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Results for “Vestibular Neuronitis”

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PubMed2001

Action mechanism of betahistine in the vestibular end organs.

Betahistine has been used to treat several vestibular disorders of both central and peripheral origin. The objective of this work was to study the betahistine action mechanism at the vestibular end organs. Experiments were carried out in wild larval axolotl (Ambystoma tigrinum). Multiunit extracellular recordings were obtained from the semicircular canal nerve using a suction electrode. Betahistine (10 microM to 10 mM, n = 32) inhibited the basal spike discharge of the vestibular afferent neurons with an IC50 of 600 microM. To define the site of action of betahistine, its interactions with antagonists of nitric oxide sintethizing enzyme, cholinergic drugs, and excitatory amino acids were studied. Betahistine 1 mM (n = 5) was coadministered with NG-nitro-L-arginine 3 microM. The action of betahistine remained as in control experiments. Betahistine 1 mM reduced the excitatory action of carbachol (200 microM, n = 5) in a 30 +/- 3.4%. Cholinergic antagonists atropine (10 microM, n = 3) and d-tubocurarine (10 microM, n = 3) did not modify betahistine actions. Betahistine 1 mM also reduced kainic acid (10 microM, n = 4) excitatory action in 45.5 +/- 9.8%. These results corroborate that betahistine has a peripheral inhibitory action in the spike discharge of the afferent neurons in the vestibule. This action seems to involve neither NO production nor modifications in the release of acetylcholine from the efferent fibers. The inhibitory action of betahistine seems to be due to a postsynaptic binding site on the afferent neurons.

Ambystoma↗
PubMed2001

Diagnostic value of vibration-induced nystagmus obtained by combined vibratory stimulation applied to the neck muscles and skull of 300 vertiginous patients.

On subjects with unilateral vestibular dysfunction, the application of a vibratory stimulation (100 Hz) to the two mastoids and the vertex, and to the right and left dorsal neck muscles produces a nystagmus directed towards the good ear in 85% of patients. Fixation must be suppressed by Frenzel's glasses or video nystagmoscopy. To be significant this nystagmus must appear in at least 3 of the 5 vibratory stimulated sites. On healthy subjects nystagmus is present in 6% of cases but never in those below 30 years. In subjects affected by central vertigo, nystagmus was elicited in 10% of cases and in subjects suffering from vertigo of unknown origin in 6% of cases. Vibration nystagmus which stops immediately after stimulation differs from head shaking nystagmus which is present in only 34% of unilateral vestibular dysfunctions. Vibration occasionally produces a pseudo-caloric nystagmus which persists after stimulation. We believe that vibratory stimulation is a useful test, quick and easy to perform. In conjunction with questionnaires, clinical examination, positional testing and the results of audiometry, it gives an immediate indication of a peripheral lesion when the vertigo is seen for the first time. With unilateral deafness, a positive test leads one to suspect an acoustic neuroma. Conversely if the test becomes negative after a vestibular neuritis when it was initially positive, it is a sign of recovery.

Adolescent↗
PubMed2002

Feeling dizzy.

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Dizziness↗
PubMed2001

Laboral outcome after acute unilateral vestibulopathy.

Sixty-five adult patients who had acute peripheral vestibulopathy (APV) were followed-up to determine their functional outcome. During the acute phase, they were treated with betahistine and mobilization. In the entire study population, APV was not significantly associated with a change in occupational activities, physical work or driving ability. Older individuals had significantly attributed a change in work to disease other than APV. Change attributed to APV occurred significantly more frequently in women than in men. The therapeutic approach seems beneficial.

Adult↗
PubMed2002

The vestibulo-ocular reflex and velocity storage in spinocerebellar ataxia 8.

The autosomal dominant spinocerebellar ataxias (SCAs) are a group of neurodegenerative diseases characterized by progressive instability of posture and gait, incoordination, ocular motor dysfunction, and dysarthria due to degeneration of cerebellar and brainstem neurons. Among the more than 20 genetically distinct subtypes, SCA8 is one of several wherein clinical observations indicate that cerebellar dysfunction is primary, and there is little evidence for other CNS involvement. The aim of the present work was to study the decay of the horizontal vestibulo-ocular reflex (VOR) after a short period of constant acceleration to understand the pathophysiology of the VOR due to cerebellar Purkinje cell degeneration in SCA8. The VOR was recorded in patients with genetically defined SCA8 during rotation in the dark. Moderate to severely affected patients had a qualitatively intact VOR, but there were quantitative differences in the gain and dynamics compared to normal controls. During angular velocity ramp rotations, there was a reversal in the direction of the VOR that was more pronounced in SCA8 compared to controls. Modeling studies indicate that there are significant changes in the velocity storage network, including abnormal feedback of an eye position signal into the network that contributes to this reversal. These and other results will help to identify features that are diagnostic for SCA subtypes and provide new information about selective vulnerability of neurons controlling vestibular reflexes.

