Cases reported "Vestibular Diseases"

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1/5. Inferior vestibular neuritis.

    Sudden, spontaneous, unilateral loss of vestibular function without simultaneous hearing loss or brain stem signs is generally attributed to a viral infection involving the vestibular nerve and is called acute vestibular neuritis. The clinical hallmarks of acute vestibular neuritis are vertigo, spontaneous nystagmus, and unilateral loss of lateral semicircular function as shown by impulsive and caloric testing. In some patients with vestibular neuritis the process appears to involve only anterior and lateral semicircular function, and these patients are considered to have selective superior vestibular neuritis. Here we report on two patients with acute vertigo, normal lateral semicircular canal function as shown by both impulsive and caloric testing, but selective loss of posterior semicircular canal function as shown by impulsive testing and of saccular function as shown by vestibular evoked myogenic potential testing. We suggest that these patients had selective inferior vestibular neuritis and that contrary to conventional teaching, in a patient with acute spontaneous vertigo, unilateral loss of lateral semicircular canal function is not essential for a diagnosis of acute vestibular neuritis.
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2/5. Patient and normal three-dimensional eye-movement responses to maintained (DC) surface galvanic vestibular stimulation.

    HYPOTHESIS: That disease or dysfunction of vestibular end organs in human patients will reduce or eliminate the contribution of the affected end organs to the total eye-movement response to DC surface galvanic vestibular stimulation (GVS). BACKGROUND: It was assumed that DC GVS (at current of 5 mA) stimulates all vestibular end organs, an assumption that is strongly supported by physiological evidence, including the activation of primary vestibular afferent neurons by galvanic stimulation. Previous studies also have described the oculomotor responses to vestibular activation. Stimulation of individual semicircular canals results in eye movements parallel to the plane of the stimulated canal, and stimulation of the utricular macula produces changes in ocular torsional position. It was also assumed that the total three-dimensional eye-movement response to GVS is the sum of the contributions of the oculomotor drive of all the vestibular end organs. If a particular vestibular end organ were to be diseased or dysfunctional, it was reasoned that its contribution to the GVS-induced oculomotor response would be reduced or absent and that patients thus affected would have a systematic difference in their GVS-induced oculomotor response compared with the response of normal healthy individuals. methods: Three-dimensional video eye-movement recording was carried out in complete darkness on normal healthy subjects and patients with various types of vestibular dysfunction, as diagnosed by independent vestibular clinical tests. The eye-movement response to long-duration bilateral and unilateral surface GVS was measured. RESULTS: The pattern of horizontal, vertical, and torsional eye velocity and eye position during GVS of patients independently diagnosed with bilateral vestibular dysfunction, unilateral vestibular dysfunction, charge syndrome (semicircular canal hypoplasia), semicircular canal occlusion, or inferior vestibular neuritis differed systematically from the responses of normal healthy subjects in ways that corresponded to the expectations from the conceptual approach of the study. CONCLUSION: The study reports the first data on the differences between the normal response to GVS and those of patients with a number of clinical vestibular conditions including unilateral vestibular loss, canal block, and vestibular neuritis. The GVS-induced eye-movement patterns of patients with vestibular dysfunction are consistent with the reduction or absence of oculomotor contribution from the end organs implicated in their particular disease condition.
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3/5. Inferior vestibular neuritis: 3 cases with clinical features of acute vestibular neuritis, normal calorics but indications of saccular failure.

    BACKGROUND: Vestibular neuritis (VN) is commonly diagnosed by demonstration of unilateral vestibular failure, as unilateral loss of caloric response. As this test reflects the function of the superior part of the vestibular nerve only, cases of pure inferior nerve neuritis will be lost. CASE PRESENTATIONS: We describe three patients with symptoms suggestive of VN, but normal calorics. All 3 had unilateral loss of vestibular evoked myogenic potential. A slight, asymptomatic position dependent nystagmus, with the pathological ear down, was observed. CONCLUSION: We believe that these patients suffer from pure inferior nerve vestibular neuritis.
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keywords = neuritis
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4/5. Unilateral vestibular neuritis with otolithic signs and off-vertical axis rotation.

    Off-vertical axis rotation (OVAR) at constant velocity is a dynamic otolith stimulus that induces horizontal and vertical eye movement responses. To determine the value of this examination as a test for unilateral otolithic hypofunction, we compared the OVAR responses of patients suffering from acute vestibular neuritis (VN) without any sign of otolith affection, with those of patients suffering from acute VN with otolithic signs. The horizontal eye movement bias component shows directional preponderance (DP) significantly higher in patients with otolithic signs than in patients not presenting them. However, as bias DP also reflects the imbalance between right and left horizontal canals activity, this greater bias DP could be explained by the more severe canals impairment-evaluated by caloric test-found in patients with otolithic signs. No significant difference can be shown on horizontal modulation. The DP of vertical modulation is significantly higher in patients presenting otolithic signs than in patients not presenting them: in the case of otolithic signs, the responses are smaller during rotations toward the affected side. Therefore, this variable could be used as an indication of unilateral otolithic hypofunction.
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ranking = 0.5
keywords = neuritis
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5/5. Idiopathic bilateral vestibular loss.

    We describe the clinical and laboratory features of 13 patients with bilateral loss of peripheral vestibular sensitivity of no known cause. In the office, screening for this condition was possible using illegible e-testing and examination of the patient for refixation saccades after brisk head movements while attempting visual fixation. diagnosis was confirmed by bilaterally reduced caloric responses (< 20 degrees/second on all 4 caloric irrigations) and abnormally low gain of the vestibulo-ocular reflex on rotational chair testing. The mean age of the patients was 68 years. We noted two patterns of symptom onset: onset associated with vertigo (10 patients) and insidious progressive disequilibrium not associated with vertigo (3 patients). Only 38% of the patients complained of subjective oscillopsia. The subjects performed poorly on platform posturography, particularly when deprived of visual and somatosensory feedback. When associated with vertigo, bilateral vestibular loss may be the result of bilateral sequential vestibular neuritis; when not associated with vertigo, disequilibrium may be caused by slow, symmetrical loss of peripheral function as a result of aging. Although the subjects in this report were elderly, idiopathic bilateral vestibular loss has been reported in patients of all ages.
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keywords = neuritis
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