Schizoid and Schizotypal Personality Disorder

P. Roussos , ... L.J. Siever , in Encyclopedia of Human Behavior (Second Edition), 2012

Smooth pursuit eye movement

SPEM measures visual tracking of smoothly moving targets, such as a pendulum. The psychophysiological study of eye movements, particularly the antisaccade task, has been proposed as a candidate endophenotype for schizophrenia. This is a result of SPEM deficits being evident in the majority of patients with chronic schizophrenia when compared with controls. Additionally, SPEM impairment is also significantly more marked in relatives of probands with schizophrenia and STPD individuals. Volunteers who were selected on the basis of poor eye-tracking accuracy had a greater prevalence of STPD diagnosis than the control group with high eye-tracking accuracy. In addition, deficits during the eye-movements task have been observed in nonclinical populations such as adult, healthy volunteers with a high degree of schizotypy. STPD patients with positive-like symptoms are likely to show elevated error rates on standard antisaccade tasks in comparison to healthy normal controls. Additionally, a recent study showed that SPEM deficits were predicted solely by the criterion of social isolation, with low accuracy trackers also reporting reduced desire for social contact. These findings support the notion of impaired SPEM in relation to negative-symptom schizotypy. However, other studies have failed to demonstrate differences in antisaccade error rates between STPD with predominantly negative-like symptoms and normal individuals. Based on this, it remains unclear whether impaired SPEM is specific to negative versus positive symptoms or instead reflects the entire schizotypal syndrome. Nevertheless, SPEM deficits are found in both STPD and schizophrenia patients, further supporting the notion of impaired SPEM as an endophenotype for schizophrenia-spectrum disorders.

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Pursuit Eye Movements

U.J. Ilg , in Encyclopedia of Neuroscience, 2009

Because smooth pursuit eye movements (SPEMs) can be executed only in the presence of a moving target, they represent an ideal behavior for studying the mechanisms of visual motion processing. Position, velocity, and acceleration of the target are extracted from the retinal image and robustly used to generate SPEMs. This motion processing is confined to a retinal frame of reference. In contrast, our motion perception during the execution of SPEMs is not based on this reference. We perceive the target moving in an external frame of reference even in the total absence of retinal image motion. Some neurons in the posterior parietal cortex of rhesus monkeys code for the target movement in space during the execution of SPEMs.

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Cerebellar Learning

Suryadeep Dash , Peter Thier , in Progress in Brain Research, 2014

4 Smooth Pursuit Adaptation

Smooth pursuit eye movements (SPEMs) are tracking eye movements used to stabilize the image of a moving object of interest on the fovea. Simply put, SPEMs can be understood as the product of a feedback circuit that translates information on retinal target motion into an appropriate eye movement response, reducing retinal image slip ( Rashbass, 1961; Robinson et al., 1986). However, the first 100–150   ms of the SPEMs are driven by uncompensated retinal target image motion due to the long latencies of visual information processing. As a consequence of the sluggishness of vision, the eye movement response evoked by the moving target starts only 100–150   ms after target motion onset (SPEM latency). In other words, the 100–150   ms of SPEMs following the onset of the eye movement are an open-loop response (SPEM initiation) whose size depends solely on the visual target motion signal and a gain parameter that specifies the transformation of the target movement into a pursuit command. How is the gain parameter chosen? The study of smooth pursuit adaptation (SPA) (see below) suggests that the expected eye movement gain governing the early closed-loop behavior is used as a reference for the open-loop gain. This seems reasonable as the probability that the movement of a natural pursuit target will substantially change in this brief period is low. As a consequence, there is a good chance that already the initial SPEM has the right velocity, thereby reducing the need for corrective saccades that would otherwise jeopardize the continuous scrutiny of the moving target. SPA refers to the short-term changes in the gain of SPEM initiation brought about by an experimental manipulation that causes a violation of the aforementioned goal to minimize the pursuit error at the time closed-loop behavior kicks in. This is achieved by exposing the observer to a sequence of trials in which the target moves at an initial constant velocity for around 100–200   ms and then steps to a new predictable velocity, stereotypically at the same point in time. The pursuit velocity evoked by the initial target velocity is changed such as to make it more similar to the target velocity after the velocity step, thereby minimizing the retinal errors prevailing at the time the loop is closed (Dash et al., 2010; Fukushima et al., 1996; Kahlon and Lisberger, 1996). If the target steps to a higher velocity, subjects learn to upregulate the pursuit gain evoked by the initial target velocity (gain-increase SPA). Correspondingly, if the target velocity steps to a lower velocity following the initial target ramp, subjects gradually learn to downregulate their initial pursuit gain (gain-decrease SPA).

