Drug treatments for eye movement disorders

PATHOGENESIS OF ABNORMAL EYE MOVEMENTS AND THEIR VISUAL CONSEQUENCES

The modern rationale for the treatment of abnormal eye movements rests on current concepts of the neurobiology of ocular motility and vision.1 In order to see clearly the details in our visual world, images must be held quite still upon the retina, especially the central, foveal part, which has the highest density of photoreceptors. In order to read, which concerns detection of high spatial frequencies, image motion should ideally be less than about 5°/s.2 If image drift substantially exceeds this limit, visual acuity will decline and the illusion that the world is moving (oscillopsia) may be experienced. Normally, three main mechanisms hold gaze (the line of sight) steady, so that our view of the world is clear and stable.2 The first is the vestibulo-ocular reflex, by which the motion detectors of the inner ear initiate eye movements to compensate for head perturbations, such as occur during locomotion. The second mechanism is “visual fixation,” which has two components: the detection of retinal image drift and programming of corrective eye movements, and the suppression of unwanted eye movements that take the eye away from the target. The third mechanism depends on a neural network that makes it possible to hold the eyes at an eccentric position (for example, in lateral gaze). Malfunction of any of these three mechanisms may cause the eyes to drift away from the object of regard; corrective, quick phases (saccades) may then redirect the fovea towards the target. Thus a definition of nystagmus is repetitive to and fro involuntary eye movements that are initiated by slow drifts of the eye.

It is important to differentiate pathological nystagmus from physiological nystagmus. During rotation of the head and body in space, both vestibular nystagmus and optokinetic nystagmus act to …