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Vestibular paroxysmia caused by contralateral tortuous vertebral artery: A case report

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 undergo...

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Detalles Bibliográficos
Autores principales: Choi, Jin Woo, Kim, Chang-Hee
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8589239/
https://www.ncbi.nlm.nih.gov/pubmed/34766594
http://dx.doi.org/10.1097/MD.0000000000027815
Descripción
Sumario: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.