Bone-conducted evoked myogenic potentials from the sternocleidomastoid muscle

The aim of this study was to show that bone-conducted clicks and short tone bursts (STBs) can evoke myogenic potentials from the sternocleidomastoid muscle (SCM) and that these responses are of vestibular origin. Evoked potential responses to bone-conducted auditory stimuli were recorded from the SCMs of 20 normal volunteers and from 12 patients with well-defined lesions of the middle or inner ear or the VIIIth cranial nerve. The subjects, who had various labyrinthine and retro-labyrinthine pathologies, included five patients with bilateral profound conductive hearing loss, two with bilateral acoustic neuroma post-total neurectomy and five with bilateral sensorineural hearing loss. Air- and bone-conducted evoked myogenic potentials in response to clicks and STBs were recorded with surface electrodes over each SCM of each subject. In normal subjects, bone- and air-conducted clicks and STBs evoked biphasic responses from the SCM ipsilateral to the stimulated ear. The bone-conducted clicks evoked short-latency vestibular-evoked myogenic potential (VEMP) responses only in young subjects or in subjects with conductive hearing loss. STBs evoked VEMPs with higher amplitude and better waveform morphology than clicks with the same acoustic intensity. Patients with total VIIIth cranial nerve neurectomy showed no responses to air- or bone-conducted click or STB stimuli. Clear VEMP responses were evoked from patients with conductive or sensorineural hearing loss. It is concluded that loud auditory stimuli delivered by bone- as well as air conduction can evoke myogenic potentials from the SCM. These responses seem to be of vestibular origin.     

Bone-Conducted Evoked Myogenic Potentials from the Sternocleidomastoid Muscle

The aim of this study was to show that bone-conducted clicks and short tone bursts (STBs) can evoke myogenic potentials from the sternocleidomastoid muscle (SCM) and that these responses are of vestibular origin. Evoked potential responses to bone-conducted auditory stimuli were recorded from the SCMs of 20 normal volunteers and from 12 patients with well-defined lesions of the middle or inner ear or the VIIIth cranial nerve. The subjects, who had various labyrinthine and retro-labyrinthine pathologies, included five patients with bilateral profound conductive hearing loss, two with bilateral acoustic neuroma post-total neurectomy and five with bilateral sensorineural hearing loss. Air- and bone-conducted evoked myogenic potentials in response to clicks and STBs were recorded with surface electrodes over each SCM of each subject. In normal subjects, bone- and air-conducted clicks and STBs evoked biphasic responses from the SCM ipsilateral to the stimulated ear. The bone-conducted clicks evoked short-latency vestibular-evoked myogenic potential (VEMP) responses only in young subjects or in subjects with conductive hearing loss. STBs evoked VEMPs with higher amplitude and better waveform morphology than clicks with the same acoustic intensity. Patients with total VIIIth cranial nerve neurectomy showed no responses to air- or bone-conducted click or STB stimuli. Clear VEMP responses were evoked from patients with conductive or sensorineural hearing loss. It is concluded that loud auditory stimuli delivered by bone- as well as air conduction can evoke myogenic potentials from the SCM. These responses seem to be of vestibular origin     

Laterality of vestibular evoked myogenic potentials

To clarify the laterality of acoustically evoked vestibulocollic reflexes with a short latency (vestibular evoked myogenic potentials, VEMPs). responses on the bilateral sternocleidomastoid muscles (SCMs) to unilateral acoustic stimulation were studied. Twenty-one healthy volunteers were enrolled. Surface electrodes were placed on the upper half of each SCM (active) and on the lateral end of the upper sternum (reference). Clicks and 500-Hz tone-bursts (95dB nHL) were used. All subjects showed positive-negative biphasic responses on the ipsilateral SCM by clicks and tone-bursts. Click-stimulation of 41 of the 42 ears did not evoke any response on the contralateral SCM. However, in one ear, positive-negative biphasic responses were evoked on the contralateral SCM. Recordings on the contralateral SCM by tone-bursts showed no response in 32 ears, small positive-negative biphasic responses in four ears, and small negative-positive biphasic responses in six ears. These findings show that VEMPs are ipsilateral-dominant, basically consistent with the hypothesis that they are of saccular origin.     

