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Neurological Basis of Saccadic Eye Movement
Saccadic eye movements can be defined as rapid eye movements that refocus a peripheral visual image on the center of the retina where it can best be seen. These rapid eye movements are designed to move the eyes as quickly as possible to meet specific demands of an individual's task and environment. Saccades have been recorded to reach speeds up to 900 degrees per second and lasting only tens of milliseconds (Kendal, Squire). Simply because these movements occur so rapidly there generally is not enough time for visual feedback to modify the course of a saccade and instead saccades follow a stereotyped profile that is largely determined by the size of the movement. One would expect saccades to be driven by visual stimuli due to its nature in the role of movement, however accurate saccades have also been elicited by other modalities such as sounds, tactile stimuli, memories of locations in space, and even verbal commands (Kendal).
There are several different types of saccades, which can be divided into two classes: voluntary and involuntary. It is also important to differentiate between the horizontal and vertical component of saccades, where information is processed in the paramedian pontine reticular formation (PPRF) and mesencephalic reticular formation respectively. For the purposes of this site and the prevalent nature of saccades during movement, we will mainly focus on the horizontal component.
Functional Anatomical Review
Saccades can be better understood by imagining these movements as a result of complex integration of both a motor system and a sensory system. Sensory systems such as the visual system process visual information coming from retinal pathways that give direct input to the superior colliculus as well as the frontal eye fields (FEF) located in the frontal lobe. Dependent on the nature of the task the oculomotor pathway that produces a saccade will inevitably reach the superior colliculus either directly or indirectly, depending if it is an involuntary or voluntary saccade, respectively. The superior colliculus is a multilayered structure of alternating gray and white layers lying on the roof of the midbrain and is divided into two functional regions: the superficial layers, and the intermediate and deep layers. Retinal ganglion cells project directly to the superficial layers and form a visual map that corresponds to specific locations of the contralateral visual field. Furthermore, the superior colliculus serves to further process visual information and is where visuomotor integration takes place.The motor signals for saccades descending from higher centers specify the location of the target, which is then transformed by pathways in the brain stem reticular formation into specific motor pathways. An overview of this general pathway can be better understood by referring to Figure 1.1 below.
Motor Circuit for Horizontal Saccades
Before we get lost in motor circuits, let us first review how we get the eyes to move where we want them to go. When thinking about a saccade there is a fast (pulse) and slow (step) component. The fast component is a result of a burst of activity in the PPRF that quickly shifts the eyes to the moving object. The slow phase, however, is generated by tonic neurons in the nucleus prepositus hypoglossi (PPH) that maintain a steady signal related to eye position, and thus holding them in place for a given amount of time. For example, say there is a moving object in the left visual field. This requires the left lateral rectus and right medial rectus to pull the eyes to the left very rapidly. One might ask how we can target these specific eye muscles?
Targeting these specific eye muscles involves ocular motor signals that are organized and transformed by interneurons in the brain stem reticular formation. The paramedian pontine reticular formation, is a key structure in the generation of horizontal saccades. Specific neurons called
are located in the PPRF that when activated have polysynaptic connections. To produce a leftward saccade, excitatory burst neurons in the left PPRF synapse on a motor neuron and interneuron in the ipsilateral abducens nucleus, that directly activates the ipsilateral lateral rectus and indirectly activates the contralateral medial rectus via the medial longitudinal fasciculus (MLF) and left oculomotor nucleus. Excitatory burst neurons also drive ipsilateral inhibitory burst neurons that inhibit the contralateral abducens and excitatory burst neurons to prevent the eyes from jumping to the right. Current research has also suggested that the medial vestibular nucleus may also have a role in inhibiting contralateral abducens neurons.
A second class of pontine cells,
cells, fire continuously when not performing saccadic eye movements. These cells are located in the nucleus of the dorsal raphe and have inhibitory effects on the contralateral burst neurons in the PPRF, and thus inhibit saccades. This inhibition must be removed in order to elicit a saccade, which can be better understood by studying yet another important structure in the control of saccades, the superior colliculus.
Control of Saccades in Superior Colliculus
As mentioned before, the superior colliculus (SC) is characterized by visual and motor layers that provide a mapping of the space around you, beginning at the fovea and moving outward to the periphery. The superior colliculus has two functional regions: the rostral and caudal regions. The rostral region has a representation of the fovea and is known as the “fixation zone”, which is suitably active during visual fixation. Neurons here inhibit the caudal region of the colliculus and also project directly to the nucleus of the dorsal raphe where they synapse on omnipause cells, which themselves inhibit saccades. The caudal region is the area that is thought to facilitate a saccade, which makes sense that neurons in the rostral region are inhibiting these neurons when not performing a saccade.
