• Home

  • Documents

  • Alaa Ali Abou-Bieh, MD*, Osama Rabie Kombar, MD · 2013. 7. 12. · media cases had their specific...
OBJECTIVE: To estimate the role of magnetic resonance imaging (MRI) scan with contrast and more recently FIESTA sequence as the single best imaging modality that can diagnose most sudden sensorineural hearing loss (SSNHL) cases. METHODS: A retrospective chart and data review study included 72 SSNHL cases between mid 2006 to mid 2008 in a tertiary referral hospital. Beside the imaging studies, data reviewed included history, clinical manifestations, audiological workup, and laboratory in- vestigations. e main outcome measure of this study was the role of MRI to approach the final diagnosis. RESULTS: A final diagnosis could be approached in 19 cases (26%). e etiologies were acoustic neuroma, Ménière’s Disease, vestibulocochlear neuritis, labyrinsitis, temporal bone fractures, round window fistula, cerebrovascular accidents, multiple sclerosis, temporal lobe meningioma, Wernicke’s encephalopathy, and leukemia. MRI, especially FIESTA sequence, could finalize the diagnosis except for traumatic cases. CONCLUSIONS: MRI can guide the diagnosis at the time of clinical presentation especially in cases with progressive and more importantly life threatening etiologies. e FIESTA imaging as a stand-alone protocol reduced the examination time and eliminated the need for contrast. MRI AS SINGLE EARLY DIAGNOSTIC MODALITY FOR SUDDEN SENSORINEURAL HEARING LOSS ETIOLOGY Alaa Ali Abou-Bieh, MD*, Osama Rabie Kombar, MD Departments of Otolaryngology* and Radiology, Faculty of Medicine, Mansoura University, Mansoura, Egypt PATIENTS AND METHODS is study included 72 cases in a retrospective manner. It reviewed all the available data and charts regards all cases of SSNHL met the study’s case inclusion criteria. ese criteria were to include any case of SSNHL presented over the period of two years, between mid 2006 to mid 2008 in a tertiary referral hospital, regardless the case presented with isolated SSNHL or other associated symptoms. e term sudden was restricted to events occurring instantaneously or developing over a period not exceeding 3 days. SSNHL was defined as at least a 30-dB sensorineural hearing loss, occurring in at least 3 frequencies. All patients were seen within 7 days of onset of hearing loss 2 . Postoperative SNHL cases and other iatrogenic cases were excluded. Data reviewed included, age, sex, smoker or not, main complaint and clinical presentation; local and systemic history and examination, laboratory results, audiological evaluation and imaging modalities used. e clinical examination included local otological examination and otomicroscopic examina- tion. e cases were considered with positive findings if there were any type of perforation and / or other pathological findings or any vestibular manifestations. Tuning fork tests also were done for each patient. Audiologial assessment included pure tone audiograms, speech testing (speech reception thresholds and speech discrimination), and otoacoustic emissions. In some cases, auditory brainstem response and vestibular function tests were also done. e laboratory investigations included the basic evaluation test battery (CBC, sedimentation rate, blood sugar, renal and liver function tests) and included specific investigations, when indicted according to the suspected etiology. Imaging studies in these cases at the time of the initial presentation or, in some cases, aſter a period from the initial presentation were also reviewed. Mostly these studies included CT scans either with or without contrast and / or MRI scans with or without contrast. e MRI technique was performed using 1.5 Tesla (GE, Signa Excite ® 1.5 T, United Kingdom), with a dedicated coil. e following sequences were done while the patient was lying on supine position, sagittal T1 WI with FOV 24, slice thickness 5 mm and slice interval about 1.5 mm, matrix 256 x 256 followed by coronal T1 WI with the same parameters but matrix 256 x 224 and then axial T2 WI with FOV 26 and slice thickness and gap as before too, yet matrix 448 x 224. High resolution axial T1 WI and axial T2 WI were then performed: FOV 18, slice thickness 3 mm and slice interval 0.3 mm. 3D FIESTA parameters were FOV 20, slice thickness 1.2 mm and locs/slab= 32. In cases where intravenous Gadolinium was used, axial T1 HR with gadolinium was obtained at FOV 18, slice thickness 3 mm and slice gap 0.3 mm. Matrix for HR axial images was 256x 224 and For FIESTA 448 x 224. e final diagnosis for all cases, which in some cases proved aſter a period of follow-up, was reviewed. e cases then could be separated into two main categories, cases in which a diagnosis could be reached and those without clear diagnosis. e role of the imaging modality used in aiding this diagnosis, were also reviewed. e main outcome measure of this study was estimating the role of MRI in investigating the possible etiologies and approaching the final diagnosis of the cases. However, because this was a retrospective study, some of the cases did not have MRI during the course of the disease or the follow-up period, therefore the study reviewed the role of MRI in the diagnosis of these cases. Statistical analysis was undertaken with the statistics program SPSS ® for Windows ® (version 5; SPSS, Inc., Chicago, IL). Student’s t test and χ2 test were used for statistical analysis of the mean values of the outcome measures and variables of the two groups. A single factor Analysis of Variance (ANOVA), using repeated Fisher exact test, was also used to study the liner representation of the means. e difference would be accepted as statistically significant if the value of P was < 0.01. ABSTRACT RESULTS e total number of the study cases was 72 cases, while reviewing the data of these cases a final diagnosis was found in 19 cases (26%). e cases were 2 acoustic neuroma cases, 3 Ménière’s disease cases, 1 case of vestibulococlear neuritis, 2 cases of labyrinthitis complicating chronic suppurative otitis media, 2 cases of longitudinal temporal bone fractures, 1 round window fistula case, 2 cerebrovascular accidents cases, 2 multiple sclerosis cases, 1 case of temporal lobe meningioma, 1 case of Wernick’s encephalopathy and 2 leukemia cases. Fiſty-three cases diagnosed as idiopathic cases. e mean ages of the study cases were 53 years (range, 17 - 73 years). ere were 40 males and 32 females. ere was no significant statistical difference regards the age distribution or sex representation (P = 0.09 and 0.02 respectively). Forty-eight cases were presented with right sided hearing loss and 24 cases had leſt sided hearing loss. Side representation showed significant difference (P = 0.008). ree cases (4%) developed contra-lateral SNHL aſter the initial presentation. Smokers were 29 cases (40% of the total study cases). Smokers were 26 males (65% of the study males) and 3 females (9% of the study females). Smokers males were statistically significant (P = 0.005). e initial presentations were hearing loss only in 23 cases (32%), hearing loss and vertigo in nine cases (12.5%), hearing loss and tinnitus in 18 cases (25%) and hearing loss, vertigo and tinnitus in 22 cases (31%). Only seven cases (10%) were presented in the first day of the complaint, and they mostly came due to vertigo rather than the hearing loss, 19 cases (26%) were presented in the second day, 24 cases (33%) were presented from third to fiſth day and 22 cases (31%) were presented on the sixth and seventh days. e hearing loss occurred suddenly in 23 cases (32%) and progressed over a period ranged from one to three days in 49 cases (68%). Eighteen cases (25%) typically presented with the hearing loss noticed upon awakening or they were awakened by an attack of sever vertigo associated with or directly followed by the hearing loss. Pain was present in two cases (3%). e pain was described as sever and located over the mastoid. Seven cases (10%) described ear fullness sensation. Only one of them diagnosed as Ménière’s disease later. Except for one of the traumatic cases, none of the cases had facial nerve weakness symptoms at the time of presentation. e two chronic suppurative otitis media cases had their specific history and manifestations at the time of presentation including the long period of otorrhea. irty-two cases (44%) were diabetics, 26 of them (81%) were on insulin therapy. Forty-five cases (62.5%) were known or discovered to be with hyperlipoproteinemia. irty-nine cases (54%) were hypertensive and on oral anti-hypertensives. Two cases (3%) were know atopic patients. One case (1%) was known leukemia case in remission phase. Another case (1%) was known hypercoagulable states patient. ree cases (4%) were hepatics. Two cases (3%) had renal impairment (one was on regular dialysis and one had renal transplantation 4 years before his presentation). One case (1%) had hypo- thyroidism. Among the study population, diabetes incidence, hyperlipoproteinemia and hypertension showed statistical significance (P = 0.005, = 0.008 and = 0.006 respectively). None of the cases was known or found to have later on any congenital malformations of the temporal bone or auditory system. All the three traumatic cases were presented with history of direct or indirect temporal bone trauma (2 cases of longitudinal temporal bone fractures due motor vehicle ac- cident and falling from height and the case of round window fistula was aſter direct slap). At the time of presentation, a history for upper respiratory tract infection or viral prodrome was obtained in 64 cases (89%). is history even was obtained in some of the cases which were diagnosed as acoustic neuroma or Ménière’s disease later on. None of the cases was known as syphilitic or HIV patients. Except for the regular use of aspirin, the tracing of ototoxic use history was very difficult due to lack of previous data and filing. Forty-nine (68%) cases were using aspirin regularly as conjunctive prophy- laxis of cerebrovascular accidents. e use of aspirin was of statistical significance (P = 0.009). ree cases (4%) were alcoholic. Apart from the tuning fork findings, most of the cases did not show specific signs. Horizontally beating toward the affected side nystagmus was present in 4 cases only (6%). One of the acoustic neuroma cases showed grade 2 facial nerve weakness aſter 10 days of initial presentation although the case was on corticosteroid treatment during this time. e two cases of labyrinthitis complicating chronic suppurative otitis media showed cholesteatoma manifestation and the two cases of longitudinal temporal bone fractures showed battle sign and tympanic membrane rupture, facial nerve involvement in one case together with other injuries. e round window fistula case presented with nystagmus, but no other clinical findings. e two cerebrovascular accidents cases, although mainly presented with hearing loss and vertigo, another neurological deficits could be detected on examination. e two multiple sclerosis cases had no other specific signs at the time of presentation. e temporal lobe meningioma case had considerable headache complaint and neuro-ophthalmic manifestation as diplopia on presentation. e case of Wernick’s encephalopathy although presented initially by vertigo, ny- stagmus and hearing loss, patient rapidly progressed into confusion and altered consciousness. e two leukemia cases, one was known case during remission period and the other discovered to have the disease only during the laboratory investigations. Besides the general laboratory test battery, certain specific laboratory investigations were done for some cases. Serological studies showed normal titers of antibodies against herpes virus including cytomegalovirus. Blood studies and bone marrow studies were also done for suspected blood diseases cases. Rheumatoid and antinuclear antigen factors were significant in one case, but still this case classified as idiopathic due to the treatment protocol. None of the cases went lumber puncture or CSF testing. e pure tone audiometry showed a flat curve in 25 cases (35%), high frequency loss in 21 cases (29%), low frequency loss in 12 cases (17%) and profound loss in 14 cases (19%). Speech discrimination was significant in four cases included the acoustic neuroma cases, the multiple sclerosis cases and the temporal lobe meningioma case. e otoacustic emissions were significant only in the vestibulococlear neuritis case, mainly to differentiate it from auditory neuropathy. Auditory brainstem response was significant only in the cases of acoustic neuroma and multiple sclerosis cases. Of the 72 cases included in the study, 63 cases (88%) had one or more imaging study at certain point of the disease course. Imaging studies of these cases at the time of the initial presentation or, in some cases, aſter a period from the initial presentation were influenced mainly by the case history and initial presentation. In addition, as a general notice, there was chronologically progressive usage of the MRI in diagnosis of cases over the reviewed period. Nineteen cases (30%) had CT scans only, 24 cases (38%) had MRI only, while 20 cases (32%) had both of them. Of the 19 cases that had CT scans only, 15 cases (79%) had the scans done during the first 48 hours of the clinical presentation. e CT scans aided the diagnosis of a case of acoustic neuroma, the two cases of labyrinthitis complicating chronic suppurative otitis media, the 2 cases of longitudinal temporal bone fractures and the two cerebrovascular accidents cases. Only three cases (12.5%) of the 24 cases that had MRI only were done during the first three days of the initial presentation, one of them aided the diagnosis of the Wernick’s encephalopathy and another one diagnosed the case of the vestibulococlear neuritis. e other 21 cases (87.5%) had the study between one week to six months. ese studies aided the diagnosis of the three Ménière’s disease cases, one of the multiple sclerosis cases and 1 of the leukemia cases. e other acoustic neuroma case, the round window fistula case, a multiple sclerosis cases, the tempo- ral lobe meningioma case and a leukemia case were diagnosed by both CT and MRI scans. According to the number of cases and the need of using more than one technique to diagnose the cases, MRI usage showed statistical significance than CT scans (P = 0.005). is was aſter the exclusion of the traumatic cases. DISCUSSION e important first step in treating patients with SSNHL is not to decide which of the plethora of treatment modalities to use, but rather to ensure that it is idiopathic 17 . Sometimes the identifiable medical problem, which the hearing loss is associated with, can be more important to the patient survival than the symptom itself 15 . In these cases, treatment should be directed toward correction of this problem more than reversing the symptom only as in idiopathic cases in which successful resolution of SSNHL will occur in a majority of patients with or without treatment 18 . e most popular theories of idiopathic SSNHL include viral infection theory, vascular insult or ischemia theory and the membrane rupture theory 1, 3, 4 - 8, 15 - 21 . Among the other etiologies of the SSNHL may be etiologies that may lead to an irreversible morbidity, either locally or systematically, as the perilymph fistula or even may endanger the patient life as the cerebro-vascular accidents and encephalopathy 22 . ese etiologies can only be diagnosed by imaging studies. In addition, the usage of imaging studies in these cases needs a reliable protocol due to the time sensitivity and the trial and error is not appropriate in these cases and sometimes the lack of detailed medical history make these studies, especially the contrast dependent types, a challenge. e role of CT scans with or without contrast versus MRI studies with different protocols in the early diagnosis of the etiology of the SSNHL was the concern of our study. ere is no doubt that in certain clinical presentations the choice and protocol of the imaging modality are clear. is is as in the cases of trauma and chronic suppurative otitis media and the clear role of CT scans in these situations. However still the dilemma is when the clinical presentation is unclear or suspicious of some serious situations as in cerebro-vascular accidents and encephalopathy or when the patient is presented with severe vertigo makes it impossible to rule out any center etiology. Moreover, this was the situation when we retrospectively reviewed the SSNHL cases presented in our ter- tiary referral hospital over two years period. Imaging studies in these cases at the time of the initial presentation varied a lot and did not follow a specific protocol. In some cases, no imaging studies were done at all at this time and elective studies were used aſter this. In some other cases, MRI scans were done at admission. While in other cases, CT scans only were done at admission and then in some cases MRI scans followed this to establish the diagnosis. erefore, the absence of clear protocol for imaging studies in an important emergency like the SSNHL was the main trigger for our study. e definition of SSNHL varied between the published literatures. Duckert and Meyerhoff 15 changed the past definition of hearing loss that occurred over a period of several seconds up to 5 to 7 days to any sensorineural hearing loss, usually unilateral, and accompanied by tinnitus in about 70 percent of patients and vertigo in 50 percent of patients. ey also used a more limited and appropriate definition of sudden that included those losses occurring instantaneously or within a matter of hours. Fetterman et al 23 , Zadeh et al 2 , Psifidis et al 24 and Yeo et al 25 , restricted the term sudden to events oc- curring instantaneously or developing over a period not exceeding 3 days and defined SSNHL as at least a 30-dB sensorineural hearing loss, occurring in at least 3 frequencies provided that patients were seen within 7 days of the onset of the hearing loss. e current study followed the same definition of SSNHL. Most cases of SSNHL develop unilaterally, and