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At least 19 recordsLinked to original sources
PubMedDate not supplied

Neural correlates of sensorineural hearing loss.

Sensorineural hearing loss is characterized by a relatively well defined set of audiological signs and symptoms such as elevated thresholds, abnormally rapid loudness growth, subjective tinnitus, poor speech discrimination, and a reduction in temporal summation of acoustic energy. Knowledge of the underlying neural mechanisms responsible for some of these auditory distortions has progressed substantially within the past 10 yrs as a result of physiological studies on hearing-impaired animals. Some of the important neurophysiological changes relevant to sensorineural hearing loss are reviewed. One important effect associated with sensorineural hearing loss is the broadening of the cochlear filtering mechanism which may influence loudness growth and the perception of complex sounds. The neurophysiological results may also provide new insights in interpreting traditional audiological data and help in developing more refined tests for fitting hearing aids or differentiating patients with sensorineural hearing loss.

Animals↗
PubMed2005

Antiphospholipid antibodies in patients with sensorineural hearing loss.

Sensorineural hearing loss can be associated with autoimmune diseases and the presence of antiphospholipid antibodies. Sixty patients (mean age 47 years, range 18-76 years) with sudden sensorineural hearing loss were studied with audiograms, stapedial thresholds, otoacoustic emissions, positional and caloric testing. The serologic testing included antibodies against phosphatidylserine and beta(2)-glycoprotein. Additionally, a group of 34 patients (mean age 65 years, range 31-81 years) with normal tension glaucoma was examined because in a previous study these patients were reported to have elevated concentrations of antiphospholipid antibodies with a coincidence of progressive sensorineural hearing loss. The baseline for antiphospholipid antibody levels was established in a control group of 40 healthy blood donors. In 12 of the 60 patients with sudden sensorineural hearing loss, levels of antiphospholipid antibodies were elevated. Antiphosphatidylserine IgM antibodies were significantly lower compared to controls and patients with the combination of hearing loss and normal tension glaucoma (Fisher's exact two-sided test, P < 0.01). Our data suggest that antibodies against beta2-glycoprotein seem to coincidence with an acute event, such as sudden sensorineural hearing loss, whereas antibodies against phosphatidylserine IgG are detectable in the prolonged sequel, such as in patients with progressive sensorineural hearing loss and normal tension glaucoma.

Adolescent↗
PubMed1985

Treatable sensorineural hearing loss.

Sensorineural hearing loss is generally felt to be an untreatable medical condition. However, in some cases, prompt diagnosis and treatment of the underlying condition may reverse the deafness. This article summarizes various treatable forms of sensorineural hearing loss and provides illustrative cases histories of patients who have had sensorineural hearing losses that were improved by medical or surgical intervention. Patients with reversible sensorineural deafness due to inadvertent aminoglycoside over-dosage, congenital cholesteatoma, Meniere's syndrome, blood coagulopathy, and perilymphatic fistula all had improvements in auditory function after medical or surgical intervention. Recent experimental studies on animals may explain the basic mechanisms behind hearing loss and recovery. Aminoglycoside ototoxicity appears to have an initial reversible step, followed by a permanent process. Early endolymphatic hydrops and fistulas may cause mechanical effects in the cochlea which can be corrected. Coagulopathy may cause hypoxia which reverses after anticoagulation. These observations reveal that animal experiments can be useful in explaining human auditory dysfunction of the reversible type.

Adult↗
PubMed1991

Macrovascular sensorineural hearing loss.

Sensorineural hearing loss (SNHL) has many etiologies including vascular sources. Vascular causes of SNHL can occur at the microvascular level. Macrovascular level may be described as arising from vessels proximal to the labyrinthine artery or those vessels that can be visualized without the aid of a microscope. Otologic symptomatology and diagnostic evaluation of the SNHL may reveal a macroscopic vascular source. Representative cases of macrovascular sensorineural hearing loss due to aneurysm, arteriovenous malformation, and vertebrobasilar artery dolichoectasia are presented.

Adult↗
PubMed2001

Sensorineural hearing loss after vibration: an animal model for evaluating prevention and treatment of inner ear hearing loss.

