scholarly journals A framework for using signal, noise, and variation to determine whether the brain controls movement synergies or single muscles

2014 ◽  
Vol 111 (4) ◽  
pp. 733-745 ◽  
Author(s):  
Mati Joshua ◽  
Stephen G. Lisberger
Keyword(s):  
Eye Movements ◽  
Brain Stem ◽  
Eye Movement ◽  
Motor Behavior ◽  
Neural Firing ◽  
Abducens Nucleus ◽  
Pursuit Initiation ◽  
Sources Of Variation ◽  
Two Measures ◽  
The Brain

We have used an analysis of signal and variation in motor behavior to elucidate the organization of the cerebellar and brain stem circuits that control smooth pursuit eye movements. We recorded from the abducens nucleus and identified floccular target neurons (FTNs) and other, non-FTN vestibular neurons. First, we assessed neuron-behavior correlations, defined as the trial-by-trial correlation between the variation in neural firing and eye movement, in brain stem neurons. In agreement with prior data from the cerebellum, neuron-behavior correlations during pursuit initiation were large in all neurons. Second, we asked whether movement variation arises upstream from, in parallel to, or downstream from a given site of recording. We developed a model that highlighted two measures: the ratio of the SDs of neural firing rate and eye movement (“ SDratio”) and the neuron-behavior correlation. The relationship between these measures defines possible sources of variation. During pursuit initiation, SDratio was approximately equal to neuron-behavior correlation, meaning that the source of signal and variation is upstream from the brain stem. During steady-state pursuit, neuron-behavior correlation became somewhat smaller than SDratio for FTNs, meaning that some variation may arise downstream in the brain stem. The data contradicted the model's predictions for sources of variation in pathways that run parallel to the site of recording. Because signal and noise are tightly linked in motor control, we take the source of variation as a proxy for the source of signal, leading us to conclude that the brain controls movement synergies rather than single muscles for eye movements.

Overlap of Saccadic and Pursuit Eye Movement Systems in the Brain Stem Reticular Formation

2001 ◽  
Vol 86 (6) ◽  
pp. 3056-3060 ◽  
Author(s):  
Yi-Jun Yan ◽  
Dong-Mei Cui ◽  
James C. Lynch
Keyword(s):  
Eye Movements ◽  
Brain Stem ◽  
Eye Movement ◽  
Saccadic Eye Movements ◽  
Point Of View ◽  
Medial Longitudinal Fasciculus ◽  
Frontal Eye Field ◽  
Neural Pathways ◽  
Eye Field ◽  
The Brain

Recent physiological studies have suggested that there are several sites of interaction between the neural pathways that control saccadic eye movements and those that control visual pursuit movements. To address the question of saccade/pursuit interaction from a neuroanatomical point of view, we have studied the connections from the smooth and saccadic eye movement subregions of the frontal eye field (FEFsem and FEFsac, respectively) to the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) in four Cebus apella monkeys. The riMLF has traditionally been considered to be a premotor center for vertical saccadic eye movements on the basis of single neuron recording experiments, microstimulation experiments, and surgical or chemical lesion experiments. We localized the functional subregions of the FEF with the use of low-threshold (≤50 μA) intracortical microstimulation. Biotinylated dextran amine or lectin from triticum vulgaris (wheat germ), peroxidase labeled, was placed into these functionally defined subregions to label anterogradely the terminals of axons that originated in the FEF. Our results demonstrate that both the FEFsem and FEFsac send direct projections to the ipsilateral riMLF. The distribution and density of labeling from the FEFsem are comparable to those from the FEFsac. The direct FEFsem-to-riMLF projection suggests a possible role of the riMLF in smooth pursuit eye movements and supports the hypothesis that there is interaction between the saccadic and pursuit subsystems at the brain stem level.