bilaterally developed disease only comprises 0.44 percent to 3.4 percent of patients with SSNHL 26 – 28 . It was reported that bilateral SSNHL is related mainly to systemic diseases as cerebro-vascular insufficiency 29 and leukemia 30 . Idiopathic bilateral SSNHL is extremely rare and its pathophysiology is not known 28 . Although the presumed causes such as viral infection, circulatory insufficiency, or labyrinthine membrane rupture, similar to the causes of the unilateral form have been raised, bilateral onset of this disease may be closely con- cerned with systemic disease 26 – 30 . In our present work, none of the cases was presented with bilateral hearing loss even in the cases that were associated with systematic etiology as cerebro-vascular accidents or leukemia. ree of the idiopathic cases were presented by SSNHL in the contra-lateral side aſter about 8 - 14 months of their initial presentation. Another two cases also of the idiopathic cases had recurrent attack of SSNHL in the same ear aſter the improvement of the hearing loss resulted from the first attack. e reviewed study data other than the proposed SSNHL etiology and imaging modalities were chosen for two main reasons, their effect or relation to the incidence and etiology of SNHL and to ensure that the results were unbiased due to certain factor. e patient’s age was found to be an important risk factor in the incidence of all types of SNHL 31, 32 . El Zir et al 31 reported that the ages over 40 were an additive risk factor for high frequencies hearing loss especially with smoking and noise exposure. However, in our present study age was of no statistical significance. e difference between age rep- resentation in the present work and published literatures might be due to that mostly cases of younger ages seeks the medical advice as they are more concerned about their hearing. In addition, in older cases the attack may pass un-noticed due associated systematic morbidity or symptoms that may be more significant or if the patient is bed ridden and reluctant to seek medical advice. Smoking and noise exposure were also found to be very important risk factors in SNHL incidence 31 - 33 . Pouryaghoub et al 33 , in a cross-sectional study that was designed to study the effect of smoking on noise induced hearing loss, observed that the percentage of workers with hearing loss was greater in smokers and they concluded that smoking could accelerate noise induced hearing loss. In our present work, male smokers were statistically significant; however, the female smokers were statistically un-significant. e available data in our study cases files did not show the history or any details about noise exposure, therefore it was not included in the analysis. e male to female incidence of SSNHL was statistically equal in the published literature 2, 32 and this was the same in the present work. Side representation in our present work showed statistical significant difference. e incidence of the SSNHL was double on the right side; this was mainly with the idiopathic cases. Although we could not fined any relevant data about side representation in the published literature, we suggested that the higher incidence of the SSNHL on the right ear was due to the use of cellular phones, mobile devices and music players by the dominant right hand. Reporting of associated SNHL with the use of these devices increased in the last years in the published literature 34 - 37 . On reviewing the published other factors that might be correlated with incidence and recovery of SSNHL, Busaba and Rauch 38 , Wilson et al 39 , Laird and Wilson 40 , and Mattox and Simmons 41 , mentioned that the interval between the onset of symptoms and initiation of therapy, severity of the hear- ing loss, presence of vertigo, reduced calorics on electronystagmography, discrimination score and shape of the audiogram came aſter the age of the patient in the order of importance. Although the present study was concerned mainly with the etiology of the SSNHL and its diagnosis rather than the prognosis, the study chose to review most of these factors, still with the aim of investigating their influence on diagnosis. From this point of view, the study cases data about the initial presentation and the time until patients sought medical advice showed some characterization of these cases according to etiology. In most of the idiopathic, multiple sclerosis, acoustic neuroma, meningioma and leukemia cases the main presentation was hearing loss only or associated with tinnitus more than with vertigo and mostly these were the case presented by hearing loss that occurred suddenly, usually the typi- cally noticed upon awakening and not associated by other symptoms as pain or fullness. ese were the cases usually presented late. While in cases diagnosed as Meniere’s disease, vestibulococlear neuritis or labyrinthitis the main presentation was vertigo associated the hearing loss or tinnitus and mostly the hearing loss progressed over the time rather than occurred suddenly with progressive associated symptoms as pain or fullness and these were the cases usually presented early due to vertigo. It was the same situation in round window fistula case, but vertigo was more sever and incidence was abrupt. In cases with central etiologies as cerebrovascular accidents and encephalopathy cases, again the vertigo and rapid deterioration were the main characteristic presentations. e important notices from all the data were that mostly the vertigo was important for patients and the main reason for very early presentation, while the tinnitus was the important complaint of late presenters, and usually late presentation and order of complaints importance for the patients mislead for approaching etiological diagnosis. An effective strategy was proposed by Kerber 49 as a key to the evaluation and management of vertigo and dizziness emergency presentations. is strategy for «ruling-out» a serious disorder, such as stroke, by «ruling-in» a peripheral vestibular disorder was based on trials to found the differences in initial presentations and characteristic features that allow for a bedside diagnosis. Although the studying of patterns of recovery was aim of Zadeh et al 2 from categorizing the audiograms into 4 sensorineural types: up-sloping, down-sloping, mid-frequency “U-shaped” and profound loss, we used the same method with the aim of recognizing the pattern of audiograms in each etiologi- cal group. Lin and Young 42, 44 reviewed 556 cases of mid-frequency sudden deafness of four audiometric configurations, flat-type, high-frequency type, low-frequency type and mid-frequency type. ey found 17 cases with retro-cochlear tumors, 10 were of mid-frequency type audiograms, four were of high-frequency type audiograms, two of flat-type audiograms and one of low-frequency type audiograms. Due to the significantly higher incidence retro-cochlear tumors with mid-frequency type audiograms, they concluded that one-third of the patients with mid-frequency sudden deafness harbor a true retro-cochlear mass lesion and hence MR imaging is mandatory in such cases. In addition, the mid-frequency SSNHL were classified by Saunders et al 45 and Noguchi et al 46 as another independent disease entity from sudden deafness, which is defined as sudden-onset sensorineural hearing loss worse in the middle frequencies (1000-2000 Hz) than in the high (4000-8000 Hz) and low frequencies (250-500 Hz), representing a U-shaped or saucer-type audiogram. e proposed mechanisms by the vestibular schwannoma may cause this hearing loss might be compression of the cochlear nerve, nerve conduction block, vascular compression, or toxic/metabolic effects of the tumor 45 - 47 . Yamasoba et al 43 found that SSNHL of low-tone hearing loss and with relative preserved high-tones hearing was mostly idiopathic sensorineural hearing loss of acute onset. Wu and Young 44 reported also that this type usually improved soon aſter the onset of symptoms (< 3 days) and tended to return to almost-normal levels. e hearing loss associated with Ménière’s disease usually involving the low frequencies and the audiogram will manifest low-frequency, inverted ‘V’ low- and high-frequency or flat SNHL. In addition, Fushiki et al 48 noticed that the low-tone idiopathic SSNHL without vertigo was recurrent and progressive to Ménière’s disease. ey retrospectively followed-up 82 patients diagnosed with idiopathic SSNHL of low-tone type without vertigo for the recurrence rate according to the results of electronystagmography (ENG) and electrocochleography (ECochG) tests at the onset of the first episode of hearing loss. e found that 40% of the patients experienced recurrent hearing loss at least 45% of them had the recurrence within 6 months from the first episode of hearing loss. In our series, results showed that most of the cases with central and retro-cochlear etiologies had flat curve or high-frequency loss, while cochlear lesions showed low-frequency loss. Idiopathic cases had now fixed pattern. Although speech discrimination and auditory brainstem response were significant in retro-cochlear lesions and the otoacustic emissions were significant in the vestibulococlear neuritis case, still finding fixed audiological pattern of characterization was not possible. Busaba and Rauch 38 found that approximately a fourth of the patients with idiopathic SSNHL had abnormal auditory brainstem responses and these were the cases with a less favorable hearing outcome compared with those with normal auditory brainstem responses, irrespective of treatment. ey presumed that the auditory brainstem response abnormality might reflect cochlear neuritis or a more extensive involve- ment of the auditory system. ey proposed that in these cases high signal intensity along the course of the eighth cranial nerve may be seen on Gadolinium-MRI, but they found that such a finding was not common, and its clinical implications were not known. Our results regard the vestibulococlear neuritis case showed the reverse, the neuritis could only be detected by the MRI and the auditory brainstem responses were not significant in this case. Our data also showed that vestibular function tests did not add final diagnosis to any case. ese tests may be of prognostic value 38 - 41 . In addition, in the current study, no attempt was done to study the follow-up periods or prognosis as the main aim was the diagnosis of etiology at the time of initial presentation. Laboratory investigations for either predisposing factors or certain specific etiologies proved to be of special importance. Laboratory work-up could be of the bedside methods for ruling-out serious disorders 49 . is is due to the short duration and availability in comparison to other methods as audio- logical or imaging investigations. Diabetes is one of the most important risk factors as it might affect the vasculature and neural system of the inner ear, leading to the hearing impairment 50 . e present work data showed that diabetes, hyperlipoproteinemia and hypertension were the most prevalent predisposing factors, which was the same found in the previously published reports 15 - 50 . In addition, laboratory work-up was the main reason to diagnosis the two serious cases of leukemia. Although the incidence of acute-onset sensorineural hearing loss as the first sign of leukemia is rare, but it was previously reported and mainly the reason for the hearing loss is inner ear hemorrhage 15 - 51 . e routine MRI technique was sufficient to diagnose two cases of MS, one case of temporal lobe meningioma, two cases of CVA, one case of Wernick’s encephalopathy, as well as two cases of leukemia. e two cases of MS we found, and were the cause of SSNHL, the findings were multiple plaques that are seen along the deep white matter and corpus callosum, specifically, multiple plaques are seen in the brain stem and one case in both cerebellar peduncles as well as leſt cerebellar hemisphere. Yamasoba et al 52 , reported a patient with definite multiple sclerosis (MS) who developed unilateral sudden hearing loss coincident with exacerbation of central nervous system symptoms. Cerebrovascular accidents with SSNHL usually are infarctions in the territory of the anterior inferior cerebellar artery (AICA) and typically involving the middle cerebellar peduncle 56, 57, 58 . In a study by Lee et al 56 , MRI could identify and localize the area of infarction in the middle cerebellar peduncle and/or infarction in the anterior inferior cerebellum in 11 of 12 patients. ey also found that SSNHL was a common sign of AICA infarction and suggested that in most cases the hearing loss and tinnitus were resulted from cochlear injury. In general, the most common mechanism of AICA infarction is by formation of atheroma or thrombus in the parent basilar artery blocking the orifice of the AICA or a dolichoectatic basilar artery, which has previously been associated with AICA stroke 59, 60. In our work, we had two cerebrovascular accident cases with typical infarction in the territory of AICA, displayed as cortical and subcortical hypointense signal during T1WI and hyperintense during T2WI seen in the middle cerebellar peduncles and anterior inferior aspect of the cerebellar hemisphere. Where as FIESTA was used to diagnose one case of vestibular neuritis, three cases of Ménière’s disease, two cases of CSOM and ototic labyrinthitis and as a confirmatory for one case of traumatic R.W fistula. Fast imaging employing steady state acquisition (FIESTA) is the sequence that employs gradients to induce a constant or steady amount of transverse magnetisation. FIESTA is a true-FISP (Fast Imaging with Steady-state Precession) sequence 61 . is sequence uses very short TRs and TEs, and produces images with high signal to noise ratios (SNR). Balanced gradients refocus transverse magnetisation at the completion of each TR cycle. e short TRs used in FIESTA imaging are essential to maintaining this spin coherence 62 . e FIESTA sequence may be thought of as a fluid-bright sequence. ese sequences are those in which fluids exhibit hyperintensity compared to surrounding tissues. When studying the CPA and basal cisterns, CSF is uniformly hyper-intense in these sequences 63 . We had two cases of AS, that were diagnosed with FIESTA technique and high resolution T1WI post contrast MRI as well in one case only. e showannoma was elicited as a well defined homogenous intensity lesion seen in CPA and internal auditory canal with isointense signal during T1WI and T2WI and showing marked homogenous enhancement during post contrast study. FIESTA images shown these lesions as isointense, yet well surrounded with hyperintense signal of the CSF, it produces, so that it appears well without need for contrast injection. ose patients whose FIESTA sequence demonstrates pathology in the CPA should be further examined by post-contrast T1-weighted sequences. In addition, in cases where gadolinium may not be administered, such as preg¬nant patients or patients with known sensitivity to gadolinium, the FIESTA sequence may be used in isolation from contrast-enhanced T1-weighted sequences to exclude AS. In these cases, the use of the FIESTA sequence would appear sufficient to exclude AS, without the need for gadolinium-enhanced sequenc¬es. is would agree with Stuckey et al, who found that in the absence of T1-weighted gadolinium-enhanced sequences, CISS images were sufficient to diagnose or exclude AS 54, 55 . Rigby 53 , added that e advantages of FIESTA imaging as a stand-alone protocol for AS include: Reduced time, no contrast administration required, detailed anatomy of he inner ear; and 3D imaging – the FIESTA images can reformatted into thinner/thicker slices, and Maximum Intensity Projec- tions (MIP) images created. In order to maintain a high level of signal to noise, the slice thickness of the T1-weighted sequences is limited to 1.5–3 mm, so characterization of small lesions is not possible. e FIESTA sequence allows sub-millimeter sections, permitting better depiction of small tumors. e study used 3D FIESTA sequence for a slice thickness of 1.2 mm, with overlap of 0.6 mm. ese fine sections allow reformatting to any slice thickness or orientation, and Maximum Intensity Projections (MIP) images. e disadvantages of FIESTA -only protocol for the exclusion or diagnosis of AS without post-Gadolinium T1-weighted scans include: further characterization by post-contrast T1-weighted images, other pathologies of inner ear may be missed; post-operative changes appear to be better demonstrated by post-contrast T1-weighted images, cystic degeneration of the AS is possible, and may be a marker of a fast growing tumour. e post-contrast sequence demonstrated this change, while the FIESTA sequence did not. Other pathologies of the CPA may be better characterised by the post-gadolinium T1-weighted images than the FIESTA sequence, including epidermoid cysts, arachnoid cysts and metastasis. Our results in the three cases of Ménière’s disease, were well diagnosed with FIESTA as it delineated the endolymphatic sac and duct in unaffected side with proper adjustment of the window width and window level, yet, it did not appear at all in the affected side. is is coinciding with results of Tan- ioka et al 64 , who stated: symptoms in Ménière’s disease are characterized by hydrops of the endolymphatic system with recurrent rupture of the membranous labyrinth. e membranous endolymphatic duct and sac are identified only with high resolution MRI (HR-MRI). In addition, Rigby 53 , stated that the fluids of the inner ear (perilymph and endolymph) appear hyper-intense on the FIESTA sequence, allowing visualization of the cochlear and semi-circular canals, which is not possible on the T1-weighted sequences in this study. In a study by Tanioka et al 65 , they found that in patients experiencing an acute episode of Ménière’s disease, the endolymphatic duct and sac were not adequately visible in the affected ear but were seen well in the unaffected ear. During remission, the endolymphatic duct and sac were not visible in pa- tients with clinically advanced disease, but were seen well in the early to intermediate stages of disease. Our results for the case of vestibular neuritis showed linear enhancement of the VIII CN along its canalicular course, mainly proximal part and in the two cases of labyrinthitis that showed patchy enhancement of the cochlea and interrupted segments of the cochlear nerve. is coincide with Lavi and Sklar 66 , who demonstrated obvious enhancement of the intracanalicular portion of the eighth cranial nerve and to less extent enhancement of the labyrinth involving the basal turn of the cochlea on the right and leſt vestibule. We had one case of traumatic R.W. fistula, that demonstrated fluid signal intensity mainly during T2WI in middle ear and that coincide with Meriot and Marsot-Dupuch 67 , they found an abnormal non-enhancing high signal T1 of the membranous labyrinthine fluid on MRI. In an attempt to put a flow chart for proceeding in diagnosis of the sudden sensoryneual HL, we suggest that MRI including FIESTA technique is the modality of choice, based on Rigby 53 , who stated that by limiting the pre- and post-contrast T1-weighted sequences to a targeted patient population (i.e. those with pathology seen on the FIESTA sequence), there are savings to be made. ese savings are in terms of: time saving; avoiding cost and risk of adverse reaction of gadolinium contrast. All may be achieved without compromise of the patient. In addition to the statements of Stuckey et al 54 and Marx et al 55 , who stated that a screening sequence for exclusion of AS should be sensitive, specific, inexpensive and non-invasive when compared to the use of gadolinium-enhanced T1-weighted sequence. By these criteria, the FIESTA sequence is an ideal tool for investigation of possible AS. So that, our idea is first to assess whole brain and presence of a mass lesion in the CPA region with routine MRI including FIESTA upon temporal bone region and skull base, so that if present, this may be sufficient and if not we must proceed into intravenous contrast administration so as to evaluate viral infection (labyrinthitis and vestibulocochlear neuritis) and other etiologies. While, if the case is traumatic or CSOM, we should to start with high resolution CT. CONCLUSIONS MRI can guide the diagnosis at the time of clinical presentation especially in cases with progressive and more importantly life threatening etiologies provided that the cases are not traumatic or chronic suppurative otitis media cases, as these are the situations where starting with high resolution CT scans is the rule. e FIESTA imaging as a stand-alone protocol reduced the examination time and eliminated the need for contrast. 