Chapter Two Ocular Motor System

2.1

Introduction The ocular motor system has evolved in parallel with the visual system so that a

number of different classes of eye movement now exist, each with a particular functional purpose (see table 2.1). Eye movements that were early to evolve keep the eye fixed on objects of interest. Amongst these eye movements are subsets that are important for helping to maintain clear vision when the head is moving (vestibular-evoked eye movements) and when the visual world is moving with respect to the head (optokineticevoked eye movements). With the evolution of the fovea, a requirement for a new repertoire of eye movements arose. Since visual acuity is greatest when an image is positioned on the fovea, eye movements that function to rapidly move the eyes towards objects of interest (saccadic eye movements) and pursue objects of interest (smooth pursuit eye movements) have evolved. Furthermore, with the evolution of frontally positioned eyes, eye movements that simultaneously keep the foveae of both eyes on objects of interest (verging eye movements) evolved.

Table 2.1 Functional classes of human eye movements (adapted from Leigh and Zee 1999).

Class

Main Function

Fixations

Hold the image of a stationary target on the fovea

Vestibular

Stabilize images on the retina during brief head movements

Optokinetic

Stabilize images on the retina during relative movement of the visual world (such as during sustained head movements)

Smooth Pursuit Hold the image of a moving target on the fovea Saccades

Rapidly redirect the line of sight towards targets of interest

Vergence

Move the eyes in opposite directions so that images of a single close target are placed simultaneously on both foveae

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In this chapter, the structure and function of the ocular motor system is reviewed, with emphasis on saccadic eye movements. The structure and function of the muscle pulleys is also considered in detail (see Demer 2004 for a comprehensive overview).

2.2

Description of Eye Movements In the scientific literature, eye movements are usually described as three-

dimensional (3-d) rotations relative to a right-handed head-fixed coordinate system (see figure 2.1 and appendix). The rotations are composed of three components – torsional, vertical, and horizontal – with the magnitude of each component depending on the extent of rotation about each of the three head-fixed base axes (see appendix). Torsional rotations are those that occur about the naso-occipital x-axis (hx in figure 2.1), with positive rotations about this axis being clockwise and negative rotations being counterclockwise according to the right-hand rule (see appendix). Vertical rotations are those that occur about the inter-aural y-axis (hy in figure 2.1), with positive rotations being downward and negative rotations being upward. Rotations about the z-axis (hz in figure 2.1) are known as horizontal rotations, with positive rotations being leftward and negative rotations being rightward.

hZ

hX

hY

Figure 2.1 Eye movements are described by rotations that have projections onto three head-fixed base axes. Rotations about the hx axis are torsional rotations. Rotations about the hy axis are vertical, while those about the hz axis are horizontal rotations. Positive rotations about each of the axes are indicated by the directions of the grey arrows (adapted from Haslwanter 1995).

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In clinical practice, eye movements are described according to an alternate nomenclature. Intorsion is torsional rotation of the eye where the upper pole of the iris moves towards the midline, whereas extorsion is torsional rotation of the eye where the upper pole of the iris moves away from the midline. Elevation refers to upward rotation of the eye, whereas depression refers to downward rotation. Abduction is horizontal rotation of the eye away from the midline, whereas adduction is horizontal rotation of the eye towards the midline.

2.3

Anatomy of the Ocular Motor System The ocular motor system consists of the central and peripheral structures

responsible for generating eye movements. A brief review of the anatomy and function of these structures is given below, along with a detailed review of the anatomy and function of the recently discovered muscle pulleys.

2.3a

Extra-Ocular Muscles

There are six muscles that move each eye: the four recti (medial, lateral, superior, and inferior), and the two oblique (superior and inferior) muscles (see figure 2.2). The recti and superior oblique muscles arise from the annular tendon (or annulus of Zinn), which is adherent to the optic nerve’s dural sheath and to the periosteum of the optic canal. The levator palpebrae superioris also originates from the annular tendon; it inserts into the upper eyelid and functions to elevate it. The recti all insert on the anterior half of the eyeball. The inferior oblique muscle arises from the inferior wall of the orbit and inserts on the posterior half of the eyeball. The superior oblique muscle, which also inserts on the posterior half of the eyeball, is unique in that its tendon passes through an antero-medially placed fibro-cartilaginous loop, the trochlea, before passing posteriorly to insert on the eyeball (see figure 2.2).

