Pretectal Complex and the Accessory Optic System

The optic tract fibers that do not synapse in the lateral geniculate nucleus are directed along the brachium of the superior colliculus toward the pretectum and the superior colliculus (Fig. 1C). The nuclei of the pretectal complex are situated within and below these fibers as they enter the dorsal portion of the brain stem at meso-diencephalic levels. The pretectal complex includes the nucleus of the optic tract, the olivary pretectal nucleus, the medial pretectal nucleus, and the posterior pre-tectal nucleus. These receive contralateral retinal efferents (Fig. 5). There is also a prominent contribution from the ipsilateral eye. There is a smaller contralateral projection from the optic tract to the medial pretectal nucleus. Other than the retina, the largest source of afferents to the pretectal nuclei is from the striate and adjacent visual association cortex, and there is also a projection from frontal eye fields and the cingulate cortex. Projections from middle temporal and middle superior temporal areas to the nucleus of the optic tract have also been demonstrated, which suggests that the nucleus may participate in smooth pursuit as well as velocity storage. Within the brain stem, the pretectal complex receives inputs from the ventral division of the lateral geniculate body, the superior colliculus, the accessory optic nuclei (medial, lateral, and dorsal terminal nuclei), and the cerebellum (dentate and interposed nuclei).

The pretectal complex provides both ascending and descending projections. The ascending efferents are primarily to the thalamic nuclei, including the intralaminar, dorsal and ventral lateral geniculate body, pulvinar, and zona incerta (subthalamus). The descending projections are clearly oculomotor and reach the interstitial nucleus of Cajal, the nucleus of the posterior commissure, the superior colliculus, the mesencephalic reticular formation, and the precere-bellar nuclei in the pons and medulla (nucleus reticularis tegmenti pontis and inferior olive, respectively). The olivary pretectal nuclei have strong projections to the contralateral Edinger-Westphal nuclei via a crossing in the posterior commissure (see the section on Edinger-Westphal nuclei for functional considerations).

The accessory optic system comprises three nuclei: medial, lateral, and dorsal terminal nuclei. These

Anterior Pretectal Nucleus Function

Figures Inputs and outputs of the pretectal complex. The degree of shading in each portion of the horizontal section through the midbrain of the monkey illustrates the distribution of transported label over the contralateral pretectal complex following an intraocular injection of tritiated amino acids. The intensity of the hatching indicates the density of the label that was transported to the pretectum from the contralateral eye. Rostral is at the top and lateral is to the right. See Table I for abbreviations. (After Hutchins and Weber, 1985.)

Figures Inputs and outputs of the pretectal complex. The degree of shading in each portion of the horizontal section through the midbrain of the monkey illustrates the distribution of transported label over the contralateral pretectal complex following an intraocular injection of tritiated amino acids. The intensity of the hatching indicates the density of the label that was transported to the pretectum from the contralateral eye. Rostral is at the top and lateral is to the right. See Table I for abbreviations. (After Hutchins and Weber, 1985.)

nuclei are located in the rostral midbrain. The dorsal terminal nucleus is located just ventral to the nucleus of the optic tract at its most lateral extension. The lateral terminal nucleus is located ventral to the dorsal terminal nucleus, just dorsal to the substantia nigra, and lateral to the red nuclei. The medial terminal nucleus is located just lateral to the central gray and ventral to the red nucleus. These structures receive separate direct retinal input via a pathway known as the transpeduncular tract, which courses on the surface of the brain stem just anterior to the superior colliculus, travels over the brachium of the superior colliculus and then posterior to the medial geniculate body, and finally runs over the surface of the cerebral peduncle to enter the brain stem at the medial edge of the peduncle where it breaks into a number of fascicles to reach each of the terminal nuclei.

