Suppression head impulse test paradigm (SHIMP) characteristics in people with Parkinson's disease compared to healthy controls.

The suppression head impulse test paradigm (SHIMP) is a newly described indicator of vestibular function which yields two measures: vestibulo-ocular reflex (VOR) gain and a saccadic response. It is an alternative and complementary test to the head impulse test paradigm (HIMP). Parkinson's disease (PD) has known saccadic and central vestibular pathway dysfunction. This paper is the first description of SHIMP VOR gain and saccade characteristic in this population. This prospective observational study measured the SHIMP VOR gain and saccade characteristics in 39 participants with idiopathic PD and compared this to 40 healthy controls (HC). The effect of group, demographic variables and SHIMP characteristics were evaluated. SHIMP VOR gains were not significantly different between groups (p = 0.10). Compared to HC, the PD group mean SHIMP peak saccade velocity was significantly reduced by an average of 77.07°/sec (p < 0.001), and SHIMP saccade response latency was longer, with an average delay of 23.5 ms (p = 0.003). SHIMP saccade peak velocity was also associated with both head impulse velocity (p = 0.002) and SHIMP VOR gain (p = 0.004) variables, but there was no significant influence of these variables when SHIMP saccade peak velocity was considered as a predictor of PD (p = 0.52-0.91). VOR gains were unaffected by PD. PD-specific saccadic dysfunction, namely reduced peak saccade velocities and prolonged response latencies, were observed in the SHIMP-induced saccade responses. VOR gain using slow phase eye velocity is preferred as the indicator of vestibular function in the SHIMPs paradigm as non-vestibular factors affected saccade peak velocity.

Static and dynamic otolith reflex function in people with Parkinson's disease.

PURPOSE: Parkinson's disease (PD) is a neurodegenerative disorder with possible vestibular system dysfunction. This study reports the transient and sustained functions of the otoliths and their reflex pathways in PD compared to healthy controls (HC) and determines if otolith function relates to previous fall history. METHODS: Forty participants with PD and 40 HC had their otolith function assessed. Transient saccular and utricular-mediated reflexes were assessed by cervical and ocular vestibular evoked myogenic potentials (cVEMPs and oVEMPs, respectively) elicited by air-conducted stimulus (clicks) and bone-conducted vibration (light tendon hammer taps). Static otolith function was assessed by the Curator Subjective Visual Vertical (SVV) test. RESULTS: Compared to HC, the PD group had significantly more absent cVEMP responses to both clicks (47.5% vs. 30%, respectively, p = 0.03) and taps (21.8% vs. 5%, respectively, p = 0.002). Only the PD group had bilaterally absent tap cVEMPs, this was related to previous falls history (p < 0. 001). In both groups, click oVEMPs were predominantly absent, and tap oVEMPs were predominantly present. The PD group had smaller tap oVEMP amplitudes (p = 0.03) and recorded more abnormal SVV responses (p = 0.01) and greater error on SVV compared to HC, p < 0.001. SVV had no relationship with VEMP responses (p = 0.14). CONCLUSIONS: PD impacts on cVEMP reflex pathways but not tap oVEMP reflex pathways. Bone-conducted otolith stimuli (taps) are more robust than air-conducted sound stimuli (clicks) for both o and cVEMPs. A lack of association between SVV and VEMP responses suggest that static and dynamic otolith functions are differentially affected in PD.

Physiology, clinical evidence and diagnostic relevance of sound-induced and vibration-induced vestibular stimulation.

PURPOSE OF REVIEW: To examine the recent literature concerning the neural basis and clinical evidence for the response of the labyrinth to sound and vibration: vestibular-evoked myogenic potentials (VEMPs) and vibration-induced nystagmus (VIN). RECENT FINDINGS: There are two streams of information from each otolith - a sustained stream (afferents with regular resting activity, signalling gravity and low-frequency linear accelerations) and a transient stream (afferents with irregular resting activity) signalling onset of linear acceleration, and sound and vibration. These irregular neurons are synchronized to each cycle of the stimulus. Neurons in the transient stream are tested by presenting sounds or vibration (500 Hz) and using surface electrodes to measure myogenic potentials from muscles activated by otolithic stimuli (VEMPs). 100 Hz vibration activates irregular canal afferents and causes a stimulus-locked VIN in patients with asymmetric canal function. These new tests of the transient system have one big advantage over older tests of the sustained system - they reliably show the effect of long-term unilateral vestibular loss. SUMMARY: The new physiological and anatomical evidence shows how sound and vibration activate otolith and canal receptors and so provides the scientific foundation for VEMPs and VIN, which are important tools for diagnosing vestibular disorders. VIDEO ABSTRACT: http://links.lww.com/CONR/A47.

Superior Canal Dehiscence Syndrome: Relating Clinical Findings With Vestibular Neural Responses From a Guinea Pig Model.