The main actions and the innervations of the six extra-ocular muscles are listed in table 2.2. The medial and lateral recti produce eye rotations that are predominantly horizontal, while the other four muscles produce combinations of vertical and torsional

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eye rotations. The six extra-ocular muscles may be divided into three agonist-antagonist pairs, where contraction of one muscle in the pair produces the same movement as relaxation of the other muscle in the pair. The medial and lateral recti make up one pair, whereas the superior and inferior recti and the superior and inferior oblique muscles make up the other two pairs.

Figure 2.2 The right orbit, and surrounding structures, viewed from the lateral aspect. The six extra-ocular muscles are labelled. The lateral rectus and optic nerve have been cut, so that medially-placed structures are visible (from Williams et al. 1989).

Table 2.2 Main actions and innervations of the extra-ocular muscles (from Kandel et al. 1991).

Muscle

Main Actions

Innervation

Medial Rectus

Adduction

Oculomotor nerve (CN III)

Lateral Rectus

Abduction

Abducens nerve (CN VI)

Superior Rectus

Elevation/Intorsion

Oculomotor nerve (CN III)

Inferior Rectus

Depression/Extorsion Oculomotor nerve (CN III)

Superior Oblique Depression/Intorsion

Trochlear nerve (CN IV)

Inferior Oblique Elevation/Extorsion

Oculomotor nerve (CN III)

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2.3b

Muscle Pulleys

Connective tissue sleeves that surround the rectus muscle tendons, close to the equator of the eyeball, have been demonstrated histologically (Demer et al. 1995). These connective tissue structures, which contain collagen, elastin, and smooth muscle, are attached to one another and to the orbital wall (Demer et al. 1995; Kono et al. 2002a). Clark et al. (2000) showed, using high-resolution magnetic resonance imaging (MRI), that these sleeves function as pulleys by keeping the paths of the rectus muscle bellies fixed in the orbit, while allowing the orientations of the tendons to vary in a manner that depends on instantaneous eye position (medial rectus data are displayed in figure 2.3).

Muscle Belly

Tendon

Pulley Location

Figure 2.3 The cross-sectional “area centroid” position of the medial rectus muscle belly and tendon, determined from MRI images, with the eye in different vertical positions. The view is from the lateral aspect. The data from the top panel are plotted in the bottom panel with corrections for supero-inferior translation. When the eye is elevated, the tendon (indicated on the right) is directed upwards, while it is directed downwards when the eye is depressed. To bring about the observed changes in tendon orientation, the pulley would have to be located within the area indicated by the dotted rectangle (adapted from Clark et al. 2000).

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The observation that the pulleys change the orientations of the rectus tendons suggests that the action of each rectus muscle depends on instantaneous eye position. For example, in the case of the medial rectus, if the subject is looking straight ahead, contraction of the muscle produces a purely horizontal rotation due to rotation of the eyeball about the head-fixed z-axis (see figure 2.4a). However, if the eye is elevated, the muscle pulley alters the pulling direction of the muscle so that the same muscle contraction produces a rotation that has horizontal and torsional components, due to a backward tilt in the eye velocity axis (see figure 2.4b).

Figure 2.4 The muscle pulley of the medial rectus keeps the muscle belly fixed in position when the eye moves from the centre of the ocular motor range (A) to an elevated position (B). However, the pulley causes the tendon pulling direction to change when the eye is elevated, resulting in a tilt in the eye velocity axis away from the head-fixed z-axis.

The finding that the pulleys bring about eye position-dependent changes in the pulling directions of the recti has prompted a number of significant modifications to theories explaining how eye movement kinematics arise (Raphan 1998; Quaia and Optican 1998; Smith and Crawford 1998; Thurtell et al. 1999; Misslisch and Tweed 2001). Indeed, the discovery of the muscle pulleys is said to have sparked an “orbital revolution” (Haslwanter 2002). The influence of the muscle pulleys on the kinematic properties of saccadic and vestibular-evoked eye movements is considered in detail in the current project, with the issue being addressed in many of the chapters of this thesis.

