Part 10
SC, after recovery, can generate saccades even in the absence of the frontal eye
fields, having its own visual inputs
Subcortical saccadic circuit
Horizontal and vertical/torsional saccadic systems are closely interconnected
Share the same cortical areas, cerebellar areas and the superior colliculus
Clear anatomical parsing of the horizontal and vertical/torsion saccadic pathways
after the SC
Due to the anatomical separation of the horizontal and vertical/torsion
EBN/IBNs
The SC is the element that contains the spatio-temporal coding for saccades
SC command is further refined by the local feedback loop and cerebellar
innervation
Contralateral saccadic commands from the SC, parsed in horizontal and
vertical/torsional commands, cross and are transmitted to the ipsilateral horizontal
and vertical/torsional LLBNs
LLBNs then connect to the ipsilateral MLBs, also called EBNs
OPNs act as gates between the two groups with a very strong inhibition on the
EBNs
Excitatory burst neurons
For horizontal saccades: located in the PPRF
For vertical/torsion saccades: located in the riMLF
The SC consists of 7 layers
Dorsal layers are “visual” with the firing related to the appearance of a target in
the cell’s receptive field
No response to the movement generated by the stimulus
Precise retinal map coming directly from the contralateral retina and the
contralateral striate cortex (V1)
Conjugate rotations of the eyes + head movement are elicited when the head is
free and the elicited movement large
There is a motor map in the motor (intermediate) layers
Each location is associated to a precise motor vector (size and direction of the
movement)
The rostral pole of the SC has cells that fire tonically during fixation
If stimulated, they suppress the execution of an impending saccade
Seems to be a reciprocal inhibition between the rostral and the caudal areas of
the SC
By interrupting, through the OPNs, the flow from the LLBNs to the EBNs they can
stop the movement while occurring
Massive bilateral SC lesions (after an acute phase of profound deficits) show a
remarkable recovery
Suggests that probably a combination of FEF and cerebellar adaptations are able
to compensate for the loss of the SC
Most significant residual effects
Hypometric movements (smaller than needed) with higher number of
corrective saccades
Decrease in the frequency of scanning saccades while looking at a visual
scene
Complete loss of express saccades during the gap paradigm
The SC is responsible for the fast acquisition of the new target in the gap
paradigm
There is a “decision making” between the visual and motor layers
There is a selection process with a “winner take all” between the visual and
motor layers with cortical involvement, most likely from the FEF through the
basal ganglia
The motor layers are not just a carbon-copy of the visual layers
Basal Ganglia
Substantia nigra pars reticulate (SNpr)
Inhibitory connections to the intermediate layers of the SC
Main input probably from the frontal and supplementary eye fields through
the caudate nucleus
Cells have elevated static firing rate; normally slow down significantly in
correspondence to the presentation of a visual target
SNpr cells two main functions with respect to the saccadic system
Exerts tonic inhibition on the SC cells with a pause associated to the behavior
they “represent”
Inhibition is GABAergic
Projection is selective; there is a match between the movement fields of
the SNpr cells and the movement field of the SC cells
SNpr cells related to that specific saccadic size/direction stop allowing
the appropriate location of the SC to fire
Play a role in the initiation of voluntary saccadic eye movements
Basal ganglia circuit is an active behavioral gateway between cortex and SC
Chemical inhibition of these areas decreases the latency of the eye movements
with a stronger bias towards reflex-like behavior
Their function is to selectively release a neuronal target from tonic inhibition
An absence of this release action (a maintenance of an elevated tonic
inhibitory action even a movement is desired) is going to interfere with the
desired movement, up to its cancellation
Loss of dopamine in Parkinson’s generates an abnormal increase in the tonic
activity of these structures
Makes the generation of the selective pause that allows the movement and
the movement itself much harder
Caudate nucleus is an integration center of information from FEF, SEF, DLPC, the
IML lamina of the thalamus, SNpc
Major projections to the SNPr and globus pallidus
Pre-saccadic activity shows a strong dependence on memory, ecpectation,
attention, and reward
Lesion of this area affects mainly memory saccades
Intramedullary lamina is believed to be a source for an efferent copy of the eye
movement to the cortical eye fields
Stimulation of the FEF elicits saccades of a given size and direction, similarly to the
SC with a latency of 30-45 ms
Movement usually oblique or horizontal
Pure vertical saccades achieved only by bilateral stimulation
Different subpopulations of cells code the visual stimulus, the movement, or both
The activity is not coding the saccadic dynamics or motor error and does not
act in normal conditions as a spatio-temporal transformer like the SC
Heavily involved in the generation of memory saccades
