|Year : 2015 | Volume
| Issue : 1 | Page : 8-13
Audiological evaluation of hearing levels in patients diagnosed with migraine
Müjde Karadag1, Emine Elif Altuntas2, Serkan Sanli3, Ismail Önder Uysal2
1 Department of Otolaryngology, Sivas Numune City Hospital, 58140 Sivas, Turkey
2 Department of Otolaryngology, School of Medicine, Cumhuriyet University Campus, 58140 Sivas, Turkey
3 Department of Neurology, School of Medicine, Cumhuriyet University Campus, 58140 Sivas, Turkey
|Date of Web Publication||10-Mar-2015|
Associate Prof. Emine Elif Altuntas
Departments of Otolaryngology, School of Medicine, Cumhuriyet University Campus, 58140 Sivas
Source of Support: None, Conflict of Interest: None
Introduction: Based on the hypothesis that neurovascular events involving in the pathophysiology of migraine can cause hearing loss by influencing blood flow of inner ear, it was aimed to determine whether migraine with or without aura in our clinics patients are at risk for hearing loss by assessing hearing levels via a high-frequency audiometry, acoustic reflex and transient otoacoustic emission responses; to discriminate whether hearing loss is cochlear or retrocochlear originated, if present; and to evaluate whether or not migraine treatment affect hearing level in patients received treatment for migraine in this study. Materials and Methods: The study included patients who were diagnosed as migraine between December 2011 and December 2012 at Neurology Department of Cumhuriyet University, Medicine School according to ICD-II classification and accepted to receive medical therapy. In all patients, hearing levels were measured at baseline and after treatment by using high-frequency audiometry, transient otoacoustic emission and acoustic reflex tests. Results: In the present study, hearing thresholds measured in the right ear was normal in migraine patients with or without aura at baseline, while mild hearing loss was detected in right ear at the frequency of 500 Hz after treatment when hearing thresholds at different frequencies were compared. This difference was significant (P < 0, 05). When hearing thresholds in right ear at baseline and after treatment was compared, mild hearing loss was detected at the frequency of 250 Hz in migraine patients with aura. This difference was significant (P < 0, 05). In migraine patients with aura, hearing was normal in all patients at baseline, while in both ears mild hearing loss was detected in 2 patients (8.7%) after treatment. This difference was not significant (P > 0, 05). Conclusion: Differently from literature, hearing loss in our patients developed at lower frequencies and after treatment. The results we obtained from our study also presented that there might be a relationship between migraine disease and sensorineural hearing loss.
Keywords: Audiometry, Hearing loss, Migraine, Transient otoacoustic emission
|How to cite this article:|
Karadag M, Altuntas EE, Sanli S, Uysal IÖ. Audiological evaluation of hearing levels in patients diagnosed with migraine. Indian J Otol 2015;21:8-13
|How to cite this URL:|
Karadag M, Altuntas EE, Sanli S, Uysal IÖ. Audiological evaluation of hearing levels in patients diagnosed with migraine. Indian J Otol [serial online] 2015 [cited 2021 Apr 15];21:8-13. Available from: https://www.indianjotol.org/text.asp?2015/21/1/8/152850
| Introduction|| |
Migraine is a primer, chronic, episodic headache, known for thousands of years, which is accompanied by neurologic, gastrointestinal and otonom changes in various combinations, and of which aural neurologic symptoms seen in one-third (1/3) of the cases are known as the characteristic features. , The most common form of migraine is "migraine without aura" and 90% of the patients with migraine have just this type of migraine. In the rest of the cases, migraine attacks with aura occur alone or together with migraine attack without aura. Migraine disease induces a series of neurologic symptoms such as vertigo, dizziness, hearing loss, tinnitus and aural ache in addition to the most common auditory symptom, phonophobia. ,,
Sensorineural hearing loss (SNHL) is related to defects in sensory end organ of cochlea or in neural transmission pathway toward the central nerve system. This defect occurs while the inner ear hearing organ converts acoustic energy into electrical energy or in the period of neural impulse' transmission to the center. However, almost 90% of SNHL is cochlear origin. SNHL may be induced by hair cell lesions, pathologies in stria vascularis, metabolic disorders in inner ear and volume balance disorders of inner ear liquids. Ototoxic drug usage, neurologic pathologies, vascular diseases, hematological diseases, viral infections, systemic bone diseases, tumors, autoimmune diseases, noise induced hearing losses and presbiacusia may be conducted among the reasons of SNHL in adult individuals. Migraine is also one of neurological diseases lead to SNHL in adults. It's known that, several hearing disorders may be seen in prodromal phase of migraine with aura. They are usually more common especially in basillier migraine types. SNHL, tinnitus, sound and speech distortions, intolerance to high noises are the most common symptoms. Hearing loss is bilateral in the half of the patients. Usually, hearing loss holds low-frequencies and shows fluctuation. Vasospasm of labyrinthine arteries might explain all of these inner ear symptoms. From this aspect, it may be confused with Meniere disease (MH). 
