|Ahead of print publication
Comparative Study of high-resolution T2-weighted turbo spin echo sequence and postcontrast three-dimensional volumetric T1-weighted sequence in evaluation of acute onset sensorineural hearing loss
Somali Pattanayak1, Amit Paliwal2, Rachit Sharma3, Vikas Sharma4, Manoj Gopinath1, Jyotindu Debnath1
1 Department of Radiology and Interventional Radiology, Army Hospital (R and R), New Delhi, India
2 Department of Radiodiagnosis, Military Hospital, Jodhpur, Rajasthan, India
3 Department of Radiodiagnosis, Military Hospital, Dehradun, Uttarakhand, India
4 Department of Otorhinolaryngology and Head and Neck Surgery, PGIMER, Chandigarh, India
|Date of Submission||29-Dec-2020|
|Date of Decision||28-May-2021|
|Date of Acceptance||28-May-2021|
Department of Radiology and Interventional Radiology, Army Hospital (R and R), Delhi Cantt - 110 010, New Delhi
Source of Support: None, Conflict of Interest: None
Purpose: Magnetic resonance imaging has revolutionized the evaluation of acute onset sensorineural hearing loss (SNHL). This study was carried out with an aim to diagnose the causes of acute onset SNHL with an attempt to compare the accuracy of high-resolution three-dimensional (3D) T2-weighted sequences with postcontrast 3D volumetric T1-weighted imaging. Materials and Methods: Two hundred and fifty-five cases of acute onset SNHL were evaluated using noncontrast sequence for brain and 3D DRIVE for seventh and eight cranial nerves. Postcontrast 3D volumetric T1 sequence was done for the whole brain. Results: Poor visualization of the semicircular canal (confirmed as labyrinthitis ossificans on computed tomography) was the most common cause of acute onset SNHL, followed by vestibular schwannoma. 3D DRIVE sequence was not able to detect seven cases of small intracanalicular vestibular schwannoma and enhancement of the seventh-eighth cranial nerves. However, these cases were detected on postcontrast sequence. Conclusion: As the sensitivity of the 3D DRIVE sequence was only 74.1%, it cannot be used as a screening tool for the evaluation of acute onset SNHL. 3D postcontrast sequence will detect even small vestibular schwannomas and inflammatory/infective causes of acute onset SNHL, which might have an impact on the management of the patient.
Keywords: Acute onset sensorineural hearing loss, high-resolution T2-weighted turbo spin echo sequence, magnetic resonance imaging, postcontrast three-dimensional volumetric T1 weighted imaging, three-dimensional DRIVE
|How to cite this URL:|
Pattanayak S, Paliwal A, Sharma R, Sharma V, Gopinath M, Debnath J. Comparative Study of high-resolution T2-weighted turbo spin echo sequence and postcontrast three-dimensional volumetric T1-weighted sequence in evaluation of acute onset sensorineural hearing loss. Med J DY Patil Vidyapeeth [Epub ahead of print] [cited 2021 Nov 30]. Available from: https://www.mjdrdypv.org/preprintarticle.asp?id=324765
| Introduction|| |
Sensorineural hearing loss (SNHL) is a common clinical presentation that is characterized by elevated bone conduction thresholds on audiometry. Various classifications of SNHL have been proposed. Schucknecht's classifies SNHL into sensory, neural, strial, and cochlear conductive types. Sudden SNHL is defined as “acute hearing loss of the sensorineural type of at least 30 dB over three contiguous frequencies that occur within a 72-h period.” The most common age of incidence of SNHL is the fourth decade of life with an annual incidence of 5–20 cases/100,000 people. Unilateral presentation is most common, however, bilateral SNHL has been reported in up to 4% of cases. Although many causes have been proposed for sudden onset SNHL, it is considered that 71%–85% of cases are “idiopathic” as the cause cannot be identified in these cases., As significant percentage of the cases is considered idiopathic, no specific treatment has been proposed. Various empirical therapies such as systemic corticosteroids, antivirals, vasodilators, and carbogen or hyperbaric oxygen have been tried out with inconsistent results. Furthermore, no specific therapy has been found superior to the others.,
Contrast-enhanced magnetic resonance imaging (MRI) with high-resolution imaging and three-dimensional (3D) turbo spin echo (TSE) high-resolution T2-weighted sequences has revolutionized the diagnostic workup of sudden SNHL, as it helps in detecting subtle changes in the inner ear and the contents of internal auditory canal.,, MRI is often used to rule out a vestibular or other rarer cause of SNHL such as other cerebellopontine (CP) tumors, demyelinating disease, and brain stem infarctions.,,,,,
MRI without gadolinium has been suggested for screening patients with asymmetric SNHL suspected to be retrocochlear. MRI can reveal abnormalities in the inner ear structures, pointing to a specific etiopathogenesis or in cases of negative imaging, SNHL is defined as idiopathic. There is a paucity of literature comparing the accuracy of 3D TSE high-resolution T2-weighted sequences compared with contrast-enhanced MRI (CEMRI).
