Neurophysiology Of Saccadic Eye Movements Biology Essay

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Eye movements are generally of two main types: one that stabilises gaze and other that shift gaze. The eye movements are divided into six functional classes; smooth pursuit, vetibulo-ocular reflex, vergence movements, gaze holding, optokinetic movements and saccadic eye movements.

Saccades are rapid eye movements that shift the line of sight between successive points of fixation (fig 3-1). Saccades include range of behaviours that encompasses voluntary and involuntary shift of fixation, quick phases of vestibular and optokinetic nystagmus, and the rapid eye movements that occur during REM sleep.

In primary visual cortex (V1, Broadmann area 17), the location of a visual stimulus is represented by the distribution of activity on the surface of the cortex: different parts of this cortical map correspond to different locations on the retina. The neural representation of the motor command for the saccade response by brainstem neurons is quite different. The ocular motoneurons encode the characteristics of the saccade in terms of their temporal discharge; the size of the saccade is proportional to the total number of discharge spikes. The ocular motoneurons lie in the third, fourth, and sixth cranial nerves and cause the extraocular muscles to move the eyes with respect to the head. This means that the brain must transform the stimulus, which is encoded in terms of the location of active neurons within visual cortex (i.e., place-coded), into the saccadic command on ocular motoneurons, which is encoded in terms of discharge frequency and duration (i.e., "temporally coded"). Furthermore, a transformation from retinal coordinates into craniotopic coordinates is necessary. The retinal coordinates are two dimensional whereas the eye rotates about three axes. (132)

Brain stem controlling generation of saccades


Electrophysiological studies of the behaviour of ocular motoneurons in monkeys have delineated the changes in innervations that accompany saccades. During a saccade a high-frequency burst of phasic activity can be recorded from the agonist ocular muscle, and as shown in experimental animals, from the corresponding ocular motoneurons. This burst of activity, the saccadic pulse of innervations, starts 8 ms before the eye starts to move (725), and generates the forces necessary to overcome orbital viscous drag so that the eye muscle and its new position against orbital elastic restoring forces. The transition between the end of the pulse of innervations and the beginning of the step of innervations is not abrupt but gradual, taking up to several hundred milliseconds. This is the slide of innervations. Hence the change in innervations accounting for saccades is actually a pulse-slide step (Fig 5-3b) (510, 573).

If one records from the antagonist muscle or its motoneurons, one finds reciprocal innervational changes (656). The antagonist muscle is silenced during the saccade by an inhibitory, off-pulse of innervation; at the end of the saccade, the antagonist assumes a new, lower level of tonic innervation, the off-step. Measurements of the muscle forces generated by extraocular muscles indicated that eyes comes to rest at the end of the saccade owing to the viscous forces of the orbital tissues rather to than any "acting braking" by the antagonist muscle (463).


Two types of neurons are critical of the brainstem network that generates Premotor commands for saccades: burst neurons and Omnipause neurons (Fig 3-9 (98). Following saccade, the eye is held in position by a tonic, step-command that is generated by the neural integrator. Classic basic and clinical studies have demonstrated that the caudal pons is important for horizontal saccades and the rostral mesencephalon for vertical saccades (206, 675). For horizontal saccades, burst neurons within the paramedian pontine reticular formation (PPRF) are essential (See box 6-3, Fig 6-1, and Fig 6-2) (311). For vertical and torsional saccades, burst neurons within the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) play the equivalent role. (see Box 6-5, fig 6-3 and Fig 6-4). Omnipause neurons lie in the nucleus raphe interpositus, in the midline of the pons (see box 6-3 and Fig 6-2).



