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Results for “Hearing Loss, Sudden”

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At least 19 recordsLinked to original sources
PubMed1996

Migraine as a cause of sudden hearing loss.

Sudden hearing loss is common, but unexplained in many cases. Although usually attributed to a viral infection of the inner ear in most patients, the abrupt onset of the hearing loss in many patients argues against a viral etiology. We present 13 cases of unexplained sudden hearing loss who meet the diagnostic criteria for migraine. All had the sudden onset of hearing loss and other neurologic phenomena that could be attributed to vasospasm, including vertigo, amaurosis fugax, hemiplegia, facial pain, chest pain, and visual aura. We suggest that vasospasm of the cochlear vasculature was the cause of the sudden hearing loss in these patients. A personal and family history of migraine should be sought in patients with sudden hearing loss and when found, a trial of antispasmodic agents should be considered.

Acute Disease↗
PubMedDate not supplied

Acoustic neuroma presenting as sudden hearing loss.

Sudden hearing loss occurs as the initial symptom in 1 to 9 per cent of all acoustic neuromas. A case of an acoustic neuroma presenting with sudden hearing loss is described. In this case, the hearing thresholds returned to normal. To the authors' knowledge, this is the first case in which an acoustic neuroma presenting with sudden hearing loss exhibited a return to normal thresholds. This suggests that such tumors may have an initial reversible effect on hearing thresholds.

Acute Disease↗
PubMedDate not supplied

Multiple sclerosis: a cause of sudden hearing loss.

Sudden hearing loss is a clinical entity which has numerous aetiologies. In cases where the aetiology is not determined, evaluation and treatment of sudden hearing loss are very difficult. A case of probable multiple sclerosis with sudden hearing loss as the initial symptom is reported. The pure-tone audiometry showed a quasi-total sensorineural hearing loss in the left ear; the left side displayed only wave I in the auditory brainstem response (ABR). Electronystagmographic examination revealed hypometric dysmetria and saccadic pursuit abnormalities. Magnetic resonance imaging (MRI) showed high-intensity lesions with multiple foci. After steroid therapy, the patient's hearing loss, vertigo and visual problems improved, but the ABR findings remained unchanged. We have decided to present this case because of the interesting ABR finding revealing the presence of wave I and the absence of all other waves after the normalization of the hearing.

Adult↗
PubMed2001

[Role of endothelial cell autoantibodies in the pathogenesis of sudden hear loss].

Sudden hearing loss can be found in systemic autoimmune diseases or it can be a symptom of an autoimmune disease of the inner ear. The present work has studied a group of patients with idiopathic sudden hearing loss to determine what role anti-endothelial cell antibodies (AECA) play as markers of immuno-mediated vasculitis of the inner ear. The study involved 32 patients with sudden deafness and 14 controls. The patients underwent otofunctional, neuroradiological, sero-microbiological and immunological testing. Using the indirect immunofluorescence technique, serum AECA were determined within 24 hours of hospitalization and three days after the onset of deafness. AECA positive patients (AECA+) were administered corticosteroid therapy (methylprednisone 1 mg/kg/die) for 1 month. A clinical follow-up was performed, including audiometry, 1 month after discharge and thereafter at three-month intervals (follow-up range: 8-18 months). AECA proved positive in 15/32 patients (47%) and in 2/14 of the controls (14%). The difference between the patients and the controls was statistically significant (p = 0.03). The 7 patient who showed no recovery after 1 month were all AECA+. None of the AECA+ patients showed other symptoms or a worsening of the hearing loss. In conclusion, the determination of non-specific autoantibodies vs. the inner ear, such as AECA, can be considered a useful clinical tool in differentiating between patients with idiopathic sudden hearing loss and those for which a diagnosis of immuno-mediated vasculitis of the inner ear is likely and for which prognosis is particularly unfavorable.

Adolescent↗
PubMedDate not supplied

Methylenetetrahydrofolate reductase gene mutations as risk factors for sudden hearing loss.

