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Objective: To investigate the patterns of motor unit firing in single motor units from the sternocleidomastoid (SCM) muscles in response to stimuli previously shown to be capable of evoking vestibulocollic reflexes (loud clicks and electrical stimulation) and to relate these to the previously described surface potentials (VEMPs, vestibular evoked myogenic potentials) evoked by the same stimuli., Methods: Eleven male subjects (30-43-years-old) were studied. Local anaesthetic was used to block the SCM and confirm that the surface potentials (p13n23) arose from it. At another time, fine wire or needle electrodes were used to record single motor unit activity and peristimulus time histograms were constructed., Results: Local anaesthetic block reduced or abolished the p13n23 response in 5 of 6 subjects. A total of 94 histograms of motor unit discharges were recorded. The excitability changes seen were always small. Loud click stimuli given ipsilaterally evoked short latency (mean 14.2 ms, uncorrected for triggering delays), and short duration (mean 3.6 ms) inhibition. Contralaterally, the effect was excitatory (latency 11.9 ms, uncorrected, mean duration 2.3 ms). For electrical stimulation, short latency inhibition occurred ipsilateral to the cathode (average latency 14.0 ms, uncorrected, mean duration 2.9 ms) and excitation occurred contralaterally., Conclusions: We confirmed that the SCM is the sole or dominant source of the VEMPs recorded from electrodes over it. Short latency, short duration motor unit firing changes are evoked in SCM by loud clicks and electrical stimulation, stimuli known to be capable of evoking vestibulocollic reflexes. VEMPs beginning with a positivity correspond to inhibition of the underlying motor unit firing and those starting with a negativity correspond to an underlying excitation, findings consistent with intracellular recordings of otolith effects. Qualitative explanations of how the surface potentials are generated by these excitability changes and relating to other properties of the surface responses are proposed., Significance: This study has shown consistent patterns of single motor unit firing which underlie VEMPs evoked by both clicks and short duration galvanic stimulation.

Objective: Following stroke, the startle reflex, mediated via the reticulospinal tract, is often facilitated. Vestibulospinal reflexes are another bulbospinal reflex, abnormalities of which may contribute to impaired body posture and stance following stroke. We recorded galvanic evoked vestibulospinal and vestibulocollic reflexes to assess whether these showed similar changes to those for startle following stroke affecting the pons and above., Methods: Twenty-four stroke subjects (aged 40-82) were studied in the vestibulospinal part of the study, 21 stroke subjects (aged 40-81 years) were studied in the vestibulocollic part, including 18 studied in both. Transmastoid galvanic (DC) current was used to stimulate the vestibular nerve. Vestibulocollic responses were recorded from the sternocleidomastoid muscles and vestibulospinal responses from over soleus in standing subjects., Results: Vestibulocollic reflex amplitudes and latencies showed no significant differences between the two sides. Similarly short latency (SL) and medium latency (ML) vestibulospinal reflexes did not differ significantly in frequency, latency or amplitude between the affected and unaffected legs., Conclusions: Vestibular reflexes are not facilitated by stroke at or above the pontine level. The exaggeration of startle by stroke may be specific to this reflex.

Objective: Vestibular responses in soleus electromyography (EMG) evoked by the sudden onset of galvanic (DC) stimulation ('on-responses') have been described in detail previously. The aim of the present study was to describe responses in soleus triggered by the termination of galvanic stimulation ('off-responses')., Methods: In 10 healthy human subjects, we studied responses to transmastoid (bilateral) stimuli of 200 ms and 2 s average duration and 3 or 4 mA intensity. We obtained both on- and off-responses using the same raw data. EMG activity was recorded onto tape while current pulses of systematically varying duration were delivered. Averaged on-responses were obtained by triggering from the beginning of the current pulses. Averaged off-responses were obtained by triggering from the termination of the current pulses., Results: Short-latency (SL) and medium latency (ML) off-responses were both obtained in all but one study. The SL and the ML components of the off-responses were present and had similar latencies and amplitudes, but opposite excitability, to the on-responses obtained with the same stimuli., Conclusions: Off-responses to galvanic vestibular stimulation can be recorded from soleus EMG. Our findings imply that vestibular SL and ML reflex responses in the legs are dependent on the change in the rate of vestibular nerve discharge, not its absolute level. Both on- and off-responses have properties appropriate to a role in maintaining body stability.