1- Mattox DE, Lyles CA. Idiopathic sudden sensorineural hearing loss. Am J Otol 1989; 10: 242 - 7. 2- Zadeh M, Storper I, Spitzer J. Diagnosis and treatment of sudden-onset sensorineural hearing loss: A study of 51 patients. Otolaryngol Head Neck Surg 2003; 128: 92 - 8. 3- Wilson WR. e relationship of the herpes virus family to sudden hearing loss: a prospective clinical study and literature review. Laryngoscope 1986; 96: 870 - 7. 4- Yamasoba T, Kikuchi S, Higo R. Sudden sensorineural hearing loss associated with slow blood flow of the vertebrobasilar system. Ann Otol Rhinol Laryngol 1993; 102: 873 - 7. 5- Biavati MJ, Gross JD, Wilson WR, et al. Magnetic resonance imaging evidence of a focal pontine ischemia in sudden hearing loss and seventh nerve paralysis. Am J Otol 1994; 15: 250 - 3. 6- Feldmann H. Sudden hearing loss with delayed onset following head trauma. Acta Otolaryngol 1987; 103: 379 - 83. 7- Harris I. Sudden hearing loss: membrane rupture. Am J Otol 1984; 5: 484 - 7. 8- Cole RR, Jahrsdoerfer RA. Sudden hearing loss: an update. Am J Otol 1988; 9: 211 - 5. 9- Berg HM, Cohen NL, Hammerschlag PE, Waltzman SB. Acoustic neuroma presenting as sudden hearing loss with recovery. Otolaryngol Head Neck Surg 1986; 94: 15 - 22. 10- Chow JM, Garcia J. Acoustic neuroma presenting as sudden hearing loss. Am J Otolaryngol 1985; 6: 115 - 9. 11- Pensak ML, Glasscock ME III, Josey AF, Jackson GC, Guyla AJ. Sudden hearing loss and cerebellopontine angle tumors. Laryngoscope 1986; 95: 1188 - 93. 12- Hallberg OE. Sudden deafness of obscure origin. Laryngoscope 1956; 66: 1237 - 67. 13- Nadol JB Jr, Weiss AD, Parker SW. Vertigo of delayed onset aſter sudden deafness. Ann Otol Rhinol Laryngol 1975; 84: 841- 6. 14- Simmons FB. eory of membrane breaks in sudden hearing loss. Arch Otolaryngol 1968; 88: 67 - 74. 15- Duckert LG, Meyerhoff WL. Sudden Hearing Loss. In: Meyerhoff WL, Liston S, Anderson RG, eds. Diagnosis and management of hearing loss. Philadelphia: W. B. Saunders; 1984: 43 - 64. 16- Tucci DL, Farmer JC Jr, Kitch RD, Witsell DL. Treatment of sudden sensorineural hearing loss with systemic steroids and valacyclovir. Otol Neurotol 2002; 23: 301 - 8. 17- Grandis JR, Hirsch BE, Wagener MM. Treatment of idiopathic sudden sensorineural hearing loss. Am J Otol 1993; 14: 183 - 5. 18- Mattox DE, Simmons FB. Natural history of sudden sensorineural hearing loss. Ann Otol Rhinol Laryngol 1977; 86: 463 - 80. 19- Fisch U. Management of sudden deafness. Otolaryngol Head Neck Surg 1983; 91: 3 - 8. 20- Einer H, Tenghorn L, Axelsson A, Edstrom S. Sudden sensorineural hearing loss and hemostatic mechanisms. Arch Otolaryngol Head Neck Surg 1994; 120: 536 - 40. 21- Simmons FB. eory of membrane breaks in sudden hearing loss. Arch Otolaryngol 1968; 88: 67 - 74. 22- Weber PC, Zbar RI, Gantz BJ. Appropriateness of magnetic resonance imaging in sudden sensorineural hearing. Otolaryngol Head Neck Surg 1997; 116: 153 - 6. 23- Fetterman BL, Saunders JE, Luxford WM. Prognosis and treatment of sudden sensorineural hearing loss. Am J Otol 1996; 17: 529 - 36. 24- Psifidis AD, Psillas GK, Daniilidis JC. Sudden sensorineural hearing loss: Long-term follow-up results. Otolaryngol Head Neck Surg 2006; 134: 809 - 15. 25- Yeo SW, Lee DH, Jun BC, Park SY, Park YS. Hearing outcome of sudden sensorineural hearing loss: Long-term follow-up. Otolaryngol Head Neck Surg 2007; 136: 221 - 4. 26- Yanagita N, Murahashi K. Bilateral simultaneous sudden deafness. Arch Otorhinolaryngol 1987; 244: 7 - 10. 27- Fetterman BL, William ML, Saunders JE. Sudden bilateral sensorineural hearing loss. Laryngoscope 1996; 106: 1347 - 50. 28- Oh JH, Park K, Lee SJ, Shin YR, Choung YH. Bilateral versus unilateral sudden sensorineural hearing loss. Otolaryngol Head Neck Surg 2007; 136: 87 - 91. 29- Lee H, Whitman GT, Lim JG. Bilateral sudden deafness as a prodrome of anterior inferior cerebellar artery infarction. Arch Neurol 2001; 58: 1287 - 89. 30- Veling MC, Windmil I, Bumpous JM. Sudden hearing loss as a presenting manifestation of leukemia. Otolaryngol Head Neck Surg 1999; 120: 954 - 6. 31- El Zir E, Mansour S, Salameh P, Chahine R. Environmental noise in Beirut, smoking and age are combined risk factors for hearing impairment. East Mediterr Health J 2008; 14: 888 - 96. 32- Brors D, Eickelmann AK, Gäckler A, Sudhoff H, Lautermann J, Dazert S, Kunstmann E. Clinical characterization of patients with idiopathic sudden sensorineural hearing loss. Laryn gorhinootologie 2008; 87: 400 - 5. 33- Pouryaghoub G, Mehrdad R, Mohammadi S. Interaction of smoking and occupational noise exposure on hearing loss: a cross-sectional study. BMC Public Health 2007; 7: 137. 34- Oktay MF, Dasdag S. Effects of intensive and moderate cellular phone use on hearing function. Electromagn Biol Med 2006; 25: 13 - 21. 35- Al-Dousary SH. Mobile phone induced sensorineural hearing loss. Saudi Med J 2007 Aug; 28: 1283 - 6. 36- Loſtis M. Sources of noise-induced hearing loss. AAOHN J 2007; 55: 476. 37- Amernik K, Kabacińska A, Tarnowska C, Paradowska-Opałka B. Acute ear trauma caused by failure of mobile phone/cellular phone. Otolaryngol Pol 2007; 61: 484 - 6. 38- Busaba NY, Rauch SD. Significance of auditory brain stem response gadolinium-enhanced magnetic resonance imaging for idiopathic sudden sensorineural hearing loss. Otolaryngol Head Neck Surg 1995; 113: 271 - 5. 39- Wilson WR, Byl FM, Laird N. e efficacy of steroids in the treatment of idiopathic sudden hearing loss. Arch Otolaryngol 1980; 106: 772 - 6. 40- Laird N, Wilson WR. Predicting recovery from idiopathic sudden hearing loss. Am J Otolaryngol 1983; 4: 161 - 4. 41- Mattox DE, Simmons FB. Natural history of sudden sensorineural hearing loss. Ann Otol 1977; 86: 463 - 80. 42- Lin YT, Young YH. Retrocochlear mass lesion in mid-frequency sudden deafness. Otolaryngol Head Neck Surg 2008; 138: 13 – 17. 43- Yamasoba T, Sugasawa M, Kikuchi S. An electrocochleographic study of acute low-tone sensorineural hearing loss. Eur Arch Otorhinolaryngol 1993; 250: 418 - 22. 44- Wu CL, Young YH. Vestibular evoked myogenic potentials in acute low-tone sensorineural hearing loss. Laryngoscope 2004; 114: 2172 - 5. 45- Saunders JE, Luxford WM, Devgan KK. Sudden hearing loss in acoustic neuroma patients. Otolaryngol Head Neck Surg 1995; 113: 23 - 31. 46- Noguchi Y, Komatsuzaki A, Nishida H. Electrocochleographic study in patients with vestibular schwannomas and U-shaped audiograms. Audiology 2000; 39: 19 - 23. 47- Friedman RA, Kesser BW, Slattery WH. Hearing preservation in patients with vestibular schwannomas with sudden sensorineural hearing loss. Otolaryngol Head Neck Surg 2002; 125: 544 - 51. 48- Fushiki H, Junicho M, Aso S, Watanabe Y. Recurrence rate of idiopathic sudden low-tone sensorineural hearing loss without vertigo: a long-term follow-up study. Otol Neurotol 2009; 30: 295 - 98. 49- Kerber KA. Vertigo and dizziness in the emergency department. Emerg Med Clin North Am 2009; 27: 39 - 50. 50- Bainbridge KE, Hoffman HJ, Cowie CC. Diabetes and hearing impairment in the United States: audiometric evidence from the National Health and Nutrition Examination Survey, 1999 to 2004. Ann Intern Med 2008; 149: 1 - 10. 51- Genden EM, Bahadori RS. Bilateral sensorineural hearing loss as a first symptom of chronic myelogenous leukemia. Otolaryngol Head Neck Surg 1995; 113: 499 - 501. 52- Yamasoba T, Sakai K, Sakurai M. Role of acute cochlear neuritis in sudden hearing loss in multiple sclerosis. J Neurol Sci. 1997; 146: 179 - 81. 53- Rigby PJ. Comparison of FIESTA and gadolinium-enhanced T1-weighted sequences in magnetic resonance of acoustic schwannoma. Radiographer 2006; 53: 11 – 21. 54- Stuckey SL, Harris AJ, Mannolini SM. Detection of acoustic schwannoma: use of constructive interference in the steady state three-dimensional MR. AJNR 1996; 17: 1219 - 25. 55- Marx SV, Langman AW, Crane RC. Accuracy of fast spin echo magnetic reso¬nance imaging in the diagnosis of vestibular schwannoma. Am J Otolaryngol 1999; 20 (4): 211–16. 56- Lee H, Sohn SI, Jung Dk, et al. Sudden deafness and anterior inferior cerebellar artery infarction. Stroke 2002; 33: 2807 – 12. 57- Amarenco P, Hauw J. Cerebellar infarction in the territory of the anterior and inferior cerebellar artery. Brain 1990; 113: 139 - 155. 58- Roquer J, Lorenzo RJ, Pou A. e anterior inferior cerebellar artery infarcts: a clinical-magnetic resonance imaging study. Acta Neurol Scand 1998; 97: 225 - 30. 59- Matsushita K, Naritomi H, Kazui S, Watanabe Y, Okazaki H, Kuriyama Y, Sawada T. Infarction in the anterior inferior cerebellar artery territory: magnetic resonance imaging and auditory brain stem responses. Cerebrovasc Dis 1993; 3: 206 - 12. 60- Amarenco P, Caplan L, Pessin MS. Vertebrobasilar occlusive disease. In: Barnett HJM, Mohr JP, Stein BM, Yatsy FM, eds. Stroke: Pathophysiology, Diagnosis and Management. 3rd ed, New York: Churchill Livingstone; 1998: 551 - 3. 61- Caplan LR. Intracranial branch atheromatous disease. Neurology 1989; 39: 1246 - 50. 62- Scheffler K. A pictorial description of steady-states in rapid magnetic resonance imaging. Concepts Magn Reson 1999; 11: 291 - 304. 63- Schaefer DJ. Safety aspects of switched gradient fields. Mag Reson Imaging Clin N Am 1998; 6: 731 - 48. 64- Tanioka H, Zusho H, Machida T, Sasaki Y, Shirakawa T. High-resolution MR imaging of the inner ear: findings in Ménière’s disease. Eur J Radiol 1992; 15: 83 - 8. 65- Tanioka H, Kaga K, Zusho H, Araki T, Sasaki Y. MR of the endolymphatic duct and sac: findings in Ménière’s disease. AJNR 1997; 18: 45 - 51. 66- Lavi ES, Sklar EM. Enhancement of the eighth cranial nerve and labyrinth on MR imaging in sudden sensorineural hearing loss associated with human Herpesvirus 1 infection: case report. AJNR 2001; 22: 1380 - 2. 67- Meriot P, Marsot-Dupuch K. Imaging of post-traumatic tinnitus, vertigo and deafness. J Radiol 1999; 80: 1780 - 7. REFERENCES Case 3: Left Meniere’s Disease. Male patient aged 25 years old presented with SSNHL and vertigo. Axial FIESTA images endolymphatic sac (arrow) is seen in the right side and not seen in the left side. Case 4: Right Labrynthitis. Female patient, 30 years old presented with severe vertigo and SSNHL. A, Axial post contrast T1WI. B, Coronal post contrast T1WI showing patchy enhancement of the cochlea and vestibule as well as proximal part of the VIII CN (arrow). C & D, Axial FIESTA images showing heterogeneous appearance of the right cochlea with linear hyperintense signals seen in consecutive images (arrows). A B C D Case 5: Right Acoustic Schwannoma. Female patient, 60 years old, presented with right SSNHL. A, Axial high resolution post contrast T1WI showing (arrow) a well-defined homogeneously enhancing lesion is noted in the CPA and internal auditory canal. B, Axial high resolution T2WI showing (arrow) same lesion as hypointense. C, Axial FIESTA shows (arrow) same lesion as hypointense yet, appears well contrasted against high signal of CSF. A B C Idiopathic Cases; 53 Diagnosed Cases; 19 Fig 1. Distribution of the study cases according to their final diagnosis. AN; 2 MD; 3 VN; 1 CSOM; 2 TBF; 2 RWF; 1 CVA; 2 MS; 2 TM; 1 E; 1 L; 2 Fig 2. Distribution of diagnosed cases according to etiology. AN: acoustic neuroma, MD: Meniere’s disease, VN: vestibulococlear neuritis, CSOM: labyrinthitis complicating chronic suppurative otitis media, TBF: longitudinal temporal bone fractures, RWF: round window fistula, CVA: cerebrovascular accidents, MS: multiple sclerosis, TM: temporal lobe meningioma, E: Wernick’s encephalopathy, L: leukemia. Role of Final Diagnosis Clinical evaluation Laboratory Investigations Audiological Evaluation MRI † Case 1 Acoustic Neuroma + - ++ +++ F Case 2 Acoustic Neuroma + - ++ F confirmed Case 1 Meniere’s disease ++ - ++ ++ F Case 2 Meniere’s disease ++ - ++ ++ F Case 3 Meniere’s disease +++ - ++ ++ F Vestibulococlear Neuritis ++ - ++ +++ F Case 1 Labyrinthitis +++ - + F confirmed Case 2 Labyrinthitis +++ - + F confirmed Case 1 TB Fracture +++ - - Not used Case 2 TB Fracture +++ - - Not used Round Window Fistula +++ - + F confirmed Case 1 CVA + - - +++ Case 2 CVA -* - - +++ Case 1 MS - - + +++ Case 2 MS + - + +++ Meningioma - - + +++ Encephalopathy ++ + + +++ Case 1 Leukemia +++ +++ + ++ Case 2 Leukemia - +++ + ++ Table 1: Role of varies diagnostic modalities in establishing the final diagnosis. (-: no role, +: minor role, ++: favorable role, +++: main role, F: FIASTA sequence) (*: the clinical presentation was misleading, †: the role of MRI was either at the time of initial presentation or during the follow-up period to confirm the diagnosis) T1 T2 Post-Contrast FIESTA MS Meningioma CVA Encephalopathy Leukemia Vestibular Neuritis Meniere’s Disease Labyrinthitis Round Window Fistula Table 2. Role of T1 T2 Post-Contrast MRI versus the FIESTA Sequence in diagnosis and conformation of various SSNHL etiologies of the study cases. INTRODUCTION Sudden sensorineural hearing loss (SSNHL) affects 1:10,000 people annually 1 . Although SSNHL is a well-recognized condition, no standard diagnosis or treatment protocol has been accepted 2 . In addition, despite extensive evaluation, an etiology can only be found in 10% to 15% of patients. Viral infections 3 , vascular compromise 4, 5 and cochlear membrane ruptures 6, 7 are a few entities associated with or hypothesized to cause SSNHL. e initial presentation of an acoustic neuroma (AN) may be SSNHL in up to 10% of cases 8 - 11 . Ménière’s disease may also present initially with SSNHL 10% of the time 11 - 13 . Other causes such as syphilis, autoimmune diseases, perilymph fistula, membrane breaks 14 or multiple sclerosis (MS) must also be considered. Certain etiologies could be ruled-out by complete history and physical examination along with certain blood tests (blood count to rule out leukemia, hypercoagulable states, and sickle cell disease; chemistry to evaluate glucose potassium and calcium levels; thyroid function tests; erythrocyte sedimentation rate; rhematoid and antinuclear antigen factors and fluorescent treponemal antibody absorbance for syphilis). Some other important etiologies as Ménière’s disease, MS, vascular or traumatic causes or ANs could not be evaluated without imaging guidance 15 . A better prognosis was found to be related to the prompt administration of steroids 16 , which in turn necessitates rapid approach to the etiology. In addition the hearing loss may be a part of a more serious situation also necessitates extensive work-up 15 . To prove an imaging modality as effective, a statistical analysis in a randomized double-blinded study must be used. Because most of cases usually are presented in a true emergency situation, such a study is not possible. To estimate the role of magnetic resonance imaging (MRI) scan with gadolinium contrast as the single best imaging modality that can diagnose most of these cases, we retrospectively reviewed charts and data of all SSNHL cases attended tertiary referral hospital and then the SSNHL etiologies results were analyzed and the role of the MRI in each of these etiologies was evaluated. A B Case 1: Multiple Sclerosis. Female patient aged 24 years old, presented with left SSNHL. A, Axial T2WI shows multiple oblong shaped hyperintense foci in pons, middle cerebellar peduncles and left cerebellar hemisphere. B, FLAIR image shows the same foci as before. B A Case 2: Left Meniere’s Disease. Axial FIESTA images (A, upper and B, lower level). The endolymphatic sac (arrow) is well seen in the right side and not seen in the left side.