Sudden hearing loss (SHL) can be caused by vascular disorders favoring impaired cochlear perfusion. Several inherited prothrombotic risk factors have been considered in the pathogenesis of vascular impairment, and the possible role of genetic alterations has recently been suggested. Methylenetetrahydrofolate reductase (MTHFR) gene mutations at nucleotides 677 and 1298 cause reduced MTHFR enzyme activity, which leads to increased homocysteine and reduced serum folate levels that are known to be involved in vascular impairment. We studied the relationship between SHL and MTHFR C677T and A1298C gene polymorphisms in 67 patients with SHL and 134 controls. Wild-type MTHFR CC677/AA1298 was significantly more frequent in the controls (P = .05), and gene mutations were significantly more frequent in the patients (P = .001; P = .001 for trend). Fifty-three patients (79.1%) and 56 controls (41.8%) (P = .012) had a double mutation (homozygosis 677TT or 1298CC; compound heterozygosis for both polymorphisms). Homocysteine levels were significantly higher and serum folate levels significantly lower in the patients than in the controls (P < .0001). These data suggest that MTHFR gene polymorphisms may be involved in the pathogenesis of SHL.

Adult↗
PubMed2006

Does a reduction of adhesion molecules by LDL-apheresis have a role in the treatment of sudden hearing loss?

Sudden hearing loss (SHL) is a highly disabling affliction that can severely affect the subject's social and relational life. Although the etiology of the complaint is still debated, it is thought that microcirculation disturbances conditioned by an endothelial dysfunction might be the main pathogenetic mechanism. Adhesion molecules favoring interaction between leukocytes and endothelial cells are early markers of endothelial damage. In the present report, we describe a case of SHL that derived evident benefit from a single session of LDL/fibrinogen apheresis, with complete hearing recovery. In this patient, in addition to reducing LDL cholesterol and fibrinogen, the circulating adhesion molecules (sE-selectin, sVCAM-1 and sICAM-1), previously present in higher than normal concentrations, were reduced by the treatment.

Blood Component Removal↗
PubMed2004

[Sudden hearing loss].

Sudden hearing loss is a reduction of sensoneurinal sound perception with a sudden onset. It is usually occurring only in one ear and without a recognizable cause. If a hearing loss is suspicioned due to otoscopic and tuning fork test findings, the patient should rapidly be sent to an ENT-specialist because of the possible consequences. After the first examinations by means of ear microscopy and audiogram further diagnostics may be necessary. If no cause is found, the idiopathic sensorineural hearing loss remains as the exclusion diagnosis. Therapy follows a polypragmatic approach based on the different theories of its origin. Therefore mainly antiinflammatory, antiviral and vasoactive drugs are applied. The high spontaneous healing rate and the still pending proof of effectiveness of all types of therapy used so far must be considered.

Age Factors↗
PubMedDate not supplied

Word deafness presenting as a sudden hearing loss.

Sudden hearing loss is a condition frequently seen in ENT departments and is usually due to otological pathology. We present a patient who described symptoms of a sudden inability to hear but who, on further questioning and investigations, had 'word deafness' due to bilateral temporoparietal infarcts. We discuss the clinical syndromes associated with these infarcts and the specific management of word deafness.

Cerebral Infarction↗
PubMed1997

Clinical applications of otoacoustic emissions in sudden hearing loss.

Sudden hearing loss (SHL) is a controversial topic for which no definitive practical guidelines exist. Studies employing vasodilators, plasma expanders, anticoagulants, and carbogen inhalations have shown no improvement over the rate of spontaneous recovery. At present, there is insufficient evidence to support medical treatment for SHL, except steroid therapy in selected patients. Distortion product otoacoustic emissions (DPOAEs) are sensitive to cochlear disorders and are absent in ischemic injury to the cochlea, but can persist in cochlear neuritis. In a prospective study of 10 patients who presented to Albany Medical Center from 1995 to 1996, three patients with intact DPOAEs at presentation had an average improvement of 33 dB in the pure-tone average (PTA) of 0.5, 1.0, and 2.0 kHz with steroid therapy, whereas five of seven patients with absent DPOAEs had no improvement in hearing despite steroid therapy in six patients. The presence of DPOAEs may be a useful prognostic factor that positively correlates with recovery from SHL.

Acoustic Stimulation↗
PubMed2005

[Up to date: therapy of sudden hearing loss].

Sudden sensorineural hearing loss is thought to be of different origin. Disturbances of microcirculation, autoimmune pathology and viral infection are among the most likely causes. The shape of the puretone audiogram can be a useful clue to its origin. Following is a description of five different forms of sudden hearing loss, its suspected pathogenesis and different therapeutic strategies recommended for the treatment of sudden hearing loss.

Anti-Inflammatory Agents↗
PubMed1983

Cochlear aqueduct radiographic anatomy in temporal bone preparations and in sudden hearing loss.

