scholarly journals New insights into vestibular-saccade interaction based on covert corrective saccades in patients with unilateral vestibular deficits

2017 ◽  
Vol 117 (6) ◽  
pp. 2324-2338 ◽  
Author(s):  
Paolo Colagiorgio ◽  
Maurizio Versino ◽  
Silvia Colnaghi ◽  
Silvia Quaglieri ◽  
Marco Manfrin ◽  
...  
Keyword(s):  
Mathematical Model ◽  
Feedback Loop ◽  
Head Rotation ◽  
Vestibular Nuclei ◽  
Slow Phase ◽  
Phase Component ◽  
Head Displacement ◽  
Corrective Saccades ◽  
Head Impulses ◽  
The Brain

In response to passive high-acceleration head impulses, patients with low vestibulo-ocular reflex (VOR) gains often produce covert (executed while the head is still moving) corrective saccades in the direction of deficient slow phases. Here we examined 23 patients using passive, and 9 also active, head impulses with acute (< 10 days from onset) unilateral vestibular neuritis and low VOR gains. We found that when corrective saccades are larger than 10°, the slow-phase component of the VOR is inhibited, even though inhibition increases further the time to reacquire the fixation target. We also found that 1) saccades are faster and more accurate if the residual VOR gain is higher, 2) saccades also compensate for the head displacement that occurs during the saccade, and 3) the amplitude-peak velocity relationship of the larger corrective saccades deviates from that of head-fixed saccades of the same size. We propose a mathematical model to account for these findings hypothesizing that covert saccades are driven by a desired gaze position signal based on a prediction of head displacement using vestibular and extravestibular signals, covert saccades are controlled by a gaze feedback loop, and the VOR command is modulated according to predicted saccade amplitude. A central and novel feature of the model is that the brain develops two separate estimates of head rotation, one for generating saccades while the head is moving and the other for generating slow phases. Furthermore, while the model was developed for gaze-stabilizing behavior during passively induced head impulses, it also simulates both active gaze-stabilizing and active gaze-shifting eye movements. NEW & NOTEWORTHY During active or passive head impulses while fixating stationary targets, low vestibulo-ocular gain subjects produce corrective saccades when the head is still moving. The mechanisms driving these covert saccades are poorly understood. We propose a mathematical model showing that the brain develops two separate estimates of head rotation: a lower level one, presumably in the vestibular nuclei, used to generate the slow-phase component of the response, and a higher level one, within a gaze feedback loop, used to drive corrective saccades.

Eye-head coordination in darkness: Formulation and testing of a mathematical model

2003 ◽  
Vol 13 (2-3) ◽  
pp. 79-91
Author(s):  
Stefano Ramat ◽  
Roberto Schmid ◽  
Daniela Zambarbieri
Keyword(s):  
Mathematical Model ◽  
Vestibular System ◽  
Sensory Information ◽  
Head Rotation ◽  
Normal Subjects ◽  
Head Movements ◽  
Vestibular Nystagmus ◽  
Ocular Reflex ◽  
Head Displacement ◽  
Vestibulo Ocular Reflex

Passive head rotation in darkness produces vestibular nystagmus, consisting of slow and quick phases. The vestibulo-ocular reflex produces the slow phases, in the compensatory direction, while the fast phases, in the same direction as head rotation, are of saccadic origin. We have investigated how the saccadic components of the ocular motor responses evoked by active head rotation in darkness are generated, assuming the only available sensory information is that provided by the vestibular system. We recorded the eye and head movements of nine normal subjects during active head rotation in darkness. Subjects were instructed to rotate their heads in a sinusoidal-like manner and to focus their attention on producing a smooth head rotation. We found that the desired eye position signal provided to the saccadic mechanism by the vestibular system may be modeled as a linear combination of head velocity and head displacement information. Here we present a mathematical model for the generation of both the slow and quick phases of vestibular nystagmus based on our findings. Simulations of this model accurately fit experimental data recorded from subjects.

