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Vestibular-Evoked Cerebral Potentials.

ABSTRACT: The human vestibular cortex has mostly been approached using functional magnetic resonance imaging and positron emission tomography combined with artificial stimulation of the vestibular receptors or nerve. Few studies have used electroencephalography and benefited from its high temporal resolution to describe the spatiotemporal dynamics of vestibular information processing from the first milliseconds following vestibular stimulation. Evoked potentials (EPs) are largely used to describe neural processing of other sensory signals, but they remain poorly developed and standardized in vestibular neuroscience and neuro-otology. Yet, vestibular EPs of brainstem, cerebellar, and cortical origin have been reported as early as the 1960s. This review article summarizes and compares results from studies that have used a large range of vestibular stimulation, including natural vestibular stimulation on rotating chairs and motion platforms, as well as artificial vestibular stimulation (e.g., sounds, impulsive acceleration stimulation, galvanic stimulation). These studies identified vestibular EPs with short latency (<20 ms), middle latency (from 20 to 50 ms), and late latency (>50 ms). Analysis of the generators (source analysis) of these responses offers new insights into the neuroimaging of the vestibular system. Generators were consistently found in the parieto-insular and temporo-parietal junction-the core of the vestibular cortex-as well as in the prefrontal and frontal areas, superior parietal, and temporal areas. We discuss the relevance of vestibular EPs for basic research and clinical neuroscience and highlight their limitations.

SUBMITTER: Nakul E

PROVIDER: S-EPMC8490637 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:VEMP abnormalities in individuals with BPPV are often reported to be associated with utricle and saccule degeneration. The aim of the present study is to assess the frequency of VEMP abnormalities using vestibular evoked myogenic potentials in individuals with Posterior canal Benign Paroxysmal Positional Vertigo (BPPV) after Epley's manoeuvre. 36 individuals (36 ears) with definite posterior canal BPPV and 36 healthy controls were considered for the present study. All the them underwent otoscopic examination, Dix-Hallpike manoeuvre to diagnose posterior canal BPPV. Further Audiological Evaluation including pure tone audiometry was carried out to rule out vestibular disorders associated with hearing loss. Epley's manoeuvre was performed on all individuals with BPPV by an experienced otorhinolaryngologist. Cervical and Ocular Vestibular Evoked Myogenic Potentials (VEMP) were used to investigate the saccule and utricle functions following Epley's manoeuvre. Cervical VEMP and ocular VEMP abnormalities were observed in 8/36 (22.22%) and 18/36 (50%) affected ears with BPPV respectively. Cervical VEMP responses were reduced in amplitude among 1/36 (2.77%) and absent in 7/36 (19.44%) of affected ears with BPPV. Ocular VEMP responses were reduced in amplitude on 11/36 (30.55%), followed by absent responses in 5/36 (13.88%) ears with BPPV. Two patients with posterior canal BPPV i.e., 4/64 (5.55%) ears had bilateral absence of ocular VEMP responses. Two ears with BPPV 2/36 (5.55%) had absence of both cervical and ocular VEMP responses in BPPV affected ear. T test showed significant difference (p?<?0.01) in the amplitude of ocular VEMP among posterior canal BPPV individuals when compared to cervical VEMP. The present study highlights individuals with Posterior canal BPPV may have otoconia dislodgement or macular degeneration of utricle, saccule, both utricle and saccule unilaterally, or bilaterally. VEMP may be useful in evaluating degeneration of both otolith organs associated with BPPV.