Loud clicks, short tone bursts, head taps and short duration transmastoid currents are all capable of activating vestibular receptors and evoking reflex changes in tonic electromyogram activity within the sternocleidomastoid muscles. Because they derive from averaged electromyograms, the responses are termed 'vestibular evoked myogenic potentials'. The earliest response ipsilateral to a loud click, p13n23, is dependent upon vestibular activation, specifically saccular afferents. These new techniques are beginning to be applied clinically. An important application is in suspected cases of the Tullio phenomenon, a condition that is characterized by a pathological reduction in click threshold. The techniques have also been applied in the assessment of otolith function, vestibular neuritis, Meniere's disease and vestibular nerve tumours (acoustic neuromas).

Objective: To describe vestibulocollic responses in sternocleidomastoid (SCM) evoked by transmastoid galvanic (DC) stimulation., Methods: We studied the averaged responses in the unrectified EMG of SCM to transmastoid galvanic stimulation (5 mA/2 ms) and also to 100 dB clicks. Two patients with Meniere's disease were studied both before and after unilateral selective vestibular nerve section., Results: Transmastoid galvanic stimulation produced a positive-negative biphasic EMG response at short latency in the SCM ipsilateral to the side of cathode placement, which resembled that which followed vestibular activation by loud clicks (p13/n23). Selective unilateral vestibular nerve section abolished this galvanic-evoked response., Conclusions: Galvanic-evoked vestibulocollic responses can be recorded in SCM. This is a new method of studying vestibular reflex function which may have application in the clinical assessment of vestibular disorders.

This study compared the effects of transmastoid galvanic stimulation with unilateral galvanic stimulation of vestibular afferents. We recorded the effects on soleus EMG occurring at short (SL) and medium (ML) latency, both in normal subjects and in patients with previous unilateral vestibular neurectomy. Unipolar cathodal and anodal stimulation on the same side produced opposite effects for both SL and ML responses. Responses to unilateral cathodal or anodal stimulation were smaller, but otherwise resembled those of transmastoid stimulation with the cathode or the anode placed on the same side, respectively. Unilateral cathodal stimulation resulted in a larger SL response, which occurred at shorter latency than unilateral anodal stimulation. With unipolar stimulation on the side of previous vestibular nerve section, typical SL and ML responses were absent. With stimulation of the intact side, the patients showed smaller SL responses than normal subjects with unilateral stimulation. The larger responses to unilateral cathodal compared to unilateral anodal stimulation are consistent with previous reports that cathodal stimulation produces an increase and anodal a decrease in vestibular nerve firing. The smaller SL responses in the patients may be a consequence of central nervous system reorganization following unilateral vestibular nerve section.

Background: Benign paroxysmal positioning vertigo (BPPV) is generally thought to be caused by canalolithiasis in the posterior semicircular canal, an organ that is innervated by the inferior vestibular nerve. We hypothesized that absent vestibular evoked myogenic potentials (VEMPs) would indicate involvement of the inferior vestibular nerve and that posterior semicircular canal-type BPPV could not develop after vestibular neurolabyrinthitis (VNL) in patients with absent VEMPs., Objective: To find out if VEMPs could be helpful in evaluating involvement of the inferior vestibular nerve in acute VNL., Design: We reviewed the VEMP findings in 47 patients (34 men and 13 women) with acute VNL, 10 of whom had then developed posterior semicircular canal-type BPPV., Results: While p13-n23, the first positive-negative peak of the VEMP, was ipsilaterally present on stimulation of the unaffected side in all patients, it was absent on the affected side in 16 patients (34%). The absence or presence of p13-n23 was independent of the results of caloric tests, pure tone audiometry, and auditory brain-stem responses. Typical posterior semicircular canal BPPV developed in 10 of the 47 patients after the acute attack of VNL, always on the same side as the neurolabyrinthitis. The p13-n23 potentials were preserved on stimulation of the affected ear in all 10 patients with BPPV., Conclusions: These results suggest that if VEMPs are absent from an ear that has suffered acute VNL, then posterior semicircular canal BPPV is unlikely to develop as a consequence of the VNL. The reason for this appears to be that the absence of VEMPs is due to involvement of the inferior vestibular nerve or involvement of the structures that it innervates.