Laterality of vestibular evoked myogenic potentials

To clarify the laterality of acoustically evoked vestibulocollic reflexes with a short latency (vestibular evoked myogenic potentials, VEMPs), responses on the bilateral sternocleidomastoid muscles (SCMs) to unilateral acoustic stimulation were studied. Twenty-one healthy volunteers were enrolled. Surface electrodes were placed on the upper half of each SCM (active) and on the lateral end of the upper sternum (reference). Clicks and 500-Hz tone-bursts (95 dB nHL) were used. All subjects showed positive-negative biphasic responses on the ipsilateral SCM by clicks and tone-bursts. Click-stimulation of 41 of the 42 ears did not evoke any response on the contralateral SCM. However, in one ear, positive-negative biphasic responses were evoked on the contralateral SCM. Recordings on the contralateral SCM by tonebursts showed no response in 32 ears, small positive-nega-tive biphasic responses in four ears, and small negative-positive biphasic responses in six ears. These findings show that VEMPs are ipsilateral-dominant, basically consistent with the hypothesis that they are of saccular origin.     

An acoustically evoked short latency negative response in profound hearing loss infants

OBJECTIVE: A large negative deflection with a 3-4 ms latency within the auditory brainstem response has been reported in some profound hearing loss ears under intense stimuli in adult subjects. The wave has been termed the N3 potential or acoustically evoked short latency negative response and it is assumed to be a vestibular-evoked potential. The purpose of the current study was to investigate the relationship between the vestibular-evoked myogenic potentials and the acoustically evoked short latency negative response in infants with a functionless cochlea and normal or impaired semicircular canal. METHODS: Seventeen 3 months old infants with profound bilateral sensorineural hearing loss had acoustically evoked short latency negative responses and vestibular-evoked myogenic potentials recorded and caloric tests performed. RESULTS: No spontaneous symptoms of vestibular dysfunction were found in the examined infants. ASNR with medium latency 3.3 ms and threshold value 80-90 dB normal hearing level was elicited from 10 ears. VEMPs were present in 12 ears. ASNRs and VEMPs were absent in two ears with normal response to caloric stimulation. No response to caloric stimulation was elicited from other two ears with normal saccular function. For the ears with absence of ASNR, four had normal VEMP and the rest were considered to have saccular afunction. Significant correlation was found between the presence of ASNRs and VEMPs. CONCLUSION: Acoustically evoked short latency negative responses could be a valuable tool for assessing vestibular function in infants with profound sensorineural hearing loss.     

The relationship between hearing loss and vestibular dysfunction in patients with sudden sensorineural hearing loss

Objective: To investigate the relationship between hearing loss and vestibular dysfunction in patients with sudden sensorineural hearing loss (SSHL).

Methods: Clinical data including the symptom of vertigo of 149 SSHL patients were investigated retrospectively. Pure tone audiometry, ocular vestibular-evoked myogenic potential (oVEMP) and cervical vestibular-evoked myogenic potential (cVEMP) evoked by air-conducted sound (ACS), and caloric test were employed for cochlear and vestibular function assessment. The relationship between hearing level and vestibular dysfunction was analyzed.

Results: The pure tone averages (PTAs) (mean?±?SD) of SSHL patients with and without vertigo were 88.81?±?21.74 dB HL and 72.49?±?21.88 dB HL (Z?=??4.411, p?=?0.000), respectively. The PTAs of SSHL patients with abnormal and normal caloric test were 84.71?±?22.54 dB HL and 70.41?±?24.07 dB HL (t?=??2.665, p?=?0.009), respectively. Conversely, vertigo and abnormal caloric results also happened more frequently in patients with profound hearing loss. However, no consistent tendency could be found among vestibular evoked myogenic potentials (VEMPs) responses or hearing loss.

Conclusions: SSHL patients with vertigo or abnormal caloric test displayed worse hearing loss; and vice versa, vertigo and abnormal caloric results happened more frequently in SSHL patients with profound hearing loss.     

