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Purpose Ocular motor abnormalities such as abnormal saccades are common in idiopathic Parkinson's disease (PD) and atypical parkinsonian syndrome, such as progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD). In this study, we describe a case of patient with PD and show a video illustrating severe delay of reflexive saccades. Observations A 68-year-old Caucasian woman with diagnosis of PD presented for evaluation of diplopia. Neuro-ophthalmic examination revealed good visual acuity in both eyes and normal optic nerves but prominent ocular motor abnormalities, including hypometric saccades, impaired smooth pursuit, and convergence insufficiency causing diplopia at near. Despite treatment with carbidopa-levodopa three times per day, she exhibited episodic, severe delay of reflexive saccades. During these episodes, the patient appeared frozen and unable to initiate reflexive saccades for 20 s or longer. This freezing of reflexive saccades was variable and occurred suddenly during exam but could be interrupted by smooth pursuit. There was no gait freezing, eyelid apraxia, or prominent exacerbation of other motor symptoms. Freezing of saccades dramatically resolved after increasing dosage of carbidopa-levodopa. Conclusions and Importance We describe a patient with dopa-responsive parkinsonian syndrome with intermittent difficulty initiating reflexive saccades mimicking ocular motor apraxia. Resolution of saccadic freezing with higher carbidopa-levodopa is consistent with ocular motor impairment as a result of degeneration and dysfunction of the dopaminergic pathways in supranuclear ocular motor control.

Knowledge about the relevance and extent of human eye movement control in the cingulate cortex to date is very limited. Experiments in non-human primates brought about evidence for a potentially central role of the dorsal bank of the cingulate sulcus in saccadic eye movements. In humans, a putative cingulate eye field (CEF) in the same region has been proposed; however, its function and location still remain controversial. Another area in the posterior cingulate cortex, the cingulate sulcus visual area (CSv), has been shown to respond to visual motion cues and also ocular motor tasks. In this study we used multi-band neuroimaging (n = 46) to comprehensively characterize oculomotor responses along the entire cingulate cortex during the most common types of eye movements. We were able to robustly localize the CEF to the anterior portion of the midcingulate gyrus. The region gave responses during all oculomotor tasks and is embedded within the ventral attention network. Area CSv, which is located in the anterior portion of the posterior cingulate gyrus, on the other hand responded to smooth pursuit and optokinetic nystagmus only. It likewise represents a node within the ventral attention network but at the same time seems to be a distinctive part of the somatomotor network. Our findings support an executive role of the CEF, suggesting a cognitive control function in maintaining and adapting different kinds of eye movements. CSv on the other hand might be an interface for relaying oculomotor, visual motion and broad sensory signals related to self-motion.

Highlights • Abnormalities of saccades, vergence and smooth pursuit have been found in PD. • SPEM abnormalities in PD consist of reduced gain and saccadic pursuit. • PD patients have normal SPEM interspersed with catch up and anticipatory saccades. • SP may reflect an inability to inhibit extraneous saccades or be a sign of executive dysfunction. • Degeneration of SNr in PD may be reason behind SPEM abnormalities in PD., Smooth pursuit eye movement (SPEM) abnormalities are commonly seen in Parkinson’s disease (PD). Both reduced speed and saccades seen during SPEM, also known as saccadic pursuit (SP), have been studied in PD. A comprehensive literature review analyzed 26 studies of SPEM and PD. It appears that a greater proportion of PD patients have SPEM abnormalities consisting of reduced SPEM gain and/or SP compared to the normal population. It is not clear whether SPEM abnormalities are present early in the disease or begin sometime during disease progression. SPEM abnormalities may be correlated with disease severity but do not fluctuate or respond to dopaminergic medication in the same manner as other motor symptoms in PD. SPEM in PD is composed of normal SPEM interspersed with SP composed of both catch up and anticipatory saccades. This differs from other neurodegenerative disorders and may be related to an inability to inhibit extraneous saccades or to increased distraction reflecting executive dysfunction. Because the basal ganglia are involved in SPEM physiology, degeneration of the SNr neurons in PD may explain abnormal SPEM in this disorder. Since dementia, aging and medication effects influence SPEM, they should be controlled for in future studies of SPEM in PD. SP is easily detected on clinical exam and may be a biomarker for the disease or for disease progression. Oculomotor testing can be an important part of the Parkinson’s exam.

