Disorders of balance often pose a diagnostic conundrum for clinicians, and a multitude of investigations have emerged over the years. Vestibular evoked myogenic potential testing is a diagnostic tool which can be used to assess vestibular function. Over recent years, extensive study has begun to establish a broader clinical role for vestibular evoked myogenic potential testing.

To provide an overview of vestibular evoked myogenic potential testing, and to present the evidence for its clinical application.

Structured literature search according to evidence-based medicine guidelines, performed between November 2008 and April 2009. No restrictions were applied to the dates searched.

The benefits of vestibular evoked myogenic potential testing have already been established as regards the diagnosis and monitoring of several clinical conditions. Researchers continue to delve deeper into potential new clinical applications, with early results suggesting promising future developments.

This study sought to establish the prevalence of vestibular disorders, migraine and definite migrainous vertigo in patients with psychiatric disorders who were referred for treatment of dizziness, without a lifetime history of vertigo.

Retrospective study.

Out-patients in a university hospital.

Fifty-two dizzy patients with panic disorders and agoraphobia, 30 with panic disorders without agoraphobia, and 20 with depressive disorders underwent otoneurological screening with bithermal caloric stimulation. The prevalence of migraine and migrainous vertigo was assessed. The level of dizziness was evaluated using the Dizziness Handicap Inventory.

Dizzy patients with panic disorders and agoraphobia had a significantly p = 0.05 regarding the prevalence of peripheral vestibular abnormalities in the group of subjects with PD and agoraphobia and in those with depressive disorders. Migraine was equally represented in the three groups, but panic disorder patients had a higher prevalence of migrainous vertigo definite migrainous vertigo. Almost all patients with a peripheral vestibular disorder had a final diagnosis of definite migrainous vertigo according to Neuhauser criteria. These patients had higher Dizziness Handicap Inventory scores. The Dizziness Handicap Inventory total score was higher in the subgroup of patients with panic disorders with agoraphobia also presenting unilateral reduced caloric responses or definite migrainous vertigo, compared with the subgroup of remaining subjects with panic disorders with agoraphobia (p < 0.001).

Our data support the hypothesis that, in patients with panic disorders (and especially those with additional agoraphobia), dizziness may be linked to malfunction of the vestibular system. However, the data are not inconsistent with the hypothesis that migrainous vertigo is the most common pathophysiological mechanism for vestibular disorders.

To investigate vestibular function in human immunodeficiency virus positive subjects.

We studied vestibular function in 60 human immunodeficiency virus positive subjects reporting dizziness. All three Center for Disease Control and Prevention categories of human immunodeficiency virus infection were represented in the study group (30 patients in class A, 20 in class B and 10 in class C). Subjects had had no previous history of acute vertigo. All subjects underwent: neurotological screening for spontaneous, positional and positioning nystagmus, using head-shaking and head-thrust (Halmagyi) tests; audiometrical examination; and electronystagmography with bithermal stimulation (Freyss' method). The results of the 30 class A subjects were compared with those of 30 human immunodeficiency virus negative patients reporting dizziness.

Abnormal otoneurological findings increased progressively from the A to C categories, particularly regarding increased central damage (3.3 per cent of class A, 35 per cent of class B and 100 per cent of class C subjects). In contrast, the incidence of peripheral vestibular disorders remained almost the same, comparing the three categories (33.3 per cent in class A and 50 per cent in classes B and C subjects). Moreover, a higher number of human immunodeficiency virus positive subjects showed abnormal otoneurological findings, compared with the dizzy, human immunodeficiency virus negative subjects.

In our opinion, a vestibular disorder may occur in human immunodeficiency virus positive patients as a result of direct viral damage, even in the early phase of infection. Central vestibular damage may be established later on, and may be linked to different causes (e.g. superinfections, vascular causes and drug toxicity).

To quantitatively evaluate the diagnostic accuracy of diagnostic tests for immunomediated hearing loss.

We searched Medline and the Cochrane Database of Systematic Reviews for potentially relevant studies.

Twenty-five studies met the inclusion criteria of this systematic review. The diagnosis of immunomediated hearing loss was based on the clinical presentation and the response to corticosteroid administration.

The following data were extracted from the selected studies and entered into a standardised database: population demographics; exclusion and inclusion criteria; diagnostic tests; sensitivity; specificity; the number of true positive, true negative, false positive and false negative values; therapy used, including dose and duration; and delay between symptom onset and therapy commencement.

This systematic review combined data from 679 patients with immunomediated hearing loss, reported by 22 research teams. Substantial heterogeneity was found among the included studies; for this reason, summary sensitivity and specificity values were not computed.

The results of diagnostic tests for immunomediated hearing loss depend on many factors, and there is a risk of potential bias. This is the first time that such a systematic review has been presented; such a review is a more rigorous method of demonstrating the utility of the available diagnostic tests.

We report a case of a 58-year-old man suffering from stiff-person syndrome and recurrent peripheral vertigo.

A case report and a review of the recent literature on stiff-person syndrome are presented.

The patient presented with recurrent episodes of vertigo with a pure peripheral pattern and with concomitant episodes of burning muscle pain, muscle twitching, weight gain and fatigue, worsening with tension or stress that also occurred in periods without vertigo. Cochlear examinations only showed presbyacusis-like hearing loss. The diagnosis of stiff-person syndrome was made with electromyographic examination and from findings in the blood and cerebrospinal fluid of high titres of anti-glutamic acid decarboxylase (GAD67) autoantibodies. In a two-year follow-up period, therapy for stiff-person syndrome abolished episodes of both stiffness and vertigo.

As far as we know, no other clinical case of acute vestibular damage with a possible correlation with anti-glutamic acid decarboxylase antibodies has been described. Peripheral vertigo possibly related to a lack of gamma aminobutyric acid underlines a possible role of gamma aminobutyric acid as a neurotransmitter in the peripheral vestibular system.