HYPOTHESIS: In superior canal dehiscence (SCD), fluid displacement of the endolymph activates type I vestibular hair cells in the crista of the affected canal and thus irregular superior canal (SC) neurons in Scarpa's ganglion, which provides the neurophysiological basis for the clinical presentation of SCD. BACKGROUND: Patients with SCD display sound- and vibration-induced vertigo/nystagmus and increased amplitudes of vestibular evoked myogenic potentials. METHODS: Extracellular recordings from n = 25 primary vestibular neurons of 16 female guinea pigs were analyzed. We recorded from the same vestibular neuron before, during and after creating the dehiscence and after closing the dehiscence. Neurobiotin labeling was employed in n = 11 neurons. RESULTS: After SCD, previously unresponsive irregular SC neurons displayed a stimulus-locked increase in discharge during application of air-conducted sound (ACS) or bone-conducted vibration (BCV) for a broad range of frequencies (ACS: 200-4000 Hz; BCV: 500-1500 Hz). This typical response was only observed for irregular SC neurons (n = 19), but not regular SC neurons, or irregular/regular horizontal canal neurons (n = 2 each), and was abolished after closing the dehiscence. Eleven irregular SC neurons responsive to ACS and/or BCV were traced back to calyx synapses in the central crista of the affected superior canal by neurobiotin labeling. CONCLUSIONS: Stimulus-locked activation of irregular SC neurons by ACS and BCV is the neurophysiological basis for sound- and vibration-induced vertigo/nystagmus and increased VEMP amplitudes in SCD. The results of the present study help to improve vestibular diagnostics in patients with suspected SCD.

The response of guinea pig primary utricular and saccular irregular neurons to bone-conducted vibration (BCV) and air-conducted sound (ACS).

UNLABELLED: This study sought to characterize the response of mammalian primary otolithic neurons to sound and vibration by measuring the resting discharge rates, thresholds for increases in firing rate and supra-threshold sensitivity functions of guinea pig single primary utricular and saccular afferents. Neurons with irregular resting discharge were activated in response to bone conducted vibration (BCV) and air conducted sound (ACS) for frequencies between 100 Hz and 3000 Hz. The location of neurons was verified by labelling with neurobiotin. Many afferents from both maculae have very low or zero resting discharge, with saccular afferents having on average, higher resting rates than utricular afferents. Most irregular utricular and saccular afferents can be evoked by both BCV and ACS. For BCV stimulation: utricular and saccular neurons show similar low thresholds for increased firing rate (around 0.02 g on average) for frequencies from 100 Hz to 750 Hz. There is a steep increase in rate change threshold for BCV frequencies above 750 Hz. The suprathreshold sensitivity functions for BCV were similar for both utricular and saccular neurons, with, at low frequencies, very steep increases in firing rate as intensity increased. For ACS stimulation: utricular and saccular neurons can be activated by high intensity stimuli for frequencies from 250 Hz to 3000 Hz with similar flattened U-shaped tuning curves with lowest thresholds for frequencies around 1000-2000 Hz. The average ACS thresholds for saccular afferents across these frequencies is about 15-20 dB lower than for utricular neurons. The suprathreshold sensitivity functions for ACS were similar for both utricular and saccular neurons. Both utricular and saccular afferents showed phase-locking to BCV and ACS, extending up to frequencies of at least around 1500 Hz for BCV and 3000 Hz for ACS. Phase-locking at low frequencies (e.g. 100 Hz) imposes a limit on the neural firing rate evoked by the stimulus since the neurons usually fire one spike per cycle of the stimulus. CONCLUSION: These results are in accord with the hypothesis put forward by Young et al. (1977) that each individual cycle of the waveform, either BCV or ACS, is the effective stimulus to the receptor hair cells on either macula. We suggest that each cycle of the BCV or ACS stimulus causes fluid displacement which deflects the short, stiff, hair bundles of type I receptors at the striola and so triggers the phase-locked neural response of primary otolithic afferents.

Neural basis of new clinical vestibular tests: otolithic neural responses to sound and vibration.

Extracellular single neuron recording and labelling studies of primary vestibular afferents in Scarpa's ganglion have shown that guinea-pig otolithic afferents with irregular resting discharge are preferentially activated by 500 Hz bone-conducted vibration (BCV) and many also by 500 Hz air-conducted sound (ACS) at low threshold and high sensitivity. Very few afferent neurons from any semicircular canal are activated by these stimuli and then only at high intensity. Tracing the origin of the activated neurons shows that these sensitive otolithic afferents originate mainly from a specialized region, the striola, of both the utricular and saccular maculae. This same 500 Hz BCV elicits vestibular-dependent eye movements in alert guinea-pigs and in healthy humans. These stimuli evoke myogenic potentials, vestibular-evoked myogenic potentials (VEMPs), which are used to test the function of the utricular and saccular maculae in human patients. Although utricular and saccular afferents can both be activated by BCV and ACS, the differential projection of utricular and saccular afferents to different muscle groups allows for differentiation of the function of these two sensory regions. The basic neural data support the conclusion that in human patients in response to brief 500 Hz BCV delivered to Fz (the midline of the forehead at the hairline), the cervical VEMP indicates predominantly saccular function and the ocular VEMP indicates predominantly utricular function. The neural, anatomical and behavioural evidence underpins clinical tests of otolith function in humans using sound and vibration.

Effect of stimulus rise-time on the ocular vestibular-evoked myogenic potential to bone-conducted vibration.

