An Overview of Otologic Migraine

Educational Objectives

The goal of this program is to improve the management of otologic migraine. After hearing and assimilating this program, the clinician will be better able to:

1. Recognize signs of atypical migraine.
2. Identify migraine triggers.
3. Elaborate on the association between migraine and Meniere’s disease and other otologic disorders.
4. Recognize the correlation between migraine and sudden hearing loss.
5. Implement effective treatment protocols for otologic migraine.

Summary

Overview: the pathophysiology of migraine involves a baseline hypersensitivity of the brain; the brain of a patient without migraine will gradually tune out repetitive sounds; a patient with migraine will begin to hear the sound at an increasingly louder level; neurotransmitters involved include glutamate, serotonin, histamine, and calcitonin gene-related peptide (CGRP); the chemical-electrical changes in the brain related to migraine are opposite to those of seizure, causing decrease in brain activity, referred to as cortical depression, which spreads within the brain and causes activation of cranial nerve (CN) V, leading to headache, potential changes in the inner ear, and central vestibular effects

Involvement of the trigeminal nerve (CN V): a study by Vass et al (1998) involved labelling the ophthalmic branch (V1) of CN V; it was found to innervate the basilar artery, anterior inferior cerebellar artery, and spiral modiolar artery; the stria vascularis had dense nerve endings from V1, indicating nerve endings inside the cochlea; Vass et al (2001) investigated changes in the inner ear in response to stimulation of CN V, specifically fluid extravasation within the cochlea; V1 was stimulated with 0.1 mA and 1 mA; almost 2.5 times more fluid extravasation within the cochlea was observed at 0.1 mA and almost 4 times more fluid extravasation at 1 mA; theoretically, activation of CN V could contribute to endolymphatic hydrops (ELH), Meniere's disease (MD), and benign positional vertigo

Incidence of migraine: ranges between 13% and 25% in the general population; the lifetime prevalence of headaches in general is >90%; among patients with migraine, 27% to 42% experience vertigo at some point; 3% to 5% of the general population experiences vestibular migraine; MD has a prevalence of 0.2%; vestibular migraine is 15 to 20 times more common than MD; in most patients, MD is also related to migraine; 36% of patients with vestibular migraine experience vertigo when they are not experiencing headaches; some patients with migraine only develop vertigo and atypical migraine symptoms

Atypical migraine: ≈60% of patients with migraine have atypical symptoms and do not fulfil International Headache Society criteria; patients may complain of neck spasms or stiffness (often unilateral), sinus headaches, pain behind the eyes, stress or caffeine headaches, or head pressure; patients may complain of sinus infections with weather changes; may experience dizziness with weather changes or with too much sound or visual motion; may continue to report symptoms after multiple sinus surgeries or report transient relief of symptoms; sinus surgery disrupts nerve endings; the nerves require ≈6 mo to grow back; this can lead to multiple sinus surgeries; computed tomography (CT) prior to initial surgery is often normal; sinus surgery can cause scarring, which can lead to sinus disease; consider migraine as a cause of sinus headaches before proceeding with sinus surgery

Migraine triggers: migraine is a genetic problem but is activated by specific triggers; stress is the most common trigger; can be psychological (eg, anxiety, conflict, death) or physical (eg, pain, upper respiratory infection, immunologic response to vaccination); sleep disturbances include interrupted sleep, too little sleep; multiple awakenings, obstructive sleep apnea (OSA), excessive sleep, and shifting sleep schedule; other triggers include head trauma, intracranial surgery, ear surgery, hormonal changes (eg, menopause, hormone replacement therapy, oral contraceptives, testosterone supplements), or dental work or other procedures that stimulate CN V; dietary factors include dehydration and hunger; patients are counseled to eat on the same schedule every day; foods containing molecules similar to neurotransmitters (eg, histamine, glutamate, tyramine) can be triggers; commonly listed migraine food triggers include caffeine, chocolate, nuts (especially peanuts), alcohol (especially red wine), cheese, and fresh bread or yeast products; tyramine accumulates in aged, canned, cured, smoked, or processed meats and fermented products; foods containing monosodium glutamate or aspartame, some vegetables (eg, lima beans), and some fruits (eg, avocados, figs, raisins, any dried fruit, bananas, citrus [rich in histamine], any overly ripened fruit [rich in tyramine]) are triggers; some individuals are triggered by intense stimulation (eg, bright lights, loud sounds), intense or repeated head motions, visual motion, weather changes, intense smells, ambient heat, cold air on the face or into the ear, and intense exercise

