Magnetic resonance imaging findings in sudden sensorineural hearing loss.
ABSTRACT To investigate the role of magnetic resonance imaging (MRI) in the diagnosis of sudden sensorineural hearing loss (SSNHL).
Fifty-four consecutive patients affected by SSNHL were investigated using brain MRI. MRI was performed with an eight-channel phased-array head coil to study the entire audiovestibular pathway and the whole brain. The protocol study consisted of a high-resolution study of the temporal bone, internal auditory canal (IAC), cerebellopontine angle (CPA), and brainstem combining 2 mm thin-slice axial T(2)-weighted two-dimensional fast spin echo (FSE) and fluid-attenuated inversion recovery (FLAIR) sequences, pre- and postcontrast (gadolinium-diethylenetriamine pentaacetic acid) administration fat-suppressed axial T(1)-weighted two-dimensional FSE sequences, and a T(2)*-weighted three-dimensional Fourier transformation-constructive interference in steady state sequence (FT-CISS) , with 0.4 mm ultrathin partitions. The rest of the brain was studied with a 4 mm axial T(2)-weighted FLAIR sequence.
Thirty-one of 54 (57%) cases of SSNHL presented with MRI abnormalities. In 6 of 54 cases, the detected abnormality was directly correlated to the clinical picture (2 labyrinthine hemorrhage, 1 cochlear inflammation, 1 acoustic neuroma, 1 arachnoid cyst of the CPA, and 1 case of white matter lesions in the pons, compatible with demyelinating plaques along the central audiovestibular nervous pathway, as the first expression of multiple sclerosis).
An extensive MRI study of the audiovestibular nervous pathway and of the whole brain, pre- and postparamagnetic contrast administration, is recommended to rule out the wide spectrum of abnormalities that can cause SSNHL.
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ABSTRACT: Magnetic resonance imaging is the gold standard in retrocochlear imaging; however, its role in management of inner ear diseases remains poorly defined. In this study, we investigate the utility of MRI in defining the nature of intracochlear pathology. A retrospective review of 11 patients with inner ear abnormalities on MRI between 2010 and 2013. Patients' diagnosis included cholesteatoma, labyrinthitis, meningitis, and intralabyrinthine schwannoma. Tertiary care hospital. T1, T2, and postcontrast signal intensities were measured within the lesion and normalized in reference to the contralateral normal cochlea. The following ratios were calculated: T1 postgadolinium lesion/contralateral cochlea, T2 lesion/contralateral cochlea and T1 lesion/contralateral cochlea. Statistical analysis was conducted using the unpaired Student's t test using IBM SPSS Statistics version 20.0.0. The relative intensity ratios were useful in defining the nature of inner ear lesion. Normalized T1 postgadolinium lesion intensities were significantly higher in the tumor group (3.98 ± 0.880 versus 1.71 ± 0.370, p < 0.0002). Normalized T1 precontrast signal intensities were higher in tumors (1.33 ± 0.200 versus 0.842 ± 0.426, p < 0.0626), and T2 values were lower in tumors (0.838 ± 0.491 versus 1.10 ± 0.305, p < 0.317); however, these did not reach significance. Intensity of gadolinium enhancement on MRI is useful in differentiation of inflammation from tumors; normalized T1 postgadolinium intensity ratio greater than 3 is strongly suggestive of intralabyrinthine tumor.Otology & neurotology: official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology 05/2014; · 1.44 Impact Factor
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ABSTRACT: Sudden hearing loss (SHL) is a frightening symptom that often prompts an urgent or emergent visit to a physician. This guideline provides evidence-based recommendations for the diagnosis, management, and follow-up of patients who present with SHL. The guideline primarily focuses on sudden sensorineural hearing loss (SSNHL) in adult patients (aged 18 and older). Prompt recognition and management of SSNHL may improve hearing recovery and patient quality of life (QOL). Sudden sensorineural hearing loss affects 5 to 20 per 100,000 population, with about 4000 new cases per year in the United States. This guideline is intended for all clinicians who diagnose or manage adult patients who present with SHL. The purpose of this guideline is to provide clinicians with evidence-based recommendations