Vestibulocochlear disorders accompany the headache in patients with migraine or may occur as aura in periods without headache. It is known that neurovascular events contribute in pathophysiology of migraine. In many studies in literature, trigeminal sensorial innervation that change vascular blood flow and vascular permeability and vasospasm of internal auditor artery channels and even migrainous infarction are suggested as the possible mechanism of cochleovestibular disorders related to migraine headaches. ,,
Migraine can cause fluctuating low-frequency hearing loss and sudden deafness. The cochlear ischemia can cause hearing loss. Based on the hypothesis that the neurovascular events which contribute to pathophysiology of migraine might affect the ear blood flow by causing changes in veins in inner ear that fed with terminal veins, and as a result they might induce SNHL; we aimed in this study to evaluate hearing levels of migraine with or without aura in our clinics patients by high-frequency audiometry, acoustic reflex and transient evoked otoacoustic emission (TEOAE) results, to determine whether these patients were at risk of hearing loss, and in case of detecting a hearing loss to discriminate whether it was cochlear or retrocochlear origin.
| Materials and Methods|| |
Fifty patients who had diagnosis of migraine with aura (Group 1) and migraine without aura (Group 2) and who accepted medical therapy in Department of Neurology between December 13, 2011 and December 13, 2012 were included in this study. Triptane group drugs were used for the therapy of all these patients. Patients included in the study were diagnosed as migraine in neurology clinic in accordance with International Classification of Diseases-II. 
We got permission from Cumhuriyet University Ethics Committee of Clinical Research for this study. Signed consent forms received from the patients included in the study.
Not accepting to come ear-nose-throat policlinic and having hearing tests, not approving to be added into the study, having otologic disease or surgery, mechanic trauma, syphilis, malignancy, acute or chronic otitis media, congenital cochlear malformation, neurological diseases (known as the cause of hearing loss), intake of any ototoxic drugs within the last month, having etiologic factors such as liver or renal failure which induces hearing loss, having radiotherapy or chemotherapy within the last month for any reason were accepted as exclusion criteria of our study. Moreover, patients who had ear infection symptoms after treatment, who were detected to have hearing loss in transmission type, who didn't keep on hearing levels follow-up or who did not want to continue to the study were also excluded from the study.
Detailed anamnesis information was recorded into prepared follow-up forms; namely otoscopic examination findings, high-frequency audiometry, TEOAE, tympanometry, acoustic reflex and hearing tests conducted both in pretreatment and posttreatment periods. All of the cases participated in the study were examined by the same researcher (MK) and their hearing tests were made by the same audiometrist (VÖ).