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The recti are known to have two histologically distinct layers (Porter et al. 1995): the inner global layer is continuous from the annular tendon to the insertion of the muscle tendon on the eyeball, while the outer orbital layer terminates posterior to the scleral insertion. Demer et al. (2000) re-examined the histology of the recti, reporting that the orbital layer of each rectus muscle actually inserts on the corresponding muscle pulley. Kono et al. (2002b) subsequently demonstrated, using high-resolution MRI, that contraction of each rectus muscle results in posterior displacement of the corresponding pulley, due to contraction of the orbital layer of the muscle (see figures 2.5 and 2.6). Relaxation of each rectus muscle results in anterior displacement of the corresponding pulley, presumably because of decreased opposition to elastic forces imposed by the pulley suspensory structures (Kono et al. 2002b). The manner in which pulley position alterations are encoded centrally is yet to be determined.

Figure 2.5 Path of the medial rectus muscle belly and tendon, from a representative subject, with the eye in four different gaze positions. Supraduction indicates elevation of the eye, while infraduction indicates depression of the eye. The inflection (arrow) in the muscle path indicates the approximate location of the muscle pulley. The muscle belly is posterior to the pulley (leftward on the graph), while the tendon is anterior to the pulley (rightward on the graph). The pulley position can be seen to alter depending on whether the eye is adducted or abducted. Contraction of the medial rectus (which leads to adduction) results in posterior displacement of its pulley, while relaxation of the medial rectus (which occurs during abduction) results in anterior displacement of its pulley (from Kono et al. 2002b).

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Figure 2.6 The orbital layer of each rectus muscle inserts into the corresponding muscle pulley (A), so that posterior displacement of the muscle pulley (arrow) is observed when the muscle contracts (B). The orientation of the eye velocity axis is not altered by retraction of the pulley in the case illustrated.

2.3c

Ocular Motor Neurons

The motor neurons to the extra-ocular muscles travel in three cranial nerves (CN): the oculomotor nerve (CN III), the trochlear nerve (CN IV), and the abducens nerve (CN VI). The oculomotor nerve provides the innervation for the inferior oblique muscle and for the superior, inferior, and medial recti (see table 2.2). The trochlear nerve innervates the superior oblique muscle, while the abducens nerve innervates the lateral rectus (see table 2.2). These nerves each have long intra-cranial courses, since they travel from the brainstem (in the posterior fossa of the cranial vault) to the orbit. The cell bodies of each of the motor neurons are located close to the midline in the brainstem, in nuclei with the same name as the corresponding nerve. Oculomotor neurons originate from the oculomotor nucleus, which is found in the midbrain at the level of the superior colliculi. The oculomotor nucleus contains a number of subnuclei, each responsible for innervating a different muscle (see figure 9-9 in Leigh and Zee 1999). Trochlear neurons originate from the contralateral trochlear nucleus, found in the midbrain at the level of the inferior colliculi, while abducens neurons originate from the ipsilateral abducens nucleus, found in the caudal pons just beneath the floor of the fourth ventricle.

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2.4

Neural Signal to the Extra-Ocular Muscles For all eye movements, the neural signal travelling to the extra-ocular muscles

conveys both position and velocity information. The final signal is derived from a raw input that is proportional to the velocity of the resulting eye movement. A position signal is obtained by integration of the input (velocity) signal. The neural components responsible for generating the position signal from the input signal have therefore come to be known as the “neural integrator”. Following the generation of a position signal, it is combined with the velocity signal to produce the signal that travels to the extra-ocular muscles to move the eyes. To a first-order approximation, Robinson (1975) described motor neuron discharge rate R as being related to eye position θ and eye velocity dθ/dt by R = k (θ − θT ) + r

dθ dt

where θT is the threshold eye position at which the neuron is recruited into activity, and k and r are constants.

Both the position and velocity components of the signal are required in order to compensate for restrictions imposed on eye movements by the orbital contents, such as forces opposing movements of the eye away from the centre of the ocular motor range and forces acting to pull the eye back towards the centre when it is positioned eccentrically. If there is no eye position signal during a period of attempted fixation, for example, the eye will drift back towards the centre of the ocular motor range due to the presence of elastic restoring forces acting on the eyeball. The complete or partial loss of the position component of the signal results from lesions of the integrator (a so-called “leaky” integrator). During attempted fixation of an eccentric target, loss of the position component of the signal is clinically evident as centripetal drift of the eye back towards the centre of the ocular motor range, which is corrected for by saccadic eye movements back to the target (so-called “gaze-evoked” nystagmus; see sections 3.9 and 8.1).