The present study was aimed at diagnosing the causes of acute onset SNHL with CEMRI and 3D TSE high-resolution T2-weighted sequences with an attempt to compare the accuracy of high-resolution 3D T2-weighted sequences with postcontrast 3D volumetric T1-weighted imaging (T1WI).
| Materials and Methods|| |
This retrospective study was carried out in the Department of Radiodiagnosis and Imaging of a zonal hospital. The clinical data of the patients were obtained from the hospital records. The study was approved by the institutional ethics committee (MH Dehradun IEC number 02/2020 dated March 14, 2020).
Patients with acute onset SNHL, unilateral or bilateral, referred for MRI from the indoor or outdoor services of the hospital formed the study group. All the clinical data were obtained from hospital records after approval from the IEC.
Two hundred and fifty-five patients of acute onset SNHL were included in the final study over a span of 4 years.
All consecutive, nonrepetitive patients over a period of 4 years with acute onset SNHL referred for MRI were taken as the study group. MRI was done within 5–10 days of onset of the symptoms.
All previously diagnosed or treated cases of CP angle tumors, postoperative cases of mastoid surgery, cases with suboptimal or nondiagnostic images, cases with magnetic resonance incompatible implants/foreign bodies, patients < 20 years of age (to avoid congenital/familial SNHL cases), chronic SNHL cases, and patients with diabetes mellitus were excluded from the study. All patients whose MRI was done after 10 days of symptom onset were excluded from the study.
A study was performed using Philips Achieva 1.5 T MRI system, Philips Medical systems Nederlands BV.
MRI was conducted using a 1.5 T MRI with a phased-array head coil. Our MRI protocol included 4 mm thick T1 (TR/TE: 450 ms and 15 ms) and T2 (TR/TE; 4000 ms and 110 ms) weighted axial images, DWI at b values 0 and 1000 s/mm2 with ADC maps, fluid-attenuated inversion-recovery (TR/TE: 11000 ms and 140 ms, TI: 2800 ms), GRE (TR/TE: 717.4 ms and 13.8 ms), T1 sagittal and T2 coronal for the entire brain. High-resolution 3D TSE T2 weighted sequences (DRIVE) was done for cranial nerves, and postcontrast 3D volumetric T1-weighted sequence was done for the entire brain. The parameters for DRIVE sequences for cranial nerves were the following: TR 1500 ms; TE 230 ms; field of view (FOV) 150 mm; flip angle 90°; matrix 272 × 206; acquiring slice thickness 1.1 mm; and reconstructed slice thickness 0.55mm. Postcontrast 3D volumetric T1-weighted images (TR/TE 7.1,3.2 ms; FOV 256mm; flip angle 8°; matrix 272 × 206; acquiring slice thickness 1.0 mm; reconstructed slice thickness 1.0 mm) were acquired after an intravenous bolus injection of a standard dose of gadobutrol (Gadovist, Bayer AG; 0.1mmol/kg of body weight) through the antecubital vein using a power injector with a rate of 1 mL/s. The images were acquired after 60 s of contrast administration. All injections were followed by a saline flush of 10 mL. Postcontrast 3D volumetric T1-weighted images were obtained for the entire brain.