Vestibular evoked myogenic potentials in patients with contralateral delayed endolymphatic hydrops

We studied vestibular evoked myogenic potentials (VEMPs) in nine patients with unilateral profound hearing loss followed by contralateral delayed hearing fluctuation and episodic vertigo. This condition has been called contralateral delayed endolymphatic hydrops. Five of nine ears with profound hearing loss (56%) showed an absence of VEMPs. One ear (11%) showed decreased responses, and three ears (33%) had normal responses. Of the ears with fluctuation of hearing, six (67%) showed an absence of responses, and three ears (33%) showed normal responses. In four patients we recorded VEMPs before and after oral administration of glycerol. Three hours after glycerol administration, two of four ears with fluctuating hearing loss showed the appearance of VEMPs although there was an absence of VEMPs before glycerol administration. These results suggested that saccular dysfunction could exist not only in the ears with profound hearing loss but also in ears with fluctuating hearing loss and that saccular endolymphatic hydrops could exist in the ears with fluctuating hearing loss. “Contralateral delayed endolymphatic hydrops” might be an appropriate term. Received: 22 March 2001 / Accepted: 11 July 2001     

人类声诱发短潜伏期负电位的研究

目的在极重度感音性聋耳的ABR检测中发现一个位于3～4ms潜伏期的"V"字形负向波形,称声诱发短潜伏期负电位(Acoustically Evoked Short Latency Negative Response,ASNR)。本研究通过大宗病例调查和临床实验来探讨ASNR的特点和起源。方法回顾性调查并分析3104例ABR检测结果,以详尽了解ASNR的出现率和特性。对20名双耳极重度感音性耳聋患者(6～62岁)和12名健康人(23～30岁)进行了ABR和前庭诱发肌源性电位(VEMP)测试。患者组包括了16名人工耳蜗植入术后的患者,植入耳在裸耳状态时可提供无功能耳蜗模型。结果判读侧重于:人工耳蜗植入耳能否诱发ASNR,以及对比在极重度感音性聋耳中ASNR组和非ASNR组的VEMP出现率及反应阈值。结果ASNR仅出现于极重度感音性聋耳,并且对强声刺激(80～120dBnHL)有依赖性。在653例极重度感音性聋患者(981耳)的ABR波形中,有80例(12.3%)117耳(11.9%)出现了ASNR。ASNR有良好的重复性,可排除伪迹干扰的可能性。ASNR具有神经电位的特征,表现在随着声刺激的增强,其潜伏期缩短而振幅增大。ASNR与ABR的波形完全不一样,无法将其解释为传统听觉神经通路产生的电位。临床实验中,3个人工耳蜗植入耳能诱发出ASNR,说明ASNR的发生与耳蜗无关。所有9个ASNR耳都诱发出VEMP,且阈值与正常对照组无统计学差异(P>0.05),提示ASNR耳具有正常的球囊功能。在非ASNR组中,三分之二没有引出VEMP,而另外三分之一虽然可以诱发出VEMP,但阈值明显较正常对照组高(P<0.01),分别提示球囊功能丧失或低下。此外,有一外半规管麻痹耳诱发出了ASNR和VEMP。结论ASNR并非伪迹,而是一种依赖强声刺激,且只出现于极重度感音性聋耳的神经电位。ASNR的出现完全依赖于正常的球囊功能,而不依赖于残余听力或者半规管功能。据此认为ASNR起源感觉器官为球囊,根据其潜伏期推测电位源自前庭神经核。     

Prediction of the nerves of origin of vestibular schwannomas with vestibular evoked myogenic potentials