Functionally the nucleus of the optic tract and the dorsal terminal nucleus are essential in the production of the slow phases of optokinetic nystagmus (OKN) to the ipsilateral side. Electrical stimulation within the nucleus of the optic tract produces nystagmus. Lesions (both electrolytic and excitotoxic) in the nucleus of the optic tract and dorsal terminal nucleus reduce the slow rise of horizontal OKN and reduce or abolish optokinetic after-nystagmus. This suggests that the indirect path for velocity storage that produces compensatory eye-in-head and head-on-body movements via the vestibular system is impaired following lesions of the nucleus of the optic tract. This suggested that one role of the nucleus of the optic tract is to stabilize gaze in space during both passive motion and active locomotion in light. These effects are probably mediated via the strong input of the nucleus of the optic tract to the dorsal cap of Kooy (i.e., via the inferior olivary climbing fiber inputs to the flocculus) because the contribution to the medial vestibular nuclei is sparse. Evidence of cells with foveal receptive fields that are sensitive to retinal slip velocity suggested a role for the nucleus of the optic tract in smooth pursuit. This idea has been strengthened by evidence of a strong efferent projection from area MT to the nucleus of the optic tract. In the cat and rabbit, the majority of neurons in the medial and lateral terminal nuclei are sensitive to motion of the visual world along the vertical (i.e., vertical OKN). These nuclei are yet to be studied in the primate.

B. Control of Horizontal Gaze in the Midbrain

The primary focus of the current discussion is to point out particular characteristics and possible functions of midbrain structures that may participate in the generation of horizontal saccades. The superior colliculus has received considerable attention in the control of rapid eye movements in both horizontal and vertical directions. A map of the contralateral field of movement has been demonstrated in the intermediate and deep layers of the primate superior colliculus using supramaximal electrical stimulation (Fig. 4). Movement fields (that is, the group of saccades that causes a cell to be activated during movements of particular size and direction) are characteristic of the neurons in the intermediate and deep layers of the superior colliculus. Cells in a particular portion of the colliculus have movement fields that correspond to the amplitude and direction of saccades electrically elicited from that site. Thus, activation of a particular group of neurons in the superior colliculus leads to the generation of an eye movement of particular size and direction. This has been called a place code. This pattern of neuronal activation is quite different from that actually required to rapidly move the eyes. The motoneurons of the abducens and oculomotor nuclei increase their discharge in relationship to the size of the upcoming movement, i.e., a temporal code. One of the primary problems that must be solved by supranuclear neurons in the midbrain oculomotor system is to change the place code activation of the SC into the temporal pattern of activity needed to rapidly shift the eyes. A second issue facing neurons arranged in a place code is how is this separated into horizontal and vertical signals required to move the eyes. The answers to both of these questions are not complete yet, but the following should provide some insight into how the brain stem performs these transformations.

The first step in solving these transformations is to reevaluate the connections of the superior colliculus with downstream structures involved in the generation of horizontal eye movement in the pontine reticular formation (Fig. 6). The superior colliculus provides both crossed mono- and polysynaptic inputs to the burst neurons in the paramedian pontine reticular formation (PPRF), the center for controlling horizontal gaze. A subgroup of burst neurons (the excitatory burst neurons) in the paramedian pontine reticular formation projects directly to the abducens nucleus, and its removal leads to a complete loss of rapid eye movement to the ipsilateral side. This signal is relayed by internuclear neurons, also located in the abducens nucleus, to the medial rectus subdivision of the oculomotor complex in the midbrain. The axons of these internuclear neurons travel in the medial longitudinal fasciculus to reach the midbrain (Fig. 6). At the same time, the excitatory burst neurons provide the

Pprf Optic Nerve

Abducens

Figure 6 Schematic diagram of the final common pathway for horizontal saccades. Supranuclear inputs to the paramedian zone of the pontine reticular formation arise from the superior colliculus and frontal eye fields in parallel. Note that X marks the location of a third nerve lesion and the filled circle is a MLF lesion. A lesion in the MLF would preserve vergence, whereas a third nerve palsy would impair vergence. See Table I for other abbreviations.