Similar to STSA, also SPA reflects changes in timing. The major difference between the two is that SPA is based on the control of eye acceleration rather than eye velocity as in the case of STSA (Fig. 1B). Specifically, during gain-decrease SPA, velocity decreases due to a decrease in peak acceleration not compensated by an increase in the duration of the initial eye acceleration pulse (Dash and Thier, 2013). On the other hand, during gain-increase SPA the acceleration profile expands (i.e., the eyes are accelerated for a longer time) while peak acceleration may increase, decrease, or stay unchanged (Dash and Thier, 2013). In other words, the kinematic changes associated with gain-increase SPA and gain-decrease SPA are not mirror symmetric, similar to the asymmetry characterizing gain-increase and gain-decrease STSA. Yet another parallel holds for the effects of fatigue. If rhesus monkeys are asked to carry out long sequences of stereotypical step-ramp smooth pursuit eye movements (Dash and Thier, 2013), they are able to maintain a constant SPEM peak velocity despite constantly declining SPEM peak acceleration. The decline in peak acceleration is compensated by an expansion of the acceleration profile (i.e., an increase in acceleration duration). These changes are analogous to the compensation of the decline in peak eye velocity by increasing movement duration in the case of a saccade resilience experiment described earlier. The decrease in peak acceleration that is observed during gain-decrease SPA may be taken as a manifestation of fatigue. On the other hand, the ability to expand the acceleration pulse in order to realize gain-increase SPA is the same one that is used to compensate SPEM fatigue (Dash and Thier, 2013) (Fig. 1B).

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Eye Movement Research

T.J. Crawford , ... C. Kennard , in Studies in Visual Information Processing, 1995

Abstract

Smooth pursuit eye movements have been widely used in clinical research in attempts to clarify the neural mechanism underlying various brain diseases. However, many of these studies are subject to two major weaknesses: a failure to control for neuropharmacological factors and an inadequately defined visual context against which the smooth pursuit tracking is measured. This paper addresses both of these issues in patients with schizophrenia or focal cortical lesions. In the first study we compared smooth pursuit eye movements in the dark in medicated and non-medicated patients fulfilling the DSM-IIIR criteria for schizophrenia, and a group of age-matched control subjects. Relative smooth pursuit eye velocity (i.e. gain) was reduced in both schizophrenic groups; however the effect was significantly greater in the neuroleptically medicated group. In the second study smooth pursuit, with and without a structured background, was compared in patients with discrete cortical lesions and normal subjects. The analysis revealed a cohort of patients manifesting a large inhibitory effect of a structured background on pursuit eye movements. Examination of CT scans showed that two regions are of particular importance in this effect: an area of parietal cortex lying within the architectonic boundaries of Brodmann's area 40 (Brodmann, 1909); and an area of white matter close to the lateral ventricles containing cortico-cortical connections. These data point strongly to the critical importance of neuropharmacological factors and the visual background conditions in studies of smooth pursuit eye movements.

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Eye Movement Research

G.U. Lekwuwa , ... M.A. Grealy , in Studies in Visual Information Processing, 1995

Introduction

Smooth pursuit eye movements are effected by two main mechanisms ( Barnes & Asselman, 1991; Barnes, Donnelly & Eason, 1987; Dallos & Jones, 1963; Bahill & McDonald, 1983). There is a basic mechanism that uses information about retinal error velocity to drive the pursuit system but has a fairly low gain. It is also known to contain a substantial time delay of approximately 100   ms (Carl & Gellman, 1987) which would naturally be expected to give rise to a large phase error. The second mechanism functions mainly in the production of predictive activity. The addition of a predictive component to the pursuit response causes the eye movements to become progressively phase advanced, and enhances the gain (Barnes & Asselman, 1991; Barnes & Grealy, 1992).

Predictive mechanisms have been postulated to consist of a predictive velocity estimator which samples and holds the gaze velocity information, and a periodicity estimator which controls the anticipatory release of stored waveforms to enhance the gain of smooth pursuit (Barnes, Donnelly & Eason, 1987; Bahill & McDonald, 1983). The neural substrate for prediction in smooth pursuit has not been clearly localised. Evidence from recordings in the flocculus of the cerebellum suggests that this might be an important site for the generation of the predictive component of pursuit (Miles & Fuller, 1975; Lisberger & Fuchs, 1978; Noda & Warabi, 1986; Noda & Warabi, 1987). However previous studies (Waterston, Barnes, & Grealy, 1992) on patients with various forms of cerebellar disease suggest that prediction is preserved in these patients.