OBJECTIVE: To determine whether the nerves of origin of vestibular schwannomas can be predicted using vestibular evoked myogenic potentials (VEMPs). STUDY DESIGN: The study was a retrospective analysis. SETTING: The ear, nose, and throat department of Tokyo Medical and Dental University. PATIENTS: Twenty-eight patients undergoing removal of vestibular schwannomas were included in the study. INTERVENTIONS: Patients underwent pure tone audiometry, VEMP testing, caloric testing, and magnetic resonance imaging preoperatively. Hearing level, caloric weakness, maximum tumor size, and the nerves of origin of tumors were compared with VEMP testing. MAIN OUTCOME MEASURE: Results of VEMP testing. RESULTS: Comparisons between VEMPs and results of the other three examinations revealed no correlations. Complete disappearance of VEMPs was observed only in patients with tumors arising from inferior vestibular nerves. Patients in whom hearing was preserved tended to have preserved VEMPs. Some patients showed damaged hearing and normal VEMP results, although with inferior vestibular schwannomas. A patient with a tumor arising from a cochlear nerve exhibited preservation of VEMP, preserved caloric response, and moderate hearing loss. CONCLUSIONS: Inferior vestibular nerve function and hearing level were reflected in VEMP results. Prediction of the nerve of origin of a tumor was possible only in certain restricted cases.     

Superficial siderosis causing retrolabyrinthine involvement in both cochlear and vestibular branches of the eighth cranial nerve

Although superficial siderosis (SS) has been clinically characterized as a combination of sensorineural hearing impairment, cerebellar ataxia and pyramidal signs, precise evaluation of the function of the eighth cranial nerve has rarely been reported. The purpose of this study was to evaluate the audiological and vestibular function. We present a patient with complaints of progressive bilateral hearing loss and gait difficulty. We evaluated the audiological and vestibular functions with auditory brainstem responses and vestibular evoked myogenic potentials (VEMPs) by clicks and galvanic stimuli. The patient showed linear hypointensities surrounding the brainstem, cerebellum and the eighth cranial nerve on T2-weighted MRI images, which is characteristic of SS. Auditory brainstem response showed only wave I in the right ear and no response in the left ear. Click VEMPs and galvanic VEMPs showed no response on either side. The results of a neuro-otological examination suggested that both audiological and vestibular dysfunction in the patient with SS is of retrolabyrinthine origin.     

Superficial siderosis causing retrolabyrinthine involvement in both cochlear and vestibular branches of the eighth cranial nerve

Although superficial siderosis (SS) has been clinically characterized as a combination of sensorineural hearing impairment, cerebellar ataxia and pyramidal signs, precise evaluation of the function of the eighth cranial nerve has rarely been reported. The purpose of this study was to evaluate the audiological and vestibular function. We present a patient with complaints of progressive bilateral hearing loss and gait difficulty. We evaluated the audiological and vestibular functions with auditory brainstem responses and vestibular evoked myogenic potentials (VEMPs) by clicks and galvanic stimuli. The patient showed linear hypointensities surrounding the brainstem, cerebellum and the eighth cranial nerve on T2-weighted MRI images, which is characteristic of SS. Auditory brainstem response showed only wave I in the right ear and no response in the left ear. Click VEMPs and galvanic VEMPs showed no response on either side. The results of a neuro-otological examination suggested that both audiological and vestibular dysfunction in the patient with SS is of retrolabyrinthine origin.     

Sacculo-collic pathway dysfunction accompanying auditory neuropathy

CONCLUSIONS: In a patient with bilateral auditory neuropathy (AN), the vestibular-evoked myogenic potential (VEMP) was probably absent because of a neuropathy involving the inferior vestibular nerve and/or its end organ, the saccule. Our result can therefore be interpreted as a concomitant unilateral sacculo-collic neuropathy. We suggest the use of more precise terms to characterize AN patients with involvement of different parts of the inner ear and its innervations. We encourage detailed vestibular assessment in patients with AN in order to assess the co-existence of any symptomatic or asymptomatic vestibular disorder. Information such as that provided in this report will be valuable for clinicians caring for this group of patients. OBJECTIVE: AN is a disorder characterized by the absence or severe impairment of auditory brainstem responses in the presence of normal cochlear outer hair cell function as revealed by otoacoustic emissions (OAEs) and/or electrocochleography (ECoG). A variety of processes and etiologies are thought to be involved in its pathophysiology. In most literature reports the auditory profile of patients with AN is discussed. However, the extent of vestibular involvement, especially that involving the saccule, is not known. We performed vestibular tests to assess the status of the saccule in a patient with AN. MATERIAL AND METHODS: One patient with AN was studied. The patient was a right-handed 21-year-old female with chief complaints of hearing loss and speech perception difficulty. RESULTS: The auditory test results were consistent with the diagnosis of AN, i.e. absent auditory brainstem responses, moderate hearing loss, an inappropriately profound speech discrimination score and the presence of OAEs and measurable cochlear microphonics on ECoG. On neurological examination, gait and balance tests were normal. Ice-water caloric testing induced a sensation of dizziness in both ears. Short tone-burst VEMPs showed no response on left-ear stimulation and a biphasic response with normal latency and amplitude on right-ear stimulation.     

