Saccadic Pathway Research Articles

Evidence for the differential efficacy of yaw and pitch gaze stabilization mechanisms in people with multiple sclerosis.

People with multiple sclerosis (PwMS) who report dizziness often have gaze instability due to vestibulo-ocular reflex (VOR) deficiencies and compensatory saccade (CS) abnormalities. Herein, we aimed to describe and compare the gaze stabilization mechanisms for yaw and pitch head movements in PwMS. Thirty-seven PwMS (27 female, mean ± SD age = 53.4 ± 12.4 years old, median [IQR] Expanded Disability Status Scale Score = 3.5, [1.0]. We analyzed video head impulse test results for VOR gain, CS frequency, CS latency, gaze position error (GPE) at impulse end, and GPE at 400 ms after impulse start. Discrepancies were found for median [IQR] VOR gain in yaw (0.92 [0.14]) versus pitch-up (0.71 [0.44], p < 0.001) and pitch-down (0.81 [0.44], p = 0.014]), CS latency in yaw (258.13 [76.8]) ms versus pitch-up (208.78 [65.97]) ms, p = 0.001] and pitch-down (132.17 [97.56] ms, p = 0.006), GPE at impulse end in yaw (1.15 [1.85] degs versus pitch-up (2.71 [3.9] degs, p < 0.001), and GPE at 400 ms in yaw (-0.25 [0.98] degs) versus pitch-up (1.53 [1.07] degs, p < 0.001) and pitch-down (1.12 [1.82] degs, p = 0.001). Compared with yaw (0.91 [0.75]), CS frequency was similar for pitch-up (1.03 [0.93], p = 0.999) but lower for pitch-down (0.65 [0.64], p = 0.023). GPE at 400 ms was similar for yaw and pitch-down (1.88 [2.76] degs, p = 0.400). We postulate that MS may have preferentially damaged the vertical VOR and saccade pathways in this cohort.

Speed-accuracy tradeoffs influence the main sequence of saccadic eye movements

Several studies have proposed that an optimal speed-accuracy tradeoff underlies the stereotyped relationship between amplitude, duration and peak velocity of saccades (main sequence). To test this theory, we asked 8 participants to make saccades to Gaussian-blurred spots and manipulated the task’s accuracy constraints by varying target size (1, 3, and 5°). The largest targets indeed yielded more endpoint scatter (and lower gains) than the smallest targets, although this effect subsided with target eccentricity. The main sequence depended on several interacting factors: saccade latency, saccade gain and target size. Early saccades, which were faster than amplitude-matched late saccades, followed the target-size dependency one would expect from a speed-accuracy tradeoff process. They had higher peak velocities and shorter durations for larger targets than for smaller targets. For late saccades, however, the opposite was found. Deviations from the main sequence also covaried with saccade gain, in line with the idea that motor noise underlies part of the endpoint variability. Thus, our data provide partial evidence that the saccadic system weighs the detrimental effects of motor noise on saccade accuracy against movement duration and speed, but other factors also modulate the kinematics. We discuss the possible involvement of parallel saccade pathways to account for our findings.

Diffusion imaging fibre tractographic analysis for auditory saccadic attention deficit (ASAD) in progression stages of Alzheimer's disease

Introduction The ability of human beings to perceive auditory stimulus in everyday acoustic environments depends on the localization and the identification of relevant sounds. Localization (or) the spatial orientation of the stimulus and relative motor output with saccadic eye and neck movements is analyzed by the tract from Auditory cortex (BA-41, 42) to Premotor Eye-Ear Field [PEEF] (BA-8b), called Auditory-saccadic pathway. Our study aimed on comparative analysis of this pathway in control adults with Alzheimer's Patients, using “Diffusion Imaging fibre Tractography”. We used 60 Diffusion Tensor Imaging (DTI) datasets (30 Males and 30 Females), between the age ranges from 55 to 100 yrs. Results Study reveals that, Bi-hemispheric deterioration of auditory saccadic pathway fibers were observed in females with AD, as compared to males. Whereas the auditory saccadic fibers are markedly increases in disease progression stages of males AD. Conclusion Present study proves the existence of neurostructural connectivity of Auditory-saccadic pathway (dorsal stream-auditory pathway) and the deterioration of this track leads to cause of Auditory saccadic attention deficit (ASAD) in Alzheimer's Patients. But, the results must to strongly evidence with functional and efficient connectivity analysis in future.