Index of suspicion for migraine: consider migraine in patients who report sensitivity to light or sound, including innocuous sounds, sensitivity to motion in the visual field, childhood or adult-onset motion sickness, space and motion discomfort, or significant nausea; ear pain or pressure are often related to migraine if other causes are ruled out; Moshtaghi et al (2018) showed aural pressure or fullness which does not resolve with the Valsalva maneuver can be related to migraine; sinus headaches with repeated normal CT or lack of response to antibiotics or nasal steroids should be considered migraine until proven otherwise; Schreiber et al (2004) found 88% of patients with chronic sinus headaches had migraine; Hwang et al (2018) showed patients with low frequency or fluctuating hearing loss or other cochlear disorders are likely to be associated with migraine; Ghavami (2015) showed that many patients with presumed MD show features of migraine; patients with recurrent benign positional vertigo who do not respond to the Epley maneuver and have negative MRI likely have migraine; patients who report dizziness with the Dix-Hallpike maneuver but have no nystagmus, with significant nausea or vomiting after an Epley maneuver, or who have immediate nystagmus on Dix-Hallpike likely have migraine

Triggering events: stress, sleep and diet are the most common triggering events; usually there is a triggering event that affects the migraine threshold level in the brain; the triggering event, such as stress, accompanied by other factors like poor sleep or hormonal changes increase the brain’s activity to a level close to the threshold; a small dietary change at that point can push the brain above its threshold; at baseline, with brain activity far from the migraine threshold, the same dietary change would not exceed the threshold; if contributing factors can be reversed, brain activity returns to baseline, and normal diet can be resumed

Continuous migraine: can occur if the patient remains above the migraine threshold for a prolonged period; migraine symptoms persist until the trigger is reversed or the migraine threshold is altered; prophylaxis elevates the threshold; trigger control helps to return brain activity to baseline; trigger control is the best long-term strategy; while the patient is having painful migraines, it is often necessary to temporarily place the patient on medication to alter the threshold sufficiently to reduce symptoms; it is easier to identify triggers when symptoms are intermittent; an episode typically occurs within 6 to 8 hr after exposure to a trigger; it is helpful to maintain trigger logs to help identify triggers; a patient may have different thresholds for different symptoms

Meniere's disease: the original papers described MD as “a cerebral state, called migraine, give place in the end to similar attacks and the deafness which arises in these circumstances would seem to us inevitably to be related to a disease of the same nature”; “we believe that it can be asserted that many so-called migraines are only the index of a morbid process leading infallibly to deafness”; Ghavami et al (2016) conducted a cohort study of 28 patients with definite MD; 68% had migraine headaches; 32% had a first degree relative with family history of migraine, certain migraine features, or ≥3 sensitivities (eg, light, sound, visual motion, weather, smell); Ghavami et al (2018) treated a cohort of patients with definite MD with a migraine protocol; treatment involved a stepwise protocol of nortriptyline and verapamil with added topiramate later; a Meniere's disease quality of life survey was conducted initially and at follow-up; 92% of patients improved from a mean of 8 episodes/mo pretreatment to 0.6 episodes/mo after treatment; patients with MD responded very well to the migraine protocol; response rate was equivalent to vestibular nerve section

Mal de debarquement syndrome (MDSS) and migraine: MDSS occurs in patients after a long boat or plane ride; in a study by Ghavami et al (2017), 15 patients with MDSS were treated with a migraine protocol, including dietary and lifestyle changes plus medication; a historical control group of 17 patients were treated with physical therapy alone; 73% were women with a mean age of 51 yr; the treatment group showed a significant reduction in visual analog scale (VAS) scores from an average of 7.6 to 1.8 compared with a reduction from 7.4 to 6.8 in the control group