The means by which the neural integrator produces a position signal from the velocity signal is a subject of controversy (see chapter 4). The neural integrator and other central pathways involved in eye movement generation are discussed in greater detail below, and in chapters 3 and 4.

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2.5

Saccadic Eye Movements Saccadic eye movements enable humans to rapidly redirect their line of sight

towards objects of interest. Saccades may be identified by their profiles, since they show a consistent relationship between their peak velocities and amplitudes (Leigh and Zee 1999). Saccades also have stereotyped 3-d kinematic properties, which will be described and discussed in detail in chapter 4. The central pathways responsible for generating saccades are considered below.

2.5a

Saccadic Command to the Extra-Ocular Muscles

Recordings from ocular motor neurons during saccadic eye movements have revealed that the neural command to the extra-ocular muscles is comprised of both phasic and tonic signals. The initial part of the signal is a high frequency burst of phasic activity, the pulse, which starts about 8ms prior to the onset of eye rotation (see figure 2.7).

Figure 2.7 The pulse-slide-step of innervation, during a 20° leftward saccade in the monkey (upper panel), is illustrated (lower panel). The data were recorded from a neuron in the left abducens nucleus. The slide is denoted by the horizontal bar (from Leigh and Zee 1999).

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The pulse functions to bring about a sudden contraction of the extra-ocular muscles, so that the eye moves quickly from one target to the next. At the completion of the eye rotation, there is a new level of tonic innervation to the extra-ocular muscles, encoded by the step (see figure 2.7). The step signal, which is generated by the neural integrator (see sections 2.4 and 2.5c), is important for holding the eye in its new position, since it helps counteract various restoring forces acting on the eyeball. The transition between the end of the pulse and the beginning of the step has come to be known as the slide, since it provides a gradual transition between the two signals.

2.5b

Brainstem Circuitry for Saccades

The command signal necessary to produce a saccadic eye movement may arise from one of a variety of cortical and brainstem structures, including the frontal eye fields, supplementary eye fields, parietal eye fields, and the rostral poles of the superior colliculi. These structures control the activity of omnipause neurons, which fire continuously, except immediately prior to and during saccades. The cell bodies of the omnipause neurons lie in the nucleus raphe interpositus, which is located in the midline of the pons between the rootlets of the abducens nerves. Constant stimulation of omnipause neurons has been shown to result in an inability to generate saccades (Westheimer and Blair 1973), since omnipause neurons inhibit the brainstem saccadic pulse generator (Strassman et al. 1987; Ohgaki et al. 1989; Nakao et al. 1991).

The neurons comprising the brainstem saccadic pulse generator are located in two anatomically distinct areas. The pulse generator for horizontal saccades is located in the caudal pons, in the paramedian pontine reticular formation (PPRF), while the pulse generator for vertical saccades is located in the rostral midbrain, in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF). The neurons whose cell bodies are located in these areas are known as excitatory burst neurons (EBNs). Omnipause neurons are inhibitory neurons that project from the nucleus raphe interpositus to the EBNs. When the omnipause neurons are inhibited by the cortical or brainstem structure that has given rise to the saccadic command signal, they stop firing and the EBNs are able to discharge. The EBNs begin to discharge at high frequency approximately 12ms prior to the onset of eye rotation. The EBNs are important for producing the pulse signal to the extra-ocular muscles and their discharge rate is, accordingly, closely correlated with the velocity of the 16

eye rotation. The EBNs also send collaterals to the neural integrator, which is responsible for generating the step component of the signal to the extra-ocular muscles. The pulse from the EBNs and the step from the neural integrator are combined in the ocular motor nuclei, to create the final eye movement signal. The firing patterns of the components of the final common saccadic pathway, and their connections, are summarized in figure 2.8.

Figure 2.8 Schematic diagram showing the brainstem components involved in the generation of saccades. The omnipause neuron (P), EBN (B), and the ocular motor neuron (OMN) are illustrated, as are their firing patterns (graphs show spike discharge and discharge rate plotted against time). Before the onset of a saccade, the omnipause neuron ceases discharging, allowing the EBN to generate a pulse. The pulse is passed to the neural integrator (NI), which generates a signal proportional to eye position. The EBN also sends a signal proportional to eye velocity directly to the ocular motor neuron; this signal is combined with the eye position signal, and the resulting signal is sent to the eye muscles, producing a saccadic eye movement (E) with the profile as illustrated in the plot of eye position against time (from Leigh and Zee 1999).