Loss of the neural integrator of the oculomotor system from brain stem lesions in monkey

1987 ◽  
Vol 57 (5) ◽  
pp. 1383-1409 ◽  
Author(s):  
S. C. Cannon ◽  
D. A. Robinson
Keyword(s):  
Eye Movements ◽  
Brain Stem ◽  
Eye Movement ◽  
Time Constant ◽  
Total Darkness ◽  
Eye Position ◽  
Neural Integrator ◽  
Head Velocity ◽  
Prepositus Hypoglossi ◽  
The Brain

Eye movement were recorded from four juvenile rhesus monkeys (Macaca mulatta) before and after the injection of neurotoxins (kainate or ibotenate) in the region of the medial vestibular and prepositus hypoglossi nuclei, an area hypothesized to be the locus of the neural integrator for horizontal eye movement commands. Eye movements were measured in the head-restrained animal by the magnetic field/eye-coil method. The monkeys were trained to follow visual targets. A chamber implanted over a trephine hole in the skull permitted recordings to be made in the brain stem with metal microelectrodes. The abducens nuclei were located and used as a reference point for subsequent neurotoxin injections through cannulas. The effects of these lesions on fixation, vestibuloocular and optokinetic responses, and smooth pursuit were compared with predicted oculomotor anomalies caused by a loss of the neural integrator. Kainate and ibotenate did not create permanent lesions in this region of the brain stem. All the eye movements returned toward normal over the course of a few days to 2 wk. Histological examination revealed that the cannula tips were mainly located between the vestibular and prepositus hypoglossi nuclei, in their rostral 2 mm, bordered rostrally by the abducens nuclei. Dense gliosis clearly demarcated the cannula tracks, but for most injections there were no surrounding regions of neuronal loss. Thus the eye movement disorders were due to a reversible, not a permanent, lesion. The time constant for the neural integrator was determined from the velocity of the centripetal drift of the eyes just after an eccentric saccade in total darkness. For intact animals this time constant was greater than 20 s. Shortly after bilateral injections of neurotoxin, the time constant began to decrease and reached a minimum of 200 ms; every horizontal saccade was followed by a rapid centripetal drift with a time constant of approximately 200 ms. For vertical eye movements, in this acute phase, the time constant was approximately 2.5 s. The vestibuloocular reflex (VOR) was drastically changed by the lesions. A step of constant head velocity in total darkness evoked a step change in eye position rather than in velocity. In the absence of the neural integrator, the step velocity command from the canal afferents was not integrated to produce a ramp of eye position (normal slow phases); rather this signal was relayed directly to the motoneurons and caused a step in eye position. The per- and postrotatory decay of the head velocity signal was decreased to 5-6 s indicating that vestibular velocity storage was also impaired.(ABSTRACT TRUNCATED AT 400 WORDS)

The Brain Stem Saccadic Burst Generator Encodes Gaze in Three-Dimensional Space

2008 ◽  
Vol 99 (5) ◽  
pp. 2602-2616 ◽  
Author(s):  
Marion R. Van Horn ◽  
Pierre A. Sylvestre ◽  
Kathleen E. Cullen
Keyword(s):  
Eye Movements ◽  
Brain Stem ◽  
Dimensional Space ◽  
Three Dimensional ◽  
Saccadic Eye Movements ◽  
Three Dimensions ◽  
Related Information ◽  
Computer Based ◽  
Different Depths ◽  
The Brain

When we look between objects located at different depths the horizontal movement of each eye is different from that of the other, yet temporally synchronized. Traditionally, a vergence-specific neuronal subsystem, independent from other oculomotor subsystems, has been thought to generate all eye movements in depth. However, recent studies have challenged this view by unmasking interactions between vergence and saccadic eye movements during disconjugate saccades. Here, we combined experimental and modeling approaches to address whether the premotor command to generate disconjugate saccades originates exclusively in “vergence centers.” We found that the brain stem burst generator, which is commonly assumed to drive only the conjugate component of eye movements, carries substantial vergence-related information during disconjugate saccades. Notably, facilitated vergence velocities during disconjugate saccades were synchronized with the burst onset of excitatory and inhibitory brain stem saccadic burst neurons (SBNs). Furthermore, the time-varying discharge properties of the majority of SBNs (>70%) preferentially encoded the dynamics of an individual eye during disconjugate saccades. When these experimental results were implemented into a computer-based simulation, to further evaluate the contribution of the saccadic burst generator in generating disconjugate saccades, we found that it carries all the vergence drive that is necessary to shape the activity of the abducens motoneurons to which it projects. Taken together, our results provide evidence that the premotor commands from the brain stem saccadic circuitry, to the target motoneurons, are sufficient to ensure the accurate control shifts of gaze in three dimensions.