Sudden sensorineural hearing loss appears to have many possible etiologic factors. Shea has presented work indicating that a large cochlear aqueduct (CA) is frequently present on the side of an idiopathic sudden sensorineural hearing loss (ISHL). However, Valvassori, on performing temporal bone tomographic studies on several hundred patients complaining of ISHL, has not found enlargement of the CA in a statistically significant number of these cases. In an attempt to resolve this discrepancy, a single blind study was performed utilizing temporal bone polytomography to evaluate the presence or absence of the CA in 22 adult patients. One-half of these patients had a history of ISHL, while the remaining patients had other complaints as an indication for tomography. In all cases, the CA was identified. The CA was felt to be enlarged in 1 patient suffering from ISHL, in the nonaffected ear of 1 patient with unilateral ISHL, and in 2 control patients. There was, therefore, no positive correlation between CA enlargement and the occurrence of ISHL. In order to further elucidate the radiologic anatomy of the CA, 9 pairs of adult temporal bones removed at autopsy were studied by polytomography after cannulation and injection of radiopaque material. Measurements of the dimensions of the CA and its radiographic anatomy are discussed and compared to measurements obtained from histopathologic evaluation of the temporal bone.

Adult↗
PubMed2001

Hyperbaric oxygen as a method of therapy of sudden sensorineural hearing loss.

Sudden hearing loss is a sensorineural hearing impairment, which develops over a period of few hours to a few days. Several theories have been proposed regarding the development of sudden sensorineural hearing loss. The incidence of sudden sensorineural hearing loss has been reported to range from 5 to 20 per 100,000 persons per year. Hearing loss is treated with drugs that provide better blood supply to the inner ear and decrease inflammation. The aim of this study is to examine the influence of hyperbaric oxygen therapy in treating sudden sensorineural hearing loss. The beneficial effects of HBO2 on sudden sensorineural hearing loss are probably achieved by an increase in the distribution of O2 dissolved per volume unit of blood circulating trough the regions affected by the lack of oxygen. Sessions were performed on 17 patients, with sudden sensorineural hearing loss that began within 10 days prior to the tests. In the hyperbaric chamber, all patients breathed 100% oxygen at 2.8 bars, for 60 minutes twice a day, either until recovered or for a maximum of 30 sessions. Of the total number of study participants, 12 were male and 5 were female, and their average age was 35.3 years (range: 18 to 68). Before the therapy, an average hearing value was obtained out of five basic frequencies. Hearing was found to be in the range of 61-93 dB in 12 patients, while 5 patients had hearing in the range of 41-60 dB. Following therapy with hyperbaric oxygen, the hearing level of 14 patients was within the range of 0-26 dB, two patients' hearing level increased to 27-40 dB, and one patient's hearing level remained in the range of 41-60 dB. The average hearing level for all patients and for all five basic frequencies was 67.8 dB before therapy, in comparison with 21.6 dB after oxygen therapy (p=0.0003). The average number of sessions in the hyperbaric chamber was 11.9 (range: 5 to 20). The therapy was taken well by all patients. The results of this study, as well as the results of similar studies performed by other authors, indicate for the necessity of performing an additional prospective, random, double-blind study of the effects of hyperbaric oxygen therapy on sudden sensorineural hearing loss, on a large number of patients.

Adolescent↗
PubMed2005

[Statistical study and clinical results by comparison of two different protocols in the treatment of sudden hearing loss].

Sudden deafness goes on being a clinical entity of unknown cause for which several theories and treatments have been proposed. We are reporting a comparative study of two different protocols that we have performed on 60 patients (divided in two groups of 30) diagnosed and admitted with sudden hearing loss between 1989 and 2003. The main goal is to prove if there is a statistical and significant difference among both, in respect of the audiologic improvement obtained, after two weeks of therapy at east. We have applied the normal approximation of Mann-Whitney's test and we can argue, after its result, our current protocol (piracetam, pentoxifiline, metilprednisolone), which includes 4 days of endovenous treatment another 10 days at home. The presence of vestibular symptoms darkens the prognosis since about 95% of the patients with them have not improved significantly (p<0.05).

Adult↗
PubMed1992

Audiometric comparison of Lassa fever hearing loss and idiopathic sudden hearing loss: evidence for viral cause.