Persistent postural perceptive dizziness (PPPD) and migraine: a study investigated a cohort of 19 patients who fulfilled migraine criteria and 17 patients who did not fulfill migraine criteria; 47% had no migraine history; 36% had migraine headache but no vestibular migraine; 17% had vestibular migraine

Hyperacusis and migraine: a cohort of 18 patients with hyperacusis were treated with a migraine protocol; 17 historical controls were treated with progressive broad band noise sound therapy; no sound therapy was used in the migraine treatment group; the Modified Khalfa Hyperacusis Questionnaire score (normal <27) decreased from an average of 32.6 to 22.2 in the treatment group compared with a decrease from 33.9 to 27.6 in the control group

Other associations: in a group of 11 patients with aural fullness, 54% had migraine headaches; after treatment with a migraine regimen, VAS scores decreased from an average of 7.2 to 1.5; visual motion sensitivity involves no stimulation to the inner ear; the issue lies in the brain, not the inner ear; pediatric patients with vertigo and a normal MRI and normal examination likely have migraine; in a cohort of 5 patients with persistent post-stapedectomy vertigo, 3 had a history of migraine, and 2 had specific pressure-sensitivity; imaging studies were performed to rule out long prosthesis and perilymphatic fistula; all patients had resolution of symptoms with migraine prophylaxis; in a group of 9 patients with acoustic neuroma and episodic vertigo, 7 had migraine that resolved completely with medical treatment; 2 had benign positional vertigo which also resolved; just because a tumor is present does not necessarily mean it is the cause of vertigo; tumor and vertigo are separate conditions; a tumor is a fixed lesion which cannot cause episodic vertigo; a tumor can cause imbalance or dizziness with rapid head motion, but not spontaneous attacks of vertigo

Migraine and sudden hearing loss (HL): Kim et al (2019) showed that patients with migraine were 50% more likely to experience sudden HL; Chu et al (2013) concluded that patients with migraine had an 80% higher chance of developing sudden HL compared with the control cohort; Jenkins et al (1987) described an association between recurrent sudden HL and migraine HA; recurrent HL, usually low frequency, is referred to as cochlear migraine; characterized by lack of dizziness, a family history of migraine, motion intolerance, history of neck stiffness, and sensitivity to pressure changes (historically called cochlear Meniere's or ELH); a study applied heavily weighted T2 and delayed imaging after administration of intravenous gadolinium to visualize changes related to ELH; the same group applied the same technique to patients with migraine and found some patients with migraine also had ELH; ELH may be an effect of damage to the inner ear rather than a cause of MD; all ELH is not MD; ELH is likely the final common pathway for damage to the inner ear or fluid extravasation in the inner ear; not necessarily the cause of symptoms but more likely an effect; speaker’s group began treating patients with sudden HL with adjuvant migraine prophylaxis in addition to oral and intratympanic steroids; generally used a combination of nortriptyline and topiramate; found migraine prophylaxis markedly improved the low frequency outcome with an average of 10 dB improvement at 250 and 500 Hz and 15 dB improvement at 1000 Hz

Treatment of migraine: the typical treatment protocol for migraine involves lifestyle changes; strict adherence to diet is important, including elimination of caffeine over a period of 1 to 2 wk; maintain a consistent sleep schedule; obtain a sleep study if OSA is suspected; medications cannot effectively treat migraine if OSA is present; avoid skipping meals; eat meals on a regular schedule; drink water, but stop drinking water 3 hr before bedtime; follow a regular exercise and meditation schedule for stress relief; initially eliminate all potential dietary triggers, then gradually reintroduce food items to identify specific triggers; all patients are started on vitamin B2 200 mg twice a day (BID) and magnesium oxide 400 mg BID; if the patient experiences diarrhea, the dose of magnesium oxide is decreased to 200 mg BID or 100 BID; if diarrhea does not resolve, the speaker may switch to magnesium glycinate; the speaker writes prescriptions for vitamin B2 and magnesium because prescription grade supplements are more consistent; over-the-counter supplements are unregulated, so the quantities of vitamins are uncertain and there may be significant variability; melatonin can help with sleep onset but not sleep maintenance; patients with problems related to sleep maintenance need to be treated for underlying causes (eg, anxiety, depression) or improve their sleep hygiene