Abstract TP368: Improving In-House Stroke Code Imaging and Treatment Times

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Erin L Ward ◽  
Gail Lighthizer ◽  
Avneesh Uppal
Keyword(s):  
Endovascular Therapy ◽  
Feedback Loop ◽  
National Guidelines ◽  
Hospital Arrival ◽  
Quality Patient Care ◽  
Improvement Plan ◽  
Code Algorithm ◽  
Response Team ◽  
The Brain ◽  
Rule Out

Background: In acute ischemic stroke, a blood vessel in the brain is blocked and brain cells die within minutes; therefore rapid recognition and treatment to restore circulation to the brain is essential. National guidelines call for a CT scan of the brain to be done within 25 minutes of hospital arrival in patients presenting with acute stroke to rule out bleeding in the brain. Findings of a hemorrhage would be a contraindication for thrombolytic therapy. Additional guidelines call for intravenous t-PA (alteplase) to be administered within 60 minutes of arrival and rapid triage to endovascular therapy in appropriate patients. Similar goals for rapid treatment should be followed for patients experiencing a stroke while in the hospital. Urgent treatment with a clot busting medication (alteplase) or with special endovascular techniques to mechanically remove a clot have been shown to improve outcomes. Purpose: A performance improvement plan was developed and initiated in January 2015 to improve the time to CT, time to t-PA administration, and time to endovascular therapy for patients having a stroke while hospitalized for other diagnoses (In-House Stroke). Method s: The following revisions were made to current practice: Mock Stroke Code Drills for In-House Stroke Code responders; creation of an In-House Stroke Code algorithm; addition of CT & MRI screening forms to In-house Stroke Code packet; development of a Stroke Code criteria checklist to assist floor nurses; implementation of a feedback loop to Stroke Code team reporting imaging and treatment times along with patient outcomes; addition of a radiology supervisor to the Stroke Code response team. Results: “Stroke Code called” to “CT initiated“< 25 minutes improved from 32% in 2013, 30% in 2014, to 60% in 2015. “Stroke Code called” to “IV t-PA (alteplase) administered” < 60 minutes improved from 0% in 2013, 25% in 2014, to 100% in 2015. “Stroke Code called” to “groin puncture for endovascular therapy” < 2 hours, 40% for 2013, 43% in 2014 to 50% in 2015. Conclusion: These interventions resulted in faster CT imaging and treatment times, thereby providing the patient with the highest quality patient care.

Role of the caudal fastigial nucleus in saccade generation. II. Effects of muscimol inactivation

1993 ◽  
Vol 70 (5) ◽  
pp. 1741-1758 ◽  
Author(s):  
F. R. Robinson ◽  
A. Straube ◽  
A. F. Fuchs
Keyword(s):  
Brain Stem ◽  
Rhesus Macaques ◽  
Fastigial Nucleus ◽  
Gamma Aminobutyric Acid ◽  
End Points ◽  
Acceleration And Deceleration ◽  
Corrective Saccades ◽  
Corrective Saccade ◽  
The Right ◽  
The Brain

1. We studied the effect of temporarily inhibiting neurons in the caudal fastigial nucleus in two rhesus macaques trained to make saccades to jumping targets. We placed injections of the gamma-aminobutyric acid (GABA) agonist muscimol unilaterally or bilaterally at sites in the caudal fastigial nucleus where we had recorded saccade-related neurons a few minutes earlier. 2. Unilateral injections (n = 9) made horizontal saccades to the injected side hypermetric and those to the other side hypometric (mean gain of 1.37 and 0.61, respectively, for 10 degrees target steps, and 1.26 and 0.81 for 20 degrees target steps; normal saccade gain was 0.96). Saccades to vertical targets showed a small but significant hypermetria and curved strongly toward the side of the injection. The trajectories and end points of all targeted saccades were more variable than normal. 3. After unilateral injections, centripetal saccades were slightly larger than centrifugal saccades (mean gains for ipsilateral saccades were 1.42 and 1.31, respectively, for 10 degrees target steps, and 1.37 and 1.15 for 20 degrees target steps). 4. Unilateral injections increased the average acceleration of ipsilateral saccades and decreased the acceleration of contralateral saccades. Injections decreased both the acceleration and deceleration of vertical saccades. 5. After dysmetric saccades, monkeys acquired the target with an abnormally high number of hypometric corrective saccades. Injection increased the average number of corrective saccades from 0.6 to 2.1 after 10 degrees horizontal target steps and from 0.8 to 2.1 after 20 degrees steps. The size of each successive corrective saccade in a series decreased, and the latency from the previous corrective saccade increased. 6. Bilateral injections (n = 2) of muscimol, in which we injected first into the left caudal fastigial nucleus and then, within 30 min, into the right, made all saccades hypermetric (mean gain for 10 degrees right, left, up, and down saccades was 1.18, 1.49, 1.43, and 1.10, respectively). Paradoxically, bilateral injection decreased both saccade acceleration and deceleration. Saccade trajectories and end points were more variable than normal. 7. To account for the effects of our injections, we propose that the activity of caudal fastigial neurons on one side normally helps to decelerate ipsilateral saccades and helps to accelerate contralateral saccades by influencing the feedback loop of the saccade burst generator in the brain stem. Without caudal fastigial activity the brain stem burst generator produces hypermetric, variable saccades. We therefore also propose that the influence of caudal fastigial neurons on the burst generator makes saccades more consistent and accurate.(ABSTRACT TRUNCATED AT 400 WORDS)

