downgaze) and spreads from one position to another. Sethi and Henson39 suggested that there is a neurological memory map to maintain a compensated stable “orthophoric” position. This memory map accounts for different amounts of adaptation at different distances contributing to the distance and near phoria measurements.

These findings explain why some patients are asymptomatic with anisometropic prescriptions. The induced prismatic effects of an anisometropic prescription are compensated for by a robust adaptation system. Patients with a weak adaptation system require prism to decrease the demand on fusional disparity vergence, which subsequently decreases vergence adaptation. The result is an apparent increase in the deviation and the need for a stronger prism. The patient appears to eat up the prism. Thus, patients with a poor ability to adapt to prism should have judicious application of prism. They should be advised of the necessity for subsequent orthoptics to improve both fusional and adaptive vergence.

With large anisometropic corrections, such as for unilateral aphakia, the prismatic deviation may be too large to be overcome by fusional vergence. Diplopia occurs without allowing for adaptation. This author believes that the large, noncomitant, vertical prism induced by the anisometropia is the deterrent to single binocular vision rather than the aniseikonia. Patients with smaller anisometropic prescriptions rely on fusional vergence to eliminate the diplopia. If adaptation is robust, the induced error does not produce symptoms. If either fusional vergence or slow fusional vergence adaptation is weak, diplopia or asthenopia will ensue. Correction will require a slab-off prism.

A similar situation occurs with an incorrectly centered ophthalmic lens. The higher the prescription the higher the induced prism. The incorrectly incorporated prism becomes adapted to. The “correction of the problem” often results in recentering of the lenses to match one’s interpupillary distance. Unfortunately, a new prismatic demand has been created which needs to be adapted to. Asymptomatic patients with prism induced secondary to incorrect optical alignment should be slowly weaned off the inappropriate optical centers. Symptomatic patients should have their optical centers properly aligned.

CONCLUSION

Vergence aftereffects are a distinct type of vergence which receives its input from fast fusional vergence, and has a long time constant. Clinically it is important in explaining changes in phoria position with sustained occlusion such as Marlow occlusion, changes in ACA ratio, decompensation of hyperphoria, changes in prismatic correction in patients who eat up prism or adapt to spectacle- induced prism, and adaptation or nonadaptation to anisometropically induced prism. Therapeutically, the adaptation mechanism can be manipulated to

overcome large horizontal and vertical deviations by judicious application of prism followed by active orthoptic therapy to build compensating fusional amplitudes followed by the reduction of prism and further therapy. When adaptation is weak, prism may be used to eliminate the demand on disparity- driven vergence. Orthoptics, on the other hand, will result in an improvement in the quality of vergence adaptation and subsequently reduce the demand on the fast fusional vergence system at a given fixation distance.

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