Saccades Generated by Disinhibiting Superior Colliculus
One might still ask how the superior colliculus actually allows for saccades to occur? This is a good question that to this day has left researchers questioning as to how it actually plays out. What is known, however, is that the basal ganglia does have effects on the SC and consequently on the outcome of saccadic eye movements. The substantia nigra pars reticulata (SNr), a major output station of the basal ganglia, controls saccades with its inhibitory connection to the SC. These cells control the SC in the same way the omnipause cells control the burst neurons in the PPRF. Again, back to our original inquiry of saccade generation, it is the suppression of SNr activity that allows for this to happen. This suppression is mediated by inhibitory input from striatal neurons in the caudate nucleus that in turn disinhibit the superior colliculus. Interestingly, this signal appears to be modulated in reward-oriented tasks. The signal tends to be larger when a reward is expected, causing SC neurons to be more active, leading to an earlier and faster saccade (Sato et al).
The fun does not stop here. We previously described the brain stem saccade generator to be the PPRF, which receives a command from the superior colliculus. It is important to note that the SC that is receiving input from the SNr, is also receiving direct excitatory projections from the frontal eye field (FEF) and posterior parietal cortex (PPC). Thus the FEF directly excites the colliculus and indirectly releases it from suppression by the SNr by exciting the caudate nucleus, which inhibits the SNr and performs a subsequent saccade! These higher saccadic control centers such as the FEF and PPC may also include supplementary or prefrontal eye fields. The FEF forms an executive center that can selectively activate neurons in the SC and therefore play a role in the selection and production of voluntary saccades. The posterior parietal cortex is involved in the visual guidance of saccades by shaping the visual inputs to the superior colliculus, and respond more vigorously when the stimulus is the target for an eye movement.
Types of Saccades
Saccades are typically classified as voluntary or involuntary saccades. Voluntary saccades are willed eye movements in response to flashing or moving stimuli or an unseen remembered target perceived on the peripheral retina. Visually guided voluntary saccades are initiated principally by the frontal eye fields with input from the parietal eye areas and prefrontal cortex. Involuntary saccades are non-visually guided eye movements that are initiated by direct retinal input to the superior colliculus. Therefore, involuntary saccades bypass both the FEF and basal ganglia in order to rapidly elicit a saccade to an unexpected movement in the peripheral regions of the visual field. The saccades of rapid eye movement (REM) sleep, and the quick phases of a nystagmus are both examples of involuntary saccades.
Functions in the Control of Movement
Saccades function to reorient the eye's position. They are ballistic movements with velocities up to 900 degrees per second. Once the movement related neurons have begun to fire saccade must be completed, even if the target has changed its position. However with such rapid speeds of transmission the delay for a second saccade to fixate the eyes on the target's new position is minimal and humans are temporarily unable to visualize their surroundings for that minuscule time period that the eye is making the saccade. Saccades function to not only fix our gaze on moving targets far off in our visual field but they also occur during the short, quick movements of reading and during the perception of stabilized retinal targets. Therefore even when we are staring at a target our eyes are performing what are called "
," very short saccades completed because the human visual system needs variety in stimulation. Research has shown that when an object is made to move in direct accordance with the movements of the eye then perception of the object quickly disappears (Martinez-Conde et al).
Microsaccades are depticted here as the straght lines and "drift" is the jagged lines. This represnets the short saccades produced to maintain variation in visual stimulation.
The brain's two tasks in completing a saccade involve monitoring the amplitude and direction of the eye's movement. This intricate process occurs in the 200 milliseconds before for any movement of the eyes towards their desired target begins. The brain calculates the target's position with respect to the fovea and uses this intended position compared to its current position to determine the necessary motor command to the extraocular muscles. Movement related neurons in the superior colliculus are direction specific. They individually fire most intensely in that 200 milliseconds before eye movement in response to a target in a specific direction. Although highly direction specific, these neurons are grouped into movement fields which fire in response to a wide range of targets with no single cell's firing being capable of really altering the direction of saccade--it is ultimately the movement field that determines amplitude and direction. The frontal eye fields also have movement related neurons which fire before and during the saccade and are more related to behavior than visual targets. This firing not only excites movement related neurons in the superior colliculus directly but it also disinhibits the substantia nigra's control on the superior colliculus' movement related neurons as well (Lee et al).