Parkinson's disease (PD) impairs somatomotor and oculomotor systems. A moving object of interest induces smooth-tracking eye movements (i.e., smooth pursuit) in normal primates, but most PD patients exhibit steplike-tracking eye movements (saccadic pursuit). Basic features of smooth pursuit are well established. To understand the nature of impaired pursuit in PD, we first briefly review some features of smooth pursuit in normal primates including eye movement tasks and neural correlates. We then review recent results showing the specific nature of impaired pursuit in PD. By comparing the results with monkey data, we deduce underlying pathophysiology. We suggest that the frontal eye fields/basal ganglia loop, first suggested by Cui, Yan & Lynch (2003), is important for efficient and automatic smooth-pursuit performance and is dysfunctional in PD. We also suggest that some PD patients with difficulty in pursuit planning have dysfunction of cerebral-cerebellar networks including supplementary eye fields and cerebellar oculomotor vermis/caudal fastigial nuclei.

Objectives Though sub-concussive impacts are common during contact sports, there is little consensus whether repeat blows affect brain function. Using a “lifetime exposure” rather than acute exposure approach, we examined oculomotor performance and brain activation among collegiate football players and two control groups. Our analysis examined whether there are group differences in eye movement behavioral performance and in brain activation during smooth pursuit. Methods Data from 21 off-season Division I football “starters” were compared with a) 19 collegiate cross-country runners, and b) 11 non-athlete college students who were SES matched to the football player group (total N = 51). Visual smooth pursuit was performed while undergoing fMRI imaging via a 3 Tesla scanner. Smooth pursuit eye movements to three stimulus difficulty levels were measured with regard to RMS error, gain, and lag. Results No meaningful differences were found for any of the standard analyses used to assess smooth pursuit eye movements. For fMRI, greater activation was seen in the oculomotor region of the cerebellar vermis and areas of the FEF for football players as compared to either control group, who did not differ on any measure. Conclusion Greater cerebellar activity among football players while performing an oculomotor task could indicate that they are working harder to compensate for some subtle, long-term subconcussive deficits. Alternatively, top athletes in a sport requiring high visual motor skill could have more of their cerebellum and FEF devoted to oculomotor task performance regardless of subconcussive history. Overall, these results provide little firm support for an effect of accumulated subconcussion exposure on brain function., Highlights • Elite collegiate football players have identical smooth eye movements in comparison to cross country runners and controls. • There is more activation in ocularmotor structures in football players in comparison to cross country runners or controls.

Conservatively, it is estimated that at least 40% of the primate brain is primarily visual machinery. It is, therefore, prudent to explore visual function carefully in mild traumatic brain injury (mTBI) beyond the ostensible reassurance offered when a patient sees with 20/20 acuity bilaterally. After mTBI, deficits in visual processing as reflected in abnormal eye teaming rather than those from direct injury to the afferent visual pathways or oculomotor nerves are far more common. Visual symptoms commonly reported after mTBI include fluctuations in visual acuity at near, headaches with visual-intensive tasks, insecure balance, a sense of being visually overwhelmed, and photophobia. These can often be related to accommodative dysfunction, loss of vergence facility, saccadic dysfunction, deficiency of smooth pursuits, and impaired visual information processing. Patients will often have difficulty verbalizing their complaints, not only because of cognitive difficulties seen after mTBI such as impaired word-finding, memory, and complex attention, but also because there are only vague terms available to the layperson for the subtle visual problems. The examiner must, therefore, ask validated questions reflecting visual processing dysfunction and perform tests that reliably identify it. Assuming normality solely based upon a healthy globe and normal visual acuity and visual field might not only be incorrect, but also can result in limited gains in other rehabilitative areas. Therapy should be integrative with providers working as a team. This chapter will not only focus on identifying, measuring and explaining visual processing concerns after mTBI but also provide guidance for the generalist encountering patients.

Combination of signals based on their reliability is an increasingly popular model for sensorimotor processing. However, how reliability is estimated, or how such estimation is affected by prolonged exposure to noisy inputs, is still unknown. In this study, we compare patients with unilateral functional amblyopia with control subjects tracking either a reliable target, or a blurry, unreliable target, in a task of repeated, sustained smooth pursuit. We provide evidence for a lower weight of visual information during smooth pursuit in amblyopic and control subjects tracking a blurry target, with no significant difference of prior information weight. In contrast, we found no evidence of lower visual information weight in the catch-up saccades of amblyopic subjects. We conclude that oculomotor performance in unilateral amblyopia mostly lays within the continuum between our control groups, without significant differences in the relative weights of prior and visual information. However, smooth pursuit exhibits additional deficits that might result from abnormal visual development.