Vestibular evoked myogenic potentials are intact after sudden deafness

OBJECTIVE: To evaluate vestibular evoked myogenic potentials (VEMPs) in cases of sudden deafness, and to confirm the noncochlear origin of the VEMPs. STUDY DESIGN: Prospective study. VEMPs, which were evoked by short tone burst (95 dB nHL) stimulation, were recorded in 20 patients with unilateral, idiopathic sudden deafness. The results of the deaf ears were compared with those of the contralateral healthy ears and the normal control ears. The relations between VEMPs and the hearing level or caloric response were then investigated. RESULTS: All 20 of the deaf ears displayed normal biphasic VEMPs. The mean latencies of p13 and n23, as well as mean amplitude p13-n23, were 15.1 +/- 2.8 msec, 20.7 +/- 3.3 msec and 25.2 +/- 12.6 microV, respectively, not significantly different to either the contralateral healthy ears (p > 0.05) or the normal control ears (p > 0.05). Five deaf ears displayed canal paresis or absent caloric response, whereas the remaining 15 ears revealed normal caloric response. CONCLUSION: All the lesioned ears of patients with idiopathic sudden deafness exhibit normal biphasic VEMPs. Neither the hearing level nor the caloric response correlated to the VEMPs.     

Changes in Ribbon Synapses and Rough Endoplasmic Reticulum of Rat Utricular Macular Hair Cells in Weightlessness

Although still the subject of discussion, vestibular-evoked myogenic potentials (VEMPs) have been considered to reflect the function of the saccular and, more recently, the cochlear tracts. To accurately determine the precise afferent pathway carrying VEMPs, we studied the outcomes of VEMPs and other examinations in patients with unilateral vestibular schwannomas. Eleven patients with unilateral vestibular schwannomas resected using a middle cranial fossa approach were included in the study. Patients underwent pure-tone threshold audiometry, caloric tests and analysis of auditory brainstem responses (ABRs) and VEMPs pre- and postoperatively. The results were compared with those obtained in patients with intact superior or inferior vestibular and cochlear nerves. Among the 11 patients studied, 4 retained their VEMPs postoperatively. Three of the 10 patients with inferior vestibular schwannomas exhibited normal VEMPs, preserved hearing levels (20 dB HL) and anatomically intact superior vestibular nerves. In all of these cases, ABRs more closely correlated with VEMPs than with caloric responses. In one of the cases with inferior vestibular schwannomas, VEMPs were preserved postoperatively and VEMP latencies were shortened, which indicates the preoperative presence of a conduction block in either the cochlear or superior vestibular nerve. VEMPs may be conducted in both the superior vestibular and cochlear nerves, as well as in the inferior vestibular nerve. Thus, evaluation of saccular nerve function should be performed carefully, especially in cases where hearing is preserved. It appears that cochlear conduction may proceed along two pathways, one direct and the other via the brainstem, but this remains to be verified.     

