Compensatory Saccades Research Articles

Eye tracking dysfunction and schizophrenia: an overview with special reference to the genetics of schizophrenia

A high prevalence of eye tracking dysfunction (ETD) among schizophrenic patients and their relatives is one of the most widely replicated findings in experimental psychopathology. Almost 25 years of research have shown the following: (1) ETD occurs in about half of schizophrenics, and is not a function of psychotic state, inattention or neuroleptic drug treatment; (2) ETD involves primarily an impairment of smooth pursuit eye movements, characterized by reduced gain and increased compensatory saccades; (3) ETD also occurs in a substantial proportion of unaffected first-degree relatives of schizophrenics, including clinically discordant co-twins of schizophrenics, suggesting that ETD is under genetic control; (4) the prevalence of ETD in relatives of schizophrenics is higher than the recurrence risk for schizophrenia. ETD is one of several traits associated with schizophrenia and genetically related to schizophrenia. The use of co-familial traits like ETD, in addition to schizophrenia, increases the power of linkage studies to find a gene(s) for schizophrenia compared with conventional methods of linkage analysis, which use only the presence of the schizophrenic psychosis as the phenotype.

“Torso Rotation” Experiments; 1: Adaptation to Motion Sickness does not Correlate with Changes in VOR Gain

Following a 30-minute exposure to an unusual motor strategy called "Torso Rotation" (TR), the signs and symptoms of motion sickness appear along with perceptual illusions during movement, gaze and postural instability, and a significantly reduced vestibulo-ocular response (VOR) gain. With repeated exposure to TR, the motion sickness disappears and gaze instability seems to be reduced. Is this apparent improvement in gaze stability associated with a reduction of the transient change in VOR gain? Motion sickness (subjective questionnaire) and VOR gain (passive step rotations in darkness) were measured before and repeatedly after TR on 7 consecutive days. Despite a complete loss of symptoms in 3 to 4 days, the transient, daily change in VOR gain remained unaffected. Furthermore, there was no increase in the use of compensatory saccades. It is concluded that adaptation to TR-induced motion sickness is not the result of a change in VOR's sensitivity to TR.

Compensatory saccades made to remembered targets following orbital displacement by electrically stimulating the dorsomedial frontal cortex or frontal eye fields of primates

If the eye-position signal during visually-evoked saccades is dependent on the dorsomedial frontal cortex (DMFC), one would expect that saccades generated to briefly presented visual targets would be disrupted after displacement of the eyes via electrical stimulation of this cortical area. Compared are compensatory saccades evoked to brief targets following stimulation of the DMFC and frontal eye fields (FEF). Compensatory saccades produced to brief targets following perturbation via the DMFC were not affected. Accordingly, electrical stimulation of the DMFC does not disrupt the eye-position signal during the execution of visually-evoked saccades.

Compensatory saccades made to remembered targets following orbital displacement by electrically stimulating the dorsomedial frontal cortex or frontal eye fields of primates

Compensatory saccades made to remembered targets following orbital displacement by electrically stimulating the dorsomedial frontal cortex or frontal eye fields of primates

Smooth pursuit performance in patients with affective disorders or schizophrenia and normal controls: analysis with specific oculomotor measures, RMS error and qualitative ratings

Smooth pursuit performance in schizophrenia and affective disorders has generally been found to be abnormal using a variety of measures. The purpose of this study was to assess patients with these disorders and normal controls in order to compare the different measures across diagnoses. Smooth pursuit was assessed using quantitative specific measures (gain, catch-up saccade rate and amplitude, square-wave jerk rate, number of anticipatory saccades and total time scored), as well as two global measures: root mean-square error (RMS) and qualitative rating. As previously reported, patients with schizophrenia had low gain, increased catch-up saccade rate and spent less time engaged in scoreable smooth pursuit than normal controls. Patients with affective disorders were not statistically different from controls on any of these measures, and had significantly higher gain than patients with schizophrenia. RMS error and qualitative rating measures were highly correlated (r = 0.87). In linear regression analyses, the quantitative specific measures were highly significant predictors of both RMS error and qualitative ratings (P < 0.0001). Linear regression analyses and a modelling study indicated that one quantitative specific measure, the percent of time engaged in scoreable smooth pursuit (total time scored), was most related to global ratings. However, RMS error and qualitative ratings were less sensitive than total time scored to the difference between controls and patients with schizophrenia. These data indicate two smooth pursuit performance deficits in schizophrenia: patients spend less time engaged in scoreable smooth pursuit and have low gain (accompanied by increased compensatory saccades) when the smooth pursuit is engaged.