Alaa Ali Abou-Bieh, MD*, Osama Rabie Kombar, MD · 2013. 7. 12. · media cases had their specific history and manifestations at the time of presentation including the long period

  • Upload
    others

  • View
    1

  • Download
    0

Embed Size (px)

Citation preview

Page 1: Alaa Ali Abou-Bieh, MD*, Osama Rabie Kombar, MD · 2013. 7. 12. · media cases had their specific history and manifestations at the time of presentation including the long period

Objective: To estimate the role of magnetic resonance imaging (MRI) scan with contrast and more recently FIESTA sequence as the single best imaging modality that can diagnose most sudden sensorineural hearing loss (SSNHL) cases. MethOds: A retrospective chart and data review study included 72 SSNHL cases between mid 2006 to mid 2008 in a tertiary referral hospital. Beside the imaging studies, data reviewed included history, clinical manifestations, audiological workup, and laboratory in-vestigations. The main outcome measure of this study was the role of MRI to approach the final diagnosis.Results: A final diagnosis could be approached in 19 cases (26%). The etiologies were acoustic neuroma, Ménière’s Disease, vestibulocochlear neuritis, labyrinsitis, temporal bone fractures, round window fistula, cerebrovascular accidents, multiple sclerosis, temporal lobe meningioma, Wernicke’s encephalopathy, and leukemia. MRI, especially FIESTA sequence, could finalize the diagnosis except for traumatic cases.cOnclusiOns: MRI can guide the diagnosis at the time of clinical presentation especially in cases with progressive and more importantly life threatening etiologies. The FIESTA imaging as a stand-alone protocol reduced the examination time and eliminated the need for contrast.

MRI AS SINGLE EARLY DIAGNOSTIC MODALITY FOR SUDDEN SENSORINEURAL HEARING LOSS ETIOLOGY

Alaa Ali Abou-Bieh, MD*, Osama Rabie Kombar, MDDepartments of Otolaryngology* and Radiology, Faculty of Medicine, Mansoura University, Mansoura, Egypt

PATIENTS AND METHODSThis study included 72 cases in a retrospective manner. It reviewed all the available data and charts regards all cases of SSNHL met the study’s case inclusion criteria. These criteria were to include any case of SSNHL presented over the period of two years, between mid 2006 to mid 2008 in a tertiary referral hospital, regardless the case presented with isolated SSNHL or other associated symptoms. The term sudden was restricted to events occurring instantaneously or developing over a period not exceeding 3 days. SSNHL was defined as at least a 30-dB sensorineural hearing loss, occurring in at least 3 frequencies. All patients were seen within 7 days of onset of hearing loss 2. Postoperative SNHL cases and other iatrogenic cases were excluded.Data reviewed included, age, sex, smoker or not, main complaint and clinical presentation; local and systemic history and examination, laboratory results, audiological evaluation and imaging modalities used. The clinical examination included local otological examination and otomicroscopic examina-tion. The cases were considered with positive findings if there were any type of perforation and / or other pathological findings or any vestibular manifestations. Tuning fork tests also were done for each patient. Audiologial assessment included pure tone audiograms, speech testing (speech reception thresholds and speech discrimination), and otoacoustic emissions. In some cases, auditory brainstem response and vestibular function tests were also done. The laboratory investigations included the basic evaluation test battery (CBC, sedimentation rate, blood sugar, renal and liver function tests) and included specific investigations, when indicted according to the suspected etiology. Imaging studies in these cases at the time of the initial presentation or, in some cases, after a period from the initial presentation were also reviewed. Mostly these studies included CT scans either with or without contrast and / or MRI scans with or without contrast.The MRI technique was performed using 1.5 Tesla (GE, Signa Excite® 1.5 T, United Kingdom), with a dedicated coil. The following sequences were done while the patient was lying on supine position, sagittal T1 WI with FOV 24, slice thickness 5 mm and slice interval about 1.5 mm, matrix 256 x 256 followed by coronal T1 WI with the same parameters but matrix 256 x 224 and then axial T2 WI with FOV 26 and slice thickness and gap as before too, yet matrix 448 x 224. High resolution axial T1 WI and axial T2 WI were then performed: FOV 18, slice thickness 3 mm and slice interval 0.3 mm. 3D FIESTA parameters were FOV 20, slice thickness 1.2 mm and locs/slab= 32. In cases where intravenous Gadolinium was used, axial T1 HR with gadolinium was obtained at FOV 18, slice thickness 3 mm and slice gap 0.3 mm. Matrix for HR axial images was 256x 224 and For FIESTA 448 x 224.The final diagnosis for all cases, which in some cases proved after a period of follow-up, was reviewed. The cases then could be separated into two main categories, cases in which a diagnosis could be reached and those without clear diagnosis. The role of the imaging modality used in aiding this diagnosis, were also reviewed. The main outcome measure of this study was estimating the role of MRI in investigating the possible etiologies and approaching the final diagnosis of the cases. However, because this was a retrospective study, some of the cases did not have MRI during the course of the disease or the follow-up period, therefore the study reviewed the role of MRI in the diagnosis of these cases.Statistical analysis was undertaken with the statistics program SPSS® for Windows® (version 5; SPSS, Inc., Chicago, IL). Student’s t test and χ2 test were used for statistical analysis of the mean values of the outcome measures and variables of the two groups. A single factor Analysis of Variance (ANOVA), using repeated Fisher exact test, was also used to study the liner representation of the means. The difference would be accepted as statistically significant if the value of P was < 0.01.

