Journal of vestibular research : equilibrium & orientation · 2019
MRI findings in vestibular paroxysmia - An observational study.
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Sivarasan Nishanth, Touska Philip, Murdin Louisa, Connor Steve
Аннотация
BACKGROUND/OBJECTIVES: Vestibular paroxysmia (VP) presents as episodic vertigo believed to be caused by neurovascular cross-compression (NVCC) of the vestibulocochlear nerve. We investigated whether NVCC occurred at a higher rate in VP, compared with controls and whether angulation of the nerve, the vessel involved and location of the point of contact were significant features.
METHODS: Retrospective analysis was conducted of MR imaging performed in patients with VP and also patients with unilateral tinnitus (in whom the asymptomatic side was used as a control). Two independent, blinded reviewers assessed each case.
RESULTS: Nine patients with VP and 20 patients with unilateral tinnitus were included. NVCC was demonstrated in all 9 VP patients (100%), compared with 9 of the controls (45%), p = 0.0049. NVCC was mostly caused by a branch of the anterior inferior cerebellar artery (AICA). Nerve angulation at the point of contact occurred in 5 of the cases (44%), but in none of the controls (specificity = 100%), p = 0.0053. There was no correlation between site of contact and VP.
CONCLUSION: Our study supports the concept of NVCC in VP and additionally suggests that nerve angulation may be a specific feature. Neurovascular contact remains a common phenomenon in asymptomatic patients and therefore correlation with neuro-otology assessment remains essential.
METHODS: Retrospective analysis was conducted of MR imaging performed in patients with VP and also patients with unilateral tinnitus (in whom the asymptomatic side was used as a control). Two independent, blinded reviewers assessed each case.
RESULTS: Nine patients with VP and 20 patients with unilateral tinnitus were included. NVCC was demonstrated in all 9 VP patients (100%), compared with 9 of the controls (45%), p = 0.0049. NVCC was mostly caused by a branch of the anterior inferior cerebellar artery (AICA). Nerve angulation at the point of contact occurred in 5 of the cases (44%), but in none of the controls (specificity = 100%), p = 0.0053. There was no correlation between site of contact and VP.
CONCLUSION: Our study supports the concept of NVCC in VP and additionally suggests that nerve angulation may be a specific feature. Neurovascular contact remains a common phenomenon in asymptomatic patients and therefore correlation with neuro-otology assessment remains essential.