Sensorineural hearing loss following a variety of acoustic trauma, including middle ear surgery, is well known. Current literature, which points to the deleterious influence of noise on the inner ear during surgery, has yet to assess the influence of vibration generated by the burr. The purpose of the study reported here was to establish an animal model that mimics drilling and can be used to explore methods of hearing loss prevention and treatment. A specially developed electromagnetic vibrator was calibrated and used in 59 guinea pigs to induce hearing loss. Both young and old guinea pigs were used. The bony external ear canal of guinea pigs were exposed to vibration or sound of varying duration and intensity. The vibration of the temporal bone and noise level in the middle ear were measured. Electrocochleography was recorded to evaluate the hearing loss. Among the young animals, 90% developed a significant threshold shift (TS > 20 dB), when vibrated with 250 Hz at an intensity of 6.2 m/s2 for 15 min. An average of 42 dB TS was observed. With 10 min exposure 63% showed a TS. The older animals vibrated for 5 min developed the same TS (mean TS 34 dB) as the young animals when vibrated for 10 min. The vibration-induced TS showed no recovery within 3 days of observation. In the contralateral ear 4 out of 5 animals showed TS > 20 dB. When exposed to sound levels exceeding the vibration-generated sound in the middle ear (119 dB at 250 Hz) only 2 out of II animals (18%) showed TS. The frequency of TS and level of TS were significantly greater in the vibrated animals than in sound-only exposed animals (p < 0.01). The degree of vibration-induced TS in the present animal model could be controlled by vibration intensity and duration. The older animals were more susceptible to vibration-induced inner-ear damage than younger animals. This model will be used in further studies to find methods for prevention and treatment of hearing loss during ear surgery.

Animals↗
PubMedDate not supplied

Sensorineural hearing loss in children with sickle cell anemia.

Various degrees of hearing loss have been associated with sickle cell anemia. Fifty-six Nigerian children 6 to 15 years old were investigated for presence, type, and degree of hearing loss. Sensorineural hearing loss greater than or equal to 25 dB in two or more frequencies was found in 12 of 56 patients (21.4%). Tympanometry was normal in all patients, but acoustic reflex was elevated or absent in seven of 12 patients with hearing loss. Analysis of the data revealed a significant association between sensorineural hearing loss and the homozygous sickle cell disease, and a significant association between hearing loss and early occurrence of vaso-occlusive crisis. This latter finding suggest that the microvasculature of the cochlea in young infants may be more susceptible to occlusion during sickle cell crisis.

Acoustic Impedance Tests↗
PubMed2006

The autoimmune characteristics of progressive or sudden sensorineural hearing loss.

Autoimmune sensorineural hearing loss (ASNHL) is a clinical syndrome that typically produces a bilateral rapidly progressive hearing loss. Autoantibodies and autoreactive T cells have been implicated in the etiopathogenesis of ASNHL. However, the identity of a specific or highly relevant inner-ear self-antigen is still required. In recent years, a role for antiphospholipid antibodies has been also suggested, assuming sudden/progressive hearing loss to be part of the primary antiphospholipid syndrome (APS). In this review, we address the need for specific diagnostic tools in order to establish an autoimmune origin for hearing loss. Moreover, the decision of whether anti-inflammatory drugs or anti-coagulation should be given is also discussed.

Antiphospholipid Syndrome↗
PubMed1983

Sudden sensorineural hearing loss.

Sudden sensorineural hearing loss is a frightening experience for the patient. The patient's worse fears concern tumors or stroke. Although the physician is often frustrated by a symptom whose cause at times is not apparent, every effort should be made to identify the causes of sudden sensorineural hearing loss and possible predisposing causes of idiopathic sudden sensorineural hearing loss. Therapy includes efforts to treat known causes either medically or surgically, to keep the patient at reduced physical activity, and depending upon the treating physician's own preference, attempts to favorably alter the ultimate prognosis through medical manipulation.

Hearing Loss, Sensorineural↗
PubMed2003

Isolated vestibular ossification after meningitis associated with sensorineural hearing loss.