Postoperative vestibular-evoked myogenic potentials in cases with vestibular schwannomas

Although still the subject of discussion, vestibular-evoked myogenic potentials (VEMPs) have been considered to reflect the function of the saccular and, more recently, the cochlear tracts. To accurately determine the precise afferent pathway carrying VEMPs, we studied the outcomes of VEMPs and other examinations in patients with unilateral vestibular schwannomas. Eleven patients with unilateral vestibular schwannomas resected using a middle cranial fossa approach were included in the study. Patients underwent pure-tone threshold audiometry, caloric tests and analysis of auditory brainstem responses (ABRs) and VEMPs pre- and postoperatively. The results were compared with those obtained in patients with intact superior or inferior vestibular and cochlear nerves. Among the 11 patients studied, 4 retained their VEMPs postoperatively. Three of the 10 patients with inferior vestibular schwannomas exhibited normal VEMPs, preserved hearing levels (20 dB HL) and anatomically intact superior vestibular nerves. In all of these cases, ABRs more closely correlated with VEMPs than with caloric responses. In one of the cases with inferior vestibular schwannomas, VEMPs were preserved postoperatively and VEMP latencies were shortened, which indicates the preoperative presence of a conduction block in either the cochlear or superior vestibular nerve. VEMPs may be conducted in both the superior vestibular and cochlear nerves, as well as in the inferior vestibular nerve. Thus, evaluation of saccular nerve function should be performed carefully, especially in cases where hearing is preserved. It appears that cochlear conduction may proceed along two pathways, one direct and the other via the brainstem, but this remains to be verified.     

Narrow internal auditory meatus: an idiopathic case confirming the origin and pathway of vestibular evoked myogenic potentials in humans

OBJECTIVE: To confirm the origin and pathway of vestibular evoked myogenic potentials (VEMPs) in humans. DESIGN: Case study. SETTING: University hospital. PATIENT: A patient with a narrow internal auditory meatus (IAM). MAIN OUTCOME MEASURES: Imaging studies and functional studies concerning the seventh and eighth cranial nerves. RESULTS: Of the 4 nerves in the IAM, all but the cochlear nerve had normal function and normal courses, despite the pronounced narrowing of the IAM. The facial nerve had a normal diameter, but the vestibular nerves were thinner. Imaging revealed that the cochlear nerve was absent or extremely thinned. Both the cochlea and the cochlear nerve showed no function in the affected ear, although the VEMPs were evoked normally. CONCLUSION: Our results definitively support the vestibular origin of VEMPs in humans.     

Vestibular-evoked myogenic potentials in three patients with large vestibular aqueduct

An enlarged vestibular aqueduct (LVA) is a common congenital inner ear anomaly responsible for some unusual vestibular and audiological symptoms. Most of the cases show bilateral early onset and progressive hearing loss in children. The gross appearance on CT scan of the inner ear is generally normal. However, precise measurements of the inner ear components reveal abnormal dimensions, which may account for the accompanying auditory and vestibular dysfunction. Despite extensive studies on hearing and the vestibular apparatus, saccular function is not studied. To our knowledge this is the first report of saccular malfunction in three patients with LVA by means of vestibular evoked myogenic potentials. Conventional audiograms revealed bilateral severe sensorineural hearing loss in two patients and mixed type hearing loss in one patient. Two of the patients complained about vertigo and dizziness but vestibular assessments of the patients showed normal results. The diagnosis had been made by high-resolution CT scans and MR images of the skull that showed LVA in the absence of other anomalies. The VEMP threshold measured from the ear with LVA in two patients with unilateral enlargement of the vestibular aqueduct was 75–80 dB nHL whereas the threshold from normal ears was 95 dB nHL. The third patient with mixed type hearing loss and bilateral LVA had VEMP responses despite a big air–bone gap in the low frequency range. The VEMP in this patient was greater in amplitude and lower in threshold in the operated ear (the patient had a tympanoplasty which did not improve her hearing). These findings and results of other patients with Tullio phenomenon and superior semicircular canal dehiscence, who also showed lower VEMP threshold, confirmed the theory of a ‘third window’ that allows volume and pressure displacements, and thus larger deflection of the vestibular sensors, which would cause the vestibular organ to be more responsive to sound and pressure changes.     