The images were read by a single radiologist. The 3D DRIVE sequence was read in isolation from postcontrast 3D volumetric T1 WI sequence to remove bias. The findings of the 3D DRIVE were compared with the CEMRI (3D volumetric T1WI). Statistical analysis was done using “R” version 3.6.1. Sensitivity, specificity, positive predictive value, negative predictive value, and diagnostic accuracy were calculated.
| Results|| |
Two hundred and fifty-five patients were included in the final study group. Out of these, 60% of the patients were males (153/255). The age and gender distribution of the cases is shown in [Table 1]. Maximum cases (26%) were in the fifth decade of life followed by the fourth decade (20%). Two hundred and thirty-nine (94%) patients presented with unilateral SNHL and 16 (6%) cases presented with bilateral SNHL.
Out of the 27 positive cases diagnosed on CEMRI, only 20 could be detected by 3D DRIVE sequence. Thus, seven cases were missed out on the noncontrast study. Subtle thickening was seen in unilateral vestibulocochlear nerve in 3D DRIVE sequence in one patient. However, no abnormal enhancement or thickening was seen in the postcontrast study. This case was taken as false positive.
In the present study, it was found that 3D DRIVE sequence has a sensitivity of 74.1%, specificity of 99.6%, positive predictive value (PPV) of 95.2%, negative predictive value (NPV) of 97.0%, and diagnostic accuracy of 96.9% [Table 2]. Out of the 27 positive cases, 12 cases (44%) had poor visualization of the unilateral membranous labyrinth, suggestive of labyrinthitis ossificans, which was further confirmed on computed tomography (which were done after taking consent from the patients). Vestibular schwannoma was detected in eight cases (29%). Tentorial meningioma compressing the left eighth nerve was detected in one case. Out of the seven false negative cases on 3D DRIVE sequence, six cases showed diffuse enhancement of seventh-eighth nerve complex on 3D postcontrast study, one of which showed bilateral involvement. No significant abnormality was detected in the DRIVE sequence in these cases. One case showed a small intracanalicular schwannoma which was seen only on postcontrast study and not on DRIVE sequence. Subtle thickening was seen in unilateral vestibulocochlear nerve in 3D DRIVE sequence in one patient. However, no abnormal enhancement or thickening was seen in the postcontrast study. This case was taken as false positive. Out of the total 255 cases, 228 (89%) cases showed no significant abnormality involving cochlear or retrocochlear complex and hence were reported negative and labeled “idiopathic.”
|Table 2: Correlation of three-dimensional DRIVE with three-dimensional postcontrast T1-weighted imaging study|
Click here to view
| Discussion|| |
Acute onset SNHL is a commonly encountered clinical condition with varying etiologies, ranging from idiopathic to CP angle tumors and multiple myeloma. MRI is the choice of imaging as the cranial nerves, posterior fossa lesions, and demyelinating plaques can be visualized in exquisite detail. The role of CEMRI has been well documented in literature.,,,
In the present study, the most common age of presentation was fifth decade (26%). Byl, in their study, have reported the maximum incidence in the fourth decade. The most common pathology in our study was poor visualization of unilateral semicircular canals (44%), which is shown in [Figure 1] and was further confirmed on limited Non-Contrast Computed Tomography (NCCT) of temporal bones. The next most common diagnosis was vestibular schwannoma, which was observed in eight cases (29%). Six out of these eight cases of vestibular schwannoma (75%) were found to be intracanalicular [Figure 2]. This finding is similar to the study conducted by Jeong et al., which reported that intracanalicular lesions constitute the maximum percentage of vestibular schwannomas in sudden onset SNHL. Tentorial meningioma was seen in one case, which was observed to compress the left eighth nerve due to mass effect on the left cerebellar hemisphere [Figure 3]. Out of the 27 positive cases, 20 were detected by 3D DRIVE sequences, which were further confirmed on 3D contrast-enhanced T1WI sequences.
