Jung Eun Shin

Frequency-tuning characteristics of cervical and ocular vestibular evoked myogenic potentials induced by air-conducted tone bursts

OBJECTIVE To better characterize both ocular and cervical vestibular evoked myogenic potentials (VEMP) responses at different frequencies of sound in 20 normal subjects. METHODS Cervical and ocular VEMPs were recorded. The intensities of sound stimulation decreased from the maximal intensity, until no responses were evoked. Thresholds, amplitudes, latencies and interaural amplitude difference ratio (IADR) at the maximal stimulation were calculated. RESULTS Both tests showed the similar frequency tuning, with the lowest threshold and highest amplitude for 500-Hz tone-burst stimuli. Sound stimulation at 500Hz showed the response rates of 100% in both tests. Cervical VEMPs showed higher incidence than ocular VEMPs. Ocular VEMP thresholds were significantly higher than those of cervical VEMP. Cervical VEMP amplitudes were significantly higher than ocular VEMP amplitudes. IADRs of ocular and cervical VEMPs did not differ significantly. CONCLUSIONS Ocular VEMP showed the similar frequency tuning to cervical VEMP. Cervical VEMP responses showed higher incidence, lower thresholds and larger amplitudes than ocular VEMP. SIGNIFICANCE Cervical VEMP is a more reliable measure than ocular VEMP, though the results of both tests will be complementary. Five hundred Hertz is the optimal frequency to use.

Vestibular abnormality in patients with Meniere's disease and migrainous vertigo.

Abstract Conclusion: Vestibular abnormality was found in 84% of patients with Menieres disease (MD) and 66% of those with migrainous vertigo (MV), even in the interictal period. Although MV does not have proven pathology like endolymphatic hydrops of MD, MV had high vestibular abnormality, suggesting that comorbid vestibular abnormality can be a cause of vertigo and needs to be pursued. Objectives: MD and MV are common disorders causing recurrent vertigo. We determined the vestibular abnormality rates using vestibular tests with objective measurements. Methods: Results of caloric, head-shaking nystagmus (HSN), and vibration-induced nystagmus (VIN) tests were analyzed in 45 patients with MD and 76 with MV. Results: The abnormal rates in MD were significantly higher than those in MV. Of 45 MD patients, 21 (47%), 32 (71%), and 24 (53%) exhibited abnormal caloric, HSN, and VIN results, respectively. Fourteen (31%) MD patients had migraine associated with vertigo, but the association was not accompanied by high rates of abnormal results in the tests. Of 76 MV patients, 19 (25%), 38 (50%), and 24 (32%) exhibited abnormal caloric, HSN, and VIN results, respectively. Overall, 84% of patients with MD and 66% with MV exhibited abnormal results on at least one test. Abnormal rates were highest in HSN, followed by VIN and the caloric test.

Results of Air Caloric and Other Vestibular Tests in Patients with Chronic Otitis Media

Objectives Air caloric results are supposed to be influenced by anatomic changes of the middle ear. The aims of our study were to evaluate the incidence and characteristics of abnormal air caloric results in patients with unilateral chronic otitis media and without any history of vertigo, and to compare caloric results with there of other vestibular function tests (VFTs). Methods Twenty five patients with unilateral chronic otitis media (COM) who were scheduled for surgery underwent VFTs preoperatively. Hearing was assessed using pure-tone audiometry and vestibular function was assessed using a set of VFTs: air caloric, head-shaking nystagmus (HSN), vibration-induced nystagmus (VIN), and subjective visual vertical (SVV) tests. Results Six patients (24%) showed pathologic canal paresis (CP) on COM-sided ears. Two patients showed pathologic CP on the contralateral side. However, both of the two showed inverted nystagmus to warm air stimulation on the COM-side and hyperactive nystagmus to cold air stimulation on the COM-side, which means that the COM-sided ear was stimulated too much. There was pathologic HSN in 12 patients (48%), pathologic VIN in 7 (28%), and pathologic SVV in 5 (20%). Overall, 20 (80%) patients showed abnormal findings through a set of VFTs. Patients with an interaural difference of bone-conduction hearing thresholds ≥10 dB tended to show more abnormal VFT results than those for whom the interaural difference of bone-conduction hearing thresholds was <10 dB. Conclusion Our data show that one-fourth of patients with unilateral COM show abnormal caloric results on the COM side. However, subclinical latent vestibular imbalances were found to be common, which might be related to the gradual vestibular involvement in inflammatory processes, regardless of the caloric results. Results of a set of VFTs should be referred to when determining vestibular imbalance in patients with COM.

