Comparison of assessment of caloric nystagmus by observation of duration and by electronystagmo-graphic measurement of slow-phase velocity

1995 ◽  
Vol 29 (2) ◽  
pp. 107-115 ◽  
Author(s):  
Linda Luxon
Keyword(s):  
Phase Velocity ◽  
Slow Phase ◽  
Slow Phase Velocity ◽  
Caloric Nystagmus

Spatial Orientation of Caloric Nystagmus in Semicircular Canal-Plugged Monkeys

2002 ◽  
Vol 88 (2) ◽  
pp. 914-928 ◽  
Author(s):  
Yasuko Arai ◽  
Sergei B. Yakushin ◽  
Bernard Cohen ◽  
Jun-Ichi Suzuki ◽  
Theodore Raphan
Keyword(s):  
Phase Velocity ◽  
Spatial Orientation ◽  
Velocity Vector ◽  
Semicircular Canals ◽  
Velocity Storage ◽  
Slow Phase ◽  
Coordinate Frame ◽  
Slow Phase Velocity ◽  
Caloric Nystagmus ◽  
Eye Velocity

We studied caloric nystagmus before and after plugging all six semicircular canals to determine whether velocity storage contributed to the spatial orientation of caloric nystagmus. Monkeys were stimulated unilaterally with cold (≈20°C) water while upright, supine, prone, right-side down, and left-side down. The decline in the slow phase velocity vector was determined over the last 37% of the nystagmus, at a time when the response was largely due to activation of velocity storage. Before plugging, yaw components varied with the convective flow of endolymph in the lateral canals in all head orientations. Plugging blocked endolymph flow, eliminating convection currents. Despite this, caloric nystagmus was readily elicited, but the horizontal component was always toward the stimulated (ipsilateral) side, regardless of head position relative to gravity. When upright, the slow phase velocity vector was close to the yaw and spatial vertical axes. Roll components became stronger in supine and prone positions, and vertical components were enhanced in side down positions. In each case, this brought the velocity vectors toward alignment with the spatial vertical. Consistent with principles governing the orientation of velocity storage, when the yaw component of the velocity vector was positive, the cross-coupled pitch or roll components brought the vector upward in space. Conversely, when yaw eye velocity vector was downward in the head coordinate frame, i.e., negative, pitch and roll were downward in space. The data could not be modeled simply by a reduction in activity in the ipsilateral vestibular nerve, which would direct the velocity vector along the roll direction. Since there is no cross coupling from roll to yaw, velocity storage alone could not rotate the vector to fit the data. We postulated, therefore, that cooling had caused contraction of the endolymph in the plugged canals. This contraction would deflect the cupula toward the plug, simulating ampullofugal flow of endolymph. Inhibition and excitation induced by such cupula deflection fit the data well in the upright position but not in lateral or prone/supine conditions. Data fits in these positions required the addition of a spatially orientated, velocity storage component. We conclude, therefore, that three factors produce cold caloric nystagmus after canal plugging: inhibition of activity in ampullary nerves, contraction of endolymph in the stimulated canals, and orientation of eye velocity to gravity through velocity storage. Although the response to convection currents dominates the normal response to caloric stimulation, velocity storage probably also contributes to the orientation of eye velocity.

scholarly journals Oculomotor Abnormalities in Friedreich's Ataxia

1979 ◽  
Vol 6 (2) ◽  
pp. 167-172 ◽  
Author(s):  
T.H. Kirkham ◽  
D. Guitton ◽  
A. Katsarkas ◽  
L.B. Kline ◽  
E. Andermann
Keyword(s):  
Phase Velocity ◽  
Friedreich’S Ataxia ◽  
Friedreich's Ataxia ◽  
Motor Deficits ◽  
Slow Phase ◽  
Stimulus Velocity ◽  
Slow Phase Velocity ◽  
Ocular Reflex ◽  
Vestibulo Ocular Reflex ◽  
Caloric Nystagmus