Readings

Abouzari M, Abiri A, Djalilian HR. Successful treatment of a child with definite Meniere's disease with the migraine regimen. Am J Otolaryngol. 2019;40(3):440-442; Charles AC, Baca SM. Cortical spreading depression and migraine. Nat Rev Neurol. 2013 Nov;9(11):637-644; Ghavami Y, Haidar YM, Moshtaghi O, Lin HW, Djalilian HR. Evaluating quality of life in patients with Meniere's disease treated as migraine. Ann Otol Rhinol Laryngol. 2018 Dec;127(12):877-887; Ghavami Y, Haidar YM, Ziai KN, et al. Management of mal de debarquement syndrome as vestibular migraines. Laryngoscope. 2017;127(7):1670-1675; Ghavami Y, Mahboubi H, Yau AY, Maducdoc M, Djalilian HR. Migraine features in patients with Meniere's disease. Laryngoscope. 2016;126(1):163-168; Hwang JH, Tsai SJ, Liu TC, Chen YC, Lai JT. Association of tinnitus and other cochlear disorders with a history of migraines. JAMA Otolaryngol Head Neck Surg. 2018;144(8):712-717; Moshtaghi O, Ghavami Y, Mahboubi H, et al. Migraine-related aural fullness: a potential clinical entity. Otolaryngol Head Neck Surg. 2018;158(1):100-102; Moshtaghi O, Sahyouni R, Lin HW, Ghavami Y, Djalilian HR. A historical recount: discovering Ménière's disease and its association with migraine headaches. Otol Neurotol. 2016;37(8):1199-1203; Naganawa S, Yamazaki M, Kawai H, Bokura K, Sone M, Nakashima T. Visualization of endolymphatic hydrops in Ménière's disease with single-dose intravenous gadolinium-based contrast media using heavily T2-weighted 3D-FLAIR. Magn Reson Med Sci. 2010;9(4):237-242; Schreiber CP, Hutchinson S, Webster CJ, Ames M, Richardson MS, Powers C. Prevalence of migraine in patients with a history of self-reported or physician-diagnosed sinus headache. Arch Intern Med. 2004;164(16):1769-1772; Teixido M, Seymour P, Kung B, Lazar S, Sabra O. Otalgia associated with migraine. Otol Neurotol. 2011;32(2):322-325; Vass Z, Shore SE, Nuttall AL, Miller JM. Direct evidence of trigeminal innervation of the cochlear blood vessels. Neuroscience. 1998;84(2):559-567; Vass Z, Steyger PS, Hordichok AJ, Trune DR, Jancso G, Nuttall AL. Capsaicin stimulation of the cochlea and electric stimulation of the trigeminal ganglion mediate vascular permeability in cochlear and vertebro-basilar arteries: a potential cause of inner ear dysfunction in headache. Neuroscience. 2001;103(1):189-201.

Disclosures

For this program, the following relevant financial relationships were disclosed and mitigated to ensure that no commercial bias has been inserted into this content: Dr. Djalilian has an equity/ownership interest in Elinava Technologies and Cactus Medical, and is a consultant to NXT Biomedical. The planning committee reported nothing relevant to disclose. In his lecture, Dr. Djalilian presents information related to the off-label or investigational use of a therapy, product, or device.

Acknowledgements

Dr. Djalilian, was recorded for Audio Digest on October 9, 2021. Audio Digest thanks Dr. Djalilian for his participation in the production of this program.

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0 CE contact hours.

Lecture ID:

OT550401

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.