ABSTRACT RESULTS

The total number of the study cases was 72 cases, while reviewing the data of these cases a final diagnosis was found in 19 cases (26%). The cases were 2 acoustic neuroma cases, 3 Ménière’s disease cases, 1 case of vestibulococlear neuritis, 2 cases of labyrinthitis complicating chronic suppurative otitis media, 2 cases of longitudinal temporal bone fractures, 1 round window fistula case, 2 cerebrovascular accidents cases, 2 multiple sclerosis cases, 1 case of temporal lobe meningioma, 1 case of Wernick’s encephalopathy and 2 leukemia cases. Fifty-three cases diagnosed as idiopathic cases.The mean ages of the study cases were 53 years (range, 17 - 73 years). There were 40 males and 32 females. There was no significant statistical difference regards the age distribution or sex representation (P = 0.09 and 0.02 respectively). Forty-eight cases were presented with right sided hearing loss and 24 cases had left sided hearing loss. Side representation showed significant difference (P = 0.008). Three cases (4%) developed contra-lateral SNHL after the initial presentation. Smokers were 29 cases (40% of the total study cases). Smokers were 26 males (65% of the study males) and 3 females (9% of the study females). Smokers males were statistically significant (P = 0.005).The initial presentations were hearing loss only in 23 cases (32%), hearing loss and vertigo in nine cases (12.5%), hearing loss and tinnitus in 18 cases (25%) and hearing loss, vertigo and tinnitus in 22 cases (31%). Only seven cases (10%) were presented in the first day of the complaint, and they mostly came due to vertigo rather than the hearing loss, 19 cases (26%) were presented in the second day, 24 cases (33%) were presented from third to fifth day and 22 cases (31%) were presented on the sixth and seventh days. The hearing loss occurred suddenly in 23 cases (32%) and progressed over a period ranged from one to three days in 49 cases (68%). Eighteen cases (25%) typically presented with the hearing loss noticed upon awakening or they were awakened by an attack of sever vertigo associated with or directly followed by the hearing loss. Pain was present in two cases (3%). The pain was described as sever and located over the mastoid. Seven cases (10%) described ear fullness sensation. Only one of them diagnosed as Ménière’s disease later. Except for one of the traumatic cases, none of the cases had facial nerve weakness symptoms at the time of presentation. The two chronic suppurative otitis media cases had their specific history and manifestations at the time of presentation including the long period of otorrhea.Thirty-two cases (44%) were diabetics, 26 of them (81%) were on insulin therapy. Forty-five cases (62.5%) were known or discovered to be with hyperlipoproteinemia. Thirty-nine cases (54%) were hypertensive and on oral anti-hypertensives. Two cases (3%) were know atopic patients. One case (1%) was known leukemia case in remission phase. Another case (1%) was known hypercoagulable states patient. Three cases (4%) were hepatics. Two cases (3%) had renal impairment (one was on regular dialysis and one had renal transplantation 4 years before his presentation). One case (1%) had hypo-thyroidism. Among the study population, diabetes incidence, hyperlipoproteinemia and hypertension showed statistical significance (P = 0.005, = 0.008 and = 0.006 respectively).None of the cases was known or found to have later on any congenital malformations of the temporal bone or auditory system. All the three traumatic cases were presented with history of direct or indirect temporal bone trauma (2 cases of longitudinal temporal bone fractures due motor vehicle ac-cident and falling from height and the case of round window fistula was after direct slap). At the time of presentation, a history for upper respiratory tract infection or viral prodrome was obtained in 64 cases (89%). This history even was obtained in some of the cases which were diagnosed as acoustic neuroma or Ménière’s disease later on. None of the cases was known as syphilitic or HIV patients. Except for the regular use of aspirin, the tracing of ototoxic use history was very difficult due to lack of previous data and filing. Forty-nine (68%) cases were using aspirin regularly as conjunctive prophy-laxis of cerebrovascular accidents. The use of aspirin was of statistical significance (P = 0.009). Three cases (4%) were alcoholic.Apart from the tuning fork findings, most of the cases did not show specific signs. Horizontally beating toward the affected side nystagmus was present in 4 cases only (6%). One of the acoustic neuroma cases showed grade 2 facial nerve weakness after 10 days of initial presentation although the case was on corticosteroid treatment during this time. The two cases of labyrinthitis complicating chronic suppurative otitis media showed cholesteatoma manifestation and the two cases of longitudinal temporal bone fractures showed battle sign and tympanic membrane rupture, facial nerve involvement in one case together with other injuries. The round window fistula case presented with nystagmus, but no other clinical findings. The two cerebrovascular accidents cases, although mainly presented with hearing loss and vertigo, another neurological deficits could be detected on examination. The two multiple sclerosis cases had no other specific signs at the time of presentation. The temporal lobe meningioma case had considerable headache complaint and neuro-ophthalmic manifestation as diplopia on presentation. The case of Wernick’s encephalopathy although presented initially by vertigo, ny-stagmus and hearing loss, patient rapidly progressed into confusion and altered consciousness. The two leukemia cases, one was known case during remission period and the other discovered to have the disease only during the laboratory investigations.Besides the general laboratory test battery, certain specific laboratory investigations were done for some cases. Serological studies showed normal titers of antibodies against herpes virus including cytomegalovirus. Blood studies and bone marrow studies were also done for suspected blood diseases cases. Rheumatoid and antinuclear antigen factors were significant in one case, but still this case classified as idiopathic due to the treatment protocol. None of the cases went lumber puncture or CSF testing.The pure tone audiometry showed a flat curve in 25 cases (35%), high frequency loss in 21 cases (29%), low frequency loss in 12 cases (17%) and profound loss in 14 cases (19%). Speech discrimination was significant in four cases included the acoustic neuroma cases, the multiple sclerosis cases and the temporal lobe meningioma case. The otoacustic emissions were significant only in the vestibulococlear neuritis case, mainly to differentiate it from auditory neuropathy. Auditory brainstem response was significant only in the cases of acoustic neuroma and multiple sclerosis cases.Of the 72 cases included in the study, 63 cases (88%) had one or more imaging study at certain point of the disease course. Imaging studies of these cases at the time of the initial presentation or, in some cases, after a period from the initial presentation were influenced mainly by the case history and initial presentation. In addition, as a general notice, there was chronologically progressive usage of the MRI in diagnosis of cases over the reviewed period. Nineteen cases (30%) had CT scans only, 24 cases (38%) had MRI only, while 20 cases (32%) had both of them. Of the 19 cases that had CT scans only, 15 cases (79%) had the scans done during the first 48 hours of the clinical presentation. The CT scans aided the diagnosis of a case of acoustic neuroma, the two cases of labyrinthitis complicating chronic suppurative otitis media, the 2 cases of longitudinal temporal bone fractures and the two cerebrovascular accidents cases. Only three cases (12.5%) of the 24 cases that had MRI only were done during the first three days of the initial presentation, one of them aided the diagnosis of the Wernick’s encephalopathy and another one diagnosed the case of the vestibulococlear neuritis. The other 21 cases (87.5%) had the study between one week to six months. These studies aided the diagnosis of the three Ménière’s disease cases, one of the multiple sclerosis cases and 1 of the leukemia cases. The other acoustic neuroma case, the round window fistula case, a multiple sclerosis cases, the tempo-ral lobe meningioma case and a leukemia case were diagnosed by both CT and MRI scans. According to the number of cases and the need of using more than one technique to diagnose the cases, MRI usage showed statistical significance than CT scans (P = 0.005). This was after the exclusion of the traumatic cases.

DISCUSSIONThe important first step in treating patients with SSNHL is not to decide which of the plethora of treatment modalities to use, but rather to ensure that it is idiopathic 17. Sometimes the identifiable medical problem, which the hearing loss is associated with, can be more important to the patient survival than the symptom itself 15. In these cases, treatment should be directed toward correction of this problem more than reversing the symptom only as in idiopathic cases in which successful resolution of SSNHL will occur in a majority of patients with or without treatment 18. The most popular theories of idiopathic SSNHL include viral infection theory, vascular insult or ischemia theory and the membrane rupture theory 1, 3, 4 - 8, 15 - 21. Among the other etiologies of the SSNHL may be etiologies that may lead to an irreversible morbidity, either locally or systematically, as the perilymph fistula or even may endanger the patient life as the cerebro-vascular accidents and encephalopathy 22. These etiologies can only be diagnosed by imaging studies. In addition, the usage of imaging studies in these cases needs a reliable protocol due to the time sensitivity and the trial and error is not appropriate in these cases and sometimes the lack of detailed medical history make these studies, especially the contrast dependent types, a challenge. The role of CT scans with or without contrast versus MRI studies with different protocols in the early diagnosis of the etiology of the SSNHL was the concern of our study. There is no doubt that in certain clinical presentations the choice and protocol of the imaging modality are clear. This is as in the cases of trauma and chronic suppurative otitis media and the clear role of CT scans in these situations. However still the dilemma is when the clinical presentation is unclear or suspicious of some serious situations as in cerebro-vascular accidents and encephalopathy or when the patient is presented with severe vertigo makes it impossible to rule out any center etiology. Moreover, this was the situation when we retrospectively reviewed the SSNHL cases presented in our ter-tiary referral hospital over two years period. Imaging studies in these cases at the time of the initial presentation varied a lot and did not follow a specific protocol. In some cases, no imaging studies were done at all at this time and elective studies were used after this. In some other cases, MRI scans were done at admission. While in other cases, CT scans only were done at admission and then in some cases MRI scans followed this to establish the diagnosis. Therefore, the absence of clear protocol for imaging studies in an important emergency like the SSNHL was the main trigger for our study.The definition of SSNHL varied between the published literatures. Duckert and Meyerhoff 15 changed the past definition of hearing loss that occurred over a period of several seconds up to 5 to 7 days to any sensorineural hearing loss, usually unilateral, and accompanied by tinnitus in about 70 percent of patients and vertigo in 50 percent of patients. They also used a more limited and appropriate definition of sudden that included those losses occurring instantaneously or within a matter of hours. Fetterman et al 23, Zadeh et al 2, Psifidis et al 24 and Yeo et al 25, restricted the term sudden to events oc-curring instantaneously or developing over a period not exceeding 3 days and defined SSNHL as at least a 30-dB sensorineural hearing loss, occurring in at least 3 frequencies provided that patients were seen within 7 days of the onset of the hearing loss. The current study followed the same definition of SSNHL. Most cases of SSNHL develop unilaterally, and bilaterally developed disease only comprises 0.44 percent to 3.4 percent of patients with SSNHL 26 – 28. It was reported that bilateral SSNHL is related mainly to systemic diseases as cerebro-vascular insufficiency 29 and leukemia 30. Idiopathic bilateral SSNHL is extremely rare and its pathophysiology is not known 28. Although the presumed causes such as viral infection, circulatory insufficiency, or labyrinthine membrane rupture, similar to the causes of the unilateral form have been raised, bilateral onset of this disease may be closely con-cerned with systemic disease 26 – 30. In our present work, none of the cases was presented with bilateral hearing loss even in the cases that were associated with systematic etiology as cerebro-vascular accidents or leukemia. Three of the idiopathic cases were presented by SSNHL in the contra-lateral side after about 8 - 14 months of their initial presentation. Another two cases also of the idiopathic cases had recurrent attack of SSNHL in the same ear after the improvement of the hearing loss resulted from the first attack. The reviewed study data other than the proposed SSNHL etiology and imaging modalities were chosen for two main reasons, their effect or relation to the incidence and etiology of SNHL and to ensure that the results were unbiased due to certain factor. The patient’s age was found to be an important risk factor in the incidence of all types of SNHL 31, 32. El Zir et al 31 reported that the ages over 40 were an additive risk factor for high frequencies hearing loss especially with smoking and noise exposure. However, in our present study age was of no statistical significance. The difference between age rep-resentation in the present work and published literatures might be due to that mostly cases of younger ages seeks the medical advice as they are more concerned about their hearing. In addition, in older cases the attack may pass un-noticed due associated systematic morbidity or symptoms that may be more significant or if the patient is bed ridden and reluctant to seek medical advice. Smoking and noise exposure were also found to be very important risk factors in SNHL incidence 31 - 33. Pouryaghoub et al 33, in a cross-sectional study that was designed to study the effect of smoking on noise induced hearing loss, observed that the percentage of workers with hearing loss was greater in smokers and they concluded that smoking could accelerate noise induced hearing loss. In our present work, male smokers were statistically significant; however, the female smokers were statistically un-significant. The available data in our study cases files did not show the history or any details about noise exposure, therefore it was not included in the analysis. The male to female incidence of SSNHL was statistically equal in the published literature 2, 32 and this was the same in the present work. Side representation in our present work showed statistical significant difference. The incidence of the SSNHL was double on the right side; this was mainly with the idiopathic cases. Although we could not fined any relevant data about side representation in the published literature, we suggested that the higher incidence of the SSNHL on the right ear was due to the use of cellular phones, mobile devices and music players by the dominant right hand. Reporting of associated SNHL with the use of these devices increased in the last years in the published literature 34 - 37.On reviewing the published other factors that might be correlated with incidence and recovery of SSNHL, Busaba and Rauch 38, Wilson et al 39, Laird and Wilson 40, and Mattox and Simmons 41, mentioned that the interval between the onset of symptoms and initiation of therapy, severity of the hear-ing loss, presence of vertigo, reduced calorics on electronystagmography, discrimination score and shape of the audiogram came after the age of the patient in the order of importance. Although the present study was concerned mainly with the etiology of the SSNHL and its diagnosis rather than the prognosis, the study chose to review most of these factors, still with the aim of investigating their influence on diagnosis. From this point of view, the study cases data about the initial presentation and the time until patients sought medical advice showed some characterization of these cases according to etiology. In most of the idiopathic, multiple sclerosis, acoustic neuroma, meningioma and leukemia cases the main presentation was hearing loss only or associated with tinnitus more than with vertigo and mostly these were the case presented by hearing loss that occurred suddenly, usually the typi-cally noticed upon awakening and not associated by other symptoms as pain or fullness. These were the cases usually presented late. While in cases diagnosed as Meniere’s disease, vestibulococlear neuritis or labyrinthitis the main presentation was vertigo associated the hearing loss or tinnitus and mostly the hearing loss progressed over the time rather than occurred suddenly with progressive associated symptoms as pain or fullness and these were the cases usually presented early due to vertigo. It was the same situation in round window fistula case, but vertigo was more sever and incidence was abrupt. In cases with central etiologies as cerebrovascular accidents and encephalopathy cases, again the vertigo and rapid deterioration were the main characteristic presentations. The important notices from all the data were that mostly the vertigo was important for patients and the main reason for very early presentation, while the tinnitus was the important complaint of late presenters, and usually late presentation and order of complaints importance for the patients mislead for approaching etiological diagnosis. An effective strategy was proposed by Kerber 49 as a key to the evaluation and management of vertigo and dizziness emergency presentations. This strategy for «ruling-out» a serious disorder, such as stroke, by «ruling-in» a peripheral vestibular disorder was based on trials to found the differences in initial presentations and characteristic features that allow for a bedside diagnosis.Although the studying of patterns of recovery was aim of Zadeh et al 2 from categorizing the audiograms into 4 sensorineural types: up-sloping, down-sloping, mid-frequency “U-shaped” and profound loss, we used the same method with the aim of recognizing the pattern of audiograms in each etiologi-cal group. Lin and Young 42, 44 reviewed 556 cases of mid-frequency sudden deafness of four audiometric configurations, flat-type, high-frequency type, low-frequency type and mid-frequency type. They found 17 cases with retro-cochlear tumors, 10 were of mid-frequency type audiograms, four were of high-frequency type audiograms, two of flat-type audiograms and one of low-frequency type audiograms. Due to the significantly higher incidence retro-cochlear tumors with mid-frequency type audiograms, they concluded that one-third of the patients with mid-frequency sudden deafness harbor a true retro-cochlear mass lesion and hence MR imaging is mandatory in such cases. In addition, the mid-frequency SSNHL were classified by Saunders et al 45 and Noguchi et al 46 as another independent disease entity from sudden deafness, which is defined as sudden-onset sensorineural hearing loss

