Initiation Of Saccadic Eye Movements Research Articles

MEMORY-CONTINGENT SACCADES AND THE SUBSTANTIA NIGRA POSTULATE FOR ESSENTIAL BLEPHAROSPASM

Essential blepharospasm and cranial dystonia are related focal dystonias of unknown aetiology. Blepharospasm induced by acute dopamine depletion in parkinsonism restricts saccade initiation possibly via the substantia nigra pars reticulata (SNpr). If essential blepharospasm and cranial dystonia similarly restrict saccades, then a selective, somatotopically arranged pathway such as the SNpr may be involved. To test this possibility memory-contingent and visually-guided saccades were measured in patients with essential blepharospasm and cranial dystonia. The latency of both forms of saccades was either significantly prolonged or excessively variable, while the accuracy and peak velocity of these fast eye movements were similar to age-matched control subjects. Essential blepharospasm and cranial dystonia alter the initiation of saccadic eye movements. Subcortical brain regions or pathways where eyelid, saccade and cranial/cervical motor control are somatotopically approximated, such as the SNpr, may be involved in blepharospasm.

Gaze-related activity of brainstem omnipause neurons during combined eye-head gaze shifts in the alert cat

Studies undertaken in head-restrained animals have long implicated the omnipause neurons (OPNs) in the initiation of saccadic eye movements. These inhibitory neurons discharge tonically but cease firing just before and during saccades in all directions. By recording from OPNs in alert behaving head-unrestrained cats, we have demonstrated that the activity of these cells is related to the displacement of the visual axis in space (gaze), which is the sum of the eye movement relative to the head and head movement relative to space. OPNs were found to exhibit a complete cessation of discharge for a period equivalent to the duration of the gaze shift, and not to the duration of either the rapid eye movement or the head movement components. In large gaze shifts, OPNs were silent even when the eye was immobile in the orbit, as long as the gaze shift was not completed. The results of this study show that OPNs are controlled by neural elements that take into account the actual position of the visual axis relative to its final desired position irrespective of the trajectory of the eye in the orbit or of whether the head is moving or not.

Saccadic eye movements following kainic acid lesions of the pulvinar in monkeys

Behavioral and anatomical experiments have suggested that the pulvinar might play a role in the generation of saccadic eye movements to visual targets. To test this idea, we trained monkeys to make visually-guided saccades by requiring them to detect the dimming of a small target. We used three different saccade paradigms. On single-step trials, saccades were made from a central fixation point (FP) to a target at 12, 24 or 36 degrees to the left or right. On overlap trials, the FP remained lit during presentation of a target at 12 or 24 degrees. On double-step trials, the target stepped first to 24 degrees, and then back to 12 degrees on the same side. Animals were trained to criterion, received kainic acid lesions of the pulvinar, and were retested on all three tasks. The lesions were very large, destroying almost all of the visually responsive pulvinar. They also encroached on the lateral geniculate nucleus, thereby producing small foveal scotomas, and this resulted in some behavioral changes, including difficulty in maintaining fixation on the target and in detecting its dimming. Results on the saccade tests suggest that the pulvinar is not crucial for initiation of saccadic eye movements. Saccade latency and amplitude were unimpaired on both single-step and overlap trials. Saccadic performance was also normal on double-step trials. In a second experiment, we measured the average length of fixations during spontaneous viewing of a complex visual scene. Fixation lengths did not differ from those of unoperated control monkeys. We suggest that the neglect, increased saccadic latencies, and prolonged fixations attributed to pulvinar damage in previous studies were probably the result instead of inadvertent damage to tectal afferents. The present results, together with single unit data, point to a role for the pulvinar not in the generation of saccades, but rather in the integration of saccadic eye movements with visual processing.

Mechanisms of visual attention revealed by saccadic eye movements

This paper summarizes recent data on the initiation of saccadic eye movement in relation to the mechanisms of visual attention. In particular, the occurrence of express saccades, defined by their extremely short reaction times, is discussed on the basis of the observation that these saccades do not occur when the subjects (man or monkey) are attending to either a fixation point or to any other visual stimulus in the periphery of their field of view including the “future” saccade target location. It is concluded that the system of visual attention can be in two states: engaged or disengaged. In order to generate a saccade or to move attention from one point to another visual attention must be in the disengaged state. The disengagement takes some time which is or is not included in the saccadic reaction time depending on whether or not visual attention is engaged at the time of the onset of the saccade target. During engaged visual attention saccades are inhibited thereby providing steady central fixation or the absence of saccades during directed peripheral attention.

Saccadic eye movements following injection of lidocaine into the superior colliculus.

Ablation of the superior colliculus (SC) has generally produced limited deficits in the initiation of saccadic eye movements, usually an increase in the latency of saccades. However, recent studies using muscimol, a GABA agonist, to block afferents to the SC showed deficits in not only latency but in amplitude and velocity of saccades as well. These greater deficits might be dependent upon the testing of saccades shortly after the damage of SC before any compensation for the deficits could develop. The present experiments tested this hypothesis by injecting a local anesthetic into SC. The anesthetic inactivated the cells entirely rather than just deafferenting them, but still allowed testing immediately after the injection. Clear deficits were observed following injection of lidocaine into the SC. The amplitudes of saccades to visual targets were shortened, and the peak velocities of the saccades were reduced even if the reduced amplitude of the saccades was taken into account. Latency of saccades usually increased. The deficits were limited to the area of the visual field that overlapped the movement fields of the cells near the injection site. If the movement fields were in the periphery, saccades to the periphery were shortened following the injection of lidocaine. If the movement fields were near the center of gaze, saccades into the area were shortened, but the monkey was able to make saccades over the visual field related to the affected area to more peripheral targets.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of the basal ganglia in the initiation of saccadic eye movements

The impetus for the study of the basal ganglia in relation to vision and eye movements comes from what one know about the connection of this structure to the superior colliculus (SC), a structure recognized as a critical station for the initiation of saccadic eye movements. One output pathway of the basal ganglia, the pars reticulata of the substantia nigra (SNr), projects to the intermediate layers of the SC. These cells in the intermediate layers discharge before saccadic eye movements when those eye movements are directed to one region of the visual field, the movement field of the cells. Stimulation of these intermediate layer cells leads to the initiation of saccadic eye movements to the area of movement field of the adjacent cells. Finally, cells in the intermediate layers of the SC have direct projections to the brainstem areas (mesencephalic reticular formation, MRF; paramedian pontine reticular formation, PPRF) where pre-oculomotor neurons are located. The SNr projection to the SC represents one of the most prominent inputs to the intermediate layers of the SC. This chapter is intended to summarize those aspects of the experiments that are related to the initiation of saccadic eye movements. After describing the general characteristics of cells in the SNr, the chapter considers a particular type of cell that discharges in relation to the initiation of saccades made to remembered targets.

Selection of visual targets for the initiation of saccadic eye movements

When a monkey uses a visual stimulus falling in the receptive field of a cell in one of the superficial layers of the superior colliculus as the target for a saccade, the response of the cell to that stimulus is frequently enhanced. The effect is selective; eye movements to other parts of the visual field are not associated with the enhancement. The selective enhancement is related to the superior colliculus and is not found in striate cortex. The selective enhancement is therefore a property of the superior colliculus branch of the visual system and is not simply a reflection of activity in the geniculo-cortical system. The enhancement in the colliculus is clear when the monkey responds to the stimulus with an eye movement to the stimulus but not when it responds with a hand movement. The enhancement is therefore dependent on the type of response made to the stimulus and is possibly specifically related to eye movements.