Unravelling the Mystery of Vestibular Paroxysmia: A Case Series

TL;DR

This paper presents four cases of vestibular paroxysmia, highlighting how MRI identifies neurovascular conflicts and how sodium-channel-blocking drugs can reduce symptoms.

Contribution

The study emphasizes the diagnostic value of MRI and the effectiveness of specific medications in managing vestibular paroxysmia.

Findings

MRI identified neurovascular conflicts in all four cases of vestibular paroxysmia.

Sodium-channel-blocking agents reduced the frequency and intensity of vertigo attacks in patients.

High-resolution imaging is crucial for distinguishing VP from other vestibular syndromes.

Abstract

Vestibular paroxysmia (VP) is a neurological disorder characterised by sudden-onset, recurrent, short-term episodes of vertigo and imbalance, often resulting from neurovascular conflict between a vascular loop and the vestibulocochlear nerve (VIII-cranial nerve). We present four cases of VP, highlighting the clinical presentation, diagnostic workup including magnetic resonance imaging (MRI), and medical management. Case 1: A 40-year-old female; MRI of the brain and internal auditory canal showed a loop of the anterior inferior cerebellar artery (AICA) coursing between the facial and vestibulocochlear nerves on the left, consistent with neurovascular conflict. Case 2: A 44-year-old male; MRI revealed a loop of the AICA indenting the left VII/VIII cranial-nerve complex at the entrance of the left internal auditory canal. Case 3: A 37-year-old female; MRI demonstrated a vascular loop at the right cerebellopontine angle, indicating neurovascular conflict. Case 4: A 39-year-old male; MRI showed a vascular loop in the left cerebellopontine angle causing modest compression of the left VII/VIII cranial-nerve complex along its posterosuperior aspect. These cases underscore the importance of high-resolution imaging in identifying neurovascular compression in VP, as well as early recognition and treatment with sodium-channel-blocking agents (carbamazepine, oxcarbazepine), which have shown efficacy in reducing attack frequency and intensity. Given the overlapping clinical features of VP with other episodic vestibular syndromes, awareness of characteristic imaging findings and therapeutic response is essential for accurate diagnosis and optimal management.

Figures