Recasting the Smooth Pursuit Eye Movement System

2004 ◽  
Vol 91 (2) ◽  
pp. 591-603 ◽  
Author(s):  
Richard J. Krauzlis
Keyword(s):  
Eye Movements ◽  
Brain Stem ◽  
Smooth Pursuit ◽  
Visual Motion ◽  
Saccadic Eye Movements ◽  
Extrastriate Cortex ◽  
High Acuity ◽  
Voluntary Eye Movements ◽  
New Perspective ◽  
The Brain

Primates use a combination of smooth pursuit and saccadic eye movements to stabilize the retinal image of selected objects within the high-acuity region near the fovea. Pursuit has traditionally been viewed as a relatively automatic behavior, driven by visual motion signals and mediated by pathways that connect visual areas in the cerebral cortex to motor regions in the cerebellum. However, recent findings indicate that this view needs to be reconsidered. Rather than being controlled primarily by areas in extrastriate cortex specialized for processing visual motion, pursuit involves an extended network of cortical areas, and, of these, the pursuit-related region in the frontal eye fields appears to exert the most direct influence. The traditional pathways through the cerebellum are important, but there are also newly identified routes involving structures previously associated with the control of saccades, including the basal ganglia, the superior colliculus, and nuclei in the brain stem reticular formation. These recent findings suggest that the pursuit system has a functional architecture very similar to that of the saccadic system. This viewpoint provides a new perspective on the processing steps that occur as descending control signals interact with circuits in the brain stem and cerebellum responsible for gating and executing voluntary eye movements. Although the traditional view describes pursuit and saccades as two distinct neural systems, it may be more accurate to consider the two movements as different outcomes from a shared cascade of sensory–motor functions.

scholarly journals Time course of spatiotopic updating across saccades

2019 ◽  
Vol 116 (6) ◽  
pp. 2027-2032 ◽  
Author(s):  
Jasper H. Fabius ◽  
Alessio Fracasso ◽  
Tanja C. W. Nijboer ◽  
Stefan Van der Stigchel
Keyword(s):  
Eye Movements ◽  
Visual System ◽  
Eye Movement ◽  
Time Course ◽  
Saccadic Eye Movements ◽  
Oculomotor System ◽  
Stimulus Onset ◽  
Oculomotor Behavior ◽  
Behavioral Studies ◽  
The Brain

Humans move their eyes several times per second, yet we perceive the outside world as continuous despite the sudden disruptions created by each eye movement. To date, the mechanism that the brain employs to achieve visual continuity across eye movements remains unclear. While it has been proposed that the oculomotor system quickly updates and informs the visual system about the upcoming eye movement, behavioral studies investigating the time course of this updating suggest the involvement of a slow mechanism, estimated to take more than 500 ms to operate effectively. This is a surprisingly slow estimate, because both the visual system and the oculomotor system process information faster. If spatiotopic updating is indeed this slow, it cannot contribute to perceptual continuity, because it is outside the temporal regime of typical oculomotor behavior. Here, we argue that the behavioral paradigms that have been used previously are suboptimal to measure the speed of spatiotopic updating. In this study, we used a fast gaze-contingent paradigm, using high phi as a continuous stimulus across eye movements. We observed fast spatiotopic updating within 150 ms after stimulus onset. The results suggest the involvement of a fast updating mechanism that predictively influences visual perception after an eye movement. The temporal characteristics of this mechanism are compatible with the rate at which saccadic eye movements are typically observed in natural viewing.

scholarly journals Isolated medial longitudinal fasciculus syndrome: Review of imaging, anatomy, pathophysiology and differential diagnosis

2017 ◽  
Vol 31 (1) ◽  
pp. 95-99 ◽  
Author(s):  
Puneet S Kochar ◽  
Yogesh Kumar ◽  
Pranav Sharma ◽  
Vikash Kumar ◽  
Nishant Gupta ◽  
...  
Keyword(s):  
Differential Diagnosis ◽  
Eye Movements ◽  
Brain Stem ◽  
Medial Longitudinal Fasciculus ◽  
Rare Occurrence ◽  
Comprehensive Review ◽  
Fiber Tracts ◽  
Imaging Characteristics ◽  
The Brain