OBJECTIVES: The negative potential at 10 msec (called n10) of the ocular vestibular-evoked myogenic potential (oVEMP) recorded beneath the eyes in response to bone-conducted vibration (BCV) delivered to the skull at the midline in the hairline (Fz) is a new indicator of otolithic, and in particular utricular, function. Our aim is to find the optimum combination of frequency and rise-time for BCV stimulation, to improve the sensitivity of oVEMP testing in the clinic. DESIGN: We tested 10 healthy subjects with 6 msec tone bursts of BCV at three stimulus frequencies, 250, 500, and 750 Hz, at rise-times ranging between 0 and 2 msec. The BCV was delivered at Fz. RESULTS: The n10 response was significantly larger at the shorter rise-times, being largest at zero rise-time. In addition, we examined the effect of stimulus frequency in these same subjects by delivering 6 msec tone bursts at zero rise-time at a range of frequencies from 50 to 1200 Hz. The main effect of rise-time was significant with shorter rise-times leading to larger n10 responses and the Rise-Time × Frequency interaction was significant so that at low frequencies (100 Hz) shorter rise-times had a modest effect on n10 whereas at high frequencies (750 Hz) shorter rise-times increased n10 amplitude substantially. The main effect of frequency was also significant: The n10 response tended to be larger at lower frequency, being largest between 250 and 500 Hz. CONCLUSIONS: In summary, in this sample of healthy subjects, the most effective stimulus for eliciting oVEMP n10 to BCV at Fz was found to be a tone burst with a rise-time of 0 msec at low stimulus frequency (250 or 500 Hz).

An indicator of probable semicircular canal dehiscence: ocular vestibular evoked myogenic potentials to high frequencies.

The n10 component of the ocular vestibular evoked myogenic potential (oVEMP) to sound and vibration stimuli is a crossed response that has enhanced amplitude and decreased threshold in patients with CT-verified superior semicircular canal dehiscence (SSCD). However, demonstrating enhanced VEMP amplitude and reduced VEMP thresholds requires multiple trials and can be very time consuming and tiring for patients, so a specific indicator of probable SCD that is fast and not tiring would be preferred. Here we report a 1-trial indicator: that the oVEMP n10 in response to a very high frequency stimulus (4000 Hz), either air-conducted sound (ACS) or bone conducted vibration (BCV), is such a fast indicator of probable SCD. In 22 healthy subjects, oVEMP n10 at 4000 Hz was not detectable; however, in all 22 CT-verified SSCD patients tested, oVEMP n10 responses were clearly present to 4000 Hz to either ACS or BCV stimuli.

Enhanced otolithic function in semicircular canal dehiscence.

The enhanced sound- and vibration-induced vestibular evoked myogenic potentials (VEMPs) and their lower threshold in patients with a thinning of the bony wall of the superior semicircular canal (superior canal dehiscence, SCD) have been interpreted as being due to the dehiscence allowing sound and vibration to activate, unusually, the receptors of the dehiscent semicircular canal. We report a patient with bilateral SCD, as verified by high resolution CT scans, who had bilaterally decreased superior semicircular canal function, as shown by rotational tests of canal function. This patient also showed enhanced VEMPs and reduced thresholds. We conclude that in this patient the enhanced VEMP responses are thus probably due to enhanced otolithic stimulation by sound and vibration after dehiscence.

The ocular vestibular-evoked myogenic potential to air-conducted sound; probable superior vestibular nerve origin.

OBJECTIVE: Intense air-conducted sound (ACS) elicits an ocular vestibular-evoked myogenic potential (oVEMP), and it has been suggested that it does so by stimulating saccular receptors and afferents in the inferior vestibular nerve and so activating a crossed sacculo-ocular pathway. Bone conducted vibration (BCV) also elicits an oVEMP probably by activating utricular receptors and a crossed utriculo-ocular pathway. Are there two separate pathways mediating oVEMPs for ACS and BCV? If saccular receptors and afferents are primarily responsible for the oVEMP to ACS, then the oVEMP to ACS should be normal in patients with reduced or absent utricular function--unilateral superior vestibular neuritis (SVN). If utricular receptors and afferents are primarily responsible for oVEMP n10, then oVEMP to ACS should be reduced or absent in SVN patients, and in these patients there should be a close relationship between the size of the oVEMP n10 to BCV and to ACS. METHODS: The n10 component of the oVEMP to 500 Hz BCV and to 500 Hz ACS was recorded in 10 patients with unilateral SVN but who had saccular and inferior vestibular nerve function preserved, as shown by their normal cVEMP responses to ACS. RESULTS: In SVN patients with normal saccular and inferior vestibular nerve function, the oVEMP n10 in response to ACS was reduced or absent. Across SVN patients there was a very close correspondence between the size of oVEMP n10 for ACS and for BCV. CONCLUSIONS: The n10 component of the oVEMP to ACS is probably mediated predominantly by the superior vestibular nerve and so most likely by utricular receptors and afferents. SIGNIFICANCE: The n10 component of the oVEMP to either ACS or BCV probably indicates mainly superior vestibular nerve function.