The Velocity Storage Mechanism of the Optokinetic Nystagmus Under Apparent Stimulus Movements in Squirrel Monkeys

1997 ◽  
Vol 7 (6) ◽  
pp. 441-451
Author(s):  
J. Kröller ◽  
F. Behrens ◽  
V.V. Marlinsky
Keyword(s):  
Steady State ◽  
Brain Stem ◽  
Apparent Movement ◽  
Squirrel Monkeys ◽  
Constant Light ◽  
Velocity Storage ◽  
Slow Phase ◽  
Stripe Pattern ◽  
Storage Mechanism ◽  
The Brain

Experiments in two awake untrained squirrel monkeys were performed to study the velocity storage mechanism during fast rise of OKN slow phase velocity. This was done by testing the monkey’s capability to perform OKN in response to a stationary-appearing stroboscopically illuminated stripe pattern of a horizontally rotating drum. Nystagmus was initially elicited during constant illumination lasting between 0.6 and 25 s. The periodicity of the stripe pattern was 2.37°. When after the constant light the flash illumination was switched on again, two types of behavior could occur, depending on the length of the constant light interval (CLI): 1) when the CLI was shorter than a threshold value of 6.2 seconds, the OKN ceased under the flash stimulation. Then a “post-OKN” occurred that increased with the length of the CLIs, indicating that the intermittently illuminated pattern did not provoke fixation suppression of OKN aftereffects. 2) when the CLI was above threshold, the OKN continued under the flash light: it will he called “apparent movement OKN.” The threshold CLI between the type 1 and the type 2 response did not depend on drum velocities between 21.5°/s and 71.3°/s. The average gain of the apparent movement OKN was 0.83 ± 0.04; gain and stability of slow phase eye movement velocity did not deviate systematically from the usually elicited OKN. OKAN after apparent movement OKN did not deviate from OKAN after constantly illuminated moving patterns. In response to the OKN initiation by a constantly illuminated pattern up to pattern velocities of 100°/s, the OKN steady state gain was reached within the first 2 or 3 nystagmus beats. We ascribe the increase of the post-OKN with CLI and the existence of a threshold constant light interval to activity-accumulation in the common velocity-to-position integrator (velocity storage) of the brain stem. Loading of the velocity storage takes place after the OKN gain has already reached the steady-state value. Apparent movement OKN could also be elicited in guinea pigs that lack an effective smooth pursuit system. We suggest that apparent movement OKN is produced by mechanisms located in the brain stem.

Statocyst-Induced Eye Movements in the Crab Scylla Serrata

1973 ◽  
Vol 59 (1) ◽  
pp. 17-38
Author(s):  
D. C. SANDEMAN ◽  
A. OKAJIMA
Keyword(s):  
Eye Movement ◽  
Contralateral Side ◽  
Scylla Serrata ◽  
Slow Phase ◽  
Fast Phase ◽  
Preferred Direction ◽  
Sensory Axons ◽  
Proprioceptive Input ◽  
Motor Neurones ◽  
The Brain

1. The sensory axons of the thread hair receptors, free hook hair receptors and most receptors of the statolith area of the crab statocyst all project to the same dorsolateral part of the brain. Large sensory receptors which innervate some hairs surrounding the statolith project to a more ventral site, and send some branches across to the contralateral side of the brain. 2. The central projections of oculomotor neurones have a characteristically open branch pattern and their dendritic field corresponds closely with that of the thread hairs. There are no branches extending to the contralateral side of the brain. 3. Intracellular responses from the motor neurones of horizontal eye-movement muscles during nystagmus show that they are probably directly inhibited during a fast-phase movement of the eye opposite to the direction in which they act. During a slow-phase eye movement opposite to their preferred direction the input to the motor neurones is diminished pre-synaptically. 4. Sets of antagonist motor neurones maintain a fairly rigid relationship to one another so that an increase in activity of one set leads to a decrease in the antagonists. Neither this, nor the onset of the fast phase of nystagmus, is governed by proprioceptive input or by the frequency of discharge of the motor neurones themselves.