Signs of Dysfunction
The superior colliculus and the frontal eye fields are responsible for the onset and direction of saccadic eye movements. A lesion in the frontal eye fields leads to a temporal inability to perform saccades to the contralateral side as well as a drifting of the eyes to the hemisphere of the lesion. Frontal eye field lesions cause persistent deficiencies in patient's ability to direct their gaze away from a target (performance of
) and to redirect their gaze to the remembered position of a target that has been removed from their visual field. A lesion in the superior colliculus temporarily alters the frequency, velocity and accuracy of saccades. These changes are transient but permanent damage results from lesions of these critical areas as well. Superior colliculus lesions cause a persistent inability to perform "
," the fastest type of saccade which normally bypasses the frontal cortex (Fischer et al, Schiller et al, 1980 & 1987). A posterior parietal lesion reduces the eyes' ability to remain undistracted from their visual target in this world of constant visual stimulation. Lesions in this area cause patient's eyes to also miss their target and vary in the amount of time necessary to reach their target (Lynch et al).
The performance of saccades can actually be indicative of dysfunction in other parts of the central nervous system. Saccades manifest themselves as quick movements to bring the eye back to correct fixation after they have drifted during a
. This occurs when a lesion to the vestibulocerebellum hinders the eyes' ability to maintain the direction of gaze. Therefore both the absence and presence of saccades can be associated with lesions to the CNS.
Vision is a complex process requiring continuous eye movement. Saccades are crucial to the human ability to see and understand what they see. If the eye cannot perform saccades the brain will not receive continual accurate visual information. Although saccades can be produced with lesions to either the frontal eye fields or the superior colliculus, damage to both regions causes an ability to produce visually guided eye movements (Schiller et al.).
Glossary of Terms
pontine cells responsible for the quick deviation of the eyes during a saccade; produce the "pulse" component. Horizontal saccades are generated by burst cells located in the paramedian pontine reticular formation and vertical saccades have burst cells located in the rostral interstitial nucleus of the medial longitudinal fasiculus in the mesencephalic reticular formation
Inhibitory burst neurons
--receive input form medium-lead burst neurons to inhibit the contralateral abducens nucleus
--pontine cells located in the dorsal raphe along the midline which receive input from the superior colliculus and project to the burst cells; they tonically fire as a means of inhibiting saccadic eye movemnets
-- short involuntary saccades produced to maintain variation in visual input during visual fixation
-- voluntary saccades away from a target that would otherwise cause a reflexive involuntary saccade
-- fastest type of saccade; visually guided
--eye movement indicative of brainstem or cerebellar dysfunction; a nodding of the eyes which entails a slow drift to one direction and a fast saccade back to the intended gaze direction
-Eye Movements by Tutis Vilis: excellent supplementary material for saccadic eye movements
- fun interactive site for eye movements
Saccades- Reflexive & Volitional.pdf
Research article on reflexive vs. volitional saccades
SEF and SEM.pdf
Research article on the role of supplementary eye field in saccadic eye movement
1. What structure is bypassed during involuntary saccades?
(a) frontal eye fields
(b) superior colliculus
(c) basal ganglia
(d) A & C
(e) B & C
(f) all of the above
2. What is not a function of the rostral region of the superior colliculus?
(a) represent the fovea as the fixation zone
(b) synapse directly on omnipause cells
(c) excite the caudal region of the superior colliculus
(d) project to the nucleus of the dorsal raphe
3. When the eye is not producing a saccade which of the following is true?
(a) the omnipause neurons inhibit the burst neurons
(b) the SNr excites the omnipause neurons
(c) the burst neurons excite the abducens nucleus
(d) A & B
(e) none of the above
4. When are saccades performed?
(a) when voluntarily fixating gaze on a new visual target
(b) when involuntarily fixating gaze on a stimulating peripheral target
(c) when staring at a picture on the wall
(d) A & B
(e) all of the above
5. When do movement related neurons fire most intensely?
(a) 200 milliseconds before eye movement in response to a target in a specific direction
(b) 200 milliseconds before eye movement in response to a target in a wide range of directions