in evaluating patients with SHL, with particular emphasis on managing SSNHL. The panel recognized that patients enter the health care system with SHL as a nonspecific, primary complaint. Therefore, the initial recommendations of the guideline deal with efficiently distinguishing SSNHL from other causes of SHL at the time of presentation. By focusing on opportunities for quality improvement, the guideline should improve diagnostic accuracy, facilitate prompt intervention, decrease variations in management, reduce unnecessary tests and imaging procedures, and improve hearing and rehabilitative outcomes for affected patients. The panel made strong recommendations that clinicians should (1) distinguish sensorineural hearing loss from conductive hearing loss in a patient presenting with SHL; (2) educate patients with idiopathic sudden sensorineural hearing loss (ISSNHL) about the natural history of the condition, the benefits and risks of medical interventions, and the limitations of existing evidence regarding efficacy; and (3) counsel patients with incomplete recovery of hearing about the possible benefits of amplification and hearing-assistive technology and other supportive measures. The panel made recommendations that clinicians should (1) assess patients with presumptive SSNHL for bilateral SHL, recurrent episodes of SHL, or focal neurologic findings; (2) diagnose presumptive ISSNHL if audiometry confirms a 30-dB hearing loss at 3 consecutive frequencies and an underlying condition cannot be identified by history and physical examination; (3) evaluate patients with ISSNHL for retrocochlear pathology by obtaining magnetic resonance imaging, auditory brainstem response, or audiometric follow-up; (4) offer intratympanic steroid perfusion when patients have incomplete recovery from ISSNHL after failure of initial management; and (5) obtain follow-up audiometric evaluation within 6 months of diagnosis for patients with ISSNHL. The panel offered as options that clinicians may offer (1) corticosteroids as initial therapy to patients with ISSNHL and (2) hyperbaric oxygen therapy within 3 months of diagnosis of ISSNHL. The panel made a recommendation against clinicians routinely prescribing antivirals, thrombolytics, vasodilators, vasoactive substances, or antioxidants to patients with ISSNHL. The panel made strong recommendations against clinicians (1) ordering computerized tomography of the head/brain in the initial evaluation of a patient with presumptive SSNHL and (2) obtaining routine laboratory tests in patients with ISSNHL.Otolaryngology Head and Neck Surgery 03/2012; 146(3 Suppl):S1-35. · 1.73 Impact Factor
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ABSTRACT: Protein kinase C-eta (PRKCH) gene has been recently identified as a susceptible risk locus for cerebral infarction and hemorrhage in the Asian populations. The inner ear artery, a usual branch of anterior inferior cerebellar artery, is an end artery with minimal collaterals, therefore, the inner ear is particularly vulnerable to ischemia. The potential association between the development of stroke and sudden sensorineural hearing loss (SSNHL) has been implied. The authors hypothesized that the PRKCH polymorphism predisposing to stroke is associated with SSNHL risk, in view of brain magnetic resonance imaging (MRI) findings. The authors compared 33 cases of prevalent SSNHL with other cases among 2188 adults aged 40 to 79 years who participated in the Study of Aging, to assess the impact of PRKCH 1425G/A polymorphism in consideration of brain MRI findings. Multiple logistic regression was used to obtain odds ratios (ORs) for SSNHL, with adjustment for other possibly influential factors under additive model of minor allele. The per-allele OR for SSNHL risk was 1.770 (95% confidence interval: 1.024-3.060) after adjustments. The effect of the 1425A-allele varied by white matter lesion (WML) status. A significant impact of the A-allele on SSNHL risk increment was observed in higher-WML group, but not in no- or mild-WML group. The 1425A-allele of PRKCH has probably contributed to the susceptibility to SSNHL, despite the etiological heterogeneity of SSNHL, and the impact of the PRKCH 1425A variation observed in this study may imply underlying vascular pathogenesis of SSNHL.Journal of neurogenetics 07/2011; 25(3):82-7. · 0.73 Impact Factor