Open AccessVestibular paroxysmia caused by contralateral tortuous vertebral artery
Author(s) -
Jin Woo Choi,
Chang-Hee Kim
Publication year - 2021
Publication title -
medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.59
H-Index - 148
eISSN - 1536-5964
pISSN - 0025-7974
DOI - 10.1097/md.0000000000027815
Subject(s) - medicine , hemifacial spasm , microvascular decompression , vertigo , tinnitus , vertebral artery , neurovascular bundle , anterior inferior cerebellar artery , nystagmus , vestibulocochlear nerve , vestibular system , vestibular nerve , surgery , audiology , facial nerve , trigeminal neuralgia , aneurysm
Rationale: Vestibular paroxysmia (VP) is characterized by spontaneous, recurrent, short, paroxysmal attacks of vertigo with or without tinnitus. Patient concerns: We report a case of paroxysmal recurrent vertigo accompanying clicking tinnitus on the left side in a 61-year-old patient. He had undergone microvascular decompression to treat the left-side hemifacial spasm 6 years prior. The patient first developed vertigo attacks about 3 years after microvascular decompression, and the attacks increased in frequency over the last 4 months. Video-nystagmography revealed a background right-beating nystagmus which was reversed every 55 seconds, to left-beating nystagmus for 17 seconds. Diagnosis: Brain magnetic resonance imaging and angiography demonstrated a compression of the cisternal segment of the left vestibulocochlear nerve between the tortuous right vertebral artery and the posterior wall of the left porus acusticus internus. Interventions and outcomes: Under the diagnosis of VP, 300 mg oxcarbazepine was administered daily, which relieved the symptoms dramatically. Lesson: The neurovascular cross-compression of the vestibulocochlear nerve by the contralateral vertebral artery tortuosity can cause VP. Periodic paroxysms of right-beating nystagmus accompanying the left-side tinnitus during vertigo attacks in our patient can be explained by secondary central hyperactivity in both vestibular and cochlear nuclei following long-standing neurovascular cross-compression.