In humans, excitatory burst neurons (EBN) lie in the PPRF, rostral to the abducens nucleus, corresponding to the medial part of the nucleus reticulus pontis caudalis (316, 681). The EBN begin discharging at a high frequency, about 12 ms prior to, and time-locked with, the horizontal component of all types of saccades and quick phases (286, 725). Electrophysiological evidence suggests that some individuals EBN in the PPRF encode saccade monocularly (i.e. movements of one eye or the other. EBN discharge preferentially for ipsilateral saccades and they appear to create the immediate Premotor command that generate the pulse of activity for horizontal saccades. Three pieces of evidence supports this hypothesis. First, during saccades, the instantaneous burst cell firing rate of EBN is closely correlated with instantaneous eye velocity, (288, 725) and the total number of spikes in the burst of activity (the integral of discharge rate) is proportional to the amplitude of the ipsilateral saccades (118). Third, a unilateral lesion within the PPRF abolishes the ability to generate ipsilateral saccades (287). Note, however that EBN in the PPRF also discharges during vertical and oblique saccades, (725) and bilateral PPRF lesions not only abolish horizontal saccades but also causes slowing of vertical saccades (273, 287).

The EBN project directly to the ipsilateral abducens nucleus, where they contact both abducens motoneurons and internuclear neurons. Abducens internuclear neurons project up the contralateral MLF, to contact the medial rectus subgroup of the contralateral oculomotor nucleus (Fig 6-1). Thus for example, during rightward horizontal saccades, the excitatory pulse reaches the ocular motoneurons from EBN in the right PPRF. The EBN also project to the perhypoglossal and vestibular nuclei, which are important for integrating the saccadic pulse into a step, to hold the eye steady at the end of the saccade. In addition, EBN also project to cell groups of the paramedian tracts (See box 6-4) which relay a copy of all ocular motor commands to the cerebellum.

Inhibitory burst neurons (IBN) for horizontal saccade have been identified just caudal to the abducens nucleus in the nucleus paragiogantocellularis dorsalis of the dorsomedial portion of the rostral medulla (315, 682). The IBN receive inhibitory inputs from Omnipause neurons and contralateral IBN; they receive contralateral excitatory inputs from the superior colliculus (689). The IBN send their axons across the midline to the contralateral abducens nucleus to inhibit contralateral abducens motoneurons and interneurons during ipsilateral saccades. Like EBN, IBN also project to the vestibular nuclei, nucleus prepostitus (neural integrator), and to cell groups of the paramedian tracts (682). One role of IBN is to silence activity in the antagonist muscle during horizontal saccade. A second role may be to help end the saccade when the eye is on target (549). The synaptic connections between EBN and IBN in the pons and medulla is postulated to form a neuronal network (Fig 3-10), in which IBN inhibits IBN, thereby forming positive feedback loops that are potentially unstable, leading to high-frequency saccadic oscillations, such as ocular flutter (553).


The EBN in the riMLF encodes the vertical and the torsional components of saccade, just as EBN in the PPRF encode the horizontal component (97, 314, 356, 736). Excitatory EBN for upward and for downward saccades appear to be intermingled in the riMLF, although their projections pathways show some differences (459, 460). Thus, it appears that upward EBN in the riMLF project only bilaterally to motoneurons, but downward EBN project only ipsilaterally (Fig 6-5). Electrophysiological studies have shown that EBN discharge most vigorously for rapid eye movements that rotate the eyeball in a plane parallel to that of a pair of reciprocally acting vertical semicircular canals (e.g., right anterior and left posterior canals) (736). For example, EBN in the right riMLF increase their discharge when the right eye extorts and the left eye intorts. While the direction of torsional is fixed for EBN on each side, the direction of vertical rotation is upward in some and downward in others. Bilateral lesions in riMLF abolish all vertical and torsional saccades (690).

Recent studies suggest that in monkey, the riMLF does not contain inhibitory burst neurons. Instead, the adjacent interstitial nucleus of Cajal, and surrounding reticular formation, contains neurons that send GABAergic projections to contralateral ocular motoneurons in CN III and IV and could turn out to be vertical IBN (311). Reciprocal connections between vertical EBN and IBN seem possible, so that a neural network similar to that possible, so that a neural network similar to that postulated for horizontal saccades could account for vertical saccadic oscillations.

