Search

Background: Vestibular migraine (VM) is a common cause of recurrent vertigo. Migraine headache preventative therapies are currently prescribed to control vertigo symptoms in VM. Clinical trials of nutraceuticals for migraine headache prevention have shown positive outcomes, but, to date, there have been no studies to assess their effectiveness in the management of VM. Aims: To report the effects of nonprescription therapy management on VM symptoms. Methods: We undertook a prospective, questionnaire‐based assessment of patients diagnosed with VM between November 2019 and August 2021 at two Sydney tertiary referral clinics. Patients were advised on optimising sleep, hydration, exercise and nutrition and instructed to use an over‐the‐counter combination product containing riboflavin 200 mg, magnesium 150 mg, coenzyme Q10 75 mg and feverfew 200 mcg. Symptom severity and frequency were assessed using the Dizziness Handicap Inventory (DHI), the Vertigo Symptom Score short‐form (VSS‐sf) and two visual analogue scales for severity (VAS‐s) and frequency (VAS‐f) before and 3 months after commencing treatment. Result: In 82 participants (78% female; mean age, 44 ± 14 years) we recorded a decrease in DHI (mean, 16.8 [95% confidence interval (CI), 12.8–20.9], VSS‐sf (9.3, 7.1–11.5), VAS‐s (3.0, 2.2–3.8) and VAS‐f (2.8, 2.1–3.4), equating to an improvement of 44.1%, 44.9%, 44.1% and 38.9% for each measure respectively. On the DHI and VSS‐sf, 41 (50%) and 44 (53.7%) patients showed improvement in their symptoms; 39 (47.6%) and 36 (43.9%) patients noted no change and two patients reported worsening. The supplement was well‐tolerated. Conclusions: The results provide preliminary evidence that VM symptom frequency and severity can be reduced by using nonprescription therapies. [ABSTRACT FROM AUTHOR]

Genomic technologies such as next-generation sequencing (NGS) are revolutionizing molecular diagnostics and clinical medicine. However, these approaches have proven inefficient at identifying pathogenic repeat expansions. Here, we apply a collection of bioinformatics tools that can be utilized to identify either known or novel expanded repeat sequences in NGS data. We performed genetic studies of a cohort of 35 individuals from 22 families with a clinical diagnosis of cerebellar ataxia with neuropathy and bilateral vestibular areflexia syndrome (CANVAS). Analysis of whole-genome sequence (WGS) data with five independent algorithms identified a recessively inherited intronic repeat expansion [(AAGGG) exp ] in the gene encoding Replication Factor C1 (RFC1). This motif, not reported in the reference sequence, localized to an Alu element and replaced the reference (AAAAG) 11 short tandem repeat. Genetic analyses confirmed the pathogenic expansion in 18 of 22 CANVAS-affected families and identified a core ancestral haplotype, estimated to have arisen in Europe more than twenty-five thousand years ago. WGS of the four RFC1-negative CANVAS-affected families identified plausible variants in three, with genomic re-diagnosis of SCA3, spastic ataxia of the Charlevoix-Saguenay type, and SCA45. This study identified the genetic basis of CANVAS and demonstrated that these improved bioinformatics tools increase the diagnostic utility of WGS to determine the genetic basis of a heterogeneous group of clinically overlapping neurogenetic disorders., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)

Objective: To deduce whether similar or distinct populations of vestibular afferents are activated by acoustic and galvanic vestibular stimulation by comparing the effectiveness of 'matched' stimuli in eliciting vestibulospinal reflexes., Methods: Twelve subjects (5 men, 7 women) underwent individual 'matching' of 2 ms tone burst and galvanic stimuli, using vestibulocollic reflexes so that corrected reflex amplitudes to tone burst and galvanic stimuli were within 10% of each other. These same intensities were then administered using 20 ms durations to determine whether they were equally effective in evoking vestibulospinal responses., Results: Corrected reflex amplitudes for vestibulocollic responses to tone burst and galvanic stimulation were not significantly different for the right (P=0.45) or left (P=0.68) sides. All subjects had vestibulospinal responses to galvanic stimulation (average intensity 4.0 mA for both sides). The short latency (SL) and medium latency (ML) components of the vestibulospinal reflexes were larger after galvanic compared to tone burst stimulation in 11 of 12 subjects (P<0.01)., Conclusions: Despite evoking equal-sized vestibulocollic reflexes, there was a clear dissociation between the magnitude of tone burst and galvanic-induced vestibulospinal reflexes. Galvanic stimulation evoked SL and ML reflexes in all subjects. Tone burst stimuli evoked only small SL reflexes and, in most cases, no ML reflexes. Acoustically-evoked vestibulocollic reflexes are likely to be due to saccular excitation. The limited effectiveness of longer tone burst stimuli to evoke ML vestibulospinal reflexes suggests that saccular afferents have, at most, only a minor role in the production of these reflexes. We conclude that galvanic stimulation is more effective in eliciting vestibulospinal reflexes than tone burst stimulation, and that the two methods activate different populations of vestibular afferents.

A 36-year-old male developed an acute right-sided weakness due to left-sided pontine infarction. Two months later, he first noticed sudden right elbow flexion in response to a loud unexpected noise. Detailed electrophysiological assessment was performed. A large, short-latency (median 39 msec), synchronous electromyographic discharge occurred in the right biceps brachii electrodes following a 50-msec, 120-dB 1-kHz tone burst, with habituation only with very short (30-second) interstimulus intervals. Less synchronous activity at longer latencies was present both in a number of right-sided arm muscles at rest and on the clinically unaffected side during a tonic voluntary contraction. We discuss possible underlying mechanisms and our reasons for considering this a focally enhanced startle response. Our report broadens the range of expression of acquired startle disorders., (Copyright 2001 Movement Disorder Society.)