Different methods have been used to assess and study the predictive component of pursuit. In one method, repeated transient stimulations are used to demonstrate the temporal characteristics of smooth pursuit eye movements (Barnes & Asselman, 1991; Barnes & Grealy, 1992; Boman & Hotson, 1988). Subjects are instructed to follow the motion of a constant velocity target during brief periods of stimulation that are separated by periods of darkness. The effect of prediction is revealed firstly by the fact that smooth pursuit eye movements become progressively phase advanced with repeated stimulation, and secondly by the observation that anticipatory eye movements occur before the onset of target motion. Prediction has also been assessed by examination of the oculomotor response when, after following a number of cycles of similar stimuli, there is an unexpected change in frequency, direction, or amplitude of target motion. Prediction is demonstrated if the eye movement following the unexpected change has velocity and timing characteristics similar to the preceding eye movements (Keating, 1991; Barnes & Asselman, 1991; Lisberger, Evinger, Johanson, & Fuchs, 1981). The same type of results can also be obtained if a predictable target is unexpectedly blanked out instead of changing the direction, velocity, or amplitude of the target trajectory (Barnes & Grealy, 1992).

In the present study we determined the presence or absence of prediction in cerebellar patients and controls by assessing their ability to build up anticipatory eye movements after repeated runs of transiently illuminated predictable stimuli.

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Clinical Examination of the Cranial Nerves

Adam Fisch , in Nerves and Nerve Injuries, 2015

Smooth Pursuit Eye Movements

Smooth pursuit eye movements allow us to keep a moving target in our fovea and clearly visualize it. Each hemisphere is responsible for ipsilateral smooth pursuit eye movements, meaning the right hemisphere detects and tracks images as they move to the right and the left hemisphere detects and tracks images as they move to the left. Within the circuitry for smooth pursuit, the contralateral cerebellum and medulla and the ipsilateral pons are involved in a double decussating pathway. M retinal ganglion cells detect the target movement: the visual system is generally divided into the pathway for detection of movement (the magnocellular (or M) pathway, which receives rod photoreceptor stimulation) and the pathway for detection of color (the parvocellar (or P) pathway, which receives cone photoreceptor stimulation). Visual detection of the target's movement from left to right is projected from the retinae to the right lateral geniculate nucleus and then to the right primary visual cortex (V1). The primary visual cortex projects to visual area V5 (the human homologue to the macaque middle temporal area), which then projects to visual area V5a (the human homologue to the macaque medial superior temporal area)—in humans, both V5 and V5a lie at the temporo-occipito-parietal junction. Visual area V5a projects to the posterior parietal cortex, which projects to the frontal eye fields. Note that many nonsequential, bidirectional connections exist within this projection pathway (it is not purely sequential and unidirectional).

The frontal eye fields (and other cortical visual areas, as well) project to the ipsilateral dorsolateral pontine nuclei (DLPN) in the high pons and the ipsilateral nucleus reticularis tegmenti pontis (NRTP) in the upper pons. The DLPN and NRTP project across midline to the contralateral cerebellum: specifically to the flocculus and paraflocculus of the vestibulocerebellum and also to the dorsal vermis. These structures project to the ipsilateral medial vestibular nucleus in the medulla, which projects to the contralateral abducens nucleus in the mid to low pons, which completes the double decussation. The abducens nucleus initiates the final common pathway.

Y-group vestibular nuclear connections to the oculomotor and trochlear nuclei also exist, which are involved in vertical pursuit movements (Figure 15.10).

Figure 15.10. Smooth Pursuit.

 Reproduced with permission from Fisch, A. Neuroanatomy: Draw it to Know it, 2nd ed. (Oxford University Press, 2012), Drawing 23–5, pg 421.

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Eye Movements

Charles J. Bruce , Harriet R. Friedman , in Encyclopedia of the Human Brain, 2002

IV.E.1 Tracking with Pursuit and Saccades

Smooth-pursuit eye movements support scrutiny of objects moving in space by matching eye velocity to target velocity in order to both reduce retinal blur of the moving object and facilitate its continued foveation. Smooth pursuit occurs when the FS selects a moving target or when a previously selected stationary target starts to move. However, target selection for pursuit also activates the saccadic system; hence, moving targets are usually tracked with a combination of smooth pursuit and saccades, with these two eye movement systems operating independently but synergistically to track the same chosen target (Fig. 2). Their synergy reflects control by separate parameters of the target's trajectory. The principal impetus for smooth pursuit is target velocity (i.e., retinal slip), and the pursuit system continuously endeavors to eliminate retinal slip by matching eye velocity to target velocity. In contrast, the principal concern of the saccade system is target position (i.e., retinal error), and saccades are intermittently generated to eliminate retinal error by foveating the target.