Air and bone conduction thresholds of patients were measured by clinical audiometer device (INTERACOUSTICS AC 40 clinical audiometer) that calibrated according to ISO standards. All audiological tests were made while other ear was masked. Pure tone hearing thresholds were measured for frequencies 0.25, 0.5, 1, 2, 4, 6, 8 and 12 kHz. For whom the pure tone threshold of hearing was up to 0-20 dBs the hearing was classified as normal, for those between 21 and 40 dBs as mild, for those between 41 and 60 dBs as moderate, for those between 61 and 80 dBs as severe, for those between 80 and 100 dBs as deep and for those over 100 dBs the hearing was classifies as total hearing loss.  After that TEOAE test was made with TEOAE device (MAICO ERO-scan TEOAE) on all patients. TEOAE testing and analysis were made by a commercial device (Maico, ERO scan analyzer, GmbH Salzufer, 13/14, 10587, Berlin Germany) that calibrated before using. During the test, disposable prop were used to close the ear canal. When testing is complete, if there was a response to TEOAE (better hearing than 30 decibels), the result was seen as "PASS" on the screen, while it was seen as "REFER" for ones that there was not any response (hearing loss range was 30 decibels or more). Screening test was repeated in the ear we get "REFER" as result. Stimulant in form of klick occurred in the frequency range 0.7-4 kHz and 83 dB/SPL (±3 dB) degree of density. This test was recorded in each session separately for the right and left ears. The results were recorded one by one in the frequency band width of 1,5-4 kHz and in 1.5, 2, 2.5, 3, 3.5 and 4 kHz frequencies for TEOAE. In the band width of 1,5-4 kHz, the average amplitude of TEOAE below 6 dB was meant that there was no response to OAE.
The inputs gathered in our study by statistical methods were uploaded to SPSS 14.0 (SPSS Inc., Chicago, IL, USA) statistic packaged software and because the parametric test assumptions couldn't be practiced, when (Kolmogorov-Smirnov) Wilcoxon test, Mann-Whitney U-test, McNemar test, parametric test assumptions were implemented, the significance of the difference between two pairs test was used for the evaluation of results. The level of significance was accepted as 0.05 and P < 0.05 were accepted as significant.
| Results|| |
The average age of 23 patients had migraine with aura (Group 1) was 30.43 ± 6.33 years (minimum-maximum 19-40); 27 (54%) had migraine without aura (Group 2) was 36.59 ± 10.6 years (minimum-maximum 21-57).
12 (24.0%) of 50 cases included in the study were male; 38 of them (76.0%) were female. 6 of the patients (26.1%) were male, 17 (73.9%) were female in Group 1; 6 (22.2%) were male and 21 (77.8%) were female in Group 2.
Hearing tests results made by TEOAE were normal in the right and the left ears of the patients included in the study both before and after treatment.
Acoustic reflex test results of the patients were normal in the right and the left ears both before and after treatment.
When pretreatment and posttreatment hearing threshold values at various frequencies (250-120,000 Hz) in both the right and the left ears of all cases included in the study were compared, the difference recorded between measurements was found statistically insignificant (P > 0.05).
Pretreatment and posttreatment hearing thresholds of the right ears of individuals in Group 1 and Group 2 at different frequencies (250-120,000 Hz) were shown in [Table 1]. The difference was found statistically insignificant. While hearing threshold of the right ear at 500 Hz was 13.04 ± 4.94 in cases of Group 1 and 11.48 ± 4.96 in Group 2 before treatment, hearing threshold at the same frequency was 15.62 ± 6.95 in Group 1 and 11.66 ± 4.59 in Group 2 cases after treatment. When both groups were compared, the change of hearing threshold of cases in pretreatment and posttreatment periods was found statistically significant (P < 0.05).
|Table 1: Comparison of hearing thresholds of the right ears of all cases included in the study at different frequencies in pretreatment and posttreatment periods |
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When we compared pretreatment and posttreatment hearing thresholds in left ears of individuals in Group 1 and Group 2 measured at various frequencies (250-120,000 Hz), the difference was found statistically insignificant (P > 0.05).