Responses of single neurons in the vestibular nerve to high-intensity clicks were studied by extracellular recording in anaesthetised guinea pigs. One hundred and two neurons in the posterior division of the superior branch or in the inferior branch of the vestibular nerve were activated at short latency by intense clicks. The latency of activation was short (median 0.9 ms) and the threshold was high: the click intensity for evoking the response of these cells was around 60 dB above the auditory brainstem response threshold. Animals were tilted and rotated to identify physiologically the sensory region of the labyrinth from which the activated neurons originated. Seventeen neurons responded to static tilt as well as clicks. These results show that vestibular receptors, probably the otoliths, respond to clicks at intensities corresponding to those used in a new clinical test of the vestibulo-collic pathway.

We studied vestibular evoked myogenic potentials in 6 patients after unilateral vestibular neurectomy and in 22 patients after unilateral vestibular neuritis and unilateral absent caloric responses. We found that the ipsilesional vestibular evoked potentials were abolished in every patient after unilateral vestibular neurectomy. In vestibular neuritis patients we found that the ipsilesional vestibular evoked potentials were absent in some but not in all cases. These findings confirm that the p13-n23 potential is of vestibular origin and also show that it is not of lateral canal origin.

Objectives: The frequency of pathologically reduced click thresholds for vestibular activation was explored in patients with the Tullio phenomenon (sound induced vestibular activation).Methods: Seven patients (eight affected ears) with symptoms of oscillopsia and unsteadiness in response to loud external sounds or to the patient's own voice were examined. In all but one patient, vestibular hypersensitivity to sound was confirmed by the fact that eye movements could be produced by pure tones of 110 dB intensity or less. Conventional diagnostic imaging was normal in all cases and three of the patients had normal middle ears at surgical exploration. Thresholds for click evoked vestibulocollic reflexes were compared with those of a group of normal subjects. Galvanic stimulation was used as a complementary method of examining the excitability of vestibular reflexes.Results: All the patients showed a reduced threshold for click activation of vestibulocollic reflexes arising from the affected ear. Short latency EMG responses to clicks were also present in posterior neck and leg muscles, suggesting that these muscles receive vestibular projections. Galvanic stimulation produced a normal pattern of body sway in four of the five patients tested.Conclusions: A pathologically reduced threshold to click activation (< or = 70 dB NHL (average normal hearing level)) seems to be a consistent feature of the Tullio phenomenon and a useful diagnostic criterion. This in turn is most likely to be due to an increased effectiveness of the transmission of sound energy to saccular receptors. Activation of these receptors probably contributed to the vestibular symptoms experienced by the patients. [ABSTRACT FROM AUTHOR]

Electromyograms (EMGs) were recorded from surface electrodes over the sternomastoid muscles and averaged in response to brief (0.1 ms) clicks played through headphones. In normal subjects, clicks 85 to 100 dB above our reference (45 dB SPL: close to perceptual threshold for normal subjects for such clicks) evoked reproducible changes in the averaged EMG beginning at a mean latency of 8.2 ms. The earliest potential change, a biphasic positive-negativity (p13-n23), occurred in all subjects and the response recorded from over the muscle on each side was predominantly generated by afferents originating from the ipsilateral ear. Later potentials (n34, p44), present in most but not all subjects, were generated bilaterally after unilateral ear stimulation. The amplitude of the averaged responses increased in direct proportion to the mean level of tonic muscle activation during the recording period. The p13-n23 response was abolished in patients who had undergone selective section of the vestibular nerve but was preserved in subjects with severe sensorineural hearing loss. It is proposed that the p13-n23 response is generated by activation of vestibular afferents, possibly those arising from the saccule, and transmitted via a rapidly conducting oligosynaptic pathway to anterior neck muscles. Conversely, the n34 and p44 potentials do not depend on the integrity of the vestibular nerve and probably originate from cochlear afferents. [ABSTRACT FROM AUTHOR]