worse in the middle frequencies (1000-2000 Hz) than in the high (4000-8000 Hz) and low frequencies (250-500 Hz), representing a U-shaped or saucer-type audiogram. The proposed mechanisms by the vestibular schwannoma may cause this hearing loss might be compression of the cochlear nerve, nerve conduction block, vascular compression, or toxic/metabolic effects of the tumor 45 - 47. Yamasoba et al 43 found that SSNHL of low-tone hearing loss and with relative preserved high-tones hearing was mostly idiopathic sensorineural hearing loss of acute onset. Wu and Young 44 reported also that this type usually improved soon after the onset of symptoms (< 3 days) and tended to return to almost-normal levels. The hearing loss associated with Ménière’s disease usually involving the low frequencies and the audiogram will manifest low-frequency, inverted ‘V’ low- and high-frequency or flat SNHL. In addition, Fushiki et al 48 noticed that the low-tone idiopathic SSNHL without vertigo was recurrent and progressive to Ménière’s disease. They retrospectively followed-up 82 patients diagnosed with idiopathic SSNHL of low-tone type without vertigo for the recurrence rate according to the results of electronystagmography (ENG) and electrocochleography (ECochG) tests at the onset of the first episode of hearing loss. The found that 40% of the patients experienced recurrent hearing loss at least 45% of them had the recurrence within 6 months from the first episode of hearing loss. In our series, results showed that most of the cases with central and retro-cochlear etiologies had flat curve or high-frequency loss, while cochlear lesions showed low-frequency loss. Idiopathic cases had now fixed pattern. Although speech discrimination and auditory brainstem response were significant in retro-cochlear lesions and the otoacustic emissions were significant in the vestibulococlear neuritis case, still finding fixed audiological pattern of characterization was not possible. Busaba and Rauch 38 found that approximately a fourth of the patients with idiopathic SSNHL had abnormal auditory brainstem responses and these were the cases with a less favorable hearing outcome compared with those with normal auditory brainstem responses, irrespective of treatment. They presumed that the auditory brainstem response abnormality might reflect cochlear neuritis or a more extensive involve-ment of the auditory system. They proposed that in these cases high signal intensity along the course of the eighth cranial nerve may be seen on Gadolinium-MRI, but they found that such a finding was not common, and its clinical implications were not known. Our results regard the vestibulococlear neuritis case showed the reverse, the neuritis could only be detected by the MRI and the auditory brainstem responses were not significant in this case. Our data also showed that vestibular function tests did not add final diagnosis to any case. These tests may be of prognostic value 38 - 41. In addition, in the current study, no attempt was done to study the follow-up periods or prognosis as the main aim was the diagnosis of etiology at the time of initial presentation.Laboratory investigations for either predisposing factors or certain specific etiologies proved to be of special importance. Laboratory work-up could be of the bedside methods for ruling-out serious disorders 49. This is due to the short duration and availability in comparison to other methods as audio-logical or imaging investigations. Diabetes is one of the most important risk factors as it might affect the vasculature and neural system of the inner ear, leading to the hearing impairment 50. The present work data showed that diabetes, hyperlipoproteinemia and hypertension were the most prevalent predisposing factors, which was the same found in the previously published reports 15 - 50. In addition, laboratory work-up was the main reason to diagnosis the two serious cases of leukemia. Although the incidence of acute-onset sensorineural hearing loss as the first sign of leukemia is rare, but it was previously reported and mainly the reason for the hearing loss is inner ear hemorrhage 15 - 51.The routine MRI technique was sufficient to diagnose two cases of MS, one case of temporal lobe meningioma, two cases of CVA, one case of Wernick’s encephalopathy, as well as two cases of leukemia.The two cases of MS we found, and were the cause of SSNHL, the findings were multiple plaques that are seen along the deep white matter and corpus callosum, specifically, multiple plaques are seen in the brain stem and one case in both cerebellar peduncles as well as left cerebellar hemisphere. Yamasoba et al 52, reported a patient with definite multiple sclerosis (MS) who developed unilateral sudden hearing loss coincident with exacerbation of central nervous system symptoms.Cerebrovascular accidents with SSNHL usually are infarctions in the territory of the anterior inferior cerebellar artery (AICA) and typically involving the middle cerebellar peduncle 56, 57, 58. In a study by Lee et al 56, MRI could identify and localize the area of infarction in the middle cerebellar peduncle and/or infarction in the anterior inferior cerebellum in 11 of 12 patients. They also found that SSNHL was a common sign of AICA infarction and suggested that in most cases the hearing loss and tinnitus were resulted from cochlear injury. In general, the most common mechanism of AICA infarction is by formation of atheroma or thrombus in the parent basilar artery blocking the orifice of the AICA or a dolichoectatic basilar artery, which has previously been associated with AICA stroke 59, 60. In our work, we had two cerebrovascular accident cases with typical infarction in the territory of AICA, displayed as cortical and subcortical hypointense signal during T1WI and hyperintense during T2WI seen in the middle cerebellar peduncles and anterior inferior aspect of the cerebellar hemisphere. Where as FIESTA was used to diagnose one case of vestibular neuritis, three cases of Ménière’s disease, two cases of CSOM and ototic labyrinthitis and as a confirmatory for one case of traumatic R.W fistula.Fast imaging employing steady state acquisition (FIESTA) is the sequence that employs gradients to induce a constant or steady amount of transverse magnetisation. FIESTA is a true-FISP (Fast Imaging with Steady-state Precession) sequence 61. This sequence uses very short TRs and TEs, and produces images with high signal to noise ratios (SNR). Balanced gradients refocus transverse magnetisation at the completion of each TR cycle. The short TRs used in FIESTA imaging are essential to maintaining this spin coherence 62. The FIESTA sequence may be thought of as a fluid-bright sequence. These sequences are those in which fluids exhibit hyperintensity compared to surrounding tissues. When studying the CPA and basal cisterns, CSF is uniformly hyper-intense in these sequences 63. We had two cases of AS, that were diagnosed with FIESTA technique and high resolution T1WI post contrast MRI as well in one case only. The showannoma was elicited as a well defined homogenous intensity lesion seen in CPA and internal auditory canal with isointense signal during T1WI and T2WI and showing marked homogenous enhancement during post contrast study. FIESTA images shown these lesions as isointense, yet well surrounded with hyperintense signal of the CSF, it produces, so that it appears well without need for contrast injection.Those patients whose FIESTA sequence demonstrates pathology in the CPA should be further examined by post-contrast T1-weighted sequences. In addition, in cases where gadolinium may not be administered, such as preg¬nant patients or patients with known sensitivity to gadolinium, the FIESTA sequence may be used in isolation from contrast-enhanced T1-weighted sequences to exclude AS. In these cases, the use of the FIESTA sequence would appear sufficient to exclude AS, without the need for gadolinium-enhanced sequenc¬es. This would agree with Stuckey et al, who found that in the absence of T1-weighted gadolinium-enhanced sequences, CISS images were sufficient to diagnose or exclude AS 54, 55.Rigby 53, added that The advantages of FIESTA imaging as a stand-alone protocol for AS include: Reduced time, no contrast administration required, detailed anatomy of he inner ear; and 3D imaging – the FIESTA images can reformatted into thinner/thicker slices, and Maximum Intensity Projec-tions (MIP) images created. In order to maintain a high level of signal to noise, the slice thickness of the T1-weighted sequences is limited to 1.5–3 mm, so characterization of small lesions is not possible. The FIESTA sequence allows sub-millimeter sections, permitting better depiction of small tumors. The study used 3D FIESTA sequence for a slice thickness of 1.2 mm, with overlap of 0.6 mm. These fine sections allow reformatting to any slice thickness or orientation, and Maximum Intensity Projections (MIP) images. The disadvantages of FIESTA -only protocol for the exclusion or diagnosis of AS without post-Gadolinium T1-weighted scans include: further characterization by post-contrast T1-weighted images, other pathologies of inner ear may be missed; post-operative changes appear to be better demonstrated by post-contrast T1-weighted images, cystic degeneration of the AS is possible, and may be a marker of a fast growing tumour. The post-contrast sequence demonstrated this change, while the FIESTA sequence did not. Other pathologies of the CPA may be better characterised by the post-gadolinium T1-weighted images than the FIESTA sequence, including epidermoid cysts, arachnoid cysts and metastasis.Our results in the three cases of Ménière’s disease, were well diagnosed with FIESTA as it delineated the endolymphatic sac and duct in unaffected side with proper adjustment of the window width and window level, yet, it did not appear at all in the affected side. This is coinciding with results of Tan-ioka et al 64, who stated: symptoms in Ménière’s disease are characterized by hydrops of the endolymphatic system with recurrent rupture of the membranous labyrinth. The membranous endolymphatic duct and sac are identified only with high resolution MRI (HR-MRI). In addition, Rigby 53, stated that the fluids of the inner ear (perilymph and endolymph) appear hyper-intense on the FIESTA sequence, allowing visualization of the cochlear and semi-circular canals, which is not possible on the T1-weighted sequences in this study. In a study by Tanioka et al 65, they found that in patients experiencing an acute episode of Ménière’s disease, the endolymphatic duct and sac were not adequately visible in the affected ear but were seen well in the unaffected ear. During remission, the endolymphatic duct and sac were not visible in pa-tients with clinically advanced disease, but were seen well in the early to intermediate stages of disease.Our results for the case of vestibular neuritis showed linear enhancement of the VIII CN along its canalicular course, mainly proximal part and in the two cases of labyrinthitis that showed patchy enhancement of the cochlea and interrupted segments of the cochlear nerve. This coincide with Lavi and Sklar 66, who demonstrated obvious enhancement of the intracanalicular portion of the eighth cranial nerve and to less extent enhancement of the labyrinth involving the basal turn of the cochlea on the right and left vestibule. We had one case of traumatic R.W. fistula, that demonstrated fluid signal intensity mainly during T2WI in middle ear and that coincide with Meriot and Marsot-Dupuch 67, they found an abnormal non-enhancing high signal T1 of the membranous labyrinthine fluid on MRI.In an attempt to put a flow chart for proceeding in diagnosis of the sudden sensoryneual HL, we suggest that MRI including FIESTA technique is the modality of choice, based on Rigby 53, who stated that by limiting the pre- and post-contrast T1-weighted sequences to a targeted patient population (i.e. those with pathology seen on the FIESTA sequence), there are savings to be made. These savings are in terms of: time saving; avoiding cost and risk of adverse reaction of gadolinium contrast. All may be achieved without compromise of the patient. In addition to the statements of Stuckey et al 54

and Marx et al 55, who stated that a screening sequence for exclusion of AS should be sensitive, specific, inexpensive and non-invasive when compared to the use of gadolinium-enhanced T1-weighted sequence. By these criteria, the FIESTA sequence is an ideal tool for investigation of possible AS.So that, our idea is first to assess whole brain and presence of a mass lesion in the CPA region with routine MRI including FIESTA upon temporal bone region and skull base, so that if present, this may be sufficient and if not we must proceed into intravenous contrast administration so as to evaluate viral infection (labyrinthitis and vestibulocochlear neuritis) and other etiologies. While, if the case is traumatic or CSOM, we should to start with high resolution CT.

