Internuclear Oculomotor Control The Final Common Pathway

Zones within the tegmental reticular formation in the brain stem serve to combine the various eye movement commands and to present an integrated set of final motor commands to the ocular motor nuclei. The PPRF refers to the zone surrounding cranial nerve Vi nucleus on either side of midline in the pontine tegmentum. This area contains burst and pause cells that are important for horizontal saccade generation. The rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), the interstitial nucleus of Cajal (iC), the nucleus of Darkschewitsch (nD), the nucleus of the posterior commissure (nPC), and adjacent portions of the mesencephalic reticular formation (MRF) probably supply burst and pause commands for vertical saccades, and pass the final innervation pattern to the nuclei of the third and fourth cranial nerves. The integration of these systems has been reviewed extensively by Leigh and Zee. y

Commands for saccades and pursuit descend in the brain stem via supranuclear eye movement pathways outlined earlier. In addition, the vestibular nuclei in the medulla and the flocculi and noduli of the cerebellum provide vestibular inputs to both the horizontal eye movement system in the PPRF and to the vertical eye movement zones of the mesencephalic reticular formation, primarily the riMLF and iC. The final command signal for saccades and pursuit movements that descend on the ocular motor nuclei is a composite of inputs from a direct pathway and a pathway through the neuronal circuitry that performs a mathematical integration on the direct signal. This neural integration is probably a distributed function with components from the cerebellum (especially flocculus and paraflocculus), the nucleus prepositus hypoglossi, and the medial vestibular nucleus (MVN) for horizontal gaze and the iC for vertical gaze. The PPRF was once thought to perform this function, but it has been established that lesions of this structure spare gaze holding, the primary function of the integrator for saccades.

Normal saccade velocity depends on normal function of burst neurons (velocity command) that provide the acceleration part of the movement. Without a proper burst, the resulting saccade is slow. The neural integrator produces a tonic step of innervation (position command) that is at just the right firing rate to sustain eye deviation at the endpoint of the saccade. When the neural integrator is leaky and produces a step innervation at too low a frequency of action potentials, the eyes reach the target accurately and with normal velocity on account of the burst. They then, however, drift back toward primary gaze, because the step or holding function is inadequate. After a certain amount of drift, a position error signal is generated calling for another saccade. This results in a repetitive cycle of saccades and back drifts that is called gaze-evoked nystagmus (see later).

When a novel visual stimulus calls for a saccadic refixation or when a command to look at a new fixation target is given, there is an obligate latent interval of between 100 and 200 milliseconds. This latent interval includes time for the visual stimulus in the peripheral field to travel along afferent pathways to the cerebral cortex, where the spatial coordinates of the object to be foveated are turned into motor commands or vectors having both direction and amplitude specifications. This computation of vectors and passage of the efferent commands to the brain stem requires additional time. It has also been postulated that the system works via intermittent data samples rather than continuous intake of afferent data. Thus, if a novel visual stimulus occurs just after a sample is taken, it will have to wait for the next sampling interval, perhaps 40 to 50 milliseconds later, before entry into the system. This could explain much of the latency variability observed for generation of individual saccades. The generation of saccades is a much more complex entity, however, and there is considerable controversy as to whether saccade vectors are calculated through intermittent or continuous sampling. It is also unclear whether saccade motor commands can be modified as the eyes are in motion during a saccade. Under ordinary circumstances, saccades behave as a ballistic movement--as with a thrown ball, the saccade trajectory is not modifiable after the movement begins. Under special test circumstances, however, it seems that some individuals are capable of modifying saccade trajectory in midflight. These special features of a few saccades in normals have not yet been adequately explained by existing models of brain stem circuitry.

Pursuit movements also depend on the combination of a velocity and position signal. When the direct innervation is not present, the eyes eventually attain the velocity of the stimulus, but the beginning acceleration to that velocity is slow. For pursuit commands, the direct pathway carries a step command, which is the velocity signal, and the neural integrator produces a ramp command that is the position signal. The slow eye movements of the vestibulo-ocular system also depend on a combined step-ramp signal for normal trajectory.

The organization of the vertical eye movement system is complex and incompletely understood at present. It appears that the riMLF contains primarily burst neurons that generate vertical saccades. Cells of iC, nD, nPC, and MRF carry the fully assembled burst-step firing pattern needed to perform saccades, pursuit, and vestibulo-ocular movements, as well as to hold the eyes in eccentric positions of gaze. Nuclei at the pontine and medullary levels are important in control of vertical eye movements. Bilateral lesions of the MLF, which carries complex ascending influences from vestibular nuclei and PPRF gaze centers, abolish vertical pursuit and VOR movements but spare saccades. Thus, the riMLF apparently has functional connections with the cerebral hemispheres independent of supranuclear pathways that operate via the PPRF. Although vertical saccades are spared with bilateral lesions of the ascending pathways, the eye position signal is abolished, and gaze paretic nystagmus occurs with upgaze and downgaze effort.

Efferents from the PPRF on one side connect with large motor cells in the ipsilateral sixth nerve nucleus for

abduction of the ipsilateral eye and with small cells in the same nucleus, which, in turn, connect via the MLF with the opposite medial rectus subnucleus of the third nerve for adduction of the contralateral eye. Thus, a contraversive (opposite direction) saccade command from the right hemisphere descends to the left PPRF, then to the left abducens nucleus for abduction of the left eye and adduction of the right eye via the right MLF. This circuitry thereby produces conjugate gaze contralateral to the hemisphere issuing the command and ipsilateral to the activated PPRF. This network is illustrated schematically with participating brain stem and hemispheric pathways for conjugate leftward gaze (Fig. 9-7 (Figure Not Available) ). Thus, the brain stem connections for ocular motility are arranged to provide conjugate gaze. Lesions affecting the internuclear gaze pathways distal to the PPRF, through the MLF, produce disconjugate gaze palsy such that only the abducting eye ipsilateral to the activated abducens nucleus has full deviation, often with dissociated or monocular nystagmus. The contralateral adducting eye moves either incompletely or slowly. The eyes, however, remain straight with parallel visual axes when viewing objects at a distance in the primary position of gaze, which distinguishes iNo from a cranial nerve III lesion or a primary defect of the medial rectus muscle, either of which causes divergence of the visual axes (exotropia) in primary gaze.


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