Opsoclonus/flutter (O/F) is a rare disorder of the saccadic system. Previously, we modeled O/F that developed in a patient following abuse of anabolic steroids. That model, as in all models of the saccadic system, generates commands to make a change in eye position. Recently, we saw a patient who developed a unique form of opsoclonus following a concussion. The patient had postsaccadic ocular flutter in both directions of gaze, and opsoclonus during fixation and pursuit in the left hemifield. A new model of the saccadic system is needed to account for this gaze-position dependent O/F. We started with our prior model, which contains two key elements, mutual inhibition between inhibitory burst neurons on both sides and a prolonged reactivation time of the omnipause neurons (OPNs). We included new inputs to the OPNs from the nucleus prepositus hypoglossi and the frontal eye fields, which contain position-dependent neurons. This provides a mechanism for delaying OPN reactivation, and creating a gaze-position dependence. A simplified pursuit system was also added, the output of which inhibits the OPNs, providing a mechanism for gaze-dependence during pursuit. The rest of the model continues to generate a command to change eye position.

This chapter covers eye movement disorders that are characterized by intact alignment but in which the eyes either have restricted motility, move too slowly, or are misdirected. In neuro-ophthalmic terminology, these include horizontal and vertical conjugate gaze limitations, voluntary smooth pursuit and saccadic deficits, and involuntary conjugate gaze deviations. These conditions tend to result from impaired supranuclear input upon the ocular motor nuclei. Thus, for the most part, third, fourth, and sixth nerve function, as well the vestibuloocular reflex, are intact except in the situations noted. In contrast, disorders in which the eyes tend to be misaligned are covered in Chapters 15 and 18 . In Chapter 17 , conditions characterized by excessive or inaccurate saccades are reviewed.

Oculomotor dysfunction may originate from physical, physiological or psychological causes and may be a marker for schizophrenia or other disorders. Observational tests for oculomotor dysfunction are easy to administer, but are subjective and transient, and it is difficult to quantify deviations. To date, video-based eye tracking systems have not provided a contextual overview of gaze data that integrates the eye video recording with the stimulus and gaze data together with quantitative feedback of metrics in relation to typical values. A system was developed with an interactive timeline to allow the analyst to scroll through a recording frame-by-frame while comparing data from three different sources. The visual and integrated nature of the analysis allows localisation and quantification of saccadic under- and overshoots as well as determination of the frequency and amplitude of catch-up and anticipatory saccades. Clinicians will be able to apply their expertise to diagnose disorders based on abnormal patterns in the gaze plots. They can use the line charts to quantify deviations from benchmark values for reaction time, saccadic accuracy and smooth pursuit gain. A clinician can refer to the eye video at any time to confirm that observed deviations originated from gaze behaviour and not from systemic errors.

For the visual system to function correctly, the eyes must be appropriately directed. This is accomplished via six extraocular muscles controlled from three cranial nerve nuclei: the oculomotor, trochlear, and abducens. Several types of eye movements are made, each requiring a different neural circuit that funnels through these nuclei. Saccades quickly change the direction of the eye, and the fovea in particular, so that detailed visual information can be acquired during fixation. Smooth pursuit eye movements point the fovea pointed at a moving target. Vergence eye movements move the eyes to compensate for target distance. The eyes also make reflexive movements in order to maintain fixation when the head or body is perturbed. These are termed optokinetic, when stimulated by the visual system, or vestibular, when initiated by signals from the inner ear. Lesions can independently affect each type of eye movement, since the circuits lie in different regions of the brain. The eyes also contain intraocular muscles: the ciliary muscle focuses the lens, and the sphincter and dilator muscles of the pupil control retinal illumination. The first two are regulated by parasympathetic paths from the Edinger-Westphal nucleus. The last is regulated by sympathetic pathways from thoracic spinal cord. The eyes are protected by the eyelids. The levator palpebrae muscle, supplied by the oculomotor nerve, lifts the eyelid, while the orbicularis oculi muscle, supplied by the facial nerve, closes it. Tests of pupil and lid reflex function allow one to assess both sensory and motor paths.