When pretreatment and posttreatment hearing thresholds in right ears of individuals in Group 1 at various frequencies (250-120,000 Hz) was compared, difference in 250 Hz was found significant (P < 0.05). On the other hand, difference in other frequencies was found statistically insignificant [Table 2]. However, hearing levels of cases were between normal limits though the posttreatment increase in hearing thresholds at 250 Hz. When we compared pretreatment and posttreatment hearing thresholds in left ears of cases in Group 1 at different frequencies (250-120,000 Hz), the difference was found statistically insignificant.
|Table 2: Comparison of hearing thresholds of the right ears at different frequencies in Group 1, in pretreatment and posttreatment periods |
Click here to view
When pretreatment and posttreatment hearing thresholds of the right and left ears of cases in Group 2 at various frequencies (250-120,000 Hz) were compared, the difference at all frequencies was found statistically insignificant.
| Discussion|| |
This study was planned based upon the hypothesis that neurovascular events contributing in migraine pathophysiology may induce a SNHL by making neurovascular changes in terminal arteries supplying the inner ear and influencing inner ear blood flow. When we evaluated all the cases in our study; while pretreatment hearing threshold in right ear at 500 Hz frequency was 13.04 ± 4.94 in Group 1 and it was 11.48 ± 4.96 in Group 2; posttreatment hearing threshold in right ear was found 15.65 ± 6.95 in Group 1 and 11.66 ± 4.59 in Group 2. This increase detected in hearing levels of Group 1 cases was found statistically significant (P < 0.05). Again in Group 1, when pretreatment and posttreatment hearing thresholds of right ear at various frequencies were compared, pretreatment hearing threshold at 250 Hz was 14.56 ± 5.41, it was found 19.13 ± 7.48 after treatment and this difference was statistically significant (P < 0.05).
It was suggested for the 1 st time by Tissot in 1778 that hearing disorders such as phonophobia and hyperacusia seen in migraine patients might be related to stress induced headache.  Hallucinations, ossilokuzi, phonophobia, hyperacusia, tinnitus, variable low-frequency hearing loss and sudden hearing loss may be counted among hearing symptoms of migraine patients. ,,,,,, Beside of these, migraine disease may cause a series of neurootologic symptoms such as vertigo, dizziness and aural ache. , Hearing symptoms in patients with migraine are less common than vestibular symptoms. ,,
Nowadays, ear-nose-throat doctors and neurologists frequently meet patients with a clinical picture including headaches similar to migraine, dizziness attacks, vertigo, ear fullness, hearing symptoms and tinnitus. These patients caused to define a new clinical entity and this entity is called by various names such as migraine related vertigo, migraine related dizziness, migraine related drowsiness, migrainous vertigo, migraine-anxiety related dizziness, migraine related cochleovestibular dysfunction. Having similar clinics with a series of other otoneurologic diseases notably the Meniere disease, these patients leaded up the otoneurologists to be more interested in researches on migraine related audio-vestibular dysfunctions. ,,,,,
Various studies in the literature suggest that migraine disease might induce permanent audio and vestibular dysfunctions. ,,, In general, it is a common approach that temporary neurologic symptoms related to migraine, which lasts longer than 4 min and shorter than 60 min are assessed as aura. The most common migraine auras consist of visual symptoms. The studies regarding metabolic activities of brain aiming at searching neurologic symptoms monitored in migraine patients also drawn attention that these symptoms might be stemming from a primary neuronal event together with seconder vascular changes such as vasospasm or vasodilation depending on the migraine phase. ,
Pathophsyology of hearing symptoms is probably related to vasospasm of small arterioles found in the cochlear or labyrinth. ,,, However, the certain mechanism linking migraine and SNHL is not known. The trigeminal sensual innervation of cochlear blood vessels in a way to change blood flow and permeability of vessels and vasospasm of internal auditory artery channels and even migrainous enfarktus are suggested as the potential mechanism of cochleovestibular dysfunctions related to migraine headaches. , The first patient who was a 62-year-old female with migraine attacks accompanied by relapsing hearing loss was reported in 1987 by Lipkin et al.  After that, Viirre and Baloh  presented a series of cases consisting 13 patients matching the migraine criteria and having unexplained SNHL and mentioned that the dysfunction in cochlear micro vessels might induce this hearing loss. Lee et al.  reporting two young patients without any other health problem than acute hearing loss accompanying migraine attacks and they suggested that hearing symptoms might be a part of prodromal symptoms of migrainous infarction. The only histopathological proof associating migraine and SNHL was offered in 2000 by Lee et al.  In the study they made a postmodern investigation on cochlear of a patient who had migraine for a long time and developed SNHL when 50-year-old, they presented that there was significant fibrosis in the stria vascularis and spiral ligament which was the characteristic finding of ischemic damage. In the light of the histopathological findings they gathered, they defended the opinion that hearing loss might result from migraine related vasospasm.