However, this division of labor is not absolute. Smooth pursuit is modestly affected by positional errors: Ongoing pursuit accelerates in response to small retinal positional errors, and it is even possible to initiate smooth pursuit with an afterimage placed near the fovea (although eccentric afterimages are usually tracked with a succession of saccades). The pursuit system also responds to the rate of change in retinal slip (i.e., acceleration). Thus, pursuit is a function of the zero-, first-, and second-order derivatives of the target's retinal image.

Conversely, the saccadic system attends to target velocity as well as location. Saccadic latency is shorter for targets moving centrifugally (away from the fixation point) and longer for targets moving centripetally. Moreover, saccades are usually directed to a predicted target location based on its position and velocity as acquired 100–200   msec before the saccadic movement starts.

Pursuit velocity ranges up to ∼100°/sec; however, pursuit gain (defined, like VO and OK gain, as eye velocity/target velocity) is generally poor for target velocities above 25°/sec. When the pursuit gain is low, the eye will persistently fall behind the target and frequent, large "catch-up" saccades will be made; however, if gain is high (∼1.0), then only a few, small saccades may be needed.

Interestingly, low smooth-pursuit gain is the principal symptom of the eye tracking dysfunction (ETD) of schizophrenia. Subsequent research has shown a cluster of oculomotor impairments that covary across the schizophrenic patient population and are often also present in first-degree relatives of schizophrenic patients. On the basis of the ETD and other cognitive aspects of schizophrenia, it has been hypothesized that schizophrenia reflects diminished frontal lobe function in general, and that the ETD specifically reflects impaired function in both the saccadic and the smooth-pursuit regions of the FEF.

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Visual and Oculomotor Functions

Stefano Da Pozzo , ... Paolo Perissutti , in Studies in Visual Information Processing, 1994

Introduction

Smooth pursuit eye movements, assuring continuous foveal fixation, allow continuous clear vision of objects moving within the visual environment ( Leigh & Zee, 1991). Conventionally, pursuit is measured during tracking of a predictable, sinusoidal target motion, while step-ramp stimulations are generally preferred to study the initiation of the smooth pursuit. A part of the abnormalities of pursuit initiation, smooth pursuit (SP) gain (slow eye velocity/target velocity) alteration and asymmetry (different gain values for nasal and temporal-directed tracking) are commonly studied, usually through sinusoidal stimulation, in a large variety of neurological diseases (Glaser, 1990; Leigh & Zee, 1991). Various studies of the effect of ocular misalignment on SP response have been conducted, but most of them were related to paralytic strabismus, particularly to abducens nerve palsy. Some studies about concomitant strabismus are however present in the literature (Sokol, Peli, Moskowitz, & Reese, 1991; Tychsen, Hurtig, & Scott, 1985; Tychsen & Lisberger, 1986), and all of them report a Smooth Pursuit System (SPS) impairment. From these studies it seems clear that in early-onset strabismus (infantile strabismus, with onset prior to the first year of life) an evident asymmetrical gain is present, which is characterized by normal values of nasal-directed and reduced values of temporal-directed pursuit gain. Tychsen and Lisberger (1986) attributed this asymmetry to a maldevelopment of visual motion processing caused by the disruption of binocular vision; in fact, binocular experience is necessary for the normal development of the visual cortex and of the pathways specialized for visual motion processing. Hence, Tychsen et al. (1985) hypothesized that the SPS impairment found in early-onset strabismus may represent a static arrest of development at an infantile stage. However, when late-onset strabismus (onset after the second year of life) was considered, conflicting findings were reported. Tychsen et al. (1985) reported that in three subjects with noninfantile strabismus (recorded at ages ranging from 7 to 29 years) pursuit gain fell within the control range of 0.90 or better and that there was no evidence of a nasal-temporal gain asymmetry. On the other hand, Sokol et al. (1991) reported that half of their 15 subjects with late-onset esotropia showed impairment of pursuit gain, resulting in reduced but symmetrical nasal-temporal values. The purpose of the present study was to measure the SPS response in subjects of pediatric age with late-onset strabismus, through a quantitative evaluation of smooth pursuit gain (SP gain) and a comparison between these values and the corresponding values obtained in orthophoric children of the same age range. In addition the global pursuit gain (GP gain) was evaluated, because there was a lack of data about this kind of measurement. The global pursuit results from the cooperation between the smooth pursuit and the saccadic systems. Furthermore, we tried to document the effect of surgery on GP and SP gains, in the attempt to determine if their objective quantification could be meaningful and helpful in pre-surgical planning for strabismus or in the evaluation of effectiveness of the post-surgical outcome.

