[ON THE EFFECT OF IONIZING RADIATIONS ON THE FUNCTION OF THE VESTIBULAR ANALYZER].
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OBJECTIVE: The study provides a qualitative evaluation of unilateral vestibulopathy by comparing otolithic and canal function, to establish possible relationships between the type of dysfunction observed and the evolving clinical pictures associated with it. STUDY DESIGN: Retrospective study of a series of cases. SETTING: Department of Medical-Surgical Specialization, Otolaryngology and Cervicofacial Surgery Division, University of Perugia, Perugia, Italy. PATIENTS: Twenty patients whose medical history showed at least one episode corresponding to the clinical parameters of acute vestibulopathy. INTERVENTIONS: Study of vestibular function by recording VEMPs and repeating canal function testing at least 6 months after the first episode of vertigo. MAIN OUTCOME MEASURES: Relationship between the type of vestibulopathy (canal and otolithic) and the clinical pictures observed. RESULTS: Paroxysmal positional vertigo, observed in 4 patients, was correlated with the presence of vestibular evoked myogenic potentials (VEMPs) and the absence of an ipsilateral canal response in all cases (100%). Persistent dizziness was observed in nine patients, and VEMPs were absent in all of them (100%); three (33.3%) showed the recovery of previously absent canal function. Comparison of responses in six patients with recurrent acute vestibulopathy showed persistent and complete loss of canal function in five cases (83.3%), whereas impairment of otolithic response was less constant (40%). CONCLUSION: The combined VEMPs-canal test study shows predictive value regarding certain evolving clinical pictures of vestibulopathy. The absence of VEMPs confirms the role of otolithic dysfunction in the onset of dizziness. Likewise, it suggests that a vestibular origin of these disorders should be considered in cases that have shown aspecific symptoms since onset, without frank vertigo and with normal vestibular response to canal function testing.
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Traumatic brain injury (TBI) in humans may cause extensive sensorimotor and cognitive dysfunction. As a result, many TBI researchers are beginning to assess behavioral correlates of histologically determined damage in animal models. Although this is an important step in TBI research, there is a need for standardization between laboratories. The ability to reliably test treatments across laboratories and multiple injury models will close the gap between treatment success in the lab and success in the clinic. The goal of this review is to describe and evaluate the tests employed to assess functional outcome after TBI and to overview aspects of cognitive, sensory, and motor function that may be suitable targets for therapeutic intervention.
CONCLUSION: Symptomatic high frequency/acceleration vestibular loss is a distinct clinical entity that can be missed on conventional ENG with caloric testing. Under certain circumstances, symptomatic patients with a high frequency/acceleration vestibular loss should undergo an MSSC study for confirmation, if required. OBJECTIVE: To document that normal electronystagmography (ENG) with conventional bithermal caloric testing is inadequate for diagnosing clinically significant high frequency/acceleration vestibular loss. MATERIAL AND METHODS: Patients with clinical symptoms and signs of persistent peripheral vestibular dysfunction despite normal conventional bithermal caloric testing on ENG underwent high frequency/acceleration horizontal magnetic scleral search coil (MSSC) eye movement studies. The clinical findings and results from audiometric tests, conventional ENG with bithermal caloric tests and MSSC tests were reviewed. RESULTS: Eleven patients were identified as having an abnormal MSSC study, indicating a high frequency/acceleration vestibular loss consistent with their clinical history despite normal or equivocal bithermal caloric responses on conventional ENG. Although valuable, ENG caloric testing evaluates lateral semicircular canal function and should be considered a non-physiological test primarily of low frequency vestibular function. High frequency/acceleration head thrust testing clinically detected a "high frequency/acceleration vestibular loss" in 8/11(72.7%) cases.
27 patients with acoustic neuroma were operated on by translabyrinthine tumor removal. At operation 8th nerve compartments were identified and removed for study. Results of the audiological test battery and vestibular tests were compared with histological state of the nerve specimens studied. The tumor appears only seldom to invade the cochlear nerve in cases with 'cochlear' hearing loss, but in the majority of cases with 'retrocochlear' hearing loss the cochlear nerve is invaded.
