Unilateral Peripheral Vestibulopathy Research Articles

A practical approach to acute vertigo

Patients complaining of symptoms of acute vertigo present a diagnostic challenge for the clinician; the main differential diagnoses are acute unilateral peripheral vestibulopathy (“vestibular neuritis”), cerebellar stroke or migraine. The...

Possible association between thyroid autoimmunity and Menière's disease

Various aetiopathological mechanisms have been postulated to be at the root of Menière's disease (MD), and some data suggest that there may be also an underlying autoimmune factor. In fact, Menière patients manifest certain characteristics that are typical of autoimmune involvement association of particular human leucocyte antigen haplotypes, the presence of antibodies against internal ear antigens. In this study, we evaluated the association between thyroid autoimmunity and MD in a non-selected group of patients. We recruited 50 consecutive MD patients and two groups as controls: group A, 82 healthy volunteers; and group B, 50 subjects suffering from acute unilateral peripheral vestibulopathy. All subjects were submitted to instrumental assessment of cochlear-vestibular function and analysis of thyroid-stimulating hormone (TSH), free triiodothyronine, free thyroxine, anti-TSH receptor antibody (TR-Ab), anti-thyroperoxidase antibody (TPO-Ab) and anti-thyroglobulin antibody (Tg-Ab) in the blood. The prevalence of autoimmune thyroiditis in group B [6/50 (12%); 66.7% TPO-Ab and 33.3% Tg-Ab] was superimposable with the healthy controls [6/82 (7%); 66.7% TPO-Ab and 33.3% Tg-Ab]. In contrast, 38% of the MD patients (P = 0.0001 versus group A and group B) had significant autoantibody levels (68.4% TPO-Ab; 15.8% TPO-Ab + TR-Ab; 10.5% Tg-Ab; 5.2% TPO-Ab + Tg-Ab). Furthermore, 14% of the MD patients were hyperthyroid under l-thyroxine therapy, while no dysfunction was seen in the control groups. Overall, our data demonstrate a significant association between MD and thyroid autoimmunity, which suggests that an autoimmune factor is involved in the aetiopathogenesis of this disease. These findings suggest that it should be useful to submit MD patients to multi-disciplinary clinical investigation.

Hyperventilation-induced nystagmus in peripheral vestibulopathy and cerebellopontine angle tumor

To determine the incidence and characteristics of hyperventilation-induced nystagmus (HIN) in cerebellopontine angle (CPA) tumors and unilateral peripheral vestibulopathy (UPV), and to elucidate differential contribution of hyperventilation to bring out vestibular asymmetry between acute and chronic phases of UPV. We recorded horizontal HIN in 33 patients with CPA tumors and 145 with UPV. The UPV included patients of either acute (7 days or less from symptom onset, n = 47) or chronic (more than 7 days from symptom onset, n = 98) phases. The incidence of HIN was higher in the CPA tumor than in the UPV group (82 vs 34%, p < 0.01) and was also higher in the acute than in the chronic UPV group (60 vs 21%, p < 0.01). Furthermore, HIN was more commonly ipsilesional (i-HIN) in the CPA tumor than in the UPV group (52 vs 8%, p < 0.01) and more commonly ipsilesional in the acute than in the chronic UPV group (21 vs 1%, p < 0.01). The patients with i-HIN and acoustic neuroma had a tendency to harbor smaller tumors and to have less severe caloric asymmetry. The contribution of hyperventilation on vestibular nystagmus differs depending on the disease phase or underlying pathologies. Our study demonstrates that hyperventilation-induced nystagmus (HIN) beating to the side of reduced caloric response, hearing impairment, or abnormal auditory brainstem response responses may be a valuable sign for bedside detection of cerebellopontine angle (CPA) tumors. CPA tumor should be a prime suspicion in patients with acute vertigo and ipsilesional HIN, especially when the vertigo accompanies hearing impairments.

Head Position Dependency of Induced Nystagmus to Ice-water Irrigation in Peripheral Vestibulopathy

Evaluation of head-position dependency during the ice-water test is essential when the test is indicated. Because ice-water irrigation (IWI) in the prone position is frequently skipped in many laboratories, we investigated the importance of evaluating position dependency in an ice-water test. Twenty-five unilateral peripheral vestibulopathy patients showing no nystagmus during warm irrigation were included. IWI was performed in supine and prone positions, and maximum slow-phase velocity and direction of nystagmus were assessed by using video nystagmography. Eleven cases showed head-position dependency and were interpreted as hypofunctional. Fourteen cases showed no dependency, suggesting the absence of end organ function. In the latter group, 6 patients showing definite nystagmus in supine position could have been misinterpreted as hypofunctional, had it not been for prone-position results. Evaluation of head position dependency by using IWI is important in the determination of lateral semicircular canal function.