SummaryA clinical neuro-opthalmo-logical and electro-oculographic study was made on fourteen patients with Friedreich's ataxia. None had evidence of optic nerve dysfunction. No patient complained of oscillopsia although all had ocular motor deficits of varying degrees, which appeared to be related to the severity of the general manifestations of the disease. The defects comprised square wave jerks, jerky pursuit with inability to maintain eccentric gaze resulting in gaze paretic nystagmus and rebound nystagmus. There was failure to suppress by fixation the vestíbulo-ocular reflex. The slow phase velocity of caloric nystagmus was always of reduced velocity. There was inability to augment the slow phase velocity of optokinetic nystagmus with increasing stimulus velocity. Abnormalities of the saccadic system were manifest particularly as hypermetria. These signs in combination are suggestive of disease involving the cere be I lar flocculus and vermis or their brain stem connections. No abnormalities were found in 17 parents or siblings.

Visual Suppression Test

1977 ◽  
Vol 86 (1) ◽  
pp. 80-85 ◽  
Author(s):  
Setsuko Takemori
Keyword(s):  
Phase Velocity ◽  
Slow Phase ◽  
Clinical Test ◽  
Visual Suppression ◽  
Slow Phase Velocity ◽  
Suppression Test ◽  
The Mean ◽  
Caloric Nystagmus ◽  
Visual Suppression Test ◽  
Normal Adults

Visual suppression of caloric nystagmus was studied in normal adults and in 98 clinical cases in order to justify the application of the procedure as a clinical test. The maximum slow phase velocity during ten seconds in darkness and the slow phase velocity during ten seconds in light were taken from the recordings and measured. The mean values of these slow phase velocities were calculated and the mean slow phase velocity in darkness was assigned a value of 100%. The value which the slow phase velocity in light subtracts from the slow phase velocity in darkness, represents the visual suppression. It was determined that visual suppression of the slow phase velocity of caloric nystagmus was 48 ± 10% in 22 normal adults. This was caused by the visual fixation mechanisms. Cases in which lesions were diagnosed in the cerebellum, such as spinocerebellar degeneration and cerebellitis, showed reduced or abolished visual suppression. The lesion side can be determined by this test. Compensation following unilateral sudden loss of inner ear function can be measured by the visual suppression test.

Vestibular Function and Motion Sickness Susceptibility: Videonystagmographic Evidence From Oculomotor and Caloric Tests

2020 ◽  
Vol 29 (2) ◽  
pp. 188-198
Author(s):  
Cynthia G. Fowler ◽  
Margaret Dallapiazza ◽  
Kathleen Talbot Hadsell
Keyword(s):  
Phase Velocity ◽  
Motion Sickness ◽  
Repeated Measures ◽  
Short Form ◽  
Vestibular Function ◽  
Slow Phase ◽  
Test Results ◽  
Normal Range ◽  
Slow Phase Velocity ◽  
Caloric Tests

Purpose Motion sickness (MS) is a common condition that affects millions of individuals. Although the condition is common and can be debilitating, little research has focused on the vestibular function associated with susceptibility to MS. One causal theory of MS is an asymmetry of vestibular function within or between ears. The purposes of this study, therefore, were (a) to determine if the vestibular system (oculomotor and caloric tests) in videonystagmography (VNG) is associated with susceptibility to MS and (b) to determine if these tests support the theory of an asymmetry between ears associated with MS susceptibility. Method VNG was used to measure oculomotor and caloric responses. Fifty young adults were recruited; 50 completed the oculomotor tests, and 31 completed the four caloric irrigations. MS susceptibility was evaluated with the Motion Sickness Susceptibility Questionnaire–Short Form; in this study, percent susceptibility ranged from 0% to 100% in the participants. Participants were divided into three susceptibility groups (Low, Mid, and High). Repeated-measures analyses of variance and pairwise comparisons determined significance among the groups on the VNG test results. Results Oculomotor test results revealed no significant differences among the MS susceptibility groups. Caloric stimuli elicited responses that were correlated positively with susceptibility to MS. Slow-phase velocity was slowest in the Low MS group compared to the Mid and High groups. There was no significant asymmetry between ears in any of the groups. Conclusions MS susceptibility was significantly and positively correlated with caloric slow-phase velocity. Although asymmetries between ears are purported to be associated with MS, asymmetries were not evident. Susceptibility to MS may contribute to interindividual variability of caloric responses within the normal range.

