In contrast to the saccadic control, the conjugate pursuit system of each hemisphere controls binocular eye movements
Figure 9-6 (Figure Not Available) Hypothetical cortical pathways involved in saccade control. The cortical relays of saccade pathways are represented by arrowheads. FEF, frontal eye field; H, hippocampal formation; OC, occipital cortex; PEF, parietal eye field; PFC, prefrontal cortex (i.e., area 46 of Brodmann); PPC, posterior parietal cortex; SC and RF, superior colliculus and reticular formation; SEF, supplementary eye field; SPI, superior parietal lobule; T, thalamus; VC, vestibulafFrom Pierrot-Deseilligny C, Rivaud S, Gaymatd B, et al: Cortical control of saccades. Ann Neurol 37:557-567, 1995.)
to the ipsilateral visual space.y Occipital visual areas (Brodmann 18 and 19) provide input on spatial vectors to the middle temporal (MT) and medial superior temporal (MST) cortexes. These areas are of primary importance in generating smooth conjugate pursuit eye movements. y , y Efferents from MT and MST travel to the FEF, posterior parietal cortex, and brain stem reticular formation. Brain stem connections undergo a double decussation, resulting in each hemisphere's controlling ipsilateral smooth pursuit eye movements. y , y Selective lesions of MST bring about bilateral reduction of pursuit gain over the entire movement field, although this is most pronounced for ipsilateral pursuit. y Optokinetic nystagmus (OKN) gain is reduced by MST lesions.y Optokinetic nystagmus occurs when a series of vertical bars or a similar pattern is passed in front of the eyes. There is a slow following phase and a rapid jerk in the opposite direction. y Selective MT lesions produce impaired initiation of pursuit with motion in either direction in the contralateral hemifield of vision. y
Large cortical lesions, involving either frontal or parietal lobes, generally are associated with ipsilateral conjugate eye deviation that lasts a few days. y In these cases, forceful eye closure may be associated with conjugate eye deviation contralateral to the lesion. y Bilateral posterior cerebral hemisphere lesions lead to Balint's syndrome, in which pursuit eye movements and OKN movements are defective in all directions and visually guided saccades have increased latency and diminished accuracy with relatively preserved intentional saccades. Involvement of angular gyrus and superior parietal cortex is thought to be responsible for the visual inattention that accompanies this syndrome. Optic ataxia refers to the inability of the patient to make accurate eye or limb movements under visual guidance. These patients also have a distinctive visual perceptual abnormality in which they cannot synthesize large visual figures that require multiple fixations to encompass. This is caused in part by the inability to make accurate saccades to the elements of the extended visual figure. This perceptual problem has been called amorphosynthesis or simultanagnosia by various authors.
Subcortical nuclei and pathways are undoubtedly important in generating smooth pursuit, although the result of focal lesions of these structures is uncertain. The thalamic pulvinar receives direct input from the retina and SC, and it projects to several cortical areas involved in the generation of eye movement. There is evidence that the pulvinar may function in visual suppression during saccades to eliminate perception of image motion as the eyes are traveling to a new fixation point. The pulvinar may also play a role in shifts in spatial attention and efference copy by which brain stem ocular motor structures provide feedback to cortical eye movement control systems about the moment-to-moment state of the eye movement. The internal medullary lamina of the thalamus receives input from brain stem nuclei, including the SC, vestibular nuclei, and nucleus prepositus hypoglossi, and provides reciprocal connections to the FEF, SEF, and PEF in the cerebral hemisphere. The clinical result of lesions involving the internal medullary lamina is uncertain. Such lesions may result in inaccuracy of memory-guided saccades, if another eye movement occurs between the saccade stimulus and the resulting saccade. Also, difficulties with disengaging fixation may occur, leading to increased saccade latency for visually guided saccades under certain stimulus circumstances. y
Thus, there is a fundamental distinction to be made between cerebral hemisphere and brain stem conjugate gaze control. At the cerebral level, the direction of the saccade control (contraversive) is opposite to the direction of the pursuit control (ipsiversive), while at the brain stem level both control ipsilateral movement. Clinical evidence demonstrates that pathways that control saccadic movements decussate caudal to the diencephalon but rostral to the pons, while the pursuit pathways either do not cross, or cross and recross. Patient studies suggest that hemisphere bidirectionality is preserved as far caudal as the thalamus and that the pursuit and saccade pathways both operate via the ipsilateral FEF outflow through the thalamus. Alternatively, the pursuit system may have pathways in the corona radiata separate from the saccade system outflow but funnel through the same region in the thalamus as the frontal system. The fact that some frontal lesions are associated with an ipsidirectional pursuit defect in conjunction with a contraversive saccade disorder supports the concept that the pursuit system outflow occurs via a common frontal-thalamic-brain stem pathway. However, the repeated observation of frontal lesions with isolated contralateral saccade disruption and normal pursuit weigh against a common pathway.
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