found to have structural lesions by MRI and all had impaired superior vestibular nerve function, with absent vestibular responses in 3 (75%) of the 4 cases.
Overall, 4 cases in our sample showed no response, 3 (75%) had abnormal MRIs and 2 of them (50%) tumors, and so absent caloric test responses require an imaging study.
However, abnormal imaging findings do not predict permanent deafness, since cases 6 and 11 both experienced hearing recovery.
When the audiovestibular test results were combined with the MRI findings, the proportion with a topographic SHL diagnosis increased from 20% to 45%.Figure 5. Isolated test results do not provide sufficient data to establish the extent of SHL involvement and hence a possible etiology. The combination of all tests was more efficient for topographic diagnosis than just audiometry and MRI. Combined assessment permits a functional evaluation that cannot be obtained with MRI alone.
Each test evaluates a different segment of the cochleo-vestibular system and permits an overview of the degree of functional or structural impairment. The auditory evoked potentials (ABRs) could be included in the audiovestibular test battery. ABR may be useful to rule out malingering and patients with psychogenic hearing loss, and may also be helpful in follow-up of SHL, especially in patients with schwannomas.REFERENCES1.
Sudden complete or partial loss of function of the octavus system in apparently normal persons. Thirty-year trends in sudden deafness from four nationwide epidemiological surveys in Japan.
Extent of lesions in idiopathic sudden hearing loss with vertigo: study using click and galvanic vestibular evoked myogenic potentials. Prognostic value of initial electronystagmography findings in idiopathic sudden sensorineural hearing loss without vertigo. Prediction of hearing outcomes by distortion product otoacoustic emissions in patients with idiopathic sudden sensorineural hearing loss. Correlation between audiovestibular function tests and hearing outcomes in severe to profound sudden sensorineural hearing loss. Magnetic resonance imaging findings in the auditory pathway of patients with sudden deafness. Effects of degree and configuration of hearing loss on the contribution of high- and low-frequency speech information to bilateral speech understanding. Reporting click-evoked and distortion-product otoacoustic emission results with respect to the pure-tone audiogram. The effect of noise bandwidth on the contralateral suppression of transient evoked otoacoustic emissions. ENT Assistant Doctor Department of Otolaryngology University of Sao Paulo School of Medicine - R.

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  2. 227 writes:
    Really keep out of cacophonous rooms.
  3. evrolive writes:
    The basket case that loud music could harm your hearing, but now scientists.