Infancy is the most dynamic part of human development. During this period, all basic sensorimotor and cognitive abilities are established. In this chapter, we will trace some of the important achievements of this development with a focus on how infants achieve predictive control of actions, i.e., how they come to coordinate their behavior with the ongoing events in the world without lagging behind. With the maturation of the brain, new possibilities that have profound effects on cognition open up. Some of them are core abilities, i.e., they function at birth or very early in development. Important examples are the structured perception of objects and surfaces and the control of arm movements. Closely after birth, infants move their arms to the vicinity of objects in front of them demonstrating that they have some control of their arms and indicating that they perceive objects as such. Another example is the rapid onset of smooth-pursuit eye movements during the second month of life and the emerging ability to predict when and where an occluded moving object will reappear. At 4 months of age, out of sight is no longer of mind. The child's sensorimotor system is especially designed to facilitate the extraction of knowledge about the world including other people. In addition, the infant is endowed with motives that ensure that the innate predispositions are transformed into a system of knowledge for guiding actions predictively. By perceiving and acting on the world, infants develop their cognition and through developmental studies; we can learn more about these processes.

In this chapter, we present the bedside assessment and laboratory tests that are available for the neuro-ophthalmologic evaluation of children and adults with cerebellar diseases. In the evaluation of a patient with cerebellar dysfunction, recognizing the pattern of ocular motor and / or vestibular impairment is often a key step to the correct diagnosis. The cerebellum is very important in processing a wide range of different eye movements, including angular vestibulo-ocular reflexes, otolith-ocular reflexes, fixation and gaze holding, smooth pursuit eye movements, saccadic eye movements, optokinetic response, ocular alignment, and vergence. Quantitative eye movement recording is now widely available in specialized clinics and medical practices, especially for testing the vestibulo-ocular reflexes. We describe the approach for assessing specific eye movements linked to cerebellar function, discuss appropriate eye movement laboratory tests, and summarize recent related research findings. In addition, for each laboratory test, we discuss its advantages, disadvantages, indications, and interpretations. Furthermore, we provide differential diagnoses for specific ocular motor and vestibular abnormalities such as slow saccades or impaired vestibulo-ocular reflexes.

A plethora of motor control challenges are presented to the oculomotor system whose primary purpose is to point the eyes to hold images stably on the fovea, the region of the retina with the highest visual acuity. The eyes can rotate in horizontal, vertical, and torsional (around the axis of gaze) directions and require the coordinated action of a total of 12 extraocular muscles. In addition, the eyes are mounted in a head that has the ability to move in roll, pitch, and yaw axes in addition to the ability to translate from side to side, and fore and aft. Positioned on the top of the body, the head is carried through three-dimensional space. Therefore, if the oculomotor system cannot solve this litany of stabilization problems, blurred, moving, or double images are presented to the visual system. Many portions of the cerebral cortex and brain stem have been committed to carry out this complex system control problem. We use a layered approach to understand the oculomotor system starting with the extraocular muscles, and working backward into the brain stem and eventually the cerebral cortex. Particular attention is devoted to control of voluntary saccades, smooth pursuit, and vergence. The longstanding dispute that was raised more than 150 years ago between Hermann von Helmholtz and Ewald Hering on whether the central nervous system synthesizes signals that control the eyes together or individually is addressed. A number of clinical applications are provided to amplify the understanding of the anatomy and neurophysiology of eye movement control.

The brain continuously maintains a current representation of its immediate surroundings. Perceptual representations are often updated when the world changes, e.g., when we notice an object move. However, we can also update representations internally, without incoming signals from the senses. In other words, we can run internal simulations of dynamic events. This ability is evident during mental object rotation. These uncontroversial observations lead to an obvious question that nevertheless remains to be answered: How does the brain control the speed of dynamic mental simulations? Is there a central rate controller or pacemaker module in the brain that can be temporarily coupled to sensory maps? We can refer to this as the common rate control theory. Alternatively, the primitive intelligence within each map could tune into the speed of recent changes and use this information to keep going after stimuli disappear. We can call this the separate rate control theory. Preliminary evidence from prediction motion experiments supports common rate control, although local predictive mechanisms may cover short gaps of < 200 ms. The putative rate controller might turn out to be the same thing as the velocity store described in smooth pursuit eye movement models and/or the pacemaker module proposed in the cognitive timing literature. Indirect neuroimaging evidence suggests rate control is a function of the core timing system in the dorsal striatum.