Isolated medial longitudinal fasciculus (MLF) syndrome due to infarction limited only to the midbrain is a rare occurrence. The MLF are a group of fiber tracts located in the paramedian area of the midbrain and pons. They control horizontal eye movements by interconnecting oculomotor and abducens nuclei in the brain stem. Such small infarcts can easily be overlooked by young neuroradiologists and trainees. In this review, we discuss the clinical and imaging characteristics, comprehensive review of the anatomy, pathophysiology, and differential diagnosis.

“One-and-a-Half” Syndrome after a Resection of a Midline Cerebellar Astrocytoma: Case Report and Discussion of the Literature

Neurosurgery ◽  
1991 ◽  
Vol 29 (5) ◽  
pp. 768-772 ◽  
Author(s):  
Herbert B. Newton ◽  
Michael E. Miner
Keyword(s):  
Brain Stem ◽  
Posterior Fossa ◽  
Rare Complication ◽  
Medial Longitudinal Fasciculus ◽  
Abducens Nucleus ◽  
Blurred Vision ◽  
Computed Tomographic ◽  
Truncal Ataxia ◽  
The One ◽  
The Brain

Abstract This report describes a rare complication after the resection of a tumor of the posterior fossa, the “one-and-a-half” syndrome. The one-and-a-half syndrome is a disturbance of horizontal eye movements in which patients have lateral gaze palsy in one direction and internuclear ophthalmoplegia in the other direction. The patient was a 54-year-old woman who developed headaches, diplopia, and blurred vision over 6 months. Computed tomographic scans and magnetic resonance imaging demonstrated an enhancing, mixed density, midline mass of the cerebellum. After a resection of the mass, an anaplastic astrocytoma, the patient complained of more severe diplopia and facial weakness. An examination disclosed a left one-and-a-half syndrome, left peripheral facial paralysis, dysarthria, dysphagia, mild left hemiparesis, dysmetria of the left upper limb, and truncal ataxia. The brain stem showed no abnormalities on postoperative computed tomographic scans. After 4 months of follow-up, the one-and-a-half syndrome had not improved, even though other signs had improved or resolved. This syndrome is caused by damage to structures within the pontine tegmentum: the medial longitudinal fasciculus, the ipsilateral paramedian pontine reticular formation, or the ipsilateral abducens nucleus. Multiple sclerosis and brain stem infarctionn are the most common causes of the one-and-a-half syndrome. Less frequently, it is caused by primary and metastatic tumors of the brain stem and cerebellum. Rarely, the one-and-a-half syndrome can develop postoperatively after the removal of tumors of the posterior fossa. The mechanism of pontine tegmental injury remains unknown.

scholarly journals Signal analysis of sleep electrooculogram

2021 ◽  
Author(s):  
Peyman Shokrollahi
Keyword(s):  
Eye Movements ◽  
Wavelet Analysis ◽  
Eye Movement ◽  
Discrete Wavelet ◽  
Linear Discriminant ◽  
Antidepressant Medications ◽  
Disease States ◽  
Movement Data ◽  
Sleep Physiology ◽  
The Brain

Measures of sleep physiology, not obvious to the human eye, may provide important clues to disease states, and responses to therapy. A significant amount of eye movement data is not attended to clinically in routine sleep studies because these data are too long, about six to eight hours in duration, and they are also mixed with many unknown artifacts usually produced from EEG signals or other activities. This research describes how eye movements were different in depressed patients who used antidepressant medications, compared to those who did not. The goal is to track antidepressant medications effects on sleep eye movements. Clinically used SSRIs such as Prozac (Fluoxetine), Celexa (Citalopram), Zoloft (Sertraline), the SNRI Effexor (Venlafaxine) have been considered in this study to assess the possible connections between eye movements recorded during sleep and serotonin activities. The novelty of this research is in the assessment of sleep eye movement, in order to track the antidepressant medications' effect on the brain through EOG channels. EOG analysis is valuable because it is a noninvasive method, and the following research is looking for findings that are invisible to the eyes of professional clinicians. This thesis focuses on quantifying sleep eye movements, with two techniques: autoregressive modeling and wavelet analysis. The eye movement detection software (EMDS) with more than 1500 lines was developed for detecting sleep eye movements. AR coefficients were derived from the sleep eye movements of the patients who were exposed to antidepressant medications, and those who were not, and then they are classified by means of linear discriminant analysis. also for wavelet analysis, discrete wavelet coefficients have been used for classifying sleep eye movements of the patients who were exposed to medication and those who were not.