A recently published prospective study on acute sensorineural deafness in Lassa fever among a West African population showed the audiometric pattern of a known virally induced hearing loss. Using the audiometric data from the patients with Lassa fever in that study, we analyzed and classified the initial hearing loss and final recovery into three groups by pure-tone average values and then did the same for 222 patients with idiopathic sudden hearing loss (SHL) in our study. Statistical analyses of the severity of initial hearing loss and the hearing recovery pattern indicate that the clinical course of our 222 patients with idiopathic SHL showed no statistically significant differences from the clinical course of the patients with Lassa fever. We found a marked difference in age, however, and a clinically significant difference in the incidence of bilateral hearing loss. In reviewing the literature on sudden sensorineural hearing loss, we found no apparent relation between severity of viral illness and initial hearing loss or subsequent recovery. Cummins et al. suggest that virally induced hearing loss in Lassa fever is linked to the host's immune response and not to the viremia. We thus propose a virally induced immune response mechanism for idiopathic sensorineural SHL. Further prospective studies are needed for verification.

Acute Disease↗
PubMed1984

Functional hearing loss presenting as sudden hearing loss: a case report.

A case of functional hearing loss presenting as sudden sensorineural hearing loss in the only hearing ear of a musician is presented. Pure-tone audiometric evaluation showed good intratest and intertest consistency. The pitfalls of diagnosis, ultimately made by brain stem evoked response audiometry, are discussed in light of the literature on sudden and functional hearing loss. Psychiatric evaluation revealed features consistent with hysterical conversion. It is argued that it is important to establish the exact etiologic agent of functional hearing loss despite the difficulty of diagnosis so that the patient may receive appropriate treatment.

Adult↗
PubMed1996

Current concepts in the diagnosis and treatment of sudden sensorineural hearing loss.

Sudden hearing loss (SHL) has been a controversial topic in the literature for the past several decades. Although much theoretical work has been done regarding its diagnosis and treatment, no useful practical guidelines exist for application to current patient management. Many authors have discussed the various treatment protocols available to treat this entity, but only a handful of dated, clinical studies supporting these treatments are available. More recent studies applying treatment protocols including vasodilators, plasma expanders, anti-coagulants, and carbogen inhalations have shown no improvement over the rate of spontaneous recovery without therapy. Except in cases of therapy directed toward known predisposing factors, there is insufficient evidence in the literature to support medical treatment for SHL, although steroid therapy appears to be useful in selected patients. Our own review of 14 patients with SHL is presented. A standard diagnostic and therapeutic approach based on a comprehensive review of the literature is described that can be applied to most patients presenting with SHL.

Administration, Inhalation↗
PubMed1980

Idiopathic sudden hearing loss.

Idiopathic sudden hearing loss is an otologic emergency with an obscure cause. It is the acute onset of hearing loss of 30 cB in three contiguous frequencies, which may occur instantaneously or progressively over several days. Suspect etiologies include viral infections, cochlear artery occlusion, rupture of the intracochlear membranes, and biochemical alterations in the metabolism maintaining the endocochlear membrane potentials. Histopathology of the temporal bone most commonly reveals atrophy of the organ of Corti and striae vascularis. Treatments proposed include close observation for spontaneous recovery, steroid theray, and combination regimens of vasodilators, steroids, diuretics, and intravenous iodinated radiocontrast material. Prognosis and recovery are related to the audiometric pattern of the hearing loss and associated symptoms. The absence of vertigo at th clinical onset and low tone hearing loss are associated with better hearing recovery.

Adult↗
PubMed1999

Anti-endothelial autoantibodies in patients with sudden hearing loss.

OBJECTIVES/HYPOTHESIS: Sudden hearing loss (HL) can be caused by autoimmune disorders localized to the inner ear or secondary to systemic immune diseases. Studies in autoimmune animal strains showing HL have reported changes in the cochlear stria vascularis. The authors investigated the presence of antiendothelial cell antibodies (AECA) to see if immune-mediated vasculitis may play a role in human sudden HL. STUDY DESIGN: A prospective study in patients with sudden HL. METHODS: Fifteen consecutive patients (mean age, 32 y) affected by sudden HL and 14 normal subjects were included. Patients with familial deafness and metabolic diseases were excluded. Extensive audiovestibular, imaging, microbiological, immunological, and routine examinations were performed. AECA were detected on rat kidney tissue sections on the sera collected at -20 degrees C. RESULTS: AECA were positive in 8 of 15 patients (53%) (2 of 5 men and 6 of 10 women), thus differing significantly from the normal control population, in which only 2 of 14 tested AECA positive (P = .023). CONCLUSIONS: In patients with sudden HL, immune-mediated vascular damage can have a pathogenetic role and AECA might represent a serological marker of vasculitis.

Adolescent↗