Isolated perverted head-shaking nystagmus in focal cerebellar infarction

Head-shaking nystagmus (HSN) refers to the nystagmus induced by head oscillation, and usually beats to the healthy side in unilateral peripheral vestibulopathy.1 It may occur from velocity storage mechanism and Ewald second law.1,2 In perverted HSN (pHSN), the nystagmus develops in the plane other than that being stimulated, i.e., downbeat or upbeat after horizontal head oscillation. pHSN has been reported in diffuse cerebellar degeneration or medullary lesion,3,4 and signifies central vestibular lesion. However, isolated pHSN from focal cerebellar lesions has not been described. A 59-year-old man reported recurrent dizziness that most often occurred from exposure to heat or after taking a hot bath and lasted several minutes without other neurologic symptoms. On initial examination, he had blood pressure of 155/95 mm Hg and fasting blood glucose of 206 mg/dL. Other physical, neurotologic, and routine laboratory examinations were normal. In view of hypertension, diabetes, and duration of the dizzy spells, he was suspected to have vertigo of vascular origin and was scheduled for brain MRI. Five days later, while …

The Active Head-Impulse Test in Unilateral Peripheral Vestibulopathy

The head-impulse test, which is sensitive and specific for detecting severe unilateral peripheral vestibulopathy, is an accepted part of the neurological examination, especially in patients with vertigo and balance disorders. To discover if the head-impulse test is just as useful diagnostically when patients are asked to rotate their own heads, the active head-impulse test, rather than when the clinician does so as in the standard passive head-impulse test. Clinical observation of compensatory saccades and search coil measurement of compensatory eye rotations, during active and passive horizontal head-impulses in 6 patients with total unilateral vestibular deafferentation. Clinical observation showed the expected compensatory saccades with rotations toward the side with the lesion with passive head-impulses but not with active head-impulses. Search coil recordings revealed 2 reasons for this. With active head-impulses not only was vestibulo-ocular reflex gain higher, but compensatory saccade latency was shorter resulting in an occult saccade that occurred during, rather than after, head rotation. Passive head-impulses are necessary to detect a severe unilateral peripheral vestibulopathy; active head-impulses will produce a false-negative result.

Dynamic body tilt in internuclear ophthalmoplegia and one-and-a-half syndrome

We report five patients presenting acutely because of diplopia and lateropulsion. Four had internuclear ophthalmoplegia and the fifth, one-and-a-half syndrome. In addition, they presented with a peculiar sign, called lateropulsion, which is a slow falling down to the side in a roll plane when sitting, standing, or walking. All five patients were adults, the first three having a history of multiple vascular risk factors. Brain CT showed a mesencephalic infarct in one patient and no pathology in the rest. Brain MRI in one patient did not show any lesion in the pontomesencephalic area. Clinically, the neuro-ophthalmological constellation of these patients pointed to tegmental medial pontomesencephalic lesions, which were associated with a dynamic lateral body tilt accompanying the oculomotor signs. In all five patients, the body tilt was contralateral (contraversive) to the clinical brainstem lesion. Their recovery was good in the short term, with improvement in the body tilt and eye movements. We suggest that body tilt in the lateral (coronal) plane could be due to a graviceptive dysfunction, occurring in the medial longitudinal fasciculus or in its surrounding structures. The body tilt observed in these patients is phenomenologically identical to that observed in acute unilateral peripheral vestibulopathy.

Impulsive testing of individual semicircular canal function.

In order to test the human angular vestibulo-ocular reflex in the dynamic range of normal head movements, we measured 3-dimensional compensatory eye-movement responses to low-amplitude (10-12 degrees), high-acceleration (3000-4000 degrees/s/s), passive, manually delivered head rotations (head "impulses") in the three planes of the semicircular canals in normal subjects, in subjects who had recovered from surgical unilateral vestibular deafferentation, and in patients after acute unilateral peripheral vestibulopathy, that is, from vestibular "neuritis." We found that canal-plane head impulses away from an intact semicircular canal, that is, toward a lesioned semicircular canal, invariably produce a vestibulo-ocular reflex with permanently low gain, typically less that 0.4 if the lesion is complete. These results are a necessary consequence of primary semicircular canal afferents being driven into inhibitory saturation by rapid angular accelerations. With practice, clinicians can learn to recognize the telltale compensatory saccades that patients with unilateral loss of semicircular canal function will make if asked to look at an earth-fixed target during head impulses in any one of the three semicircular canal planes.

Individual semicircular canal function in superior and inferior vestibular neuritis.

To examine the concept of selective superior and inferior vestibular nerve involvement in vestibular neuritis by studying the distribution of semicircular canal (SCC) involvement in such patients. Vestibular neuritis was traditionally thought to involve the superior and inferior vestibular nerves. Recent work suggests that in some patients, only the superior nerve is involved. So far there are no reported cases of selective involvement of the inferior vestibular nerve. The authors measured the vestibuloocular reflex from individual SCC at natural head accelerations using the head impulse test. The authors studied 33 patients with acute unilateral peripheral vestibulopathy, including 29 with classic vestibular neuritis and 4 with simultaneous ipsilateral hearing loss, 18 healthy subjects and 15 surgical unilateral vestibular deafferented patients. In patients with preserved hearing, eight had deficits in all three SCC, suggesting involvement of the superior and inferior vestibular nerves. Twenty-one had a lateral SCC deficit or a combined lateral and anterior SCC deficit consistent with selective involvement of the superior vestibular nerve. Two patients with ipsilateral hearing loss had normal caloric responses and an isolated posterior SCC deficit on impulsive testing. The authors propose that these two patients had a selective loss of inferior vestibular nerve function. Vestibular neuritis can affect the superior and inferior vestibular nerves together or can selectively affect the superior vestibular nerve.