OBJECTIVE: Sensorineural hearing loss after bacterial meningitis is common. It is thought to be secondary to cochlear inflammation from direct bacterial seeding through the cochlear aqueduct. Although cochlear ossification with or without vestibular involvement is common, isolated vestibular ossification is rare. We review our recent experience with isolated vestibular ossification associated with profound sensorineural hearing loss and the implication for cochlear implantation in this population. STUDY DESIGN: Retrospective case review. SETTING: Academic tertiary referral center. PATIENTS: Patients referred with profound sensorineural hearing loss after bacterial meningitis with evidence of ossified vestibular labyrinth but normal cochleae on computed tomographic scanning were included in the study. INTERVENTIONS We review the history, imaging findings, operative intervention, and operative findings in this series of patients. MAIN OUTCOME MEASURES Clinical history, imaging findings, operative intervention, and operative findings. RESULTS: Three patients with isolated vestibular ossification without computed tomographic evidence of cochlear osteoneogenesis were identified. Two of these patients subsequently underwent cochlear implantation with the Clarion device with complete insertion of the electrode array. Intraoperatively, one patient had isolated scala tympani ossification and the implant electrode array was placed within the scala vestibuli. CONCLUSION: A pattern of sensorineural hearing loss and isolated ossification of the vestibular system without radiographic evidence of cochlear involvement may be seen after bacterial meningitis. In these patients, magnetic resonance imaging scanning should be performed, because computed tomographic scanning may not always detect cochlear ossification. Cochlear implantation is feasible in these patients.

Adult↗
PubMed2003

Autoimmune sensorineural hearing loss.

Autoimmune sensorineural hearing loss has been increasingly recognized as a clinical entity since its description by McCabe in 1979. Recognition and proper management of this condition is important, as it is one of the very few forms of sensorineural hearing loss that can be successfully treated by medical therapy. Recent studies have provided experimental evidence to suggest that immune processes can cause sensorineural hearing loss in animals and humans. However, antigenic targets within the inner ear are diverse and as a result conclusive evidence for specific autoimmune damage to the inner ear has been elusive. This review focuses on the recent progress in understanding of the aetio-pathogenesis of autoimmune hearing loss along with a description of the various clinical conditions in which they occur. Recent advances in the laboratory diagnosis and management of this interesting condition are also described.

Autoimmune Diseases↗
PubMed1988

Sudden sensorineural hearing loss.

Sudden sensorineural hearing loss has many causes and treatments. The family physician can identify the hearing loss, perform audiometry, identify likely systemic causes and counsel the patient on the prognosis. Most patients are ultimately found to have idiopathic sensorineural hearing loss, and the spontaneous recovery rate is high. If no improvement occurs within one month, evaluation to rule out tumor is recommended.

Adolescent↗
PubMed1994

Surgical decompression of Chiari I malformation for isolated progressive sensorineural hearing loss.

Progressive sensorineural hearing loss has been associated with Chiari type I malformation. Retrocochlear features on auditory brainstem response testing have been reported; however, debate exists over the exact location of the defect. Surgical decompression may be beneficial if brainstem or vascular compression have played a significant role in the pathophysiology of the hearing loss. Lack of specific audiologic data before and after surgical decompression has kept surgical decision making theoretic. This report presents the case of a 10-year-old boy with a progressive, asymmetric sensorineural hearing loss without other neurologic abnormalities. He underwent a posterior fossa decompression that resulted in stable hearing over the 2 years he was followed postoperatively. Preoperative and postoperative audiologic and evoked response features are described, and the rationale for operating with symptoms limited to hearing loss is discussed.

Arnold-Chiari Malformation↗
PubMed1997

CT screening for temporal bone abnormalities in idiopathic bilateral sensorineural hearing loss.

Bilateral sensorineural hearing loss can be caused by a variety of temporal bone abnormalities including primary cochlear otosclerosis, local and systemic bony diseases and some metabolic conditions. These may be identified using computerized tomography (CT), with attenuation recordings taken across the cochlear capsule (CT densitometry). Eighty patients with bilateral sensorineural hearing loss were screened over a period of six and a half years using this technique, and only three cases (3.8 per cent) of treatable disease were detected. Positive yields may be increased by screening selected cases with other clinical or biochemical stigmata of temporal bone disease.