The extraretinal signal from the pursuit-eye-movement system: Its role in the perceptual and the egocentric localization systems

The accuracy of perceptual judgment of the distance of a moving target tracked at various velocities by pursuit eye movements was examined in relation to the amount of two types of eye movement (smooth pursuit eye movement and compensatory saccade) involved in eye tracking. The perceptually judged distance became shorter as the amount of pursuit-eye-movement component in eye tracking increased. A detailed analysis of the eye-movement data and the size of perceptual underestimation indicated that the underestimation was mainly caused by inaccurate extraretinal information derived from the pursuit-eye-movement system, which underestimated the distance at a constant ratio, irrespective of the velocity of tracking. Egocentric localization was not affected by the mode of eye movements, indicating that the egocentric localization system functions without interference from the inaccurate information from the pursuit-eye-movement system.

Contribution of the otoliths to the calculation of linear displacement.

1. The present work is a quantitative study of the eye movements induced by linear translation when the subject is instructed to stabilize his gaze on a memorized earth-fixed target. These experiments may allow a better understanding of the central processing of otolithic signals. 2. Human subjects were submitted to either sinusoidal or step-like horizontal linear displacements along the interaural (Y)-axis in darkness, seated in a cart moving along a linear track. Each subject's head was fixed by a helmet secured to the cart. They were asked to keep their eyes on an earth-fixed memorized target at 63 cm from them on the X-axis. 3. During sinusoidal motion, a combination of low smooth compensatory eye movements and of compensatory saccades allowed the subjects to track the memorized target. The linear model of the responses of five subjects (seven sessions) exhibited a near-ideal slope of 1.14 (range 0.84-1.58). Two subjects did not compensate properly for their displacement. The mean "vestibular-saccadic" (VS) gain (ratio of overall eye movement peak-peak amplitude versus head displacement amplitude) was 1.52 +/- 0.80 (SD), showing an overestimation of head displacement. 4. The otolith-ocular reflex (OOR) mean gain values (ratio of slow phase cumulated peak-peak amplitude versus head displacement amplitude) were about 0.13 degrees/cm. This value is 5 times higher than what has been reported in the literature, probably due to the fact that the target was at a short distance. 5. The number of saccades occurring during sinusoidal stimulations varied according to the different subjects. They were obviously compensatory saccades and not quick phases. They indicate that although the gain of the OOR was small, the brain has computed the adequate desired eye position. 6. During steplike head displacements in darkness, although the OOR gain was also small, seven of the eight subjects could stabilize their gaze with a mean VS gain of 1.01 +/- 0.70. The linear model for the pooled responses of these subjects exhibited a slope of 0.82. 7. When subjects were instructed not to move their eyes during the translation, three of the five examined could still correctly reproduce the head movement amplitude with saccades, even as late as 50 s after motion had stopped. This indicates that head displacement was stored with the adequate metrics and could be used to drive the saccadic system. 8. Bilabyrinthectomized patients could not perform any adequate gaze stabilization. This shows that the observed performance was of vestibular origin.

Long-term deficits of goal-directed vestibulo-ocular function following total unilateral loss of peripheral vestibular function.

Brief whole-body movements (+/- 5 to 170 degrees/s peak velocity; approximately equal to 0.5 s duration), applied during 1.44-s intervals of total darkness while subjects "looked" at a just-viewed target, were used to examine vestibulo-ocular function in 3 patients who had compensated to total unilateral loss of peripheral vestibular function. We found that the combined effects of slow-phase and saccadic eye movements both tended to keep the eyes stabilized on the unseen target. Compensatory slow-phases elicited during rapid head movements ipsilateral to (i.e., towards) the lesion were only about 60% as effective as those elicited during rapid contralateral movements. Compensatory gaze-correcting saccades tended to supplement deficient slow-phase movements, especially during rapid ipsilateral head movement. However, the gaze-correcting effect of saccades was only about half of the required for perfect stabilization. Thus, two functional vestibular deficits were observed during rapid ipsilateral head movements: (1) reduced slow-phase stabilization, and (2) reduced saccadic ability to adequately supplement the deficient slow phases. However, overall vestibular functional capability, as assessed by observation of the net effect of both slow phases and saccades, was much better than would be indicated by conventional observation of slow-phase movements alone.