Influence of Canal Paresis and Compensation on Gain and Time Constant of Nystagmus Slow-phase Velocity to Yaw-axis Rotation

In order to assess the influence of canal paresis and compensation on the yaw-axis rotatory chair test parameters gain and time constant, a study was conducted in 435 patients diagnosed with unilateral peripheral vestibulopathy. Patients were grouped according to the amount of canal paresis found in the caloric test and by the result of a bedside examination of the vestibulo-ocular reflex (VOR). The time constant of the VOR diminishes as canal paresis increases and, when using a high-velocity sinusoidal test, there is a similar reduction in gain. Mean time constant was reduced when rotations were to the side of the lesion (ipsilesional) and to the normal (contralesional) and differences between both rotations were found for 21-80% canal paresis. Ipsilesional gain was significantly less than contralesional gain, which had a normal result independent of the amount of canal paresis; differences between them were significant when canal paresis was > 41%. Spontaneous nystagmus significantly influenced the appearance of asymmetries in gain and time constant in the tests performed while, with high-velocity sinusoidal rotation, gain was found to be significantly different for ipsilesional and contralesional rotations in non-acute symptomatic patients.

일측성 전정기능장애 환자에서의 온도안진검사, Velocity Step Test, 동적자세검사 사이의 상관관계

Background and Objective: The advent of rotation test and computed dynamic posturography, along with the caloric test has endowed the physician with an amazing insight into the pathophysiology of the vestibular system. The purpose of this study is to investigate the relationship of the three vestibular function tests in unilateral peripheral vestibulopathy according to compensation. Materials and Methods: Among 612 patients who have received vestibular function test in Asan Medical Center, from January to December in 1998, this study was performed on 121 patients who showed canal paresis of 20% or more in caloric test. The patients who showed symmetry in SHA test (slow harmonic acceleration test) were defined as compensated group (n = 82), and the patients who showed asymmetry in SHA test were defined as uncompensated group (n= 39). To investigate the relationship of the three vestibular function tests, the canal paresis was used as parameter for the caloric test, the SCEP-DP (Slow cumulative eye position-directional preponderance) and Tc-DP (time constant-directional preponderance) for the velocity step test, and the equilibriun score of vestibular function for the posturography. Results: There were close relationships between canal paresis and SCEP-DP (r=0.59 in uncompensated group, r=0.39 in compensated group), between canal paresis and Tc-DP (r=0.53 in uncompensated group, r=0.42 in compensated group) and between SCEP-DP and Tc-DP (r=0.83 in uncompensated group, r=0.49 in compensated group). Equilibrium score of vestibular function showed a minute correlation with SCEP-DP in compensated group (r=-0.2) and no correlation with the others. There was a close relationship between SHA test and posturography in deciding compensation or not (p&lt;0.05 by ????2-test). Conclusion: We have found a close relationship of canal paresis, SCEP-DP and Tc-DP regardless of compensation. Equilibrium score of vestibular function showed a minute correlation with SCEP-DP in compensated group and no correlation with the others. We have also found a close relationship between SHA test and posturography in deciding compensation or not. J Clinical Otolaryngol 2000;11:53–59)

What Inner Ear Diseases Cause Benign Paroxysmal Positional Vertigo?

Benign paroxysmal positional vertigo (BPPV) originating from the posterior semicircular canal (pSCC) is a common vestibular disorder that is easy to diagnose and usually easy to treat. The majority of patients with BPPV have no known inner ear disease; they have ?primary? or ?idiopathic? BPPV. However, a minority does have objective evidence of an inner ear disease on the same side as the BPPV and this group has ?secondary? or ?symptomatic? BPPV. Previous publications differ on the prevalence of secondary BPPV and about the types of inner ear diseases capable of causing it. In order to determine what proportion of patients have secondary as opposed to primary BPPV and which inner ear diseases are capable of causing secondary BPPV, we searched our database for the 10-year period from 1988 to 1997 and found a total of 2847 patients with BPPV. Of these, 81 (3%) had definite pSCC-BPPV secondary to an ipsilateral inner ear disease. Sixteen had Menière's disease, 24 had an acute unilateral peripheral vestibulopathy, 12 had a chronic unilateral peripheral vestibulopathy, 21 had chronic bilateral peripheral vestibulopathy and 8 had unilateral sensorineural hearing loss. It seems that any inner ear disease that detaches otoconia and yet does not totally destroy pSCC function can cause BPPV and that a case can be made for audiometry and caloric testing in all patients with BPPV.