|Figure 1: A 26-year-old male presenting with acute onset right-sided sensorineural hearing loss. (a) Three-dimensional DRIVE sequence – the right semicircular canals were not visualized in entirety. (b) Confirmatory limited NCCT showing encroachment of bony areas into the right semicircular canals with their poor visualization suggestive of labyrinthitis ossificans|
Click here to view
|Figure 2: A 22-year-old female presenting with left-sided acute onset sensorineural hearing loss. (a) Three-dimensional DRIVE image showing predominantly intracanalicular vestibular schwannoma with small cisternal extension. (b) Confirmatory postcontrast image|
Click here to view
|Figure 3: A 50-year-old female presenting with acute onset left-sided sensorineural hearing loss. (a) Sagittal contrast-enhanced T1-weighted imaging showing left tentorial meningioma with infra as well as supratentorial extension. (b and c) Three-dimensional DRIVE and axial contrast-enhanced T1-weighted imaging showing compression and displacement of the left cerebellar hemisphere and brain stem anteriorly which are in turn compressing on the left seventh eight nerve complex|
Click here to view
Six cases (2%) showed diffuse enhancement of seventh-eighth nerve complex on postcontrast study, one of which showed bilateral involvement. These cases were not detected in 3D DRIVE sequence, as no significant thickening of the nerves was seen. Hence, these cases could have been missed out in the absence of contrast study. One case showed a small intracanalicular schwannoma which was seen only on postcontrast study and not on DRIVE sequence [Figure 4]. One case of subtle thickening of the seventh and eighth nerve complex was seen in the 3D DRIVE sequences, which was not detected in the 3D postcontrast study. This was categorized as false-positive case. Therefore, 3D DRIVE sequence was able to detect 20 of the 27 positive cases accurately, giving it a sensitivity of 74.1%, specificity of 99.6%, PPV of 95.2%, NPV 97.0%, and diagnostic accuracy of 96.9%. As the sensitivity of the sequence is 74.1%, which is not very high, it cannot be used as a screening tool for the evaluation of acute onset SNHL, as it will miss out some cases. Hence, it is recommended that postcontrast study be done in all cases of acute onset SNHL. This is in difference to study conducted by Ryan et al., which advocated MRI without gadolinium as a screening modality for patients with asymmetric SNHL suspected to be retrocochlear.
|Figure 4: A 67-year-old male presenting with acute onset right-sided sensorineural hearing loss. (a) Axial contrast-enhanced T1-weighted imaging showing small right intracanalicular vestibular schwannoma. (b) Three-dimensional DRIVE sequence showed no significant abnormality|
Click here to view
Empirical therapy is started in patients with vascular or inflammatory pattern on MRI, as no study has yet investigated different treatment protocols based on MRI findings, especially in inflammatory causes. Hence, the role of detecting inflammatory cause of SNHL in the form of enhancing nerve roots remains debatable.
Mainstay of treatment of acute onset SNHL continues to be oral administration of corticosteroids,, even though other treatment modalities such as hyperbaric oxygen therapy, antivirals, vasodilators, and vasoactive substances continue to be used with variable outcomes. Moreover, it is advisable that the imaging is done as soon as possible after the patient presents, before starting of corticosteroids to avoid the masking effects.
This study has a few limitations. First, this being a retrospective study, clinical correlation was not done with audiometry and no follow-up of the cases was done, regarding the treatment. Second, the findings of this study will not be applicable to patients with deranged renal parameters, in whom contrast cannot be administered. As the images were read by a single radiologist, possibility of observer bias cannot be ruled out. However, the pre- and post-contrast images were read at separate occasions and in isolation to minimize the bias.
| Conclusion|| |
Various causes of SNHL can be detected on MRI, which can alter the management, though majority of cases continue to be idiopathic. It is recommended that 3D volumetric CEMRI is used in all cases of acute onset SNHL apart from regular sequences and 3D high resolution T2-weighted sequence. This will help us in diagnosing the inflammatory/infective causes and small intracanalicular schwannomas, which can otherwise be missed out on high-resolution T2WI sequence.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Liu H, Zhou K, Zhang X, Peng KA. Fluctuating sensorineural hearing loss. Audiol Neurootol 2019;24:109-16.
Rauch SD. Clinical practice. Idiopathic sudden sensorineural hearing loss. N Engl J Med 2008;359:833-40.
Byl FM Jr. Sudden hearing loss: Eight years' experience and suggested prognostic table. Laryngoscope 1984;94:647-61.
Chau JK, Lin JR, Atashband S, Irvine RA, Westerberg BD. Systematic review of the evidence for the etiology of adult sudden sensorineural hearing loss. Laryngoscope 2010;120:1011-21.