In the migraine cohort study of Chu et al.,  including migraine patients looking for active medical assistance and patient population gathered from National Health Insurance Research Database, migraine was founded related to increase of SNHL risk when two cohort were composed by minimalizing the difference as much as possible in terms of vascular risk factors such as accompanier major cardiovascular diseases and serebrovascular diseases. In Chu et al.,  study, SNHL developed during the follow-up in 134 (0.3%) of 51.400 subjects, it also developed in 43 (0.4%) subjects of migraine cohort and 91 subjects of matched control cohort (Fisher exact test, P < 0.001).
The average onset ages of SNHL in the migraine (45.1 years old) and the matched cohorts (45.72 years old) were founded similar (P < 0.76).
In this study, by using the Kaplan-Meier estimations, it has been showed that the cumulative incidence of SNHL in the migraine cohort was significantly higher than that in the matched cohort (log rank < 0.002). The incidence rate of SNHL in the migraine cohort was detected as 81.6 (95% confidence interval [CI]: 81.3-81.9) and that in the matched cohort was detected as 45.7 (95% CI: 45.5-45.9)/100,000 person-years. The migraine cohort had a greater risk of developing sudden SNHL than the matched cohort (incidence rate ratio < 1.8; 95% CI: 1.22-2.61; P < 0.01). The nationwide population-based cohort study of Chu et al.  showed that the migraine cohort had 1.8 times greater risk of developing SNHL than the matched cohort. According to Chu et al.,  their study is the first to demonstrate that migraine was associated with an increased risk of idiopathic SNHL and incidence rate of SNHL in the control cohort was higher than that in the previous epidemiologic studies. ,,,
In the study Bayazıt et al.  made, pure tone hearing threshold in migraine patients decreased at high-frequencies between 6 and 8 kHz, but pure tone hearing was not influenced between 0,5 and 4 kHz. On the other hand, slight hearing loss detected in the cases participated in our study at low-frequencies and these results we gathered don't have any similarity with the results of Bayazıt et al.,  study on 20 patients with migraine in 2001. We are of the opinion that making certain comments about the reason of this difference wouldn't be appropriate since we do not have histopathologic inputs.
In our study, it is detected that SNHL developed in migraine patients with aura in the period they have been taking treatment at low-frequencies. These findings show similarity with the results of Chu et al.  study. However, differently from Chu et al.  study, it is interesting in our cases that the hearing loss developed after having migraine treatment. We are of the opinion that this difference should be evaluated with prospective studies which will include results from long term treated cases and quantitatively more patients.
We are of the opinion that, the SNHL at low-frequencies which occurred during the follow-ups of our cases might be due to the hearing loss in migraine induced from pathophysiologic changes to become irreversible as the attacks repeat or the repeating migraine attacks to be permanent in time just as it is in Meniere disease.
