Ординатура / Офтальмология / Английские материалы / The Neurology of Eye Movements_Leigh, Zee_2006

ated neurologic deficits, saccade velocities are usually normal in divergence paralysis (i.e., abducens nerve palsies are not the cause).129 If necessary, such cases can be treated successfully with bilateral surgical resection of the lateral rectus muscles.

SUMMARY

1.Vergence movements rotate the eyes in opposite directions to enable binocular fixation of a single object.Vergence movements occur in response to several distinct stimuli. Fusional

(disparity) vergence movements are stimulated when images from one object fall on noncorresponding retinal elements in the two eyes. Accommodative vergence movements are stimulated by retinal blur. Another important stimulus for vergence is the sense of nearness (proximal vergence), which may be abstracted from cues such as size and motion. These stimulus-induced changes of vergence are superimposed upon an underlying level of vergence tone (tonic vergence). Vergence is also under a degree of voluntary control. Under normal circumstances, fusional and accommodative vergence are tightly coupled, each affecting the other through neural cross-linkage. Vergence movements occur synkinetically with accommodation of the lens and pupillary constriction (the near triad).

2.When performed without accompanying saccades, vergence movements are slow and show an approximately negative exponential waveform. Under most natural circumstances, how ever, vergence movements are used in combination with saccades to place the images of an object on both foveae, or with pursuit to keep the images of a moving object on both foveae. When vergence is conjoined with saccades, the change in relative alignment is much faster than with vergence movements made alone (Fig- 8-2).

3.During a vergence movement from a far to a near target, ocular motoneurons show a phasic-tonic (velocityposition) change in innervation (Fig. 8-4). Premotor vergence neurons of three major types lie in the midbrain, dorsal and lateral to the oculomotor nuclei. They encode vergence velocity, vergence position, or a combination of both signals.

4.The maintenance of both static and dynamic ocular alignment is under long-term adaptive control to ensure that with every change of gaze, the lines of sight of both eyes are promptly brought to the fixation target and kept there (Fig. 8-7).

5.Abnormal vergence eye movements should be differentiated from disorders of conjugate eye movements induced by convergence. Conver- gence-retraction nystagmus, which is common with midbrain lesions, isprimarily a disorder of saccades in which attempted upgaze elicits rapid, bilateral, nearly simultaneous phasic adduction with contraction. Divergence nystagmus (slow phases convergent, quick phases divergent) may be a sign of lesions at the craniocervical junction. Bilateral sixth nerve palsies must be differentiated from divergence palsy and from voluntary spasm of the near reflex, which is recognized by the accompanying miosis and full range of movement during monocular viewing or vestibulo-ocular testing.

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