Executive functions are cognitive processes that critically involve the frontal lobes and enable us to accomplish goals and make decisions in everyday life. Since eye movements are key determinants of what information reaches our brain and higher cortical centers, they are central to executive functions. Eye movements can be more reflexive (automatic) or more voluntary (willful). Voluntary eye movements especially, have become an important tool with which to measure different aspects of executive functions in many human disorders. They also have been critical in differentiating subtypes and evaluating medication or treatment efficacy in clinical populations.

Six muscles control the movements of each eye, allowing two broad categories of movements: gaze-stabilization and gaze-shifting movements. Gaze-stabilization movements act to compensate for movements of the head and body, acting to stabilize the image of the visual world on the retina. Gaze-shifting movements shift the fovea into alignment with objects of interest in the visual world. Eye movements are controlled by three cranial nerve nuclei (the oculomotor (III), trochlear (IV), and abducens (VI)), which together control the six eye muscles. The oculomotor system provides an excellent model for understanding the principles of movement control.

The extraocular muscles have many anatomic, physiologic, and molecular characteristics distinct from those of other striated muscles. These characteristics, which likely developed in response to the specialized demands placed on the extraocular muscles (including tonic position-maintaining contractures, conjugate smooth pursuit and saccades, and dysconjugate vergence movements) may account for the often predictable involvement or sparing of extraocular muscle in specific pediatric neuromuscular disorders. Extraocular muscle dysfunction in neuromuscular disease typically presents with ptosis, ophthalmoplegia, or incomitant strabismus, or a combination of these symptoms, which can assist the clinician in formulating differential diagnoses for neuromuscular conditions. This chapter reviews the unique features of the oculomotor system and the neuromuscular disorders affecting it.

Smooth pursuit (SP) maintains visual acuity of slow-moving objects by keeping their image near the fovea. SP impairment is recognized by saccadic pursuit and occurs toward the side of lesions at the parietal, occipital, and temporal lobe junction (area V5); the frontal eye field and their projections to the basal pontine nuclei; paraflocculus; and caudal cerebellar vermis. Retinotopic SP impairment occurs in the visual hemifield contralateral to damage to areas V5 or V1. Craniotopic SP defects occur contralateral to the orbital midposition after acute unilateral cerebral damage. Omnidirectional saccadic pursuit is a sensitive sign of diffuse brain disease.

In order to ameliorate the consequences of ego motion for vision, human and nonhuman observers generate reflexive, compensatory eye movements based on visual as well as vestibular information, helping to stabilize the images of visual scenes on the retina despite ego motion. And in order to fully exploit the advantages of foveal vision, they make saccades to shift the image of an object onto the fovea and smooth pursuit eye movements to stabilize it there despite continuing object movement relative to the observer. With the exception of slow visually driven eye movements, which can be understood as manifestations of relatively straightforward feedback systems, most eye movements require a direct conversion of sensory input into appropriate motor responses in the absence of immediate sensory feedback. Hence, in order to generate appropriate oculomotor responses, the parameters linking input and output must be chosen suitably. Moreover, as the parameters may change from one manifestation of a movement to the next, for instance because of oculomotor fatigue, the choices should also be quickly modifiable. This chapter will present evidence showing that this fast parametric optimization, understood as a functionally distinct example of motor learning, is an accomplishment of specific parts of the cerebellum devoted to the control of eye movements. It will also discuss recent electrophysiological results suggesting how this specific form of motor learning may emerge from information processing in cerebellar circuits.

Eye movements evolved to serve vision in two ways. Gaze-holding eye movements keep images of the world fairly still on the retina during natural activities, such as locomotion. Gaze-shifting eye movements point the retinal fovea, which corresponds to best vision, at features of interest in the environment. A good deal is known about how the brain controls eye movements. Consequently, eye movements are often used as experimental tools in the neurosciences and as diagnostic signs at the bedside. Animal models of eye movement disorders have led to development of new treatments for patients with impaired vision.

The analysis of well-defined behaviors that require the cerebellum has helped reveal many key mechanisms operating in the cerebellum to mediate learning and feed-forward prediction. These systems include eyelid conditioning, adaptation of the vestibuloocular reflex, smooth pursuit eye movements, and arm-reaching tasks. This review focuses specifically on the variety of findings that have come from the use of eyelid conditioning to study the cerebellum. Phenomena discussed include sites and rules for plasticity, temporal coding and mechanisms of timing, cerebellar control of climbing fibers and its role in bidirectional learning, extinction of conditioned responses, and the phenomenon of savings.