Therefore, we believe that there is a need for researches covering prospective and histopathologic evaluations adequate to present whether hearing loss progresses in migraine patients with aura or not, and if it progresses to present by which pathophysiologic mechanisms it happens.
Otoacoustic emission tests enable us to describe the cochlear component of hearing disorder and to monitor objectively the changes that cannot be detect with other audiologic methods in case of cochlea. DPOAE tests refer to normally functioning cochlea in migraine patients between 1 and 4 kHz frequencies. In another study, the DPOAEs tested between the ranges of 1 and 6 kHz didn't presented any abnormality in migraine patients without aura, beside of that the DPOAEs in migraine patients with aura presented lower amplitudes only at 5 kHz frequency area. Regarding the sensitivity of DPOAE to high-frequencies, detecting disfunctioning at 5 kHz suggests that abnormal outer hair cell function in the basal turn of the cochlea in migraine patients with aura.  In our study, we did not detect any abnormality during TEOAE tests made before and after treatment in Group 1 and Group 2.
| Conclusion|| |
The outputs of many studies in the literature and even of our study point out that there is a correlation between migraine disease and SNHL. For this reason, it will be useful to investigate both SNHL patients' migraine amnesis and migraine patients' complaint of hearing loss. The findings we gathered from our study bring into mind that doctors should be careful for migraine patients with aura regarding SNHL.
According to our literature searches, there isn't any cohort study made in our country on hearing loss of migraine patients until 2012. The results we reached point out that SNHL may develop in migraine patients at low-frequencies even though they have medical therapy. Hearing loss at low-frequencies which occurred through the follow-ups made us think that pathophysiologic changes inducing hearing loss in migraine might be irreversible or repeating migraine attacks might cause pathologic changes inducing hearing loss to be permanent. But, our evaluations include short time follow-ups and histopathologic changes occur in the cochlea were not taken into consideration. Therefore, we are of the opinion that there is a need for prospective studies in the future which will include an enhanced number of patients who will have had medical treatment for a longer time and will also search whether hearing loss shows progression or not, and if there is a progression, will include histopathologic evaluations indicating which pathophysiologic mechanisms it emerges with.
| References|| |
Vural O. Headache. Ertaº M. Migraine. Turk Clin J Intern Med 27 Neurol Spec Top Headache 2003;1:116-23.
Ferrari MD. Migraine. Lancet 1998;351:1043-51.
Lance JW. Current concepts of migraine pathogenesis. Neurology 1993;43:S11-5.
Olsson JE. Neurotologic findings in basilar migraine. Laryngoscope 1991;101:1-41.
Viirre ES, Baloh RW. Migraine as a cause of sudden hearing loss. Headache 1996;36:24-8.
Akyildiz N. Ear diseases and micro surgery. Ankara: Bilimsel Medicine; 2002. p. 4-5.
Katsarava Z, Giffin N, Diener HC, Kaube H. Abnormal habituation of 'nociceptive' blink reflex in migraine - Evidence for increased excitability of trigeminal nociception. Cephalalgia 2003;23:814-9.
Kayan A, Hood JD. Neuro-otological manifestations of migraine. Brain 1984;107:1123-42.
Headache Classification Subcommittee of the International Headache Society. The international classification of headache disorders. 2 nd
edition. Cephalalgia 2004;24 Suppl 1:16-151.
Guidelines for screening for hearing impairment and middle-ear disorders. Working Group on Acoustic Immittance Measurements and the Committee on Audiologic Evaluation. American Speech-Language-Hearing Association. ASHA Suppl. 1990;(2):17-24.
Sachs OW. Migraine: The evolution of a common disorder. 1 st
ed. London: Faber and Faber; 1970.
Rubin D, McAbee GN, Feldman-Winter LB. Auditory hallucinations associated with migraine. Headache 2002;42:646-8.
Whitman BW, Lipton RB. Oscillocusis: An unusual auditory aura in migraine. Headache 1995;35:428-9.