A model-based theory on the signal transformation for microsaccade generation

The eyes are continuously fluctuating even during fixation. The fluctuations are called miniature eye movements and consist of microsaccades, drifts, and tremors. It has been revealed that these miniature eye movements aid our vision; they improve the visibility of high spatial frequency components, and prevent retinal adaptation during fixation. Although the functional roles of the miniature eye movements have gradually been uncovered, their generation mechanism remains a mystery. Here, we focused on microsaccades, and constructed a neuronal network model to explore their generation mechanism. Several lines of evidence ensure that microsaccades and saccades share the same neuronal circuitry because they fall on the same main sequence, a relationship between their amplitudes and peak velocities. In the saccade pathway, saccade commands generated in the superior colliculus are relayed to motoneurons via burst neurons (BNs) and the integrator network. The BNs are inhibited by omnipause neurons (OPNs) except when saccades are generated. We configured a model for microsaccades based on the well-defined saccade neuronal pathway including tonic neurons, BNs, OPNs, the integrator network, and the eye plant. The model successfully reproduced various characteristics of microsaccade: square-wave jerk, single-sided microsaccades, and the main sequence. Moreover, during microsaccades, BNs showed low-rate spikes due to a partial release from the OPN inhibition. These results suggest that microsaccades are generated when BNs are partially, but not completely, released from tonic inhibition by OPNs during fixation, in contrast to the generation of ordinary saccades in which OPNs pause firing and release BNs from their strong inhibition.

Identifying sites of saccade amplitude plasticity in humans: transfer of adaptation between different types of saccade

To view different objects of interest, primates use fast, accurate eye movements called saccades. If saccades become inaccurate, the brain adjusts their amplitudes so they again land on target, a process known as saccade adaptation. The different types of saccades elicited in different behavioral circumstances appear to utilize different parts of the oculomotor circuitry. To gain insight into where adaptation occurs in different saccade pathways, we adapted saccades of one type and examined how that adaptation affected or transferred to saccades of a different type. If adaptation of one type of saccade causes a substantial change in the amplitude of another, that adaptation may occur at a site used in the generation of both types of saccade. Alternatively, if adaptation of one type of saccade transfers only partially, or not at all, to another, adaptation occurs at least in part at a location that is not common to the generation of both types of saccade. We produced significant amplitude reductions in memory-guided, delayed, targeting and express saccades by moving the target backward during the saccade. After memory-guided saccades were adapted, the amplitude of express, targeting and delayed saccades exhibited only a partial reduction. In contrast, when express, targeting, or delayed saccades were adapted, amplitude transfer to memory-guided saccades was more substantial. These results, combined with previously published data, suggest that there are at least two sites of adaptation within the saccadic system. One is used communally in the generation of express, targeting, delayed and memory-guided saccades, whereas the other is specific for the generation of memory-guided saccades.

Oculomotricity parameters in digital nystagmography among children with and without learning disorders

The saccadic pathway involves numerous regions of the brain cortex, the cerebellum and the brainstem. Saccadic movement latency, velocity and precision parameters assess the efficacy of central nervous system (CNS) control over rapid eye movements. Very few disorders which alter the CNS are missed when these parameters are carefully measured using a computer. Pendular tracking assesses the integrity of the oculomotor system in controlling slow eye movements - vulnerable to CNS and vestibular system dysfunctions. Optokinetic nystagmus represents a stereoceptive response which compensates environment movements by psycho-optical inputs. AIMS: to compare the oculomotricity values found in children with and without learning complaints. MATERIALS AND METHODS: prospective study. We included in the study 28 children of both genders, within the age range between 8 and 12 years, with learning disorders (study group) and 15 without (control group). We carried out the fixed and randomized saccadic movement tests, pendular tracking study and optokinetic nystagmus. RESULTS: There was a statistically significant difference between the groups concerning the randomized saccadic movement velocity parameters and in the pendular tracking test. CONCLUSION: The children with learning disorders presented alterations in some oculomotricity tests when compared to children without complaints.

Oculomotricity parameters in digital nystagmography among children with and without learning disorders

SummaryThe saccadic pathway involves numerous regions of the brain cortex, the cerebellum and the brainstem. Saccadic movement latency, velocity and precision parameters assess the efficacy of central nervous system (CNS) control over rapid eye movements. Very few disorders which alter the CNS are missed when these parameters are carefully measured using a computer. Pendular tracking assesses the integrity of the oculomotor system in controlling slow eye movements - vulnerable to CNS and vestibular system dysfunctions. Optokinetic nystagmus represents a stereoceptive response which compensates environment movements by psycho-optical inputs.Aimsto compare the oculomotricity values found in children with and without learning complaints.Materials and Methodsprospective study. We included in the study 28 children of both genders, within the age range between 8 and 12 years, with learning disorders (study group) and 15 without (control group). We carried out the fixed and randomized saccadic movement tests, pendular tracking study and optokinetic nystagmus.ResultsThere was a statistically significant difference between the groups concerning the randomized saccadic movement velocity parameters and in the pendular tracking test.ConclusionThe children with learning disorders presented alterations in some oculomotricity tests when compared to children without complaints.

