Individual semicircular canal function in superior and inferior vestibular neuritis

Aw, Swee T.; Fetter, M.; Cremer, Phillip D.; Karlberg, Mikael; Hálmagyi, G. Michael

doi:10.1212/wnl.57.5.768

Cited by 208 publications

(178 citation statements)

References 19 publications

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“…Only 1/3 of the patients of Hong et al showed abnormal cervical VEMPs, suggesting that visual vertical measurements may be superior to cervical VEMPS in identifying vestibular neuritis. Since in most patients vestibular neuritis spares the inferior division of the vestibular nerve (Aw, Fetter, 2001;Fetter and Dichgans, 1996;Schmid-Priscoveanu, Straumann, 1999), a higher sensitivity for utricular tests, such as vibration induced oVEMP or the visual vertical, than of saccular tests, such as cervical VEMPs evoked by air conducted sound, is expected. Indeed, it has recently been reported that in a large sample of patients with unilateral vestibular loss, the SVV during eccentric rotation in patients was significantly more asymmetric than cervical VEMPS (Schonfeld, Helling, 2010).…”

Section: Discussionmentioning

confidence: 99%

Relative diagnostic value of ocular vestibular evoked potentials and the subjective visual vertical during tilt and eccentric rotation

Valko

Hegemann

Weber

et al. 2011

Clinical Neurophysiology

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Straumann, D; Bockisch, C J (2010with the visual vertical during whole-body roll tilt and eccentric rotation in healthy subjects and patients with unilateral vestibular loss, to determine which test was most sensitive in discriminating impaired utricle function. Methods:OVEMPs and the visual vertical were measured in 11 patients and 11 healthy subjects. Visual vertical was measured during roll tilts between -9.6 and 9.6°, and during rotation at 400°/s with the head upright and the vertical rotation axis located between ±3.5 cm from the head center.Results: OVEMPs in patients were strikingly asymmetric, whereas they were approximately symmetric in healthy subjects. Patients showed impaired visual vertical gain during eccentric rotation and increased errors for both roll tilt and eccentric rotation tests. OVEMPs were superior at discriminating between patients and healthy subjects, although eccentric rotation performed nearly as well. Conclusions:OVEMPs provide a powerful test for discriminating between healthy subjects and patients with chronic unilateral vestibular loss, and testing the visual vertical testing during eccentric rotation was superior to testing during whole-body roll tilt.Significance: OVEMPs are easier to administer, less demanding on patients, and in general are more effective at identifying chronic unilateral vestibular loss than visual vertical measurements.

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Section: Discussionmentioning

confidence: 99%

Relative diagnostic value of ocular vestibular evoked potentials and the subjective visual vertical during tilt and eccentric rotation

Valko

Hegemann

Weber

et al. 2011

Clinical Neurophysiology

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“…Maximum errors were <2%. The search coil signals were computed in three dimensions in rotation vectors and Euler angles as position and velocity in space/head fixed coordinates (Aw et al 2001Fahey et al 2008;Weber et al 2008). …”

Section: Head and Eye Movement Recordings And Analysismentioning

confidence: 99%

“…We characterized the vestibular function and its conduction pathways with mechanically and electrically evoked vestibular stimuli. We used the HIT to assess individual semicircular canal function (Aw et al 2001); air-conducted click evoked ocular and cervical VEMPs to assess the otolith functions (Taylor et al 2011) and EVS to examine the vestibular conduction pathway latency, and low and high frequency response of the vestibular system . Ocular motor abnormalities were investigated with volitional horizontal and vertical saccades, vergence, and smooth pursuit (Fahey et al 2008).…”