Acute pharmacological lesions cause an immediate oculomotor scotoma (the
abolition of any kind of saccades in the area affected by the lesion)
Main effects are increased saccadic latency and inaccuracy of visual and
memory saccades coded in that area (relatively minor effects)
Main feature of the supplementary eye fields is that it seems to code complex
(learned) saccadic behaviors, like anti-saccades and sequences of saccades
Lesions can inhibit a subject from executing a learned sequence of saccades
Dorsolateral prefrontal cortex seems to be involved in the holding of the memory of
where a memory saccade is going to be directed; similar effect for anti-saccades
Damage is mainly affecting memory saccades and anti-saccades
FEF, SEF, and DLPC can be seen as cortical supervisor/decision makers of the
saccadic system
Capable of generating complex motor behaviors
Decisions are transmitted to the basal ganglia and the SC, eventually
overwriting (when needed) the reflexive behavior of the SC
Parietal areas are NOT directly involved in the generation of saccadic eye movement
Responsible for the spatial reorganization for the sensory space when you move
Posterior parietal cortex contains cells that respond to visual stimuli and discharge
after saccades have been made
Also critical in the programming of complex movements, like saccadic gaze (eye
+ head) shifts toward selected targets, eye, head, and hand coordination that
require a spatial frame of reference
Acute unilateral posterior parietal lesions cause contralateral inattentions
Bilateral lesions are associated with Balint’s syndrome
Area LIP is a critical for a number of eye movements
Discharges before a saccade and there is coding of eye position
Their visual response field shifts in order to anticipate the change in visual frame
reference associated with the incoming eye movement
They seem to code the info where to go next in a memory saccade
Main effect of lesions is a prolonged latency of visually-guided saccades
during gap and overlap trials
Patient is also unable to respond to double-step tasks
NRTP
Contains neurons that discharge in relation to a variety of eye movements
Lesions cause torsional errors
Dorsal vermis
The amount and duration of stimulation in the dorsal vermis directly modulates
the saccadic dynamics and size
Plays a role in the fine tuning of the saccadic response
The control is on the pulse part of the saccade (because there is no postsaccadic drift)
Unilateral damage causes marked ipsilateral hypometria and mild
contralateral hypermetria
With longer latencies for ipsilateral saccades and abolition of express
and anticipatory saccades
Adaptation of saccades to modified visual correspondence is lost after
damage to the dorsal vermis
Fastigial Nucleus
Actual adaptation center
Outputs project to practically all subcortical saccadic structures
Discharge ~8ms before the movement with a contralateral component and
around the end of the saccade with generally an ipsilateral component
Gives an additional acceleration drive to the burst neurons for contralateral
saccades and an additional late brake during ipsilateral ones
Bilateral lesions produce marked hypermetria in all saccades
Complete cerebellectomy affects the pulse component of the saccade with
hypermetria
Also major post-saccadic drift (pulse-step mismatch)
Cerebellum can almost completely compensate for the loss of the SC or the FEF
(but not both)
Saccadic abnormalities
Main features quantified in a saccadic response are
Gain, defined as the ratio between the size of the movement executed and
the required size
Duration, defined as the distance between two given velocity thresholds
Peak velocity (deg/s)
Post-saccadic drifts
Latency
Presence of saccadic intrusions: presence of involuntary saccades while the
subject is fixating
Pulse dysmetria
Pulse lasting too much (overshoot, hypermetria)
Pulse lasting too little (undershoor, hypoemetria)
Pulse with a low gain but with an abnormally low peak velocity
Pulse with too much gain, with an abnormally high peak velocity
Memory saccades, saccades in the dark, saccades during decreased alertness, and
during vergence eye movements are often slower than normal visually-elicited
saccades
Abnormally slow saccades are usually associated with problems in the generation or
maintenance of the saccadic pulse in the saccadic bursters
More central disorders (involving SC or FEF) also generate slower saccades
Gaze-evoked nystagmus is usually a sign of loss of the neural integrator
The saccadic system detects the error and generates another saccade and the
cycle repeats: nystagmus
In the pulse-step mismatch there is still a neural integrator but the integrator gain is
altered
Two other common aspects are difficulties in generating a saccade or the generation
of saccades when not wanted (saccadic intrusions)
Significantly longer latencies or no saccades are usually signs of cortical
problems
Saccadic intrusions mean the inability of a subject to suppress unwanted
saccades
When the overshoot is very large, the subject is not able to reach the target and
engages in an oscillatory pattern called macrosaccadic oscillations
Macrosaccadic oscillations are a typical expression of huge hypermetria (often
associated with cerebellar disease)
Look at graph