Lawrence R, Thevasagayam R. Controversies in the management of sudden sensorineural hearing loss: An evidence-based review. Clin Otolaryngol 2015;40:176-82.
Conlin AE, Parnes LS. Treatment of sudden sensorineural hearing loss: I. A systematic review. Arch Otolaryngol Head Neck Surg 2007;133:573-81.
Stachler RJ, Chandrasekhar SS, Archer SM, Rosenfeld RM, Schwartz SR, Barrs DM, et al
. Clinical practice guideline: Sudden hearing loss. Otolaryngol Head Neck Surg 2012;146:S1-35.
Kim TY, Park DW, Lee YJ, Lee JY, Lee SH, Chung JH, et al
. Comparison of inner ear contrast enhancement among patients with unilateral inner ear symptoms in MR images obtained 10 minutes and 4 hours after gadolinium injection. Am J Neuroradiol 2015;36:2367-72.
Berrettini S, Seccia V, Fortunato S, Forli F, Bruschini L, Piaggi P, et al
. Analysis of the 3-dimensional fluid-attenuated inversion-recovery (3D-FLAIR) sequence in idiopathic sudden sensorineural hearing loss. JAMA Otolaryngol Head Neck Surg 2013;139:456-64.
Zhu H, Ou Y, Fu J, Zhang Y, Xiong H, Xu Y. A comparison of inner ear imaging features at different time points of sudden sensorineural hearing loss with three-dimensional fluid-attenuated inversion recovery magnetic resonance imaging. Eur Arch Otorhinolaryngol 2015;272:2659-65.
Portmann M, Dauman R, Duriez F, Portmann D, Dhillon R. Modern diagnostic strategy for acoustic neuromas. Arch Otorhinolaryngol 1989;246:286-91.
Biavati MJ, Gross JD, Wilson WR, Dina TS. Magnetic resonance imaging evidence of a focal pontine ischemia in sudden hearing loss and seventh nerve paralysis. Am J Otol 1994;15:250-3.
Franklin DJ, Coker NJ, Jenkins HA. Sudden sensorineural hearing loss as a presentation of multiple sclerosis. Arch Otolaryngol Head Neck Surg 1989;115:41-5.
Hagiwara M, Roland JT, Wu X, Nusbaum A, Babb JS, Roehm PC, et al
. Identification of endolymphatic hydrops in Ménière's disease utilizing delayed postcontrast 3D FLAIR and fused 3D FLAIR and CISS color maps. Otol Neurotol 2014;35:e337-42.
Ryan M, Weissman JL, Kaylie D. Is Gadolinium contrast enhancement necessary in screening MRI for asymmetric sensorineural hearing loss? Laryngoscope 2015;125:783-4.
Jeong KH, Choi JW, Shin JE, Kim CH. Abnormal magnetic resonance imaging findings in patients with sudden sensorineural hearing loss: Vestibular schwannoma as the most common cause of MRI abnormality. Medicine (Baltimore) 2016;95:e3557.
Hegarty JL, Patel S, Fischbein N, Jackler RK, Lalwani AK. The value of enhanced magnetic resonance imaging in the evaluation of endocochlear disease. Laryngoscope 2002;112:8-17.
Whitaker S. Idiopathic sudden hearing loss. Am J Otol 1980;1:180-3.
Conte G, Berardino FD, Sina C, Zanetti D, Scola E, Gavagna C, et al
. MR imaging in sudden sensorineural hearing loss. Time to talk. Am J Neuroradiol 2017;38:1475-9.
Moskowitz D, Lee KJ, Smith HW. Steroid use in idiopathic sudden sensorineural hearing loss. Laryngoscope 1984;94:664-6.
Wilson WR, Byl FM, Laird N. The efficacy of steroids in the treatment of idiopathic sudden hearing loss. A double-blind clinical study. Arch Otolaryngol 1980;106:772-6.
Lee JW, Park YA, Park SM, Kong TH, Park SY, Bong JP, et al
. Clinical features and prognosis of sudden sensorineural hearing loss secondary to intralabyrinthine hemorrhage. J Audiol Otol 2016;20:31-5.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2]