If humans try to pursue a moving target, the nervous system uses predictions to overcome some of the nervous systems delays. It is therefore possible for the eyes to pursue a target with virtually no delay and to make accurate catch-up saccades to moving targets. Another example of a delay is the latency of a saccade made in response to a target step. Due to imperfect pursuit, the retinal error will change during this latency. The aim of the present study was to investigate whether step-induced saccades take into account this change. To vary this change in retinal error, the gain of the pursuit eye movement was manipulated successfully by adding a patterned background in one condition and a concomitant hand tracking in another. The increased gain of the pursuit eye movements in the hand tracking condition significantly modified the change in retinal error during the latency. However, no significant differences in saccadic amplitude were found between conditions. We conclude that these step-induced saccades are generated independently of the gain of the pursuit eye movement.

The neural centers in the cerebral hemispheres, both cortex and basal ganglia, involved in the generation of saccadic and smooth pursuit eye movements have been well delineated in terms of their location and function. For the generation of saccades these include the frontal eye fields, the supplementary eye field, and the intraparietal sulcus, and in the basal ganglia the caudate nucleus and the substantia nigra, pars compacta. The generation of pursuit eye movements involves the middle temporal (area V5) and medial superior temporal areas and the frontal eye field. These centers and their connections are disturbed not only in acute and chronic lesions such as cerebral infarction, but also in a wide variety of neurodegenerative diseases. In certain of these conditions, such as patients with cortical dementias and basal ganglia disorders, correct interpretation of the resulting eye movement abnormalities can contribute to differentiating between a range of differential diagnoses.

There are six extraocular muscles innervated by three cranial nerves, 3, 4, and 6 serving to control simple eye movements. While the nuclei for these cranial nerves are located in the brainstem, there are supranuclear networks residing in varied regions of the brain that provide the complex and precise instructions insuring the ability to maintain a target upon the fovea of the retina (thus clear vision) under varying circumstances. The term supranuclear is appropriate to designate these systems, as they functionally reside above and provide input to the ocular motor neurons.

Eye movement abnormalities are common in movement disorders and may offer insight into neural mechanisms, assist with diagnosis, or result in visual complaints in the setting of normal visual function. The role of the basal ganglia in eye movement control and eye movement abnormalities common in various movement disorders are discussed.

Publisher Summary This chapter reviews that the shared goal of all components of the ocular motor system is to maintain clear, single vision by placing and maintaining an object of visual interest on the fovea, the retinal region, with the highest density of photoreceptors and the best visual acuity. Several functional classes of eye movements coexist to meet this shared goal. These include saccades, smooth pursuit, vergence, optokinetic responses, and vestibular reflexes. It discusses that separate premotor or supranuclear command networks exist for initiation and modulation of each functional class of eye movements. These premotor networks converge upon a “final common pathway” that includes the ocularmotoneuron, the neuromuscular junction, and the final effector organ of eye movements— that is, the extraocular muscle. The chapter also reviews that the complexity and the variety of demands that the ocular motor system must meet in order to maintain stable vision require complex anatomy and physiology at every level from extraocular muscle to cortical ocular motor regions.

Publisher Summary This chapter discusses that the testing of ocular motor functions is an important step in the diagnosis of vestibular and balance disorders for three reasons: First, most of these disorders are associated with the disorders of eye movements. Second, the classification of the eye movement disorder will often lead to localization of the neural structures involved. Third, eye movement disorders can cause impaired vision or dizziness, and thus might impair balance. The chapter outlines the technology and equipment needed for clinical electronystagmography (ENG), its basic recording and calibration procedures, possible artifacts, and its advantages and disadvantages versus clinical bedside tests. It also describes the testing procedures and interpretation for three categories of ocular motor functions: (1) stability of gaze; (2) smooth pursuit eye movements and optokinetic nystagmus; and (3) saccadic eye movements. For vertical eye movements, positive angles correspond to gaze up and negative angles to gaze down. It is assumed that the eye position is digitally available for numerical differentiation to obtain eye velocities.