Postlesional Vestibular Reorganization in Frogs: Evidence for a Basic Reaction Pattern After Nerve Injury

2001 ◽  
Vol 85 (6) ◽  
pp. 2643-2646 ◽  
Author(s):  
Fumiyuki Goto ◽  
Hans Straka ◽  
Norbert Dieringer
Keyword(s):  
Nerve Injury ◽  
Vestibular Nuclei ◽  
Reaction Pattern ◽  
Similar Process ◽  
Spatial Response ◽  
Sensory Modalities ◽  
Basic Reaction ◽  
Afferent Inputs ◽  
Motor Maps ◽  
The Brain

Nerve injury induces a reorganization of subcortical and cortical sensory or motor maps in mammals. A similar process, vestibular plasticity 2 mo after unilateral section of the ramus anterior of N. VIII was examined in this study in adult frogs. The brain was isolated with the branches of both N. VIII attached. Monosynaptic afferent responses were recorded in the vestibular nuclei on the operated side following ipsilateral electric stimulation either of the sectioned ramus anterior of N. VIII or of the intact posterior vertical canal nerve. Excitatory and inhibitory commissural responses were evoked by separate stimulation of each of the contralateral canal nerves in second-order vestibular neurons. The afferent and commissural responses of posterior vertical canal neurons recorded on the operated side were not altered. However, posterior canal-related afferent inputs had expanded onto part of the deprived ramus anterior neurons. Inhibitory commissural responses evoked from canal nerves on the intact side were detected in significantly fewer deprived ramus anterior neurons than in controls, but excitatory commissural inputs from the three contralateral canal nerves had expanded. This reactivation might facilitate the survival of deprived neurons and reduce the asymmetry in bilateral resting activities but implies a deterioration of the original spatial response tuning. Extensive similarities at the synaptic and network level were noted between this vestibular reorganization and the postlesional cortical and subcortical reorganization of sensory representations in mammals. We therefore suggest that nerve injury activates a fundamental neural reaction pattern that is common between sensory modalities and vertebrate species.

Intranasal Oxytocin has sympathoexcitatory effects on vascular tone in healthy males

2020 ◽  
Author(s):  
Moritz Meusel ◽  
Magdalena Herrmann ◽  
Felix Machleidt ◽  
Klaas Franzen ◽  
Reinhard Vonthein ◽  
...  
Keyword(s):  
Feedback Loop ◽  
Vascular Tone ◽  
Total Activity ◽  
Double Blind ◽  
Fasting Period ◽  
Intracerebral Administration ◽  
Baroreflex Function ◽  
Drug Challenge ◽  
The Brain ◽  
Healthy Males

Objective: Oxytocin appears to be involved in the neuroendocrine regulation of sympathetic blood pressure (BP) homeostasis. In animals, intracerebral administration of oxytocin induces BP-relevant sympathetic activation. In humans, central nervous effects of oxytocin on BP regulation remain unclear. Intranasal administration supposedly delivers oligopeptides like oxytocin directly to the brain. We investigated the effects of intranasal oxytocin on sympathetic vascular baroreflex function in humans using microneurographic techniques. Methods: In a balanced, double-blind cross-over design oxytocin or placebo was administered intranasally to 12 lean healthy males (age 25±4 years). MSNA was assessed microneurographically before (pre), 30-45 (post-I) and 105-120 minutes (post-II) after oxytocin administration. Baroreflex was challenged via graded infusions of vasoactive drugs and correlation of BP with MSNA and heart rate (HR) defined baroreflex function. Experiments were conducted in the afternoon after a 5h fasting period. Results: After oxytocin, resting MSNA (burst rate and total activity) showed significant net-increases from pre to post-II compared to placebo (∆-increase: +4.3±1.2 (oxytocin) vs. +2.2±1.4 burst/min (placebo), ANOVA p<0.05; total activity 184±11.5% (oxytocin) vs. 121±14.3% (placebo), ANOVA; p=0.01). This was combined with a small but significant net-increase in resting diastolic BP, while systolic and mean arterial BP or HR as well as baroreflex sensitivity at vasoactive drug challenge were not altered. Conclusion: Intranasally administered oxytocin induced vasoconstrictory sympathoactivation in healthy male humans. The concomitant increase of diastolic BP was most likely attributable to increased vascular tone. This suggests oxytocin-mediated upward resetting of the vascular baroreflex setpoint at centers superordinate to the mere baroreflex-feedback-loop.

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