A Model of Visual-Vestibular Interaction in Cerebellar Disorders

ORL ◽  
1984 ◽  
Vol 46 (6) ◽  
pp. 302-309 ◽  
Author(s):  
Nils Gunnar Henriksson ◽  
Carsten Wennmo ◽  
Ilmari Pyykkö ◽  
Lucyna Schalén
Keyword(s):  
Visual Vestibular Interaction ◽  
Cerebellar Disorders

Validity and limitation of manual rotational test to detect impaired visual–vestibular interaction due to cerebellar disorders

2005 ◽  
Vol 32 (1) ◽  
pp. 23-28 ◽  
Author(s):  
Norihiko Murai ◽  
Kazuo Funabiki ◽  
Yasushi Naito ◽  
Juichi Ito ◽  
Hidenao Fukuyama
Keyword(s):  
Visual Vestibular Interaction ◽  
Cerebellar Disorders

scholarly journals The critical need to develop tools assessing cerebellar reserve for the delivery and assessment of non-invasive cerebellar stimulation

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Mario Manto ◽  
Shinji Kakei ◽  
Hiroshi Mitoma
Keyword(s):  
Daily Practice ◽  
Clinical Applications ◽  
Non Invasive ◽  
Very High ◽  
Cerebellar Disorders ◽  
Cerebellar Stimulation

AbstractNon-invasive cerebellar stimulation (NICS) aims to modulate cerebello-cerebral loops and cerebro-spinal loops, both for research and clinical applications. It is of paramount importance to establish and validate morphological and functional tools to quantify cerebellar reserve, defined as the capacity for restoration and compensation to pathology of the cerebellum. Using NICS without efforts to estimate cerebellar reserve will end up in conflicting results due to the very high heterogeneity of cerebellar disorders encountered in daily practice.

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.

P.0550 The BALB/c mutant female mice of the nox3 gene as a model to investigate vestibular and cerebellar disorders

2021 ◽  
Vol 53 ◽  
pp. S404-S405
Author(s):  
K.E. Kiataqui ◽  
S.R. Massironi ◽  
C.C. Mori ◽  
T.B. Kirsten ◽  
E. Bondan ◽  
...  
Keyword(s):  
Female Mice ◽  
Mutant Female ◽  
Cerebellar Disorders

Visual-Vestibular Interaction Hypothesis for the Control of Orienting Gaze Shifts by Brain Stem Omnipause Neurons

2007 ◽  
Vol 97 (2) ◽  
pp. 1149-1162 ◽  
Author(s):  
Mario Prsa ◽  
Henrietta L. Galiana
Keyword(s):  
Brain Stem ◽  
Head Movements ◽  
Gaze Control ◽  
Gaze Shifts ◽  
Gaze Shift ◽  
Switching Mechanism ◽  
Interaction Hypothesis ◽  
Visual Vestibular Interaction ◽  
Motor Error ◽  
Gaze Position

Models of combined eye-head gaze shifts all aim to realistically simulate behaviorally observed movement dynamics. One of the most problematic features of such models is their inability to determine when a saccadic gaze shift should be initiated and when it should be ended. This is commonly referred to as the switching mechanism mediated by omni-directional pause neurons (OPNs) in the brain stem. Proposed switching strategies implemented in existing gaze control models all rely on a sensory error between instantaneous gaze position and the spatial target. Accordingly, gaze saccades are initiated after presentation of an eccentric visual target and subsequently terminated when an internal estimate of gaze position becomes nearly equal to that of the target. Based on behavioral observations, we demonstrate that such a switching mechanism is insufficient and is unable to explain certain types of movements. We propose an improved hypothesis for how the OPNs control gaze shifts based on a visual-vestibular interaction of signals known to be carried on anatomical projections to the OPN area. The approach is justified by the analysis of recorded gaze shifts interrupted by a head brake in animal subjects and is demonstrated by implementing the switching mechanism in an anatomically based gaze control model. Simulated performance reveals that a weighted sum of three signals: gaze motor error, head velocity, and eye velocity, hypothesized as inputs to OPNs, successfully reproduces diverse behaviorally observed eye-head movements that no other existing model can account for.

A non-linear model for visual-vestibular interaction during body rotation in man

1980 ◽  
Vol 36 (3) ◽  
pp. 143-151 ◽  
Author(s):  
R. Schmid ◽  
A. Buizza ◽  
D. Zambarbieri
Keyword(s):  
Linear Model ◽  
Body Rotation ◽  
Visual Vestibular Interaction ◽  
Non Linear
Sign in / Sign up

Export Citation Format

Share Document