Combined eye–head movements are commonly used to redirect the visual axis (gaze) in space. This article reviews recent advances in understanding the neural control of gaze with particular emphasis on four key issues: (1) the interactions that occur among multiple oculomotor subsystems (e.g., saccadic, pursuit, and or/vestibular), (2) the pathways that control orienting head movements, (3) the neural mechanisms that transform gaze commands into eye and head movements, and (4) the importance of integrated feedback in preserving gaze accuracy. The implications of these experimental findings are then considered in relation to current theoretical models of gaze control.

The cerebellum plays a key role in the ‘on-line’ generation and the long-term calibration of all types of eye movements. The flocculus and paraflocculus assure that images are held steady on the fovea: impaired gaze holding, spontaneous vertical nystagmus, impaired pursuit and abnormal amplitude, and direction of vestibulo-ocular reflexes are signs of lesions here. The nodulus and ventral uvula modulate the amplitude and the axis of eye rotation of the response to the low-frequency (sustained) components of head rotation: prolonged vestibular responses and periodic alternating nystagmus are signs of lesions here. The dorsal vermis and underlying posterior fastigial nuclei calibrate saccade amplitude and pursuit initiation. Saccadic dysmetria is the hallmark sign of lesions here. The cerebellum also assures that both static and dynamic ocular alignment is optimized for binocular foveal vision.

Primates use a combination of saccadic and smooth pursuit eye movements to maintain the central high-acuity region of their retinas on stationary and moving objects of interest. Many of the neural circuits that generate the precise control of these two eye movement systems are found in the central core of the brain stem. The organization of these brain stem circuits is reviewed here with the use of schematic summaries that outline the control principles and the neural groups involved. Although the schematic models of these two systems use simple engineering approximations, the review stresses throughout that the actual systems involve highly parallel, distributed neural processing to carry out their eye-movement control function. Separate schematics are used to explain control in the two systems, but modern research has shown that the two systems share many common neural elements in their brain stem circuitry. These shared elements, as well as the elements unique to each system, are discussed.

Voluntary eye movements serve to shift the center of gaze from one point of interest to another in an individual’s surroundings (saccadic eye movements) or to maintain the image of a moving object on the fovea so it can be tracked accurately with the eyes (pursuit eye movements). These two types of eye movements are controlled by largely separate neural circuits, although there is some overlap. Both classes of eye movements are controlled at the highest level by cortico-cortical networks which project to generally separate structures in the brain stem but project to similar regions in the cerebellum and basal ganglia.

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.

Executive functions are cognitive processes that critically involve the frontal lobes and enable us to accomplish goals and make decisions in everyday life. The brain regions responsible for some executive functions (spatial attention and memory) overlap with brain regions necessary for eye movements. Eye movements can be more reflexive (automatic) or more voluntary (willful). Voluntary eye movements, especially, have become an important tool with which to measure different aspects of executive functions in many human disorders. They also have been critical in differentiating subtypes and evaluating medication or treatment efficacy in clinical populations.

The optokinetic response (OKR) supports the vestibuloocular reflex (VOR) in maintaining stable gaze during constant-velocity or low-acceleration head movements by producing eye movements in the direction of visual motion. The optimal stimulus for producing an OKR is large-field visual motion. Visual signals carried in optokinetic pathways also play a major role in adjusting the gain of the VOR in response to developmental, age-related, or pathological challenges. The OKR of frontal-eyed mammals is sensitive to postnatal binocular visual experience, development of cortical binocularity, and maturation of descending visual cortical connections to the pretectum and nuclei of the accessory optic system.

Eye tracking dysfunction (ETD) is one of the most widely replicated behavioral deficits associated with psychotic disorders. It is also over-represented in clinically unaffected first-degree relatives. Here, we provide an overview of research related to the specificity and co-familiality of ETD, the effects of medications, brain imaging findings, and the pathophysiology of this impairment. The evidence suggests that ETD involves both higher-order structures and early parts of the pursuit pathway. Localizing behavioral paradigms used in the fMRI environment can help to clarify the neural systems involved and to disambiguate predictive and sensorimotor factors.

The supplementary eye fields (SEFs) are located in dorsomedial frontal cortex and contribute to high-level control of eye movements. Recordings in the SEF reveal neural activity related to vision, saccades, and fixations, and electrical stimulation in the SEF evokes saccades and fixations. Inactivations and lesions of the SEF, however, cause minimal oculomotor deficits. The SEF thus processes information relevant to eye movements and influences critical oculomotor centers but seems unnecessary for generating action. Instead, the SEF has overarching, subtle functions that include limb-eye coordination, the timing and sequencing of actions, learning, monitoring conflict, prediction, supervising behavior, value-based decision making, and the monitoring of decisions.