Abducens

Figure 6 Schematic diagram of the final common pathway for horizontal saccades. Supranuclear inputs to the paramedian zone of the pontine reticular formation arise from the superior colliculus and frontal eye fields in parallel. Note that X marks the location of a third nerve lesion and the filled circle is a MLF lesion. A lesion in the MLF would preserve vergence, whereas a third nerve palsy would impair vergence. See Table I for other abbreviations.

same burst signal to the neurons of the nucleus prepositus hypoglossi. This structure is responsible for changing this pulse of activity (most closely associated with eye velocity) into a prolonged step of activity that is most closely related to eye position. This step response is then relayed back to the abducens nucleus and is responsible for holding the eyes steady at the new position. The abducens motoneurons provide an axon that reaches the lateral rectus muscle, which moves the eye toward the temporal side. Similarly, the oculomotor motoneurons provide an axon that travels in the oculomotor nerve to reach the medial rectus muscle, which moves the eye toward the nose. The combination of the PPRF, abducens nucleus, oculomotor nucleus, nucleus prepositus hypo-glossi, medial rectus muscle, lateral rectus muscle, and medial longitudinal fasciculus is called the final common pathway responsible for the generation of horizontal saccadic eye movements.

Despite the clear connections of the final common pathway, how the superior colliculus directs eye movement control remains unclear. Work in the monkey suggests that the superior colliculus neurons provide monosynaptic connections to the long-lead burst neurons and not the excitatory burst neurons of the PPRF. In fact, most papers suggest that the input to the excitatory burst neurons of the PPRF is polysynaptic and not monosynaptic. The activity of long-lead burst neurons (LLBNs) is not uniform. Instead, a subgroup of LLBNs discharges only for particular directions (e.g., horizontal) of ipsilateral eye movements (directional LLBNs), whereas other LLBNs discharge for eye movements of very specific amplitude regardless of direction (i.e., vector long-lead burst neurons). As a result, one could generate a horizontal eye movement by projections of superior colliculus neurons to a select subgroup of vector LLBNs, which in turn activate the directional LLBNs and subsequently activate the excitatory burst neurons that project to the abducens nucleus. This scheme would explain the transformation from spatial coordinates in the superior colliculus to temporal coordinates in the excitatory burst neurons, as well as the selection of just the horizontal component of movement from a group of neurons that encodes both horizontal and vertical saccade directions.

Surprisingly, removal of the superior colliculus produces only minor eye movement deficits. An increased latency for saccades and the elimination of express saccades (i.e., saccades with latencies <160 msec) are seen, but there are no changes in saccade accuracy. Following injections of the GABA agonist muscimol, which produces temporary inacti-vation of the intermediate and deep layers of the SC, saccade trajectory becomes curved and most saccades are hypometric (i.e., they fall short of the target). However, bilateral removal of both the superior colliculus and the neocortical frontal eye fields produces persistent deficits in the generation of rapid eye movements in all directions. This suggests that there are two pathways for saccade signals originating in the cerebral cortex to reach the paramedian pontine reticular formation: (1) a superior-colliculus-depen-dent route and (2) an extracollicular route. These experimental findings have been confirmed by clinical experience. No clinical oculomotor syndrome has been associated with damage to the superior colliculus alone. In fact, one patient examined following removal of an angioma in the superior colliculus showed increased latency for contralateral saccades, and these movements were hypometric.

On the other hand, damage (i.e., electrolytic lesion, stroke, or tumor) to the mesencephalic reticular formation is associated with distinct problems in contraversive horizontal saccades and ipsilateral smooth pursuit. One possibility is that mesencephalic reticular formation lesions interrupt the direct projections from the frontal eye fields to the paramedian pontine reticular formation. However, as pointed out earlier, these fibers are sparse. Midbrain lesions could also interrupt fibers from the nuclei of the posterior commissure to the paramedian pontine reticular formation or other parts of the reticular formation. More likely, corticobulbar projections from the frontal eye fields and parietal cortex reach the mesencephalic reticular formation and nuclei of the posterior commissure, and these structures relay them to the PPRF.

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Responses

  • tamica mcnew
    What does the pretectal area do in brain?
    3 months ago

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