Barry M. Seemungal

Vestibular Perception following Acute Unilateral Vestibular Lesions

Little is known about the vestibulo-perceptual (VP) system, particularly after a unilateral vestibular lesion. We investigated vestibulo-ocular (VO) and VP function in 25 patients with vestibular neuritis (VN) acutely (2 days after onset) and after compensation (recovery phase, 10 weeks). Since the effect of VN on reflex and perceptual function may differ at threshold and supra-threshold acceleration levels, we used two stimulus intensities, acceleration steps of 0.5°/s2 and velocity steps of 90°/s (acceleration 180°/s2). We hypothesised that the vestibular lesion or the compensatory processes could dissociate VO and VP function, particularly if the acute vertiginous sensation interferes with the perceptual tasks. Both in acute and recovery phases, VO and VP thresholds increased, particularly during ipsilesional rotations. In signal detection theory this indicates that signals from the healthy and affected side are still fused, but result in asymmetric thresholds due to a lesion-induced bias. The normal pattern whereby VP thresholds are higher than VO thresholds was preserved, indicating that any ‘perceptual noise’ added by the vertigo does not disrupt the cognitive decision-making processes inherent to the perceptual task. Overall, the parallel findings in VO and VP thresholds imply little or no additional cortical processing and suggest that vestibular thresholds essentially reflect the sensitivity of the fused peripheral receptors. In contrast, a significant VO-VP dissociation for supra-threshold stimuli was found. Acutely, time constants and duration of the VO and VP responses were reduced – asymmetrically for VO, as expected, but surprisingly symmetrical for perception. At recovery, VP responses normalised but VO responses remained shortened and asymmetric. Thus, unlike threshold data, supra-threshold responses show considerable VO-VP dissociation indicative of additional, higher-order processing of vestibular signals. We provide evidence of perceptual processes (ultimately cortical) participating in vestibular compensation, suppressing asymmetry acutely in unilateral vestibular lesions.

Visual Dependency and Dizziness after Vestibular Neuritis

Symptomatic recovery after acute vestibular neuritis (VN) is variable, with around 50% of patients reporting long term vestibular symptoms; hence, it is essential to identify factors related to poor clinical outcome. Here we investigated whether excessive reliance on visual input for spatial orientation (visual dependence) was associated with long term vestibular symptoms following acute VN. Twenty-eight patients with VN and 25 normal control subjects were included. Patients were enrolled at least 6 months after acute illness. Recovery status was not a criterion for study entry, allowing recruitment of patients with a full range of persistent symptoms. We measured visual dependence with a laptop-based Rod-and-Disk Test and severity of symptoms with the Dizziness Handicap Inventory (DHI). The third of patients showing the worst clinical outcomes (mean DHI score 36–80) had significantly greater visual dependence than normal subjects (6.35° error vs. 3.39° respectively, p = 0.03). Asymptomatic patients and those with minor residual symptoms did not differ from controls. Visual dependence was associated with high levels of persistent vestibular symptoms after acute VN. Over-reliance on visual information for spatial orientation is one characteristic of poorly recovered vestibular neuritis patients. The finding may be clinically useful given that visual dependence may be modified through rehabilitation desensitization techniques.

A practical approach to acute vertigo

Patients complaining of symptoms of acute vertigo present a diagnostic challenge for the clinician; the main differential diagnoses are acute unilateral peripheral vestibulopathy (“vestibular neuritis”), cerebellar stroke or migraine. The head impulse test is useful in the acute situation because, of these three diagnostic alternatives, it will only be positive in patients with vestibular neuritis. A history of acute vertigo and hearing loss suggests Ménière’s disease but the clinician must be wary of anterior inferior cerebellar artery strokes which may cause audiovestibular loss due to peripheral vestibulocochleal ischaemia, although the accompanying brainstem signs should remove diagnostic ambiguity. We also discuss other less common vertigo diagnoses that may be referred to the neurologist from the acute general hospital take. As ever in neurology, a careful history and focussed examination is necessary in the evaluation and management of acute vertigo.

[Vestibular migraine: diagnostic criteria: consensus document of the Bárány Society and the International Headache Society].

This paper presents diagnostic criteria for vestibular migraine, jointly formulated by the Committee for Classification of Vestibular Disorders of the Bárány Society and the Migraine Classification Subcommittee of the International Headache Society (IHS). The classification includes vestibular migraine and probable vestibular migraine. Vestibular migraine will appear in an appendix of the third edition of the International Classification of Headache Disorders (ICHD) as a first step for new entities, in accordance with the usual IHS procedures. Probable vestibular migraine may be included in a later version of the ICHD, when further evidence has been accumulated. The diagnosis of vestibular migraine is based on recurrent vestibular symptoms, a history of migraine, a temporal association between vestibular symptoms and migraine symptoms and exclusion of other causes of vestibular symptoms. Symptoms that qualify for a diagnosis of vestibular migraine include various types of vertigo as well as head motion-induced dizziness with nausea. Symptoms must be of moderate or severe intensity. Duration of acute episodes is limited to a window of between 5 minutes and 72 hours.

