causes the slope of the fixation disparity curve to flatten and eliminates asthenopia.3537 If orthoptics flattens the curve enough and sustained vergence skills (isometric) are developed, the curve may also be shifted.

Wick and London38 have developed a system of analysis based on measurements made under binocular testing. They take into account not only open loop findings (phoria, vergence amplitudes, ACA ratio, CAC ratio, and proximal vergence), but also binocular closed negative feedback ioop findings (binocular proximal convergence, accommodative lag, accommodative facility testing, and slow vergence adaptive changes).

It should be remembered that all the methods for binocular vision analysis previously described ignore certain components of the patient’s behavior which must be accounted for. For example, accommodative and vergence testing often create discomfort irrespective of their measured amplitude. The effort to sustain binocular vision during testing is not easily quantified and so is usually ignored. Clinically, the patient who displays asthenopia after measurements of accommodation and vergence amplitudes is most often the patient who benefits from orthoptic therapy.

Other commonly ignored factors include: (1) individual pain thresholds, (2) total amount of time spent at near tasks, (3) total amount of time spent at near tasks without a break, (4) amount of visual detail, and (5) cognitive demand. Last but not least, most of the vergence studies cited assume that open loop data can be applied to closed ioop accommodative-vergence functioning. Though a more comprehensive accommodative-vergence analysis, as proposed by Wick and London, is more accurate, it is not complete because the above described variables have not been accounted for.

Vergence Adaptation with Physiological Change

Concomitant-type vergence adaptation effects are important in maintaining binocular alignment changes that occur over time. Sethi and Henson39 have shown that adaptation increases when the prism is introduced in small steps. Each small step reaches a larger proportional amount of adaptation which is additive to the preceding step. Sethi40 postulated that small step adaptation may account for gradual physiological changes in ocular position that occur with both age-related and slowly advancing pathological processes. For example, with advancing presbyopia, vergence as a direct result of accommodation decreases, thus causing the near phoria to become more divergent or exophoric. This increases the demand on the fusional convergence system which results in constant output from the slow vergence adaptor. Thus, adaptation serves to eliminate the increased demand on fusional vergence which results from a loss of accommodative vergence. Clinically, this may be seen in patients who present with orthophoria or a small exophoria on an initial cover test but who, with prolonged

repeated occlusion, demonstrate an increasing divergent deviation. Prolonged sustained vergence maintains vergence adaptation, whereas prolonged repeated cover testing eliminates fusion and, consequently, vergence adaptation with its long time course.

Similar adaptive findings would be expected to occur with enophthalmos, which increases with age, tumor-generated proptosis, and slowly increasing exophthalmos secondary to Graves’ disease. Rapidly occurring paresis secondary to trauma, vascular accidents, etc., results in diplopia and lacks slow vergence adaptation.

Often, patients with congenital deviations such as a congenital superior oblique paresis or congenital facial asymmetries (resulting in one orbit being higher than the other) are relatively orthophoric or demonstrate significantly less vertical deviation than expected. The binocular system of these patients may decompensate in later years. They must be differentiated from the person with a newly acquired superior oblique palsy who has no adaptation. Patients with congenital superior oblique paresis often show, with repeated occlusion, a slowly increasing vertical deviation. Their opposing infraduction is usually much greater than the expected findings, i.e., 4”. Also, the amount of prism needed to eliminate the diplopia is much less than expected.

Cooper4’ has described a treatment regimen for decompensated vertical deviations. He prescribes. the minimal amount of vertical prism to eliminate diplopia by stimulating fusional vergence. This is followed by orthoptic therapy to improve horizontal fusional amplitudes. Upon normalization of horizontal fusion amplitudes the prism is reduced in 2pd steps to encourage adaptation followed by subsequent orthoptic treatment. Often the prism can be eliminated entirely. The full amount of vertical prism measured is prescribed in cases of recently acquired deviations in order to eliminate diplopia; then the clinician should attempt to decrease the prism slowly and encourage adaptation.

Cooper believes that vergence therapy should include: (1) slow ramp vergence training to improve fusional vergence; (2) continuous ramp therapy to improve the vergence reflex which eliminates constantly changing disparity vergence signals; (3) jump or step vergence to improve recovery once sensory fusion is lost; and (4) sustained vergence training (isometric) to improve adaptation.42 Slow, continuous, and step vergence therapy must be practiced with various binocular stimuli until these skills become an effortless, automated reflex.

Noncomitant Vergence Adaptation

As mentioned previously, Henson and Dharamshi43 and Sethi and Henson39 have shown that noncomitant disparity induced by anisometropia results in adaptation across the entire oculomotor field. Adaptation is maximal where binocular experience usually occurs (primary position and

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