A new method for evaluating lateral semicircular canal cupulopathy

Persistent direction‐changing positional nystagmus (DCPN) during the supine head‐roll test is a typical finding of cupulopathy. The aim of this study was to introduce a simple method of evaluating patients with cupulopathy (light cupula and heavy cupula), which is performed in a seated position, and investigate its diagnostic utility and use for lateralization.

Sudden sensorineural hearing loss with simultaneous positional vertigo showing persistent geotropic direction-changing positional nystagmus.

Objectives To characterize the clinical features of patients who simultaneously developed ipsilateral sudden sensorineural hearing loss (SSNHL) and positional vertigo showing geotropic direction-changing positional nystagmus (DCPN) on a supine head-roll test, and to address the possible pathophysiology of the disease. Study Design Retrospective case series review. Methods We conducted a retrospective case series study in 17 patients with SSNHL and simultaneous positional vertigo showing geotropic DCPN. Results All 17 patients showed persistent geotropic DCPN without latency in the supine head-roll test. The intensity of nystagmus was stronger when the patient’s head was turned to the lesion side of SSNHL in 15 of 17 patients. We sought to identify a null plane in nine patients, and the null plane was identified on the same side as the SSNHL in all nine patients, which was thought to be caused by the “light cupula” of the lateral semicircular canal in the same ear as the SSNHL. Conclusion A light cupula mechanism may be one of the causes of positional vertigo in patients with SSNHL. In these cases, persistent geotropic DCPN is observed in the supine head-roll test and the null plane can be identified on the same side as the hearing loss.

Clinical manifestations in patients with herpes zoster oticus

Patients with herpes zoster oticus (HZO) may exhibit diverse symptoms regarding cochleovestibular dysfunction. This study investigated the clinical manifestations of HZO by comparing symptoms associated with dysfunctions of the 7th and 8th cranial nerves (CN VII and VIII, respectively). This study is a retrospective case series. Eighty-one patients with HZO who had dysfunction of CN VII or VIII were included in this study. Electroneuronography (ENoG) values were compared among patient groups with facial weakness. Patients with ipsilateral facial weakness (62 of 81) were more common than those without. Among 81 patients, those with facial weakness, hearing loss, and vertigo were most common, and only 1 patient had vertigo without hearing loss or facial weakness. Most patients with vertigo also had hearing loss (28 of 30), and patients without hearing loss did not have vertigo (19 of 21). While patients with vertigo had worse ENoG values than those without vertigo, ENoG values were not significantly different between patients with and without hearing loss. In conclusion, various clinical manifestations of CN VII and VIII dysfunction are possible in patients with HZO. Patients with vertigo had worse ENoG values than those without, which may indicate that vertigo reflects more severe facial nerve degeneration in HZO patients with facial weakness.

“Light cupula” involving all three semicircular canals: A frequently misdiagnosed disorder

Though benign paroxysmal positional vertigo (BPPV) is the most common vestibular disorder causing positional vertigo, patients with typical positional vertigo in which the findings of positional nystagmus do not meet the diagnostic criteria for BPPV are often encountered in the clinic. Recently a concept of the light cupula was introduced, which accounts for some of positional vertigo. Under a normal condition in which the specific gravity of the cupula is same as that of the surrounding endolymph, semicircular canals (SCCs) are not influenced by the gravity. The light cupula, which indicates cupula with lower specific gravity than the surrounding endolymph, is characterized by persistent geotropic direction-changing positional nystagmus (DCPN) without latency on the supine head-roll test and the presence of a null plane. Unless the duration and pattern of positional nystagmus are carefully examined, the light cupula can be misdiagnosed as other types of BPPV. We present a patient with light cupula on the right side who reported recurrent episodes of positional vertigo and had been diagnosed as BPPV with multiple canal involvement (posterior and lateral SCCs) on the opposite side. In this study, we present the mechanism of typical positional nystagmus patterns in patients with light cupula involving all of the unilateral SCCs, and discuss the possible causes of misdiagnosis of the light cupula.