In additions to their projections to ocular motoneurons in the CN III and CN IV nuclei, vertical EBN also send axons collaterals to the interstitial nucleus of Cajal (Fig 6-4 and Box 6-6) (459, 60). The latter structure appears to contain not only vertical IBN, but also burst-tonic neurons, thus contributing to the velocity-to-position integrator for vertical and torsional eye movements. This scheme is supported by the results of pharmacological inactivating the interstitial nucleus of Cajal; vertical and torsional saccades can still be made, but there is centripetal post-saccadic drift, indicating impaired vertical gaze-holding (131).


Omnipause cells lies in the nucleus raphle interpostitus, which is located in the midline between the rootlets of the abducens nerves (fig 6-2) (99,379). Omnipause neurons utilize glycine as their neurotransmitter, consistent with their inhibitory function. An important crossed projection to the Omnipause cell region arises from the rostral pole ("fixation zone") of the superior colliculus (11, 220, 221). Additional projections to the Omnipause neurons are from the frontal eye fields, (677) the supplementary eye field, (631) the central mesencephalic reticular formation, the long-lead burst neurons in the rostral pons and midbrain, (627) and the fastigial nucleus (490). Omnipause cells send inhibitory projections, which are mainly crossed, to EBN in the pons, to IBN in the medulla, and to the riMLF (481, 500).

Omnipause neurons discharge continuously except immediately before and during saccades, when they pause. They stop discharging during saccades in any direction. When Omnipause cells are experimentally stimulated in the monkey, the animal is unable to make saccades or quick phases in any direction, although other types of movements, such as vestibular slow phases, can still be elicited (755). If Omnipause cells are stimulated during a saccade, the eye decelerates abruptly in mid-fight (fig 3-11) (349, 350). Based on these findings, it appears that Omnipause cells tonically inhibit all burst cells, and when a saccade is called for, the Omnipause cells themselves must be inhibited to permit the burst cells to discharge. By acting as an inhibitory switch, Omnipause cells help maintain the necessary synchronization of the activity of premotor saccadic burst neurons to drive the yes rapidly during the saccade and to keep the eyes still when the saccade is over.

Expremental lesions with excitotoxins or muscimol in the Omnipause region casue slow horizontal and vertical saccades (339, 662. This effect is perhaps surprising, given the "high gain" properties of burst neurons, and one prediction of lesioning the "saccadic switch" would be uncontrollable saccadic oscillations, such as opsoclonus. An explanation for slow saccade may be that Omnipause neurons exert paradoxical influence on burst neurons. Since they are glycinergic, Omnipause neurons normal inhibit burst neurons. However it has been shown that glycine can actually facilitate NMDA receptors currents. It has been postulated that when burst neurons synchronously receive a trigger signal from long-lead burst neurons and cessation of Omnipause discharge, the result is a post-inhibitory rebound that produces the high acceleration typical of saccades (447, 448). Thus, if Omnipause neurons are lesioned, there will be no glycine to enhance the NMDA receptor current (i.e., no post-inhibitory rebound) and saccades will be slower, depending solely on inputs from long-lead burst neurons.

Intracellular electrophysiological studies indicate that omnipause neurons receive a powerful inhibitory input that completely turns them off just before a saccade is initiated (770); this has been attributed to a "trigger signal", perhaps driven by inputs from the rostral pole of the superior colliculus. After this initial inhibition, the level of membrane hyperpolarisation of omnipause neurons is temporally linked with current eye velocity, and this sustained hyperpolarisation keeps omnipause neurons "off" for the remainder of the saccade.

Since the discharge of excitatory burst neurons is also correlated with eye velocity during the saccade, they may be the source of sustained hyperpolarisation of omnipause neurons via local inhibitory neurons called latch neurons (Fig 3-9). Certain PPRF neurons have been identified that might serve as latch neurons (444).