Visually evoked slow eye movements, visual-vestibular interaction, and infratentorial lesions

1983 ◽  
Vol 91 (1) ◽  
pp. 76-80 ◽  
Author(s):  
Carsten Wennmo ◽  
Nils Gunnar Henriksson ◽  
Bengt Hindfelt ◽  
Ilmari PyykkÖ ◽  
MÅNs Magnusson
Keyword(s):  
Eye Movements ◽  
Phase Velocity ◽  
Brain Stem ◽  
Smooth Pursuit ◽  
Maximum Velocity ◽  
Slow Phase ◽  
Slow Phase Velocity ◽  
Velocity Gain ◽  
Visual Vestibular Interaction ◽  
Slow Eye Movements

The maximum velocity gain of smooth pursuit and optokinetic, vestibular, and optovestibular slow phases was examined in 15 patients with pontine, 10 with medullary, 10 with cerebellar, and 5 with combined cerebello — brain stem disorders. Marked dissociations were observed between smooth pursuit and optokinetic slow phases, especially in medullary disease. A cerebellar deficit enhanced slow phase velocity gain during rotation in darkness, whereas the corresponding gain during rotation in light was normal.

Monocular Nystagmic Responses to Caloric Stimulation

1979 ◽  
Vol 88 (1) ◽  
pp. 79-85 ◽  
Author(s):  
James W. Wolfe
Keyword(s):  
Phase Velocity ◽  
Rhesus Monkeys ◽  
Cold Water ◽  
Normal Subjects ◽  
Closed Circuit ◽  
Slow Phase ◽  
Vestibular Nystagmus ◽  
Differential Activation ◽  
Slow Phase Velocity ◽  
Left And Right

Twenty-five normal subjects and 173 clinical patients received standard bithermal caloric testing. Vestibular nystagmus was evaluated for cumulative slow phase velocity from the summated horizontal eye recording and independent recording of the left and right eye. These data revealed that cold water stimulation produced more intense activation of the ipsilateral eye. Simultaneous closed-circuit video and D.C. electro-oculographic recordings from eight normal rhesus monkeys in response to cold water irrigations confirmed the fact that this stimulus leads to differential activation of the extraocular muscles. A possible explanation for this finding is discussed.

Efficacy of histaminergic drugs in experimental motion sickness

2008 ◽  
Vol 17 (5-6) ◽  
pp. 313-321
Author(s):  
E.I. Matsnev ◽  
E.E. Sigaleva
Keyword(s):  
Phase Velocity ◽  
Healthy Volunteers ◽  
Motion Sickness ◽  
Slow Phase ◽  
High Susceptibility ◽  
Double Blind ◽  
Slow Phase Velocity ◽  
Betahistine Dihydrochloride ◽  
The Mean ◽  
Oculomotor Activity

The purpose of this investigation was to evaluate the efficacy of the histaminergic drug "Betahistine dihydrochloride" in experimental motion sickness in 10 healthy volunteers (mean age 19.4 y.o.) with high susceptibility to motion sickness. Motion sickness was modeled using Coriolis (precession) accelerations (cumulative Coriolis stimulation test – CCST). Each subject took 32 mg of "Betahistine dihydrochloride" or placebo under "double – blind" conditions 1 hour before testing. The duration and slow phase velocity of the post-rotational nystagmus, the pursuit eye tracking test, and the latency, velocity and accuracy of saccades were estimated. The tolerability level of the CCST in volunteers in the betahistine series was shown to be significantly (p < 0.001) higher, as compared to placebo and baseline. The mean illusory sensations score for the experimental series was significantly lower than that in the placebo and baseline series (p < 0.01). It was found that "Betahistine" demonstrated antimotion sickness efficacy and improved oculomotor activity (increased gain during pursuit movements, faster and more accurate saccades).

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