Neuro-otological emergencies.

Purpose of the reviewPhysicians find acute vertigo a diagnostic challenge. This article review recent evidence outlining the clinical presentation of acute central and peripheral dizzy syndromes and suggest when clinicians may consider acute neuro-imaging. Recent findingsRecent evidence highlights the difficulty that acute vertigo may sometimes pose to the clinician. For example, migrainous vertigo may have oculomotor abnormalities suggestive of either central neurological or peripheral vestibular dysfunction. Furthermore, vertebrobasilar stroke syndromes may mimic peripheral disorders such as vestibular neuritis, or when there is hearing involvement may be misdiagnosed as Menieres disease. In addition to the need for identifying serious conditions in acute vertigo, recent evidence suggests that early steroid treatment in vestibular neuritis may improve long term outcome. Further trials regarding symptomatic outcome are required, however, before routine use of steroids can be recommended in this condition. SummaryRecent findings have not made the assessment of acute vertigo any easier for the nonspecialist. Although the commonest vertigo syndromes are benign, serious conditions such as stroke may masquerade as a peripheral labyrinthine disorder and conversely benign conditions such as migrainous vertigo may have clinical characteristics of central disorders. These findings re-emphasize the need for a thorough clinical evaluation of the acutely dizzy patient.

The effect of single session bi-cephalic transcranial direct current stimulation on gait performance in sub-acute stroke: A pilot study

PURPOSE Non-invasive brain stimulation with transcranial direct current stimulation (tDCS) modulates cortical excitability and improves upper limb motor performance when applied to chronic stroke patients. The objective was to evaluate whether tDCS can influence gait function in sub-acute stroke patients. METHODS We assessed the effect of single session, bi-cephalic tDCS on gait performance in 14 subacute patients with stroke involving the cerebral hemisphere (2-8 weeks post-stroke) in a double-blinded, sham-controlled study. Patients were randomly allocated to receive either active (n = 7) or sham (n = 7) tDCS. The anodal electrode was placed on the scalp over the ipsilesional lower limb primary motor cortex and the cathode was placed over the contralesional leg motor cortex. Gait performance was measured using the Timed Up and Go test and the Performance Oriented Mobility Assessment before and after active or sham tDCS. RESULTS The tDCS group was significantly quicker in the Timed Up and Go test in the tDCS group, compared to the sham group (p = 0.018). The Performance Oriented Mobility Assessment was not different between groups (p = 0.897). CONCLUSIONS This is the first study to examine the effects of tDCS on gait in stroke patients in the sub-acute stage. Active tDCS improved gait performance (Timed Up and Go) in stroke patients, despite no changes to limb biomechanics of the hemiparetic side (Performance Oriented Mobility Assessment), as compared to sham stimulation. These results suggest that tDCS could be used as a therapeutic adjunct for gait rehabilitation following stroke.

Posterior parietal rTMS disrupts human Path Integration during a vestibular navigation task

In contrast to vision, the neuro-anatomical substrates of vestibular perception are obscure. The vestibular apparati provide a head angular velocity signal allowing perception of self-motion velocity. Perceived change of angular position-in-space can also be obtained from the vestibular head velocity signal via a process called Path Integration (so-called since displacement is obtained by a mathematical temporal integration of the vestibular velocity signal). It is unknown however, if distinct cortical loci sub-serve vestibular perceptions of velocity versus displacement (i.e. Path Integration). Previous studies of human brain activity have not used head motion stimuli hence precluding localisation of vestibular cortical areas specialised for Path Integration distinct from velocity perception. We inferred vestibular cortical function by measuring the disrupting effect of repetitive transcranial magnetic stimulation on the performance of a displacement-dependent vestibular navigation task. Our data suggest that posterior parietal cortex is involved in encoding contralaterally directed vestibular-derived signals of perceived angular displacement and a similar effect was found for both hemispheres. We separately tested whether right posterior parietal cortex was involved in vestibular-sensed velocity perception but found no association. Overall, our data demonstrate that posterior parietal cortex is involved in human Path Integration but not velocity perception. We suggest that there are separate brain areas that process vestibular signals of head velocity versus those involved in Path Integration.

Vestibular Activation Differentially Modulates Human Early Visual Cortex and V5/MT Excitability and Response Entropy

Head movement imposes the additional burdens on the visual system of maintaining visual acuity and determining the origin of retinal image motion (i.e., self-motion vs. object-motion). Although maintaining visual acuity during self-motion is effected by minimizing retinal slip via the brainstem vestibular-ocular reflex, higher order visuovestibular mechanisms also contribute. Disambiguating self-motion versus object-motion also invokes higher order mechanisms, and a cortical visuovestibular reciprocal antagonism is propounded. Hence, one prediction is of a vestibular modulation of visual cortical excitability and indirect measures have variously suggested none, focal or global effects of activation or suppression in human visual cortex. Using transcranial magnetic stimulation-induced phosphenes to probe cortical excitability, we observed decreased V5/MT excitability versus increased early visual cortex (EVC) excitability, during vestibular activation. In order to exclude nonspecific effects (e.g., arousal) on cortical excitability, response specificity was assessed using information theory, specifically response entropy. Vestibular activation significantly modulated phosphene response entropy for V5/MT but not EVC, implying a specific vestibular effect on V5/MT responses. This is the first demonstration that vestibular activation modulates human visual cortex excitability. Furthermore, using information theory, not previously used in phosphene response analysis, we could distinguish between a specific vestibular modulation of V5/MT excitability from a nonspecific effect at EVC.