Animals with foveal vision use a combination of pursuit and saccadic eye movements when exploring their visual surroundings. The two types of movements must be tightly coordinated to effectively improve the ability to see. This article reviews findings from behavioral and electrophysiological studies that clarify the neural mechanisms that accomplish this coordination. Current evidence points to shared mechanisms for gating the two movements and for selecting a common target stimulus. Although cortical circuits are involved, brainstem regions such as the superior colliculus play a prominent role in target selection for both pursuit and saccades.

Classically, saccadic and pursuit systems were considered largely independent. However, on the basis of cat and primate studies, scientists accumulated evidence showing that the two oculomotor systems are intimately linked. It was demonstrated that both saccadic and pursuit systems use position and velocity inputs and share common initiation, cancellation, and target-selection mechanisms. Moreover, neuronal populations in several cortical and subcortical brain areas were shown to convey both saccade and pursuit signals. This article discusses all these results, showing that saccade and pursuit systems are much more integrated than previously thought. © 2009 Elsevier Ltd All rights reserved. ispartof: Encyclopedia of Neuroscience pages:421-428 ispartof: pages:421-428 status: published

To track a small visual target in 3-D space, the two eyes have to move in different directions and/or at different velocities. This tracking might be accomplished by a disjunctive pursuit system, which uses separate motion processing of each individual eye but no disparity signal (hypothesis 1), or by the conjugate pursuit and the vergence system (hypothesis 2). To test the validity of the two hypotheses we recorded eye movements in five healthy human subjects with the scleral search-coil method. A small dim laser stimulus was presented on an earth horizontal platform. A position-ramp stimulus was presented in eight different directions: rightward or leftward, convergence or divergence, or a combination of them. We compared a fusible with an un-fused and a monocular viewing condition to assess whether a disparity signal is needed for 3-D tracking. Fusion was prevented by a vertical prism. We compared the monocular with the prism viewing condition to examine the effect of retinal motion signals of either one or both eyes on the tracking performance in the absence of disparity signals. Results revealed severe impairment of tracking in depth, while tracking in pure horizontal directions remained unaffected during the prism and monocular as compared to the binocular viewing condition. These data support hypothesis 2.

The vestibulo-ocular reflex (VOR) mechanism triggers eye movements as a result of head motion in order to keep gaze stationary relative to the world. However, in order to shift the direction of the gaze along with head motion, the VOR mechanism must be overridden ("cancelled"). Two mechanisms have been proposed to explain this cancellation: a reduction of the VOR gain or activation of smooth pursuit (SP) eye movements in the opposite direction. We studied VOR cancellation using the magnetic search coil in six spinocerebellar ataxia type 3 (SCA-3) and four episodic ataxia type 2 (EA-2) patients, conditions that are known to have degraded SP but different degrees of VOR impairment. Abnormal VOR was found in two of the four EA-2 patients and all of the SCA-3 patients. All subjects possessed residual VOR, although when tested using head thrusts it was almost negligible in the SCA-3 patients. The EA-2 patients showed essentially no SP and the SCA-3 patients had poor SP. However, for all patients, the gain during VOR cancellation was comparable to normals. These results provide additional evidence that SP cancellation of the VOR cannot be the sole mechanism utilized in overriding the VOR in these patients.

Publisher Summary This chapter discusses acquired ocular motility disorders and nystagmus. Eye movement disorders may be considered in two categories: those that cause incomplete eye movements (ophthalmoparesis) and those that cause excessive eye movements (saccadic intrusions and nystagmus). Central to an understanding and correct diagnosis of abnormal eye movements is the evaluation of ocular alignment, ocular motility, and each functional class of eye movements: optokinetic, vestibular, vergence, smooth pursuit, and saccades. Ophthalmoparesis is caused by the dysfunction of extraocular muscles, the neuromuscular junction, cranial nerves, cranial nerve nuclei, and internuclear and supranuclear connections. The initial pathologic eye movement in nystagmus is a slow drift of the eye away from the desired position, whereas the initial pathologic eye movement in saccadic intrusions is an inappropriate saccade that intrudes on fixation. The identification of the characteristics of nystagmus (physiologic versus pathologic and jerk versus pendular) is necessary for diagnostic evaluation and treatment.