Project description:IntroductionCervical vestibular evoked myogenic potentials (cVEMPs) provide an objective measure of the integrity of the sacculo-collic pathway leading to their widespread use as a clinical tool in the diagnostic vestibular test battery. Though the application of cVEMPs in preclinical models to assess vestibular function, as performed in relevant clinical populations, remains limited. The present study aimed to establish a rodent model of cVEMP with standardized methods and protocols, examine the neural basis of the responses, and characterize and validate important features for interpretation and assessment of vestibular function.MethodsWe compared air-conducted sound (ACS)-evoked VEMPs from the sternocleidomastoid muscles in naïve Brown Norway rats. A custom setup facilitated repeatable and reliable measurements which were carried out at multiple intensities with ACS between 1 and 16 kHz and over 7 days. The myogenic potentials were identified by the presence of a positive (P1)-negative (N1) waveform at 3-5 ms from the stimulus onset. Threshold, amplitude, and latency were compared with intensity- and frequency-matched responses within and between animals.ResultscVEMP responses were repeatedly evoked with stimulus intensities between 50-100 dB SPL with excellent test-retest reliability and across multiple measurements over 7 days for all frequencies tested. Suprathreshold, cVEMP responses at 90 dB SPL for 6-10 kHz stimuli demonstrated significantly larger amplitudes (p < 0.01) and shorter latencies (p < 0.001) compared to cVEMP responses for 1-4 kHz stimuli. Latency of cVEMP showed sex-dependent variability, but no significant differences in threshold or amplitude between males and females was observed.DiscussionThe results provide a replicable and reliable setup, test protocol, and comprehensive characterization of cVEMP responses in a preclinical model which can be used in future studies to elucidate pathophysiological characteristics of vestibular dysfunctions or test efficacy of therapeutics.

Project description:Objective: The objective of our study was to investigate the potential association between the occurrence of benign paroxysmal positional vertigo (BPPV) and saccular dysfunction using cervical vestibular evoked myogenic potentials (cVEMP) testing. Methods: The databases including Pubmed, Embase, and CENTRAL were systemically searched for case-control literatures investigating saccular dysfunction using cVEMP testing in BPPV patients compared with healthy controls. The literatures were published up to 16 April 2019 and were limited to the English language. All statistical processes were carried out using software Review Manager, version 5.3. Subgroup analysis and sensitive analysis were performed simultaneously. Results: Of the 12 case-control studies confirmed for meta-analysis, p13 latency of cVEMP was assessed in 8 studies, n23 latency in 6 studies, amplitude in 5 studies, asymmetry ratio (AR) in 3 studies, proportion of absent response in 9 studies, and abnormal cVEMP in 8 studies. Compared with healthy controls, the p13 mean latency of cVEMP was longer (MD = 0.88, 95% CI = 0.64-1.12, p < 0.00001), the mean amplitude was lower (SMD = -0.60, 95% CI = -0.80 to -0.41, p < 0.00001), and the proportions of absent response (OR = 8.76, 95% CI = 2.28-33.61, p = 0.002), and abnormal cVEMP (OR = 7.47, 95% CI = 4.65-12.01, p < 0.00001) were higher in BPPV patients. But there was no significant difference in the n23 mean latency (MD = 0.37, 95% CI = -0.23-0.98, p = 0.22) and the AR of cVEMP (MD = 3.95, 95% CI = -4.75-12.65, p = 0.37) between BPPV patients and healthy controls. In the sub-group analysis based on age, only the result of the proportion of absent response of cVEMP indicated a significant difference existed (p = 0.002) between the studies with age-matched controls (OR = 2.78, 95% CI = 1.09-7.10, p = 0.03) and the studies without age-matched controls (OR = 53.85, 95% CI = 10.09-287.13, p < 0.00001). In the sub-group analysis of the proportion of abnormal cVEMP according to the diagnostic criteria of abnormal cVEMP, the result indicated no significant difference existed between the four groups (p = 0.61, I 2 = 0%). In the sensitivity analysis, we obtained the consistent results after removing each study sequentially. Conclusion: The meta-analysis reveals that saccular dysfunction may be associated with BPPV occurrence, and neural degeneration in the saccular macula may be a potential pathogenesis for BPPV.

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Vestibular-Evoked Cerebral Potentials.

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