Symptomatic Recovery in Miller Fisher Syndrome Parallels Vestibular–Perceptual and not Vestibular–Ocular Reflex Function

Unpleasant visual symptoms including oscillopsia and dizziness may occur when there is unexpected motion of the visual world across the subjects retina (“retinal slip”) as in an acute spontaneous nystagmus or on head movement with an acute ophthalmoplegia. In contrast, subjects with chronic ocular dysmotility, e.g., congenital nystagmus or chronic progressive external ophthalmoplegia, are typically symptom free. The adaptive processes that render chronic patients asymptomatic are obscure but may include a suppression of oscillopsia perception as well as an increased tolerance to perceived oscillopsia. Such chronic asymptomatic patients display an attenuation of vestibular-mediated angular velocity perception, implying a possible contributory role in the adaptive process. In order to assess causality between symptoms, signs (i.e., eye movements), and vestibular–perceptual function, we prospectively assessed symptom ratings and ocular-motor and perceptual vestibular function, in a patient with acute but transient ophthalmoplegia due to Miller Fisher Syndrome (as a model of visuo-vestibular adaptation). The data show that perceptual measures of vestibular function display a significant attenuation as compared to ocular-motor measures during the acute, symptomatic period. Perhaps significantly, both symptomatic recovery and normalization of vestibular–perceptual function were delayed and then occurred in a parallel fashion. This is the first report showing that symptomatic recovery of visuo-vestibular symptoms is better paralleled by vestibular–perceptual testing than vestibular–ocular reflex (VOR) measures. The findings may have implications for the understanding of patients with chronic vestibular symptoms where VOR testing is often unhelpful.

Intratympanic methylprednisolone versus gentamicin in patients with unilateral Ménière's disease: a randomised, double-blind, comparative effectiveness trial

BACKGROUND Ménières disease is characterised by severe vertigo attacks and hearing loss. Intratympanic gentamicin, the standard treatment for refractory Ménières disease, reduces vertigo, but damages vestibular function and can worsen hearing. We aimed to assess whether intratympanic administration of the corticosteroid methylprednisolone reduces vertigo compared with gentamicin. METHODS In this double-blind comparative effectiveness trial, patients aged 18-70 years with refractory unilateral Ménières disease were enrolled at Charing Cross Hospital (London, UK) and Leicester Royal Infirmary (Leicester, UK). Patients were randomly assigned (1:1) by a block design to two intratympanic methylprednisolone (62·5 mg/mL) or gentamicin (40 mg/mL) injections given 2 weeks apart, and were followed up for 2 years. All investigators and patients were masked to treatment allocation. The primary outcome was vertigo frequency over the final 6 months (18-24 months after injection) compared with the 6 months before the first injection. Analyses were done in the intention-to-treat population, and then per protocol. This trial is registered with ClinicalTrials.gov, number NCT00802529. FINDINGS Between June 19, 2009, and April 15, 2013, 256 patients with Ménières disease were screened, 60 of whom were enrolled and randomly assigned: 30 to gentamicin and 30 to methylprednisolone. In the intention-to-treat analysis (ie, all 60 patients), the mean number of vertigo attacks in the final 6 months compared with the 6 months before the first injection (primary outcome) decreased from 19·9 (SD 16·7) to 2·5 (5·8) in the gentamicin group (87% reduction) and from 16·4 (12·5) to 1·6 (3·4) in the methylprednisolone group (90% reduction; mean difference -0·9, 95% CI -3·4 to 1·6). Patients whose vertigo did not improve after injection (ie, non-responders) after being assessed by an unmasked clinician were eligible for additional injections given by a masked clinician (eight patients in the gentamicin group vs 15 in the methylprednisolone group). Two non-responders switched from methylprednisolone to gentamicin. Both drugs were well tolerated with no safety concerns. Six patients reported one adverse event each: three in the gentamicin group and three in the methylprednisolone group. The most common adverse event was minor ear infections, which was experienced by one patient in the gentamicin group and two in the methylprednisolone group. INTERPRETATION Methylprednisolone injections are a non-ablative, effective treatment for refractory Ménières disease. The choice between methylprednisolone and gentamicin should be made based on clinical knowledge and patient circumstances. FUNDING Ménières Society and National Institute for Health Research Imperial Biomedical Research Centre.