Cerebellum↗
PubMedDate not supplied

[Cyclotropia after unilateral vestibular damage].

UNLABELLED: Influence of unilateral peripheral vestibular lesion on cyclotorsion of both eyes was assessed by fundus photography. Control group was composed of 24 healthy individuals. Ten patients suffering from Acute Unilateral Peripheral Vestibulopathy (AUPV), which is the other name for vestibular neurolabyrinthitis, were examined at the beginning of the disease, and again after one year. Also 3 patients were examined that had undergone unilateral vestibular neurectomy about 10 years ago. In this paper we propose measurement of a single angle that defines tilt in the roll plane of both eyes at the same time. We propose this measurement of cyclotorsion of both eyes only after peripheral lesions because here vestibular influence is the same on both eyes (contrary to central lesions). RESULTS: 1) Both eyes tilt in healthy population varies equally around zero, from 5 degrees left to 5 degrees right; 2) Both eyes tilt in AUPV patients at the beginning of the disease was oriented to the side of the lesion 12.3 degrees in average which significantly differs from healthy subjects. Here, because of present nystagmus component in the roll plane taking only 1 photograph may result in error up to 5 degrees. Therefore, we took 5 photographs of each eye and calculated arithmetic mean; 3) Both eyes tilt in AUPV patients after one year has elapsed was 1.06 degrees to the lesion side and did not significantly differ from healthy subjects; 4) Vestibular neurectomy patients 10 years later showed 2 degrees tilt to the side of the lesion which also did not significantly differ from healthy subjects. CONCLUSIONS: One year after AUPV and 10 years after vestibular neurectomy central compensation significantly diminished pathological cyclotorsion of both eyes. At the beginning of AUPV several photographs have to be taken (we recommend 5) to avoid error up to 5 degrees due to marked nystagmus component in roll plane. We recommend measurement and calculation of both eyes tilt angle as only one parameter that defines peripheral vestibular lesion influence on cyclotorsion of both eyes.

Adult↗
PubMed2002

Vestibular symptoms as a complication of sildenafil: a case report.

Potential vasodilator side effects of sildenafil such as headache, flushing, dyspepsia, heartburn, nasal congestion, dizziness and visual changes have been frequently observed. We report a 79-year-old man who developed severe vestibular neuritis-like symptoms (horizontal nystagmus with rotatory components and vomiting) two hours after taking 50 mg sildenafil. Additionally, the patient complained of tinnitus in both ears. Internal and neurological examination revealed no pathological findings and the patient had no history of cardiovascular disease. The symptoms lasted for 24 hours and then resolved completely. All of the patient's complaints indicated a drug-related phenomenon. This drug related adverse reaction should be included in the long list of potential side effects of sildenafil.

Adverse Drug Reaction Reporting Systems↗
PubMed2003

Vestibular evoked myogenic potentials in response to skull taps for patients with vestibular neuritis.

In recent years it has been demonstrated that loud clicks generate short latency vestibular evoked myogenic potentials (VEMP). It has also been demonstrated that skull tap stimulation evokes similar VEMP. In the present study, the differences between the click-induced and the skull-tap induced VEMP were studied in 18 patients at onset of vestibular neuritis. Gentle skull taps were delivered manually above each ear on the side of the skull and on the forehead midline. The muscular responses were recorded over both sternocleidomastoid muscles using skin electrodes. Abnormal skull tap VEMP were found in the majority of the patients (10/18, 56%). However, only 4/18 (22%) showed asymmetry in the click-induced VEMP. The high percentage of abnormal skull tap VEMP might suggest that this response is not only dependent on the inferior division of the vestibular nerve, because the inferior division of this nerve is usually spared in vestibular neuritis. Moreover, the patients with abnormal skull tap VEMP differed from those with normal VEMP in their settings of the subjective visual horizontal with static head tilt in the roll plane. This might suggest that skull tap VEMP are (also) related to utricular function.

Acoustic Stimulation↗