AUTHOR=Goldschagg Nicolina , Brem Christian , Strupp Michael 

TITLE=Case report: Bitter vertigo

JOURNAL=Frontiers in Neurology

VOLUME=Volume 13 - 2022

YEAR=2022

URL=https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2022.1028597

DOI=10.3389/fneur.2022.1028597

ISSN=1664-2295

ABSTRACT=Background: There are many causes of episodes of vertigo and very few causes of episodes of changes in taste, and the combination of the two is very rare. Here we describe a patient with recurrent short episodes of vertigo, in combination with simultaneous episodes of recurrent paroxysmal dysgeusia and an altered feeling on the left side of face. The symptoms were caused by a compression of the vestibulo-cochlear nerve and the facial nerve due to a dolichoectasia of the basilar artery. 
Methods: The patient was diagnosed in our routine clinical practice and underwent a complete neurological and neuro-otological examination, including video head impulse test, caloric irrigation, ocular and vestibular evoked myogenic potentials, acoustic evoked potentials, neuro-orthoptic examination as well as cranial MRI and MR-angiography. The patient was seen twice for follow-up.
Case: A 71-year-old patient primarily presented with a two-year history of recurrent short episodes of spinning vertigo. Each of these episodes began with an altered feeling on the left side of the face, followed by a bitter taste on the left half of the tongue and subsequently vertigo lasting for up to 15 seconds. The frequency of attacks was high: up to 80 times per day. Laboratory tests revealed signs of a peripheral vestibular deficit on the left side. There were no signs of sensory or motor deficits or of altered taste between the episodes. An MRI of the brain showed an elongated basilar artery leading to an indentation of the facial and vestibulocochlear nerve on the left side. 
Conclusion: We propose a neurovascular compression in the proximal part of two cranial nerves due to pulsatile compression by the elongated basilar artery with ephatic discharges as the cause of the recurrent episodes. Consistent with this theory of ephatic discharges, treatment with the sodium channel blocker lacosamide over six months with a final dosage of 200 mg per day p.o. led to a significant reduction of the attack frequency and intensity. This treatment option with a sodium channel blocker should therefore not only be considered in vestibular paroxysmia but also in cases of paroxysmal dysgeusia.