following respective components of the deviation:

accommodative-vergence, proximal vergence, and vergence aftereffects. DE patients with high gradient ACA’s who show minimal effects with occlusion should not have as a surgical goal alignment or overcorrection. Surgery, if used, should under- correct the deviation followed by vision training to compensate for the residual deviation. The goal should be to create strong vergence adaptation coupled with reflex fusional vergence.

Treatment of DE patients with normal ACA’s also requires improvement of both fusional vergence amplitudes and slow vergence to reduce the load on the fusional vergence mechanism. A strong slow vergence system results in an apparent change in the tonic position of the eyes, i.e., orthophorization, and a decrease in the distance-near ACA ratio measurement. Surgical correction appears to be most successful when both fusional and adaptive vergence components are eliminated.

After orthoptic therapy, rapid alternate cover testing often shows a reduction in any deviation. This change in tonic position has often been taken as evidence of a change in the neurological gain of the ACA cross-link system (increase in the ACA ratio). However, because prolonged occlusion eliminates this effect, alteration of the slow vergence system must be involved in the change. Thus, strong fusional vergence training in the direction opposite to the phoria should result in a reduction in the apparent phoria (orthophorization) and a reduction in the load on phasic disparity-driven fusional vergence.30

Adaptation to Prescribed Prism

Carter31 described a patient who was prescribed compensating prisms for a moderate exophoria. After a short period of time the patient exhibited the original phoria while wearing the prism. According to Carter there was a “shift in the fusion free position to maintain the same demand on fusional convergence that existed prior to wearing the prism.” This phenomenon of adaptation has been described as “eating up the prism” and occurs for horizontal and vertical phorias. Eating up the prism is a direct result of elimination of fusional disparity by prism with a subsequent increase in adaptation.

Carter described another patient given a prescription for an asymptomatic 1 pd left hyperphoria. Upon reevaluation 1 month later, the patient measured 1 pd left hyperphoria through the prismatic prescription that he was wearing. A new prescription was given incorporating the additional prism. A subsequent recheck 3 weeks later again revealed 1.5k left hyperphoria. The spectacles already had

2 pd of vertical prism; thus the patient was really manifesting 3.5 pd of left hyperphoria. Carter removed the prism. Retesting 1 week later revealed 1.5 pd hyperphoria without any symptoms.

Patients similar to the one described by Carter, who appear to be eating up the prism, are actually

adapting to the prism. Clinically, these patients may be identified by having them wear the prism for 20 min in a trial frame. If the patients adapt, relieving prisms are contraindicated. Thus, short- term evaluations are valid because the process of adaptation does not disappear with long-term wearing of prisms. Carter suggested that patients with good adaptation are usually asymptomatic, whereas those with poor sensory fusion are usually symptomatic due to poor vergence adaptation. Carter suggested that patients who are symptomatic and demonstrate poor vergence adaptation would benefit from prismatic correction. North and Henson32 have confirmed Carter’s findings that symptomatic patients demonstrate poor vergence adaptation, i.e., slow fusional vergence.

Orthophorization

Adaptation is probably responsible for the leptokurtic distribution of distance phorias. Morgan33 noted that 76% of all patients have a distance phoria between 1 pd of esophoria and 3 pd of exophoria. Adaptation serves to eliminate the apparent phoria through the feedback mechanism from the disparity vergence system. After initial motor fusion subsequent to disparity vergence, slow fusional vergence with its long-time decay maintains the eyes in alignment over a period of time. The resulting orthophorization may be disrupted by prolonged occlusion. If fusional vergence and vergence adaptation are improved with orthoptics, there should be a reduction of the apparent phoria or orthophorization.

Slow fusional vergence is probably responsible for maintaining ocular alignment during blinking. Short or long blinks disrupt sensory fusion, but have little or no effect on the slow fusional vergence signal. Therefore, upon opening the eyes after blinking or sleep, one would expect alignment of the eyes even in the presence of a high phoria. One may conclude that the fast sytem is responsible for initiation of sensory fusion, whereas the slow fusional vergence system is responsible for maintaining oculomotor position over time.

Binocular Analysis

These findings show that Maddox analysis or graphical analysis needs to include both proximal and the important slow (adaptation) vergence controller system. The above findings suggest that the ability of the binocular system to maintain comfortable binocular vision at a given fixation distance is related to the strength of the slow vergence system.

Schor34 believes that the shape of the fixation disparity forced vergence curve is reciprocally related to vergence. adaptation; i.e., the flatter the curve the better the vergence adaptation. Large associated phorias would represent a steady-state error for the fast vergence system. If adaptation is weak, the position of the fixation disparity curve may be altered with prism or surgery. Orthoptics