Impairment of Static Vestibular Function Is Limited in Patients with Sudden Sensorineural Hearing Loss with Vertigo

Sudden sensorineural hearing loss with vertigo (SSNHL_V) and vestibular neuritis (VN) are common neuro-otologic disorders that cause acute spontaneous vertigo. The SSNHL_V and VN lesion sites are thought to be within the labyrinth and the vestibular nerve, respectively. Neurolabyrinthitis of a viral origin is the most commonly accepted etiology of SSNHL_V, and neural degeneration due to viral infection (predominantly in the superior vestibular nerve) is thought to be responsible for the pathophysiology of VN. The objective of this study was to compare the static vestibular imbalance between SSNHL_V and VN patients during the acute stage of the disease. We compared the results of spontaneous nystagmus (SN), subjective visual vertical (SVV), and canal paresis (CP) between SSNHL_V and VN patients within 10 days from the onset of vertigo. Significant SN was observed in 58% of SSNHL_V and 90% of VN patients (p < 0.001), and abnormal SVV was observed in 10% of SSNHL_V and 78% of VN patients (p < 0.001). However, CP values were not significantly different between the 2 groups (50.8 ± 19.7% in SSNHL_V and 57.1 ± 18.9% in VN). In conclusion, significant SN and abnormal SVV are less frequently encountered in SSNHL_V than in VN even though the caloric test did not reveal significant differences at the acute stage.

Hyperventilation-Induced Nystagmus in Patients with Vestibular Neuritis in the Acute and Follow-Up Stages

Objective: Our purposes were to characterize hyperventilation-induced nystagmus (HVIN) in patients with unilateral vestibular neuritis (VN) through follow-up examinations and to determine the effects of hyperventilation on vestibular imbalance in patients with VN. Materials and Methods: The horizontal eye movements in 35 patients with acute VN were recorded. The eye movements were analyzed and the maximum value of slow-phase eye velocity (SPV) was obtained during and after hyperventilation. Nineteen of 35 patients underwent follow-up examinations around 7 weeks later. When spontaneous nystagmus was present, the SPV of spontaneous nystagmus was subtracted from that of HVIN. A maximum SPV of HVIN of ≧4°/s was considered abnormal. The direction and SPV of HVIN were analyzed. Results: The incidence of HVIN in patients with VN was significantly higher in the acute stage (18 of 35; 51%) than the follow-up stage (4 of 19; 21%). The direction of HVIN present in the follow-up stage was entirely towards the contralesional side (contralesional HVIN). However, the direction of HVIN in the acute stage was mixed, towards the contralesional side (10 of 35; 28%) and towards the ipsilesional side (8 of 35; 23%). The SPVs (49 ± 56°/s) of ipsilesional HVIN were significantly greater than the contralesional HVIN in the acute stage (8 ± 3°/s). Robust nystagmus (SPV ≧25°/s) was entirely ipsilesional HVIN, which was observed only in the acute stage. Conclusions: Our findings indicate that hyperventilation can result in aggravation of vestibular imbalance in the acute and follow-up stages in different ways. Hyperventilation resulted in contralesional HVIN in both the acute and follow-up stages, each in approximately a fourth of the patients, which suggests a disruption of central static compensatory mechanisms. However, ipsilesional HVIN was elicited only in the acute stage (in approximately a fourth of the patients). About half of the patients with ipsilesional HVIN showed robust responses, which is a characteristic finding, suggesting a transient intense increase in vestibular activity on the lesional side.

Clinical Significance of Vibration-Induced Nystagmus

The aims of the study were to characterize the vibration-induced nystagmus (VIN) in patients with unilateral vestibular neuritis (VN) and Ménière’s disease (MD), and to clarify the clinical significance of VIN by comparing it with caloric results in patients with VN and MD. We recorded eye movements from 22 VN patients and 24 MD patients using unilateral 100-Hz vibration on the mastoid bone. Eye movements were analyzed and the maximum value of slow-phase eye velocity was obtained during vibration on each mastoid. The average value of slow-phase velocities was calculated. Spontaneous nystagmus was subtracted from the slow-phase velocity, whenever it was present. A canal paresis (CP) greater than 25% was considered pathologic. All but one VN patient showed pathologic CP with the direction of the slow-phase eye movement of VIN toward the lesioned side. Fifteen (63%) out of 24 MD patients showed VIN with the slow-phase eye movement directed to the lesioned side. Pathologic CP was present in 9 (38%) out of 24 MD patients and 8 of them showed slow-phase eye movements of VIN directed to the lesioned side. There were also 8 other MD patients who showed slow-phase eye movement of VIN directed to the intact side. Among them, 3 patients with the slow-phase eye movement more than 5°/s showed CP on the intact side. The amplitude of slow-phase eye velocity showed a significant correlation with CP in patients with either VN or MD. There was no significant difference in the slope of the regression lines between the VN and MD groups. Our results suggest that VIN may probe imbalance of canal responses to low-frequency stimulation similar to the caloric test. It also shows that VIN can help in detecting vestibular imbalance using a stimulation mechanism different from the caloric test. The VIN test can be helpful in determining the lesioned side in patients with VN; however, it has some limitations in localizing the lesioned side in patients with MD.