(c) 200 milliseconds before eye movement in response to a moving target
6. What are the results of a lesion to the frontal eye field?
(a) permanent inability to perform express saccades
(b) permanent inability to perform antisaccades
(c) a drifting of the eyes to the hemisphere of the lesion
(d) temporal inability to perform saccades to the contralateral side
(e) A B & C
(f) B C & D
(g) all of the above
7. What are the results of a lesion to the superior colliculus?
(a) temporarily alteration of the frequency, velocity and accuracy of saccades
(b) permanent inability to perform antisaccades
(c) permanent inability to perform express saccades
(d) A & B
(e) B & C
(f) C & A
8. Saccade centers in the brainstem are indirectly receiving input from
(a) broadman's area 6
(b) superior colliculus
(c) ventral streams
(d) substantia nigra compacta
(e) none of the above
9. Saccadic eye movements are an important function in the regulation of human movement and typically occur in the horizontal plane. The following would be an example of this:
(a) watching a train pass by
(b) walking on the road and quickly looking up at an airplane passing above you
(c) posing for a family picture and suddenly become distracted by uncle Larry in the periphery and insist at looking at what he is doing
(d) all of the above
1. Saccadic eye movements that result from non-visually guided target are controlled and generated in the same cortical and brainstem areas as REM sleep and the quick phase of the nystagmus.
Simply because these movements occur so rapidly there generally is not enough time for visual feedback to modify the course of a saccade and instead saccades follow a stereotyped profile that is largely determined by the size of the movement.
3. An individual with a lesion in the ipsilateral Medial Longitudinal Fasciculus (MLF) would not be able to generate a complete saccade.
4. The velocity at which you perform a saccade can be controlled in voluntary, or visually-guided saccades.
5. Tonic neurons in the nucleus of dorsal raphe are located in the brainstem and are responsible for holding the eyes in the desired position after the initial burst of activity from the rostral superior colliculus.
6. Output from the omnipause neurons is modulated by the superior colliculus and is what releases burst neurons in the PPRF from inhibition and allows for saccades to be generated.
7. Vision is an active process where the eyes are never still and consequently the eyes are constantly making "mini" jumps, or microsaccades to receive the visual field.
8. Saccades are a result of both sensory and motor information including input and output to and from somatosensory receptors in the periphery.
9. Reading this wikipage is an example of performing successive saccades.
10. After reviewing this page and successfully learning the neurological control and regulation of saccades, you are going to tell everyone you know and explain to them how and why we generate saccadic eye movements.
Short Answer Questions:
1.) What structures are involved in voluntary but not involuntary saccades?
2.) What are the differences between express saccades, microsaccades and antisaccades?
3.) What is the function of an omnipause neuron when the eyes are not generating saccades?
Describe the neurological mechanism behind performing a voluntary horizontal saccade.
( D C D E A F F E C)
1.) Frontal eye fields, posterior parietal cortex, substantia nigra reticula, caudate
2.) Express saccades are the most rapid saccades and they like antisaccades are voluntary. Antisaccades are to foveate away from a distracting stimulus while microsaccades are very short involuntary saccades done to maintain variation in visual stimulation to the brain.
3.) To inhibit burst neurons from firing and producing saccades. Omnipause neurons put the brakes on saccade generation.
To perform a voluntary horizontal saccade the frontal eye fields and the posterior parietal cortex excite the caudate which excites the Substantia Nigra Reticula (SNr). The SNr inhibits the superior colliculus which then inihibits the omnipause neurons of the dorsal raphe so that the burst neurons of the paramedian pontine reticular formation are released from inhibition and they can excite the abducens nuclei. The abducens then directly excites the ipsilateral lateral rectus muscle of the eye and through the medial longitudinal fasiculus excites the contralateral medial rectus muscle. The eye then makes a quick movement (up to 900 degrees per second) to foveate the new target. The prepositus hypoglossi is then responsible for maintaining the eye’s position, keeping it from drifting back to where it was. Even once you fixate on your desired target your eyes are still performing microsaccades to maintain variation in visual stimulation.
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Journal of Neurophysiology
Edelman A, Xu KZ, (2009). Inhibition of voluntary saccadic eye movement commands by abrupt visual onsets.
Journal of Neurophysiolgy.
Fischer B, Ramsberger E. Human express saccades: extremely short reaction times of goal directed eye movements. Exp Brain Res (1984) 57:191-195
Kandel ER, Schwartz JH, Jessell TM (2000).
Principles of Neuroscience.
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Lynch JC, McLaren JW, (1989). Deficits of visual attention and saccadic eye movements after lesions of parieto-occipital cortex in monkeys.
Journal of Neurophysiology
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Essentials of Clinical Neuroanatomy and Neurophysiology.
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Sato M, Hikosaka O, (2002). Role of primate substantia nigra pars reticulata in reward-oriented saccadic eye movement.
Journal of Neuroscience.
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Journal of Neurophysiology.
- jiggly eye balls
saccade reaction time
--- microsaccade picture
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