CONCLUSIONS

MRI can guide the diagnosis at the time of clinical presentation especially in cases with progressive and more importantly life threatening etiologies provided that the cases are not traumatic or chronic suppurative otitis media cases, as these are the situations where starting with high resolution CT scans is the rule. The FIESTA imaging as a stand-alone protocol reduced the examination time and eliminated the need for contrast.

1- Mattox DE, Lyles CA. Idiopathic sudden sensorineural hearing loss. Am J Otol 1989; 10: 242 - 7. 2- Zadeh M, Storper I, Spitzer J. Diagnosis and treatment of sudden-onset sensorineural hearing loss: A study of 51 patients. Otolaryngol Head Neck Surg 2003; 128: 92 - 8.3- Wilson WR. The relationship of the herpes virus family to sudden hearing loss: a prospective clinical study and literature review. Laryngoscope 1986; 96: 870 - 7.4- Yamasoba T, Kikuchi S, Higo R. Sudden sensorineural hearing loss associated with slow blood flow of the vertebrobasilar system. Ann Otol Rhinol Laryngol 1993; 102: 873 - 7.5- Biavati MJ, Gross JD, Wilson WR, et al. Magnetic resonance imaging evidence of a focal pontine ischemia in sudden hearing loss and seventh nerve paralysis. Am J Otol 1994; 15: 250 - 3.6- Feldmann H. Sudden hearing loss with delayed onset following head trauma. Acta Otolaryngol 1987; 103: 379 - 83.7- Harris I. Sudden hearing loss: membrane rupture. Am J Otol 1984; 5: 484 - 7.8- Cole RR, Jahrsdoerfer RA. Sudden hearing loss: an update. Am J Otol 1988; 9: 211 - 5.9- Berg HM, Cohen NL, Hammerschlag PE, Waltzman SB. Acoustic neuroma presenting as sudden hearing loss with recovery. Otolaryngol Head Neck Surg 1986; 94: 15 - 22.10- Chow JM, Garcia J. Acoustic neuroma presenting as sudden hearing loss. Am J Otolaryngol 1985; 6: 115 - 9.11- Pensak ML, Glasscock ME III, Josey AF, Jackson GC, Guyla AJ. Sudden hearing loss and cerebellopontine angle tumors. Laryngoscope 1986; 95: 1188 - 93.12- Hallberg OE. Sudden deafness of obscure origin. Laryngoscope 1956; 66: 1237 - 67.13- Nadol JB Jr, Weiss AD, Parker SW. Vertigo of delayed onset after sudden deafness. Ann Otol Rhinol Laryngol 1975; 84: 841- 6.14- Simmons FB. Theory of membrane breaks in sudden hearing loss. Arch Otolaryngol 1968; 88: 67 - 74.15- Duckert LG, Meyerhoff WL. Sudden Hearing Loss. In: Meyerhoff WL, Liston S, Anderson RG, eds. Diagnosis and management of hearing loss. Philadelphia: W. B. Saunders; 1984: 43 - 64.16- Tucci DL, Farmer JC Jr, Kitch RD, Witsell DL. Treatment of sudden sensorineural hearing loss with systemic steroids and valacyclovir. Otol Neurotol 2002; 23: 301 - 8.17- Grandis JR, Hirsch BE, Wagener MM. Treatment of idiopathic sudden sensorineural hearing loss. Am J Otol 1993; 14: 183 - 5.18- Mattox DE, Simmons FB. Natural history of sudden sensorineural hearing loss. Ann Otol Rhinol Laryngol 1977; 86: 463 - 80. 19- Fisch U. Management of sudden deafness. Otolaryngol Head Neck Surg 1983; 91: 3 - 8.20- Einer H, Tenghorn L, Axelsson A, Edstrom S. Sudden sensorineural hearing loss and hemostatic mechanisms. Arch Otolaryngol Head Neck Surg 1994; 120: 536 - 40.21- Simmons FB. Theory of membrane breaks in sudden hearing loss. Arch Otolaryngol 1968; 88: 67 - 74.22- Weber PC, Zbar RI, Gantz BJ. Appropriateness of magnetic resonance imaging in sudden sensorineural hearing. Otolaryngol Head Neck Surg 1997; 116: 153 - 6.23- Fetterman BL, Saunders JE, Luxford WM. Prognosis and treatment of sudden sensorineural hearing loss. Am J Otol 1996; 17: 529 - 36. 24- Psifidis AD, Psillas GK, Daniilidis JC. Sudden sensorineural hearing loss: Long-term follow-up results. Otolaryngol Head Neck Surg 2006; 134: 809 - 15.25- Yeo SW, Lee DH, Jun BC, Park SY, Park YS. Hearing outcome of sudden sensorineural hearing loss: Long-term follow-up. Otolaryngol Head Neck Surg 2007; 136: 221 - 4.26- Yanagita N, Murahashi K. Bilateral simultaneous sudden deafness. Arch Otorhinolaryngol 1987; 244: 7 - 10.27- Fetterman BL, William ML, Saunders JE. Sudden bilateral sensorineural hearing loss. Laryngoscope 1996; 106: 1347 - 50.28- Oh JH, Park K, Lee SJ, Shin YR, Choung YH. Bilateral versus unilateral sudden sensorineural hearing loss. Otolaryngol Head Neck Surg 2007; 136: 87 - 91.29- Lee H, Whitman GT, Lim JG. Bilateral sudden deafness as a prodrome of anterior inferior cerebellar artery infarction. Arch Neurol 2001; 58: 1287 - 89.30- Veling MC, Windmil I, Bumpous JM. Sudden hearing loss as a presenting manifestation of leukemia. Otolaryngol Head Neck Surg 1999; 120: 954 - 6.31- El Zir E, Mansour S, Salameh P, Chahine R. Environmental noise in Beirut, smoking and age are combined risk factors for hearing impairment. East Mediterr Health J 2008; 14: 888 - 96.32- Brors D, Eickelmann AK, Gäckler A, Sudhoff H, Lautermann J, Dazert S, Kunstmann E. Clinical characterization of patients with idiopathic sudden sensorineural hearing loss. Laryn gorhinootologie 2008; 87: 400 - 5.33- Pouryaghoub G, Mehrdad R, Mohammadi S. Interaction of smoking and occupational noise exposure on hearing loss: a cross-sectional study. BMC Public Health 2007; 7: 137.34- Oktay MF, Dasdag S. Effects of intensive and moderate cellular phone use on hearing function. Electromagn Biol Med 2006; 25: 13 - 21.35- Al-Dousary SH. Mobile phone induced sensorineural hearing loss. Saudi Med J 2007 Aug; 28: 1283 - 6.36- Loftis M. Sources of noise-induced hearing loss. AAOHN J 2007; 55: 476.

37- Amernik K, Kabacińska A, Tarnowska C, Paradowska-Opałka B. Acute ear trauma caused by failure of mobile phone/cellular phone. Otolaryngol Pol 2007; 61: 484 - 6.38- Busaba NY, Rauch SD. Significance of auditory brain stem response gadolinium-enhanced magnetic resonance imaging for idiopathic sudden sensorineural hearing loss. Otolaryngol Head Neck Surg 1995; 113: 271 - 5.39- Wilson WR, Byl FM, Laird N. The efficacy of steroids in the treatment of idiopathic sudden hearing loss. Arch Otolaryngol 1980; 106: 772 - 6.40- Laird N, Wilson WR. Predicting recovery from idiopathic sudden hearing loss. Am J Otolaryngol 1983; 4: 161 - 4.41- Mattox DE, Simmons FB. Natural history of sudden sensorineural hearing loss. Ann Otol 1977; 86: 463 - 80.42- Lin YT, Young YH. Retrocochlear mass lesion in mid-frequency sudden deafness. Otolaryngol Head Neck Surg 2008; 138: 13 – 17.43- Yamasoba T, Sugasawa M, Kikuchi S. An electrocochleographic study of acute low-tone sensorineural hearing loss. Eur Arch Otorhinolaryngol 1993; 250: 418 - 22.44- Wu CL, Young YH. Vestibular evoked myogenic potentials in acute low-tone sensorineural hearing loss. Laryngoscope 2004; 114: 2172 - 5.45- Saunders JE, Luxford WM, Devgan KK. Sudden hearing loss in acoustic neuroma patients. Otolaryngol Head Neck Surg 1995; 113: 23 - 31.46- Noguchi Y, Komatsuzaki A, Nishida H. Electrocochleographic study in patients with vestibular schwannomas and U-shaped audiograms. Audiology 2000; 39: 19 - 23.47- Friedman RA, Kesser BW, Slattery WH. Hearing preservation in patients with vestibular schwannomas with sudden sensorineural hearing loss. Otolaryngol Head Neck Surg 2002; 125: 544 - 51.48- Fushiki H, Junicho M, Aso S, Watanabe Y. Recurrence rate of idiopathic sudden low-tone sensorineural hearing loss without vertigo: a long-term follow-up study. Otol Neurotol 2009; 30: 295 - 98.49- Kerber KA. Vertigo and dizziness in the emergency department. Emerg Med Clin North Am 2009; 27: 39 - 50.50- Bainbridge KE, Hoffman HJ, Cowie CC. Diabetes and hearing impairment in the United States: audiometric evidence from the National Health and Nutrition Examination Survey, 1999 to 2004. Ann Intern Med 2008; 149: 1 - 10.51- Genden EM, Bahadori RS. Bilateral sensorineural hearing loss as a first symptom of chronic myelogenous leukemia. Otolaryngol Head Neck Surg 1995; 113: 499 - 501.52- Yamasoba T, Sakai K, Sakurai M. Role of acute cochlear neuritis in sudden hearing loss in multiple sclerosis. J Neurol Sci. 1997; 146: 179 - 81.53- Rigby PJ. Comparison of FIESTA and gadolinium-enhanced T1-weighted sequences in magnetic resonance of acoustic schwannoma. Radiographer 2006; 53: 11 – 21.54- Stuckey SL, Harris AJ, Mannolini SM. Detection of acoustic schwannoma: use of constructive interference in the steady state three-dimensional MR. AJNR 1996; 17: 1219 - 25.55- Marx SV, Langman AW, Crane RC. Accuracy of fast spin echo magnetic reso¬nance imaging in the diagnosis of vestibular schwannoma. Am J Otolaryngol 1999; 20 (4): 211–16.56- Lee H, Sohn SI, Jung Dk, et al. Sudden deafness and anterior inferior cerebellar artery infarction. Stroke 2002; 33: 2807 – 12.57- Amarenco P, Hauw J. Cerebellar infarction in the territory of the anterior and inferior cerebellar artery. Brain 1990; 113: 139 - 155.58- Roquer J, Lorenzo RJ, Pou A. The anterior inferior cerebellar artery infarcts: a clinical-magnetic resonance imaging study. Acta Neurol Scand 1998; 97: 225 - 30.59- Matsushita K, Naritomi H, Kazui S, Watanabe Y, Okazaki H, Kuriyama Y, Sawada T. Infarction in the anterior inferior cerebellar artery territory: magnetic resonance imaging and auditory brain stem responses. Cerebrovasc Dis 1993; 3: 206 - 12.60- Amarenco P, Caplan L, Pessin MS. Vertebrobasilar occlusive disease. In: Barnett HJM, Mohr JP, Stein BM, Yatsy FM, eds. Stroke: Pathophysiology, Diagnosis and Management. 3rd ed, New York: Churchill Livingstone; 1998: 551 - 3.61- Caplan LR. Intracranial branch atheromatous disease. Neurology 1989; 39: 1246 - 50.62- Scheffler K. A pictorial description of steady-states in rapid magnetic resonance imaging. Concepts Magn Reson 1999; 11: 291 - 304.63- Schaefer DJ. Safety aspects of switched gradient fields. Mag Reson Imaging Clin N Am 1998; 6: 731 - 48.64- Tanioka H, Zusho H, Machida T, Sasaki Y, Shirakawa T. High-resolution MR imaging of the inner ear: findings in Ménière’s disease. Eur J Radiol 1992; 15: 83 - 8.65- Tanioka H, Kaga K, Zusho H, Araki T, Sasaki Y. MR of the endolymphatic duct and sac: findings in Ménière’s disease. AJNR 1997; 18: 45 - 51.66- Lavi ES, Sklar EM. Enhancement of the eighth cranial nerve and labyrinth on MR imaging in sudden sensorineural hearing loss associated with human Herpesvirus 1 infection: case report. AJNR 2001; 22: 1380 - 2.67- Meriot P, Marsot-Dupuch K. Imaging of post-traumatic tinnitus, vertigo and deafness. J Radiol 1999; 80: 1780 - 7.