Absorptiometry, Photon↗
PubMed2006

Internal auditory canal stenosis in congenital sensorineural hearing loss.

OBJECTIVE: Sensorineural hearing loss (SNHL) due to internal auditory canal (IAC) stenosis with hypoplasia of the cochleovestibular nerve is a rare disorder. The diagnosis of the IAC stenosis requires both high resolution computed tomography scan (HRCT) and magnetic resonance imaging (MRI). METHODS: A retrospective review over 6 years in an academic tertiary referral center was performed. RESULTS: Six patients with congenital SNHL were diagnosed with congenital IAC stenosis. Four had unilateral and two had bilateral IAC stenosis after imaging. MRI showed hypoplastic vestibulocochlear nerve in all cases. CONCLUSIONS: This paper highlights the importance of imaging in diagnosing IAC stenosis and detecting the presence of cochleovestibular nerve in cases of congenital SNHL.

Child↗
PubMed2002

Interferon-gamma production to inner ear antigens by T cells from patients with autoimmune sensorineural hearing loss.

Autoimmune sensorineural hearing loss (ASNHL) typically produces bilateral rapidly progressive loss of hearing over a few days or weeks, but may also produce sudden loss over a few hours. The diagnosis is made by excluding ototoxicity, systemic disease, and other factors that mimic ASNHL and by showing a therapeutic response to corticosteroid treatment. Antibody production and T-cell proliferative responses to inner ear antigens have been implicated in the etiopathogenesis of ASNHL. In the current study, we have extended these autoimmune investigations by determining the frequencies of inner ear specific IFN-gamma producing T cells in peripheral blood mononuclear cells (PBMC) from ASNHL patients and from age- and sex-matched control subjects. ELISPOT analysis showed that 25% of ASNHL patients have significant increased frequencies of inner ear specific IFN-gamma producing T cells in their PBMC. All control subjects were relatively unresponsive. Our results implicate inner ear specific IFN-gamma producing proinflammatory T cells in the pathogenesis of ASNHL.

Adult↗
PubMed2001

A follow-up study of patients suffering from sudden sensorineural hearing loss.

Sudden sensorineural hearing loss (S-SNHL) is a common problem with a high recovery rate. However, little is known of the long-term prognosis of affected patients. The purpose of this follow-up study was to evaluate the long-term hearing results of S-SNHL patients. The sample consisted of 168 patients with S-SNHL treated with carbogen inhalation and/or anticoagulant therapy during the period 1982-89. A questionnaire was sent to these patients, and audiological investigations were carried out in a selection of these patients in 1997. Comparison of the different treatment methods showed that the difference observed in improvement of hearing was statistically significant between the carbogen inhalation and anticoagulant treatment groups. The hearing improvement achieved was stable for, on average, 8 years of follow-up. During the follow-up period, Ménière's disease was diagnosed in only 1 of the 116 patients who answered the questionnaire and no cases of acoustic neurinoma were diagnosed, indicating that establishment of a careful patient history and clinical and audiological investigations are sufficient for the diagnosis of S-SNHL. In general, the hearing improvement achieved in S-SNHL patients is stable during long-term follow-up.

Administration, Inhalation↗
PubMed2005

ELISPOT determination of interferon-gamma T-cell frequencies in patients with autoimmune sensorineural hearing loss.

Autoimmune sensorineural hearing loss (ASNHL) is the most common cause of sudden hearing loss in adults. Although the etiopathogenesis of this disease is unclear, it is widely believed that antibody and/or T-cell responses directed against inner ear-specific proteins may mediate ASNHL. Using the enzyme-linked immunospot (ELISPOT) assay, we have recently found that many patients with ASNHL have increased frequencies of peripheral blood T-cells capable of producing interferon (IFN)-gamma in response to a homogenate of human inner ear tissue. Our studies may ultimately lead to the identification of inner ear-specific autoimmune targets in ASNHL, and our ELISPOT approach may be particularly useful in supporting the diagnosis of this disease entity. In the current chapter we detail how to use the ELISPOT assay for measuring frequencies of IFN-gamma-producing T-cells in patients with ASNHL.

Adult↗