Reversible Peripheral Vestibular Deficit due to Migraine

Dear Editor, Acute attacks of vestibular migraine (VM) can present with diverse neuro-otological[1] and oculomotor manifestations showing involvement of central, peripheral, or both vestibular systems. Various theories/hypotheses like cortical spreading depression, trigeminal neurogenic inflammation, channelopathies, and vasospasm of the internal auditory artery have been put forward to explain various clinical, oculomotor, and neuro-otological findings in ictal and inter-ictal periods. Peripheral audio-vestibular findings are usually thought to be due to vasospasm of the internal auditory artery. A 62-year-old male presented with history of recurrent attacks of vertigo since the age of 20 years. A typical attack used to start with heaviness of the head followed by flashes of light in front of eyes, followed 5 min later by vertigo and 15 min later by occipital or left-sided headache. Headache and vertigo would remain for 15 min, followed by vomiting, after which he would get relief, but heaviness of the head would persist for 4–5 h. He would sleep and get up afresh. These attacks used to occur at intervals of 6 months to 2 years. Caloric test and magnetic resonance imaging (MRI) done 2 years back after one such attack were normal. The last attack occurred 1 day before presentation to us, when after the morning walk, he had sudden unprovoked spinning while lying supine. He slept for 2–3 h and got up afresh. There was history of tinnitus and hearing impairment in the left ear from last 3 years. Pure tone audiometry revealed moderate sensorineural hearing loss in the left ear. His father also suffered from migraine headaches and recurrent attacks of vertigo associated with headaches for many years. During history taking at the first visit, the patient had a sudden attack of vertigo and was complaining of spinning. Right beat nystagmus (RBN) increasing on right gaze [Video 1] was recorded and could be observed for 30 min. Head impulse test (HIT) [Video 2] was positive to the left side. {"href":"Single Video Player","role":"media-player-id","content-type":"play-in-place","position":"float","orientation":"portrait","label":"Video 1","caption":"","object-id":[{"pub-id-type":"doi","id":""},{"pub-id-type":"other","content-type":"media-stream-id","id":"1_x5f3izdi"},{"pub-id-type":"other","content-type":"media-source","id":"Kaltura"}]} {"href":"Single Video Player","role":"media-player-id","content-type":"play-in-place","position":"float","orientation":"portrait","label":"Video 2","caption":"","object-id":[{"pub-id-type":"doi","id":""},{"pub-id-type":"other","content-type":"media-stream-id","id":"1_1tn9g67n"},{"pub-id-type":"other","content-type":"media-source","id":"Kaltura"}]} Videonystagmography performed during the attack revealed RBN (Slow phase velocity [SPV]- 5°) [Figure 1a], which increased in intensity on removal of fixation (SPV- 20°) [Figure 1b] and on right gaze. Cold caloric test [Figure 2] revealed very weak response in the left ear. On head shaking [Figure 1c] for 10 s, the intensity of RBN increased (SPV- 9°) and was replaced 40 s later by persistent left beat nystagmus (LBN) recorded for more than 1 min, but did not disappear even after waiting for 10 min. Meanwhile, his subjective spinning also decreased a lot. Then, on hyperventilation for 60 s, LBN increased in intensity (SPV 8°–20°). This LBN persisted on all positional tests without any change in its character. HIT [Figure 3] remained positive to the left side. LBN persisted even 1 h after examination. MRI of the brain with fast imaging employing steady-state acquisition of the inner ear and brainstem was unremarkable. Thinking of it as preexisting dead left ear with superimposed attack of VM, he was started on propranolol and flunarizine. Re-examination done 11 days later did not reveal any spontaneous [Video 3] or gaze-evoked nystagmus. Mild RBN was present on head shaking and on hyperventilation. HIT became negative [Figure 4 and Video 4] with no refixation saccades. Patient is under treatment for the last 9 months. He is completely symptom free, and HIT is negative on both sides.Figure 1: Videonystagmography tracings showing (a) Spontaneous right beat nystagmus (with fixation); (b) spontaneous right beat nystagmus (without fixation); (c) right beat nystagmus converting into persistent left beat nystagmus after head shakingFigure 2: Videonystagmography tracings showing Cold caloric test showing hypoactive left earFigure 3: Videonystagmography tracings showing Positive head impulse test to the left sideFigure 4: Videonystagmography tracings showing Head impulse test negative on both sides {"href":"Single Video Player","role":"media-player-id","content-type":"play-in-place","position":"float","orientation":"portrait","label":"Video 3","caption":"","object-id":[{"pub-id-type":"doi","id":""},{"pub-id-type":"other","content-type":"media-stream-id","id":"1_h6pbtvth"},{"pub-id-type":"other","content-type":"media-source","id":"Kaltura"}]} {"href":"Single Video Player","role":"media-player-id","content-type":"play-in-place","position":"float","orientation":"portrait","label":"Video 4","caption":"","object-id":[{"pub-id-type":"doi","id":""},{"pub-id-type":"other","content-type":"media-stream-id","id":"1_hwnlrbor"},{"pub-id-type":"other","content-type":"media-source","id":"Kaltura"}]} This patient was a typical case of definite VM according to International classification of headache disorders (ICHD)-3 criteria, having recurrent attacks of vertigo accompanied with aura and headaches. One such attack of vertigo incidentally occurred in front of us, during which we could notice peripheral type of RBN and positive HIT to the left side, indicating peripheral vestibular deficit on the right side. This RBN first increased and later got converted to persistent LBN after head shaking. We think he was having persistent asymptomatic LBN in the background and developed symptomatic RBN along with positive HIT to the left side during the acute attack of vertigo he suffered in front of us. He responded well to treatment for migraine and on subsequent visits, he had no spontaneous nystagmus and vertigo and HIT also became negative, indicating the reversible nature of peripheral vestibular injury he suffered during the acute attack of VM. Direction-fixed horizontal RBN, increasing on right gaze, on removal of fixation, and also on head shaking, along with positive HIT to the left along with absent response on cold caloric test on the left side, indicated it to be due to peripheral vestibular lesion. This case is unique in the sense that the reversible nature of peripheral injury during acute attack of VM could be demonstrated in this case. Other authors[2-4] have reported positive HIT in various studies, but they did not mention about its reversible nature and whether HIT became negative after the acute attack. Our finding of unilateral canal paralysis is in agreement with those of other authors.[1-4] It is a known phenomenon that damage to the inner ear, in cases of migraine, can lead to permanent hearing loss,[5] as was seen on the left side in this case. Both central as well as peripheral neuro-otological findings indicating peripheral vestibular dysfunction have been reported during acute attacks of VM by others also.[5] Peripheral vestibular and auditory deficits, for example, sudden episodes of hearing loss and/or vertigo during an acute attack of VM,[1] can occur due to vasospasm of the internal auditory artery or its branches,[2,5,6] leading to transient ischemia of the inner ear or brainstem, similar to retinal vasospasm observed in retinal migraine. Audiovestibular symptoms may also arise by trigeminal neurogenic inflammation in the labyrinth.[2] We have presented a rarely demonstrable reversible peripheral vestibular deficit during an acute attack of VM, thought usually to be due to vasospasm of the internal auditory artery, a branch of the anterior inferior cerebellar artery. VM, otherwise a central nervous system disorder, should be considered as an important cause of peripheral vestibular deficits seen in such cases and managed accordingly. Declaration of patient consent Informed written consent was obtained from patient for writing and publication of the clinical information, videos, and images. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.