REFERENCES

Case 3: Left Meniere’s Disease.Male patient aged 25 years old presented with SSNHL and vertigo. Axial FIESTA images endolymphaticsac (arrow) is seen in the right side and not seen in the left side.

Case 4: Right Labrynthitis.Female patient, 30 years old presented with severe vertigo and SSNHL.

A, Axial post contrast T1WI.B, Coronal post contrast T1WI showing patchy

enhancement of the cochlea and vestibule as well as proximal part of the VIII CN (arrow).

C & D, Axial FIESTA images showing heterogeneous appearance of the right cochlea with linear hyperintense signals seen in consecutive images (arrows).

A B

C D

Case 5: Right Acoustic Schwannoma.Female patient, 60 years old, presented with right SSNHL.A, Axial high resolution post contrast T1WI showing (arrow) a well-defined homogeneously enhancing lesion is noted in the CPA and internal auditory canal. B, Axial high resolution T2WI showing (arrow) same lesion as hypointense.C, Axial FIESTA shows (arrow) same lesion as hypointense yet, appears well contrasted against high signal of CSF.

A B

C

Idiopathic Cases; 53

Diagnosed Cases; 19

Fig 1. Distribution of the study cases according to their final diagnosis.

AN; 2

MD; 3

VN; 1

CSOM; 2

TBF; 2RWF; 1

CVA; 2

MS; 2

TM; 1

E; 1

L; 2

Fig 2. Distribution of diagnosed cases according to etiology.AN: acoustic neuroma, MD: Meniere’s disease, VN: vestibulococlear neuritis, CSOM: labyrinthitiscomplicating chronic suppurative otitis media, TBF: longitudinal temporal bone fractures, RWF: round window fistula, CVA: cerebrovascular accidents, MS: multiple sclerosis, TM: temporal lobe meningioma, E: Wernick’s encephalopathy, L: leukemia.

Role of Final Diagnosis Clinical

evaluationLaboratory

InvestigationsAudiologicalEvaluation MRI†

Case 1 Acoustic Neuroma + - ++ +++ F

Case 2 Acoustic Neuroma + - ++ F

confirmed Case 1 Meniere’s

disease ++ - ++ ++ F

Case 2 Meniere’s disease ++ - ++ ++ F

Case 3 Meniere’s disease +++ - ++ ++ F

Vestibulococlear Neuritis ++ - ++ +++ F

Case 1 Labyrinthitis +++ - + Fconfirmed

Case 2 Labyrinthitis +++ - + Fconfirmed

Case 1 TB Fracture +++ - - Not used Case 2 TB Fracture +++ - - Not used

Round Window Fistula +++ - + Fconfirmed

Case 1 CVA + - - +++ Case 2 CVA -* - - +++ Case 1 MS - - + +++ Case 2 MS + - + +++

Meningioma - - + +++ Encephalopathy ++ + + +++ Case 1 Leukemia +++ +++ + ++ Case 2 Leukemia - +++ + ++

Table 1: Role of varies diagnostic modalities in establishing the final diagnosis. (-: no role, +: minor role, ++: favorable role, +++: main role, F: FIASTA sequence) (*: the clinical presentation was misleading, †: the role of MRI was either at the time of initial presentation or during the follow-up period to confirm the diagnosis)

T1 T2 Post-Contrast FIESTAMSMeningiomaCVAEncephalopathyLeukemia

Vestibular Neuritis Meniere’s Disease LabyrinthitisRound Window Fistula

Table 2. Role of T1 T2 Post-Contrast MRI versus the FIESTA Sequence in diagnosis and conformation of various SSNHL etiologies of the study cases.

INTRODUCTION

Sudden sensorineural hearing loss (SSNHL) affects 1:10,000 people annually 1. Although SSNHL is a well-recognized condition, no standard diagnosis or treatment protocol has been accepted 2. In addition, despite extensive evaluation, an etiology can only be found in 10% to 15% of patients. Viral infections 3, vascular compromise 4, 5 and cochlear membrane ruptures 6, 7 are a few entities associated with or hypothesized to cause SSNHL. The initial presentation of an acoustic neuroma (AN) may be SSNHL in up to 10% of cases 8 - 11. Ménière’s disease may also present initially with SSNHL 10% of the time 11 - 13. Other causes such as syphilis, autoimmune diseases, perilymph fistula, membrane breaks 14 or multiple sclerosis (MS) must also be considered. Certain etiologies could be ruled-out by complete history and physical examination along with certain blood tests (blood count to rule out leukemia, hypercoagulable states, and sickle cell disease; chemistry to evaluate glucose potassium and calcium levels; thyroid function tests; erythrocyte sedimentation rate; rhematoid and antinuclear antigen factors and fluorescent treponemal antibody absorbance for syphilis). Some other important etiologies as Ménière’s disease, MS, vascular or traumatic causes or ANs could not be evaluated without imaging guidance 15. A better prognosis was found to be related to the prompt administration of steroids 16, which in turn necessitates rapid approach to the etiology. In addition the hearing loss may be a part of a more serious situation also necessitates extensive work-up 15.To prove an imaging modality as effective, a statistical analysis in a randomized double-blinded study must be used. Because most of cases usually are presented in a true emergency situation, such a study is not possible. To estimate the role of magnetic resonance imaging (MRI) scan with gadolinium contrast as the single best imaging modality that can diagnose most of these cases, we retrospectively reviewed charts and data of all SSNHL cases attended tertiary referral hospital and then the SSNHL etiologies results were analyzed and the role of the MRI in each of these etiologies was evaluated.

Case 1: Multiple Sclerosis.Female patient aged 24 years old, presented with left SSNHL.

A, Axial T2WI shows multiple oblong shaped hyperintensefoci in pons, middle cerebellar peduncles and left cerebellar hemisphere.

B, FLAIR image shows the same foci as before.

A

B

Case 1: Multiple Sclerosis.Female patient aged 24 years old, presented with left SSNHL.

A, Axial T2WI shows multiple oblong shaped hyperintensefoci in pons, middle cerebellar peduncles and left cerebellar hemisphere.

B, FLAIR image shows the same foci as before.

A

B

Case 2: Left Meniere’s Disease.Axial FIESTA images (A, upper and B, lower level). The endolymphatic sac (arrow) is well seen in the right side and not seen in the left side.B

ACase 2: Left Meniere’s Disease.Axial FIESTA images (A, upper and B, lower level). The endolymphatic sac (arrow) is well seen in the right side and not seen in the left side.B

A

Computer Engineering Rabie A. Ramadan Lecture 1. 2 Welcome Back

Computer Engineering Rabie A. Ramadan Lecture 1. 2 Welcome Back

Documents
Smoking-related ILDs By Gamal Rabie Agmy, MD, FCCP Professor of Chest Diseases,Assiut University

Smoking-related ILDs By Gamal Rabie Agmy, MD, FCCP Professor of Chest Diseases,Assiut University

Documents
CV of Professor Gamal Mohamed Rabie Agmy - aun.edu.eg · CV of Professor Gamal Mohamed Rabie Agmy Contact informations: Name : Gamal Mohamed Rabie Agmy Ghereyany National number:

CV of Professor Gamal Mohamed Rabie Agmy - aun.edu.eg · CV of Professor Gamal Mohamed Rabie Agmy Contact informations: Name : Gamal Mohamed Rabie Agmy Ghereyany National number:

Documents
Microprocessor Dr. Rabie A. Ramadan Al-Azhar University Lecture 4

Microprocessor Dr. Rabie A. Ramadan Al-Azhar University Lecture 4

Documents
Introduction to Algorithms Rabie A. Ramadan rabie@rabieramadan.org . rabieramadan.org 6 Ack : Carola Wenk nad Dr. Thomas Ottmann tutorials

Introduction to Algorithms Rabie A. Ramadan [email protected] . rabieramadan.org 6 Ack : Carola Wenk nad Dr. Thomas Ottmann tutorials

Documents
Web Design Rabie A. Ramadan, PhD 2

Web Design Rabie A. Ramadan, PhD 2

Documents
Microprocessor Dr. Rabie A. Ramadan Al-Azhar University Lecture 6

Microprocessor Dr. Rabie A. Ramadan Al-Azhar University Lecture 6

Documents
Introduction to Algorithms Rabie A. Ramadan rabie@rabieramadan.org . rabieramadan.org 3 Some of the sides are exported from different sources

Introduction to Algorithms Rabie A. Ramadan [email protected] . rabieramadan.org 3 Some of the sides are exported from different sources

Documents
Dr./ Ahmed Mohamed Rabie Sayedstaff.du.edu.eg/upfilestaff/1058/101058_a1544631339... · 2018-12-12 · Dr./ Ahmed Mohamed Rabie Sayed 1. 2. 3 Operating system : is a set of programs

Dr./ Ahmed Mohamed Rabie Sayedstaff.du.edu.eg/upfilestaff/1058/101058_a1544631339... · 2018-12-12 · Dr./ Ahmed Mohamed Rabie Sayed 1. 2. 3 Operating system : is a set of programs

Documents
Image Synthesis Rabie A. Ramadan, PhD 7. 2 Image Rasterization

Image Synthesis Rabie A. Ramadan, PhD 7. 2 Image Rasterization

Documents
Computer and Network Security Rabie A. Ramadan Lecture 2

Computer and Network Security Rabie A. Ramadan Lecture 2

Documents
Advanced Programming Rabie A. Ramadan Rabie@rabieramadan.org 7

Advanced Programming Rabie A. Ramadan [email protected] 7

Documents
Advanced Programming Rabie A. Ramadan Rabie@rabieramadan.org 2

Advanced Programming Rabie A. Ramadan [email protected] 2

Documents
Dr./ Ahmed Mohamed Rabie Sayedstaff.du.edu.eg/upfilestaff/1058/101058_a1489659230__lecture.5._.pdf · Dr./ Ahmed Mohamed Rabie Sayed 1. 2. 3 HTML Web Page Template Header Body. 4

Dr./ Ahmed Mohamed Rabie Sayedstaff.du.edu.eg/upfilestaff/1058/101058_a1489659230__lecture.5._.pdf · Dr./ Ahmed Mohamed Rabie Sayed 1. 2. 3 HTML Web Page Template Header Body. 4

Documents
Computer Organization Rabie A. Ramadan Lecture 3

Computer Organization Rabie A. Ramadan Lecture 3

Documents
Data Warehouse Fundamentals Rabie A. Ramadan, PhD 6

Data Warehouse Fundamentals Rabie A. Ramadan, PhD 6

Documents
Rabie .mi.united arab emirats journy towards excellenc

Rabie .mi.united arab emirats journy towards excellenc

Education
Advanced Computer Architecture and Parallel Processing Rabie A. Ramadan Rabie@rabieramadan.org http:

Advanced Computer Architecture and Parallel Processing Rabie A. Ramadan [email protected] http:

Documents
Dr./ Ahmed Mohamed Rabie Sayedstaff.du.edu.eg/upfilestaff/1058/101058_a1583493757__lecture.5._.pdf · Dr./ Ahmed Mohamed Rabie Sayed 1. 2. 3 Eyedropper Tool 1-7 Fill color

Dr./ Ahmed Mohamed Rabie Sayedstaff.du.edu.eg/upfilestaff/1058/101058_a1583493757__lecture.5._.pdf · Dr./ Ahmed Mohamed Rabie Sayed 1. 2. 3 Eyedropper Tool 1-7 Fill color

Documents
Introduction to Computer Hardware - Rabie Ramadan

Introduction to Computer Hardware - Rabie Ramadan

Documents
Web Design Dr. Rabie A. Ramadan 1

Web Design Dr. Rabie A. Ramadan 1

Documents
Image Synthesis Rabie A. Ramadan, PhD 6. 2 3D Images

Image Synthesis Rabie A. Ramadan, PhD 6. 2 3D Images

Documents
Dr Rabie 331S06 Introd Mod1

Dr Rabie 331S06 Introd Mod1

Documents
Introduction to Java Rabie A. Ramadan rabie@rabieramadan.org

Introduction to Java Rabie A. Ramadan [email protected]

Documents
Computer Orgnization Rabie A. Ramadan Lecture 6. DataPath

Computer Orgnization Rabie A. Ramadan Lecture 6. DataPath

Documents
Lecture 5 Introduction to Electronics Rabie A. Ramadan rabieramadan@gmail.com

Lecture 5 Introduction to Electronics Rabie A. Ramadan [email protected]

Documents
Data Warehouse Fundamentals Rabie A. Ramadan, PhD 5

Data Warehouse Fundamentals Rabie A. Ramadan, PhD 5

Documents
Introduction to Sensor Networks Rabie A. Ramadan, PhD Cairo University rabie@rabieramadan.org 2

Introduction to Sensor Networks Rabie A. Ramadan, PhD Cairo University [email protected] 2

Documents
Data Warehouse Fundamentals Rabie A. Ramadan, PhD 2

Data Warehouse Fundamentals Rabie A. Ramadan, PhD 2

Documents
Microprocessor Dr. Rabie A. Ramadan Al-Azhar University Lecture 3

Microprocessor Dr. Rabie A. Ramadan Al-Azhar University Lecture 3

Documents