Section: Introductionmentioning

confidence: 99%

Vestibular and Saccadic Abnormalities in Gaucher’s Disease

et al. 2013

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Gaucher's disease (GD) is a hereditary lysosomal storage disease characterized by abnormal deposition of glucocerebroside due to the enzyme glucocerebrosidase deficiency, resulting in multi-organ pathology. GD type III has a progressive neurological involvement. We studied the vestibular and saccadic abnormalities in GD type III to determine if these parameters may be useful for assessing neurological involvement. We evaluated the vestibular and saccadic responses of two siblings with genetically identified GD type III on enzyme replacement therapy. Vestibular functions were assessed with the head impulse test (HIT), vestibular evoked myogenic potentials (VEMPs), and electrical vestibular stimulation (EVS). Saccadic functions were investigated with volitional horizontal and vertical saccades to AE20. Three-dimensional head and eye movements were recorded with dual-search coils and VEMP with surface electrodes. HIT showed impaired individual semicircular canal function with halved angular vestibuloocular reflex (VOR) gains and absent horizontal refixation saccade. Ocular and cervical VEMPs to air-conducted clicks were absent in the older sibling, and only cervical VEMP was present in the younger sibling indicating otolithic dysfunction. EVS showed prolonged onset latency and attenuated tonic and phasic responses suggesting impaired neural conduction and vestibular function. Horizontal saccadic velocity was miniscule (<30 /s) and multiple back-to-back saccades with saccade-vergence interaction were utilized to minimize eye position error in the older sibling. Vertical saccades were slightly abnormal, but vergence and smooth pursuit were normal in both siblings. Our findings suggest that GD affected the vestibular nuclei in addition to the paramedian pontine reticular formation. These vestibular and saccadic abnormalities may be useful biomarkers to monitor neurological deterioration.

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“…Nevertheless, it can be inferred by testing the subjective visual horizontal, an easy test that can be done in any clinical neurophysiology department. 23 In some patients the disorder only affects the superior vestibular nerve and spares the inferior division of the vestibular nerve 24 so that the patient with vestibular neuritis is able to develop BPPV, presumably as a consequence of otoconia being shed from the utricle into the duct of the posterior semicircular canal.…”

Section: Acute Vestibular Neuritismentioning

confidence: 99%

Diagnosis and management of vertigo

Halmagyi

2005

Clinical Medicine

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-Vertigo is an illusion of rotation due to a disorder of the vestibular system, almost always peripheral. In the history it must be distinguished from pre-syncope, seizures and panic attacks. A single attack of acute, isolated spontaneous vertigo lasting a day or more is due either to vestibular neuritis or cerebellar infarction; distinguishing between the two requires mastery of the head impulse test. Recurrent vertigo is mostly due to benign paroxysmal positioning vertigo (BPPV), Menière's disease or migraine. With a good history, a positional test, an audiogram and a caloric test, it is usually possible to distinguish between these. BPPV is the single most common cause of recurrent vertigo and can usually be cured immediately with a particle repositioning manoeuvre. Posterior circulation ischaemia very rarely causes isolated vertigo attacks and when it does the attacks are brief and frequent and the history is short. KEY WORDS What vertigo is and is notVertigo is an illusion of rotation caused by asymmetry of neural activity between the left and right vestibular nuclei. This can be induced in anyone• by simply spinning them at constant speed for about 20 seconds and then suddenly stopping them• by heating or cooling one labyrinth, as happens in the caloric test• by otoconial particles (calcium-containing debris: literally 'earstones') moving along semicircular canal duct, as happens in benign paroxysmal positional vertigo (BPPV). It can also be produced by sudden unilateral destruction of a normal vestibular end-organ, nerve or nucleus or vestibulo-cerebellum, a structure that normally inhibits the ipsilateral vestibular nucleus. (Bilateral simultaneous vestibular destruction does not produce vertigo -in fact, a patient with bilateral vestibular loss will never again experience vertigo from unilateral or asymmetrical vestibular stimulation.)Vertigo is always temporary. Even after the vestibular nerve on one side has been surgically severed, the resulting vertigo (and nystagmus) will abate within a few days. This is not because the vestibular nerve has re-anastomosed but because profound neurochemical changes occuring in the brainstem during the process of vestibular compensation restore symmetrical vestibular nucleus activity. Vertigo is always made worse by head movement; thus patients who are 'dizzy all the time' and are happy to move around whilst dizzy do not have vertigo.Patients with aural vertigo should not lose consciousness but some patients cannot give confident and convincing answers to such simple questions as 'Did it feel as if you were losing balance or as if you were losing consciousness? Did you feel as if you were going to pass out or fall over?' Patients with vertigo might lose consciousness if they have been vomiting a lot, or if they incurred a head injury when they fell.Witness descriptions are not much help in identifying vertigo, but can be helpful in identifying other paroxysmal disorders such as seizure and syncope. Whereas panic attacks, especially with hyperventilation, co...

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Individual semicircular canal function in superior and inferior vestibular neuritis

Abstract: Vestibular neuritis can affect the superior and inferior vestibular nerves together or can selectively affect the superior vestibular nerve.

Cited by 208 publications

References 19 publications

Relative diagnostic value of ocular vestibular evoked potentials and the subjective visual vertical during tilt and eccentric rotation

Relative diagnostic value of ocular vestibular evoked potentials and the subjective visual vertical during tilt and eccentric rotation

Vestibular and Saccadic Abnormalities in Gaucher’s Disease

Diagnosis and management of vertigo

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