The PPRF is predominantly involved in the generation of horizontal saccades. EBNs from the PPRF project to abducens motor neurons and internuclear neurons, which are both located in the ipsilateral abducens nucleus in the pons. The internuclear neurons decussate and then pass via the contralateral medial longitudinal fasciculus (MLF) to

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synapse on motor neurons in the medial rectus subnucleus of the oculomotor nucleus in the midbrain. Thus, a pulse signal from the EBNs in the PPRF will result in contraction of the ipsilateral lateral rectus and contralateral medial rectus muscles, bringing about an ipsilateral horizontal saccade. Similarly, electrical stimulation of the PPRF results in an ipsilateral horizontal saccade (Cohen and Komatsuzaki 1972), while a lesion in the PPRF will result in an inability to generate ipsilateral horizontal saccades (Cohen et al. 1968).

The riMLF is important for the generation of the vertical and torsional components of saccades (Büttner et al. 1977; Büttner-Ennever and Büttner 1978; King and Fuchs 1979; Vilis et al. 1989). The EBNs from the riMLF project to motor neurons in both the oculomotor and trochlear nuclei. Collaterals are also passed to the neural integrator (see section 2.5c). Since EBNs that are responsible for generating upward and downward eye movements are located on both sides of the midbrain, a unilateral lesion will only result in a mild deficit in the ability to generate vertical saccades, while a lesion that involves both sides will abolish all vertical saccadic eye movements.

2.5c

Neural Integrator

The neural integrator generates the eye position signal from the eye velocity signal. The neural substrate for the neural integrator was identified by single-unit recording studies and by studying the effects of lesions on eye movement kinematics. The structures implicated include the medial vestibular nucleus (MVN), the nucleus prepositus hypoglossi (NPH), and the interstitial nucleus of Cajal (INC). The flocculus and paraflocculus of the cerebellum have also been implicated, since their ablation results in a decrease in the ability to hold steady gaze (Takemori and Cohen 1974; Zee et al. 1981; Waespe et al. 1983).

The production of the horizontal component of the eye position signal is thought to occur in the MVN (Miles 1974) and NPH (Lopez-Barneo et al. 1982). The NPH, which is medial to the MVN in the medulla, receives afferents from and projects to virtually all of the structures in the brainstem and cerebellum involved in ocular motor function (Belknap and McCrea 1988; see table 2.3). Cannon and Robinson (1987) confirmed that both the MVN and the NPH are important for the production of the horizontal eye position signal. After placing chemical lesions in both areas, they found that any 18

subsequent eye movements followed a course that was proportional to the predicted eye velocity only.

Table 2.3 Major connections of the NPH (adapted from Leigh and Zee 1999).

Inputs

Outputs

Vestibular nuclei:

Vestibular nuclei:

-

-

MVN

MVN

Contralateral NPH

Contralateral NPH

Brainstem reticular formation:

Brainstem reticular formation:

-

medullary reticular formation

-

medullary reticular formation

-

PPRF

-

PPRF

-

riMLF

-

INC

-

INC

Ocular motor nuclei

Ocular motor nuclei

Cerebellum

Cerebellum

Others:

Others:

-

raphe nuclei

-

raphe nuclei

-

nucleus of the optic tract

-

dorsal cap of inferior olive

The INC, a structure in the midbrain reticular formation, is thought to be important in the production of both the vertical and torsional components of the eye position signal (King et al. 1980, 1981; Fukushima 1987, 1991; Crawford et al. 1991; Crawford 1994). It receives neural input from the vestibular nuclei (via the MLF) and the riMLF. The INC sends output signals to the ocular motor nuclei (Steiger and BüttnerEnnever 1979), the vestibular nuclei, and to the NPH (Cannon and Robinson 1987; Fukushima 1991). The NPH is also involved in producing the vertical eye position signal (Baker 1977; Cannon and Robinson 1987).

Since the neural integrator produces an eye position signal from the eye velocity signal, it performs, in effect, a velocity-position transformation (Tweed and Vilis 1987). The neural integrator is also known, therefore, as the velocity-position integrator.