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The purpose of this study was to investigate the relationship of vestibular function to motor proficiency, including balance, in children with hearing impairments. Thirteen children with normal hearing and 29 children with hearing impairments, ranging in age from 7 to 13 years, were classified into categories based on vestibular function using neuro-otologic measures (ie, vestibulo-ocular reflex function and posturography). Children in each category were tested for motor proficiency using clinical assessment measures (eg, balance, muscle tone, and coordination). The test results indicated that the children with hearing impairments and normal peripheral vestibular function (n = 7) exhibited normal motor proficiency, including balance. The children with hearing impairments and loss of peripheral vestibular sensitivity (n = 19) also demonstrated normal motor proficiency, except for balance ability. The children with hearing impairments and sensory organization deficits (n = 3), however, exhibited motor deficits in many areas. The results of this study indicate that motor proficiency in children with hearing impairments depends on vestibular function. Interventions for motor deficits in children with hearing impairments, therefore, must consider vestibular function as well as motor performance.
This study examined the effects of ice water caloric stimulation on H-reflex amplitude in normal subjects and three complete spinal cord-injured patients. H-reflexes were obtained by stimulating the tibial nerve at the popliteal fossa and recording the H-response from the gastrocnemius muscle. All normal subjects who experienced nystagmus or vertigo demonstrated significant augmentation in H-reflex amplitude with ice water irrigation of the ear canal. In the three spinal cord-injured patients, there was no significant change of H-reflex with the ice water stimulus. The results suggest that descending tracts in the anterior spinal cord must be functional to demonstrate caloric augmentation of H-reflexes. In patients with spinal cord injury, it may be possible to predict the recovery of motor function using this test together with other clinical signs of neurological function.
This study was designed to assess the utility of otolith-ocular reflex testing in patients with complete unilateral peripheral vestibular deficits. Ten subjects were given a clinical vestibular test battery (ENG & vertical rotation) and research oriented tests of otolith function including dynamic posturography with head tilt and earth-horizontal axis rotation with otolith-visual interactions. Clinical tests confirmed the presence of a vestibular deficit and the side of the lesion. The results suggested the following: posturography during head tilt is not a reliable means of detecting unilateral peripheral vestibular dysfunction, while earth-horizontal axis rotation is a reliable means of assessing asymmetric otolith function. The Bias response during earth-horizontal axis rotation was significantly less during rotation ipsilateral to the lesioned ear compared to contralateral rotation while the Mod response was normal. The optokinetic test results in these subjects were normal while otolith-visual interactions were symmetrically reduced in these patients.
Chronic states of methylmercurialism were induced in squirrel monkey subjects. Principal neurological signs included ataxia, abnormal gait, incoordination and amaurosis. Although slight to moderate vacuolization occurred in supporting cell layers of the cristae and maculae, receptor cell function was essentially normal. Except for a lowered cold threshold, bithermal caloric-induced nystagmus was not significantly different from control values. Pre and postrotatory (Barany chair) tests revealed a reduction only in frequency related variables. The development of spontaneous and positional nystagmus (sometimes with eyes open) coupled with the behavioral signs and the evidence of normal receptor response suggested cerebellar dysfunction. Severe pathologic changes were present in the cerebral cortex, but no lesions were found in the cerebellar cortex. Substantial neuronal degeneration and gliosis, however, were observed in several subcortical nuclei, including cerebellar and vestibular nuclei.
The effect of betahistine on the vestibulo-ocular reflex (VOR) was assessed in 12 patients suffering from paroxysmal vertigo. Only patients who responded to betahistine treatment were admitted to the study in order to increase the probability of quantifying the effect of the drug on vestibular function. Patients received placebo or 16, 32 or 64 mg betahistine orally under double-blind conditions. Vestibular function was tested a few minutes before intake, and 1, 2, 3, 4, 6 and 8 h after intake, by torsion swing stimulus in the dark, visuo-vestibular interaction upon simultaneous visual and vestibular stimulation and high frequency passive head shaking. Betahistine significantly affected the velocity gain of low and high frequency VOR. The reduction in gain was maximal about 4 h after administration of the 16 mg dose in the torsion swing experiment and the 32 mg dose in the head shaking experiment. Above these doses, the effect on velocity gain was less marked. Betahistine had no effect on visuo-vestibular interaction or nystagmus duration during low frequency torsion. These results suggest that betahistine has a complex action on H3 receptors and that the site of action may be in the vestibular nuclei.