Acute Vestibular Syndrome from Demyelinating Lesions (P02.247)

Abstract

Objective: Describe the frequency, clinical characteristics, and lesion location of acute vestibular syndrome (AVS) patients caused by demyelinating disease. Background Multiple sclerosis (MS) is known to cause dizziness and vertigo. Prior reports suggest acute vertigo in MS results from lesions in the intra-pontine portion of the 8 th nerve fascicle. It is unclear whether demyelinating AVS mimics vestibular neuritis closely. Design/Methods: Prospective case series (1999-2011). Consecutive AVS patients (vertigo, nystagmus, nausea/vomiting, head-motion intolerance, unsteady gait) with ≥1 stroke risk factor underwent structured bedside examination and neuroimaging (almost all by MRI). Repeat imaging was obtained in patients with normal imaging but clinical signs suggestive of a central lesion. We identified demyelinating causes based on clinical, imaging, and laboratory features. Results: Of 160 AVS presentations, only 4% (n=6) were due to demyelinating disease (with stroke and vestibular neuritis the most common diagnoses). Five had an acute MS plaque likely responsible for the clinical syndrome. Lesion location varied – 3 inferior cerebellar peduncle; 1 medulla, 1 medial longitudinal fasciculus; 1 midbrain. None had lesions in the intra-pontine 8 th nerve fascicle. Three were first presentations (i.e., clinically isolated demyelinating syndrome), while the others were known MS. All had central oculomotor signs (upbeat nystagmus, internuclear ophthalmoplegia, seesaw nystagmus, skew deviation, or direction-changing, gaze evoked horizontal nystagmus). In one patient (inferior cerebellar peduncle lesion), the only central sign was a normal head impulse test of vestibular function. All patients with demyelinating AVS symptomatically improved with steroid therapy. Conclusions: Demyelinating disease was an uncommon cause of AVS in our study. It might be more frequent in a less selected AVS cohort. Symptomatic lesions were in locations other than the anticipated 8 th -nerve root entry zone. The majority of patients had relatively obvious oculomotor signs, making differentiation from vestibular neuritis more straightforward. Disclosure: Dr. Pula has received personal compensation for activities with Bayer, Teva, Lundbeck, and Novartis as a speaker. Dr. Kattah has received personal compensation for activities with Biogen Idec as a consultant. Dr. Kattah has received personal compensation in an editorial capacity for Bayer Pharmaceuticals Corporation. Dr. Newman-Toker has nothing to disclose.