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Currently, there are two main hypotheses that attempt to explain how the velocityposition integrator works, based on the implications of modelling studies. Tweed and Vilis (1987) proposed a “quaternion” integrator model of the velocity-position transformation, whereas Schnabolk and Raphan (1994) have proposed a “vector” integrator model. These two models are described and extensively discussed in chapter 4.

2.5d

Cerebellar Influences on Saccades

The cerebellum has a role in determining the metrics of saccadic eye movements, since total cerebellectomy results in marked saccadic dysmetria (Optican and Robinson 1980). In addition, an inability to hold steady gaze at the end of a saccade (post-saccadic drift) is observed following cerebellectomy (Optican and Robinson 1980). The role of several regions of the cerebellum in bringing about normal saccades is considered below (see Robinson and Fuchs 2001 for a review of the subject).

The dorsal vermis, consisting of lobules VI and VII (see figure 6.1), is thought to be important in determining saccadic metrics (Selhorst et al. 1976; Optican and Robinson 1980). The dorsal vermis receives inputs from the caudal nucleus reticularis tegmenti pontis (cNRTP), PPRF, vestibular nuclei, NPH, and inferior olivary nucleus; the major projection of the dorsal vermis is to the caudal fastigial nucleus (Yamada and Noda 1987). Pharmacological lesions of the dorsal vermis result in hypometric ipsilateral saccades, hypermetric contralateral saccades, and gaze deviation away from the side of inactivation (Sato and Noda 1992). Ablative lesions result in similar abnormalities (Takagi et al. 1998). Bilateral lesions result in hypometria of all horizontal saccades and an increase in saccadic latency (Barash et al. 1999).

The caudal fastigial nucleus also has a role in determining saccadic metrics (Optican and Robinson 1980; Vilis and Hore 1981). It receives inputs from the dorsal vermis, inferior olivary nucleus, and frontal eye fields and superior colliculus (via the cNRTP); it projects to the omnipause neurons, EBNs, and superior colliculus (Noda et al. 1990). Unilateral pharmacological lesions of the caudal fastigial nucleus result in hypermetric ipsilateral saccades and hypometric contralateral saccades, whereas bilateral lesions result in hypermetria of all horizontal saccades (Robinson et al. 1993). Caudal

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fastigial nucleus lesions also result in saccades that are more variable in amplitude when compared with normal saccades (Robinson et al. 1993).

The flocculus and paraflocculus are important for ensuring that steady gaze is maintained at the end of a saccadic eye movement, since lesions of these structures result in post-saccadic drift (Zee et al. 1981). The post-saccadic drift that occurs at the end of saccadic eye movements in subjects with floccular/parafloccular lesions is thought to be mainly due to abnormal matching of the pulse and step signals.

2.6

Summary The ocular motor system has two general functions: to keep the eyes fixed on

targets of interest, and to move the eyes from one target to another. Several classes of eye movement have evolved so that these functions may be fulfilled in a variety of situations. Amongst these classes of eye movement are vestibular-evoked eye movements, which keep the eyes fixed on a target during brief head movements, and saccadic eye movements, which rapidly move the eyes from one target to another target of interest.

Normal eye movements come about as a result of coordinated contraction and relaxation of the six extra-ocular muscles, which are innervated by cranial nerves III, IV, and VI. Both eye position and eye velocity signals must be conveyed in these nerves, to bring about normal eye movement trajectories and to ensure that the eye remains fixed on the target of interest following the eye movement. In the case of saccadic eye movements, the eye velocity signal is generated by the EBNs in the brainstem. The EBNs also send collaterals to the neural integrator, which generates the eye position signal. The eye velocity and eye position signals are then combined in the ocular motor nuclei prior to being relayed to the extra-ocular muscles.

Recent studies of orbital anatomy have demonstrated the presence of muscle pulleys, which are connective tissue sleeves that surround the rectus tendons near their insertions on the eyeball. The pulleys change the pulling directions of the tendons in a manner that depends on the instantaneous eye position. The discovery of these structures

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has prompted a revision of theories attempting to explain how eye movements are programmed and, hence, how their 3-d kinematic properties arise (see chapter 4). As there is a comparison between the kinematic properties of saccadic and vestibular-evoked eye movements in the current project, a description of the anatomy and physiology of the vestibular system is presented in chapter 3.

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