Biomedical Engineering Reference
In-Depth Information
Generally, saccades recorded for any size magnitude are extremely variable, with wide
variations in the latent period, time to peak velocity, peak velocity, and duration. Further-
more, this variability is well coordinated by the neural controller. Saccades with lower peak
velocity are matched with longer saccade durations, and saccades with higher peak velocity
are matched with shorter saccade durations. Thus, saccades driven to the same destination
usually have different trajectories.
13.9 SACCADE NEURAL PATHWAYS
Clinical evidence, lesion, and stimulation studies all point toward the participation of
vitally important neural sites in the control of saccades, including the cerebellum, superior
colliculus (SC), thalamus, cortex, and other nuclei in the brain stem, and that saccades are
driven by two parallel neural networks [10, 11, 15, 18, 50]. From each eye, the axons of
retinal ganglion cells exit and join other neurons to form the optic nerve. The optic nerves
from each eye then join at the optic chiasm, where fibers from the nasal half of each retina
cross to the opposite side. Axons in the optic tract synapse in the lateral geniculate nucleus
(a thalamic relay) and continue to the visual cortex. This portion of the saccade neural
network is concerned with the recognition of visual stimuli. Axons in the optic tract also
synapse in the SC. This second portion of the saccade neural network is concerned with
the location of visual targets and is primarily responsible for goal-directed saccades.
Saccadic neural activity of the SC and cerebellum, in particular, have been identified as
the saccade initiator and terminator, respectively, for a goal-directed saccade. The impact
of the frontal eye field and the thalamus, while very important, have less important roles
in the generation of goal-directed saccades to visual stimuli. The frontal eye fields are
primarily concerned with voluntary saccades, and the thalamus appears to be involved
with corrective saccades. Figure 13.57 shows the important sites for the generation of a
conjugate goal-directed horizontal saccade in both eyes. Each of the sites and connections
detailed in Figure 13.57 is fully supported by physiological evidence. Some of these neural
sites will be briefly described herein, with abbreviations provided in Table 13.2.
The Paramedian Pontine Reticular Formation (PPRF) has neurons that burst at frequencies
up to 1,000 Hz during saccades and are silent during periods of fixation, and neurons that fire
tonically during periods of fixation. Neurons that fire at steady rates during fixation are
called tonic neurons (TN) and are responsible for holding the eye steady. The TN firing
rate depends on the position of the eye (presumably through a local integrator type network).
The TNs are thought to provide the step component to the motoneuron. There are two types
of burst neurons in the PPRF: the long-lead burst neuron (LLBN) and a medium-lead burst
neuron (MLBN). During periods of fixation, these neurons are silent. The LLBN burst at least
12 ms before a saccade and the MLBN burst less than 12 ms (typically 6-8 ms) before the
saccade. The MLBNs are connected monosynaptically with the Abducens Nucleus.
The two types of neurons in the MLBN are the excitatory burst neurons (EBN) and the
inhibitory burst neurons (IBN). The EBN and IBN labels describe the synaptic activity upon
the motoneurons; the EBNs excite and are responsible for the burst firing, and the IBNs
inhibit and are responsible for the pause. A mirror image of these neurons exists on both
sides of the midline. The IBNs inhibit the EBNs on the contralateral side.