scholarly journals Signal analysis of sleep electrooculogram

2021 ◽  
Author(s):  
Peyman Shokrollahi
Keyword(s):  
Eye Movements ◽  
Wavelet Analysis ◽  
Eye Movement ◽  
Discrete Wavelet ◽  
Linear Discriminant ◽  
Antidepressant Medications ◽  
Disease States ◽  
Movement Data ◽  
Sleep Physiology ◽  
The Brain

Measures of sleep physiology, not obvious to the human eye, may provide important clues to disease states, and responses to therapy. A significant amount of eye movement data is not attended to clinically in routine sleep studies because these data are too long, about six to eight hours in duration, and they are also mixed with many unknown artifacts usually produced from EEG signals or other activities. This research describes how eye movements were different in depressed patients who used antidepressant medications, compared to those who did not. The goal is to track antidepressant medications effects on sleep eye movements. Clinically used SSRIs such as Prozac (Fluoxetine), Celexa (Citalopram), Zoloft (Sertraline), the SNRI Effexor (Venlafaxine) have been considered in this study to assess the possible connections between eye movements recorded during sleep and serotonin activities. The novelty of this research is in the assessment of sleep eye movement, in order to track the antidepressant medications' effect on the brain through EOG channels. EOG analysis is valuable because it is a noninvasive method, and the following research is looking for findings that are invisible to the eyes of professional clinicians. This thesis focuses on quantifying sleep eye movements, with two techniques: autoregressive modeling and wavelet analysis. The eye movement detection software (EMDS) with more than 1500 lines was developed for detecting sleep eye movements. AR coefficients were derived from the sleep eye movements of the patients who were exposed to antidepressant medications, and those who were not, and then they are classified by means of linear discriminant analysis. also for wavelet analysis, discrete wavelet coefficients have been used for classifying sleep eye movements of the patients who were exposed to medication and those who were not.

scholarly journals Challenges when diagnosing locked-in syndrome following TBI: The Story of U.P. a Clinical Puzzle

2019 ◽  
Vol 4 (3) ◽  
Keyword(s):  
Eye Movements ◽  
Brain Stem ◽  
Language Therapy ◽  
Verbal Responses ◽  
Complete Paralysis ◽  
Traumatic Subarachnoid Haemorrhage ◽  
Eye Movement Tracking ◽  
Cognitive Problems ◽  
The Brain ◽  
Movement Tracking

Background and aims: Locked-in syndrome (LIS) is a rare neurological disorder; patients with LIS are awake, conscious with normal or nearly normal cognitive functioning. They cannot produce speech, facial or limb movements with complete paralysis of all voluntary muscles except for those controlling eye movements. LIS is associated with lesions of the brain stem and the pons, with 60% of people having sustained a stroke. LIS following traumatic brain injury (TBI) is rare; brain stem lesion plus cortical damage makes diagnosis of LIS challenging. Method: We describe U.P, a 42 year old man who sustained a TBI. A CT scan showed traumatic subarachnoid haemorrhage with a pre-pontine bleed. Awake, conscious, presenting with right sided paralysis and severe left sided paresis;U.P could produce voluntary horizontal eye movement, tracking people and stimuli of interest. Vertical eye movements emerged later, reading simple instructions and following commands. Results: U.P could use eyebrow movements for “yes” and a slight head shake for “no”. He could read some written instructions; non-verbal responses were inconsistent and sometimes unreliable. Discussion: Based on assessments from speech and language therapy and neuropsychology with U.P, we discuss LIS plus additional cognitive problems and the difficulties with diagnosing LIS following TBI.

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