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The Cerebellum: From Embryology to Diagnostic Investigations

Alexander A. Tarnutzer , ... Michael S. Salman , in Handbook of Clinical Neurology, 2018

Recording the OKR in adults with cerebellar disease

Both SPEM and SEM contribute to the OKR, which is modulated by the cerebellum. Cerebellar structures contributing to the OKR include the ocular motor vermis, the flocculus, and the deep cerebellar nuclei (Dieterich et al., 2000). The OKR may be assessed quantitatively using different devices that provide moving high-contrast patterns covering both central and peripheral visual fields. While traditionally studied in a rotating chair with an optokinetic drum, more recently virtual-reality goggles provide the opportunity to modulate the direction and properties of the optokinetic stimulus. Impaired or even abolished OKR has been observed in cerebellar neurodegeneration (Baloh et al., 1975; Zee et al., 1976; Yee et al., 1979). OKR cross-coupling (i.e., the optokinetic stimulus elicits eye movements different from the plane of stimulation, e.g., a horizontal optokinetic stimulus elicits vertical eye movements) has also been described (Walker and Zee, 1999). As for SPEM, vertical OKR gains for upward movements are higher than for downward movements in cerebellar disorders, e.g., in late-onset Tay–Sachs disease (Rucker et al., 2004).

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Visual and Oculomotor Functions

John A. Waterston , ... Madeleine A. Grealy , in Studies in Visual Information Processing, 1994

Introduction

Abnormalities of smooth pursuit (SP) eye movements have been well described in patients with cerebellar ataxia (Baloh, Yee, & Honrubia, 1986; Wennmo, Hindfelt, & Pyykko, 1983; Zee, Yee, Cogan, Robinson, & Engel, 1976), and have also been reported in patients with Parkinson's disease (PD) (Corin, Elizan, & Bender, 1972; Gibson, Pimlott, & Kennard, 1987; Melville Jones & De Jong, 1976; White, Saint-Cyr, Tomlinson, & Sharpe, 1983). Although the role of the cerebellum in the generation of SP eye movements has been well established in neurophysiological studies (Lisberger & Fuchs, 1978; Miles & Fuller, 1975; Suzuki, Noda, & Kase, 1981; Zee, Yamazaki, Butler, & Gucer, 1981), no such role has been established for the dopaminergic neurons in the substantia nigra which are affected in PD (Kennard & Lueck, 1989), and the exact etiology of the reported pursuit deficits in these patients is unclear.

Optimal SP performance requires the successful interaction of two feedback mechanisms. The closed-loop, visual feedback pathways are able to correct eye velocity on the basis of retinal velocity error, but predictive strategies are also necessary to minimize the inherent feedback delays which exist in the visuo-motor pathways, and might be expected to influence performance particularly during high frequency, predictable target motion. In mildly affected patients with cerebellar disease, SP abnormalities may only be evident at higher frequencies of target motion (Zee et al., 1976), suggesting that the predictive mechanisms might be selectively involved in these patients. However, this aspect has not been adequately examined in cerebellar disease. In PD, it has been proposed that prediction is intact on the basis of near normal phase changes during sinusoidal pursuit (Bronstein & Kennard, 1985; Flowers & Downing, 1978; Melville Jones & De Jong, 1976), but performance during pursuit of unpredictable target motion has received little attention.

To document the frequency-response performance characteristics in these two patient populations we have examined their pursuit performance during predictable, sinusoidal target motion across a broad frequency band in order to quantify the SP defect.

We have also investigated the SP responses with pseudo-random target motion so as to examine the relationship of the predictive mechanisms to the generalized disturbance of pursuit. In previous studies of normal subjects during pursuit of pseudo-random target motion consisting of the sum of two or more sinusoids, it has been shown that the slow-phase eye-velocity gains for each of the lowest frequency sinusoids progressively declines as the stimulus is made less predictable by increasing the frequency of the highest frequency component above a critical level of 0.4 Hz (Barnes & Ruddock, 1989). Further breakdown in the SP response can also be seen when the velocity of the high-frequency component is increased in relation to the velocity of the other frequency components. This pattern of response has been attributed to the activity of a predictive velocity estimation mechanism which preferentially enhances the gain at the highest frequency.

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