What is adapted in saccadic adaptation?

What is adapted in saccadic adaptation?

Effect of Pharmacological Inactivation of Nucleus Reticularis Tegmenti Pontis on Saccadic Eye Movements in the Monkey

The superior colliculus (SC) provides signals for the generation of saccades via a direct pathway to the brain stem burst generator (BG). In addition, it sends saccade-related activity to the BG indirectly through the cerebellum via a relay in the nucleus reticularis tegmenti pontis (NRTP). Lesions of the oculomotor vermis, lobules VIc and VII, and inactivation of the caudal fastigial nucleus, the cerebellar output nucleus to which it projects, produce saccade dysmetria but have little effect on saccade peak velocity and duration. We expected similar deficits from inactivation of the NRTP. Instead, injections as small as 80 nl into the NRTP first slowed ipsiversive saccades and then gradually reduced their amplitudes. Postinjection saccades had slower peak velocities and longer durations than preinjection saccades with similar amplitudes. Contraversive saccades retained their normal kinematics. When the gains of ipsiversive saccades to 10 degrees target steps had fallen to their lowest values (0.28 +/- 0.19; mean +/- SD; n = 10 experiments), the gains of contraversive saccades to 10 degrees target steps had decreased very little (0.82 +/- 0.11). Eventually, ipsiversive saccades did not exceed 5 degrees , even to 20 degrees target steps. Moreover, these small remaining saccades apparently were made with considerable difficulty because their latencies increased substantially. When ipsiversive saccade gain was at its lowest, the gain and kinematics of vertical saccades to 10 degrees target steps exhibited inconsistent changes. We argue that our injections did not compromise the direct SC pathway. Therefore these data suggest that the cerebellar saccade pathway does not simply modulate BG activity but is required for horizontal saccades to occur at all.

Saccade-related activity in the parietal reach region.

In previous experiments, we showed that cells in the parietal reach region (PRR) in monkey posterior parietal cortex code intended reaching movements in an eye-centered frame of reference. These cells are more active when an arm compared with an eye movement is being planned. Despite this clear preference for arm movements, we now report that PRR neurons also fire around the time of a saccade. Of 206 cells tested, 29% had perisaccadic activity in a delayed-saccade task. Two findings indicate that saccade-related activity does not reflect saccade planning or execution. First, activity is often peri- or postsaccadic but seldom presaccadic. Second, cells with saccade-related activity were no more likely to show strong saccadic delay period activity than cells without saccade-related activity. These findings indicate that PRR cells do not take part in saccade planning. Instead, the saccade-related activity in PRR may reflect cross-coupling between reach and saccade pathways that may be used to facilitate eye-hand coordination. Alternatively, saccade-related activity may reflect eye position information that could be used to maintain an eye-centered representation of intended reach targets across eye movements.

Monocular and binocular mechanisms in saccade generation

The target article retains the traditional account of saccades as conjugate eye movements. However, recent single-unit recordings of premotor cells in the saccade pathway (excitatory burster neurons [EBNs]) found that they do not encode conjugate eye velocity, but rather, monocular eye velocity. These data argue against the traditional concept of saccades as inherently conjugate. Instead, they suggest a monocular mechanism in the sensorimotor transformation stage of saccade generation. This commentary will discuss the implications of these data for the saccade generation model proposed in Findlay &amp; Walker's target article.

Geotropic ocular deviation with skew and absence of saccade in Creutzfelt-Jackob disease

Three patients with Creutzfelt-Jakob disease (CJD) showed characteristic ocular manifestations. The head was turned left or right with the eyes deviated downward and skewed. When the head was turned to one side, the eyes very slowly deviated to that side. In addition, spontaneous ocular movements were very slow with no saccadic component early in the apathetic stage. Caloric stimulation produced tonic deviation to the appropriate side without nystagmus. At autopsy one patient showed lesions compatible with the panencephalopathic type of CJD. Although bilateral pretectal areas had marked gliosis, other nuclei and structures associated with oculomotor system in the brainstem, including the oculomotor, trochlear, abducens, vestibular and perihypoglossal nuclei, medial longitudinal fasciculus and para-median pontine reticular formation were preserved. These patients had a supranuclear disorder, probably caused by combined disruption of the direct and indirect frontal eye field to the brainstem pathways plus impairment of the superior colliculus-mediated saccade pathways.