Sacculo-collic pathway dysfunction accompanying auditory neuropathy

Conclusions. In a patient with bilateral auditory neuropathy (AN), the vestibular-evoked myogenic potential (VEMP) was probably absent because of a neuropathy involving the inferior vestibular nerve and/or its end organ, the saccule. Our result can therefore be interpreted as a concomitant unilateral sacculo-collic neuropathy. We suggest the use of more precise terms to characterize AN patients with involvement of different parts of the inner ear and its innervations. We encourage detailed vestibular assessment in patients with AN in order to assess the co-existence of any symptomatic or asymptomatic vestibular disorder. Information such as that provided in this report will be valuable for clinicians caring for this group of patients. Objective. AN is a disorder characterized by the absence or severe impairment of auditory brainstem responses in the presence of normal cochlear outer hair cell function as revealed by otoacoustic emissions (OAEs) and/or electrocochleography (ECoG). A variety of processes and etiologies are thought to be involved in its pathophysiology. In most literature reports the auditory profile of patients with AN is discussed. However, the extent of vestibular involvement, especially that involving the saccule, is not known. We performed vestibular tests to assess the status of the saccule in a patient with AN. Material and methods. One patient with AN was studied. The patient was a right-handed 21-year-old female with chief complaints of hearing loss and speech perception difficulty. Results. The auditory test results were consistent with the diagnosis of AN, i.e. absent auditory brainstem responses, moderate hearing loss, an inappropriately profound speech discrimination score and the presence of OAEs and measurable cochlear microphonics on ECoG. On neurological examination, gait and balance tests were normal. Ice-water caloric testing induced a sensation of dizziness in both ears. Short tone-burst VEMPs showed no response on left-ear stimulation and a biphasic response with normal latency and amplitude on right-ear stimulation.     

Short tone burst-evoked myogenic potentials on the sternocleidomastoid muscle: are these potentials also of vestibular origin?

OBJECTIVES: To show that short tone bursts (STBs) evoke myogenic potentials from the sternocleidomastoid muscle (SCM) that are of vestibular origin. DESIGN: Evoked potential activity was recorded from the SCMs of normal volunteers and from patients with vestibulocochlear disorders. SETTING: This outpatient study was conducted at the Department of Otolaryngology, University of Tokyo, Tokyo, Japan. SUBJECTS: Nine normal volunteers and 30 patients (34 affected ears) with vestibulocochlear disorders were examined. INTERVENTION: Diagnostic. OUTCOME MEASURES: Sound-evoked myogenic potentials in response to STBs were recorded with surface electrodes over each SCM. Responses evoked by STBs in patients were compared with responses evoked by clicks. RESULTS: In all normal subjects, STBs (0.5, 1, and 2 kHz) evoked biphasic responses on the SCM ipsilateral to the stimulated ear; the same was true for clicks. Short tone bursts of 0.5 kHz evoked the largest responses, while STBs of 2 kHz evoked the smallest. In patients with vestibulocochlear disorders, responses to STBs of 0.5 kHz were similar to responses evoked by clicks. Thirty (88%) of the 34 affected ears demonstrated the same results with 0.5-kHz STBs and with clicks. Responses were present in patients with total or near-total hearing loss and intact vestibular function. Conversely, patients with preserved hearing but with absent or severely decreased vestibular function had absent or significantly decreased myogenic potentials evoked by STBs. CONCLUSIONS: Short tone bursts as well as clicks can evoke myogenic potentials from the SCM. Myogenic potentials evoked by STBs are also probably of vestibular origin.     

Saccular damage in patients with high-frequency sensorineural hearing loss

Subjects with high frequency sensorineural hearing loss (HF-SNHL) without retrocochlear pathology are those group which certainly encountered inner ear damaging factors. This study was designed to evaluate the effects of cochlear damaging factors on the sacculocollic pathway. Fifty patients (76 ears) with varying degrees of HF-SNHL but without clinical manifestations of vestibular pathology tested for vestibular evoked myogenic potentials (VEMP). The results were compared with those of 18-healthy referents (32 ears) examined in the same way. Subjects with HF-SNHL greater than 40 dB HL showed significantly more saccular deterioration, estimated as negative VEMP responses than did the referents. This suggests subclinical disturbances of the vestibular system especially of the saccule in these patients. The underlying mechanism may be simultaneous damage to both the cochlea and saccule by the same factors.