Seidman MD, Jacobson GP. Update on tinnitus. Otolaryngol Clin North Am 1996;29:455-65.
Parker W. Migraine and the vestibular system in adults. Am J Otol 1991;12:25-34.
Lee H, Lopez I, Ishiyama A, Baloh RW. Can migraine damage the inner ear? Arch Neurol 2000;57:1631-4.
Kuritzky A, Ziegler DK, Hassanein R. Vertigo, motion sickness and migraine. Headache 1981;21:227-31.
Harker LA, Rassekh C. Migraine equivalent as a cause of episodic vertigo. Laryngoscope 1988;98:160-4.
Brantberg K, Trees N, Baloh RW. Migraine-associated vertigo. Acta Otolaryngol 2005;125:276-9.
Cass SP, Furman JM, Ankerstjerne K, Balaban C, Yetiser S, Aydogan B. Migraine-related vestibulopathy. Ann Otol Rhinol Laryngol 1997;106:182-9.
Battista RA. Audiometric findings of patients with migraine-associated dizziness. Otol Neurotol 2004;25:987-92.
Furman JM, Sparto PJ, Soso M, Marcus D. Vestibular function in migraine-related dizziness: A pilot study. J Vestib Res 2005;15:327-32.
Lempert T, Neuhauser H. Migrainous vertigo. Neurol Clin 2005;23:715-30, vi.
Lipkin AF, Jenkins HA, Coker NJ. Migraine and sudden sensorineural hearing loss. Arch Otolaryngol Head Neck Surg 1987;113:325-6.
Cutrer FM, Baloh RW. Migraine-associated dizziness. Headache 1992;32:300-4.
Kaube H, Knight YE, Storer RJ, Hoskin KL, May A, Goadsby PJ. Vasodilator agents and supracollicular transection fail to inhibit cortical spreading depression in the cat. Cephalalgia 1999;19:592-7.
Aurora SK, Welch KM. Migraine: Imaging the aura. Curr Opin Neurol 2000;13:273-6.
Färkkilä M. The pathophysiology of migraine. Ann Med 1994;26:7-8.
Nomura Y. Diagnostic criteria for sudden deafness, mumps deafness and perilymphatic fistula. Acta Otolaryngol Suppl 1988;456:7-8.
Lee H, Whitman GT, Lim JG, Yi SD, Cho YW, Ying S, et al.
Hearing symptoms in migrainous infarction. Arch Neurol 2003;60:113-6.
Chu CH, Liu CJ, Fuh JL, Shiao AS, Chen TJ, Wang SJ. Migraine is a risk factor for sudden sensorineural hearing loss: A nationwide population-based study. Cephalalgia 2013;33:80-6.
Lin HC, Lee HC, Chao PZ, Wu CS. The effects of weather on the incidence of sudden sensorineural hearing loss: A 5-year population-based study. Audiol Neurootol 2006;11:165-71.
Byl FM. Seventy-six cases of presumed sudden hearing loss occurring in 1973: prognosis and incidence. Laryngoscope 1977;87:817-25.
Rauch SD. Clinical practice. Idiopathic sudden sensorineural hearing loss. N Engl J Med 2008;359:833-40.
Klemm E, Deutscher A, Mösges R. A present investigation of the epidemiology in idiopathic sudden sensorineural hearing loss. Laryngorhinootologie 2009;88:524-7.
Bayazit Y, Yilmaz M, Mumbuç S, Kanlikama M. Assessment of migraine-related cochleovestibular symptoms. Rev Laryngol Otol Rhinol (Bord) 2001;122:85-8.
Bolay H, Bayazit YA, Gündüz B, Ugur AK, Akçali D, Altunyay S, et al.
Subclinical dysfunction of cochlea and cochlear efferents in migraine: An otoacoustic emission study. Cephalalgia 2008;28:309-17.
[Table 1], [Table 2]