Eye movements induced by pontine stimulation: interaction with visually triggered saccades.

1. Rhesus monkeys were trained to look to brief visual targets presented in an otherwise darkened room. On some trials, after the visual target was extinguished but before a saccade to it could be initiated, the eyes were driven to another orbital position by microstimulation of the paramedian pontine reticular formation. If, as current models of the saccadic system suggest, a copy of the motor command is used as a feedback signal of eye position, failure to compensate for stimulation-induced movements would indicate that stimulation occurred at a site beyond the point from which the eye position signal was derived. 2. Animals compensated for perturbations of eye position induced by stimulation of most pontine sites by making saccades that directed gaze to the position of the visual target. With stimulation at other pontine sites, compensatory saccades did not occur. 3. Pontine stimulation sometimes triggered, prematurely, impending visually directed saccades. The direction and amplitude of the premature movement depended upon the location of the briefly presented visual target. The amplitude of the premature movement was also a function of the interval between the stimulation train and the impending saccade. These data suggest that input signals for the horizontal and vertical pulse/step generators develop gradually during the presaccadic interval. Saccade trigger signals need to be delayed until the formation of these signals is completed. 4. The implications of these findings for models of the saccadic system are discussed. Robinson's local feedback model of the saccadic system can explain compensation for pontine stimulation-induced changes in eye position but cannot easily account for the failure to compensate for perturbations in eye position produced by stimulation at other sites. Modified versions of Robinson's model, which assume that the input signal to the pulse/step generator is the desired displacement of the eye, can account for both compensation and the failure to compensate since two separate neural integrators are employed. However, these models ignore kinematic arguments that commands to the extraocular muscles must specify the absolute position of the eye in the orbit rather than a relative movement from a previous position.

Spatial localization of saccade targets. II. Activity of superior colliculus neurons preceding compensatory saccades.

1. Rhesus monkeys were trained to look to brief visual targets presented in an otherwise darkened room. Single-unit activity was recorded from the superior colliculus (SC) during the performance of two tasks for which successful completion was contingent on the combination of retinal-error and eyeposition signals. The first task required successive eye movements to serially flashed targets, each of which was extinguished prior to the initial eye movement. In the second task, electrical stimulation of the SC, delivered during the interval between target offset and saccade onset, drove the eyes to another position in the orbit, thereby requiring a compensatory saccade. The major purpose of this experiment was to determine whether or not neurons in the SC discharging before visually triggered saccades also discharge before saccades compensating for stimulation-induced perturbations in eye position. 2. Tungsten microelectrodes were introduced into the SC bilaterally. Extracellular unit activity was monitored until a cell with saccade-related activity was isolated in one colliculus and stimulation of the opposite colliculus elicited an eye movement. After a movement field was plotted for the unit, its behavior during the double-saccade and compensatory saccade tasks was evaluated. Target coordinates were arranged such that the vector of the second or compensatory movement was in the movement field of the particular unit under investigation. 3. We found that 49 of the 50 cells studied discharged before all saccades in their movement field, regardless of the type of trial that produced the saccade. The one neuron that did not fire before saccades compensating for the stimulation-induced movement was shown to require prior activation by a visual stimulus within its movement field. 4. The burst of activity occurring before compensatory saccades on stimulation trials was usually less vigorous than the burst preceding control saccades to a direct visual target. 5. Results are interpreted as supporting the hypothesis that the intermediate layers of the SC contain a spatial map of motor error, the vector of the saccade required to move the eyes to a desired orbital position. This implies that input signals reaching the intermediate layers of the SC may also be encoded in motor coordinates and that the SC may represent a site where signals from different sensory modalities are translated into a common motor frame of reference.

Inhibition of central vestibular neurons from the contralateral labyrinth and its mediating pathway.

Inhibition of central vestibular neurons from the contralateral labyrinth and its mediating pathway.