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Binocular Vision &
Eye Muscle Surgery Qtrly°


response (48). A sudden disparity vergence stimuli, induced by a change in fixation or by prism, results in an initial fast fusional vergence response. Ogle & Prager (43) pointed out the purpose of the slow adaptive response is to eliminate the stress of the large demand on the fast fusional vergence system. The reduction in the demand on the fast system occurs as a result of a negative feedback loop in the fusional system. An increase in the slow adaptive system results in a decrease in demand on the fast vergence system making it easier for the fast system to respond to subsequent disparities
(49).

Slow vergence or vergence aftereffects, extensively described by Schor (48) and Sethi (49), are not only important to the normal person in reducing the oculomotor error but are extremely important in the DEX(T) and somewhat less important in the basic X(T). This mechanism is most likely responsible for the decrease in the apparent XT at near (both temporally and spatially) where both enhanced stereopsis and fusional detail result in sustained binocularity. Slow vergence with its long time constant is most likely responsible for alignment after blinking, thus eliminating diplopia in patients with significant phorias, i.e., DEX(T) (50).
Disruption or elimination of slow fusion or vergence aftereffects may be achieved by sustained occlusion of one eye, since the slow vergence receives its input (negative feedback) information from the fast (disparity driver) or fusional vergence system. Slow vergence or vergence adaptation has been measured and found to be either complete or incomplete. Sustained or repeated occlusion results in a significant increase in the size and temporal characteristics of the deviation in those patients who have strong slow vergence systems. Slow vergence reduces the deviation in DEX(T) more at near, since binocular stimuli, i.e., size, complexity and disparity cues, are stronger, resulting in stronger disparity vergence and slow vergence. Sethi & Henson (51) have shown that the slow vergence system responds differently at different viewing distances to maintain a consistent oculomotor phoria. These vergence aftereffects tend to be larger at near and in downgaze. Slow vergence movements, also, result in orthophorization with an antimetropic prescription across the whole oculomotor field, i.e., with induced spectacle prism there is no alteration in the measured phoria in different position of gazes (51,52).
Sethi & Henson (51) postulated that there is a cortical memory map for each position in the motor field which is associated with a specific amount of innervation to maintain binocular vision. In patients where the slow adaptive vergence system is weak or incomplete, occlusion will have a minimum effect on the angle of deviation. Thus, one would predict that the more often Ihe exotropic patient deviates, the greater the propensity of the deviation to appear as a basic XT and the weaker the slow vergence system. Inclusion of slow vergence into a block design control system analysis as described by Hung (53) and Cooper (50) is presented in Figure 5, next page.
Scobee (54) in 1952 reported that 24 hours of
occlusion increases the near deviation in a substantial
Major Review: Intermittent Exotropia; Basic and Divergence Excess Type
J.
Cooper, MS, OD and N. Medow, MD
Summer of 1993 Volume 8 (No.3): 185.216
Figure 3 (Cooper & Medow): Simnultaneous recordings with an infrared optometer and eye movement monitor as DEX(T) changes fixation from a 1.5 D stimnulus to a 3.0 D stimnulus. Top three traces are from a true DEX(T), e acc is the accommodative recording and e em is the eye movement position. The bottomn three recordings are from a simnulated DEX(T); note the dynamic overshoots present during response. (Reprinted with permission from cooper J, Ciuffreda K, Kruger P: Stimnulus and response AC/A ratios in intermittent exotropia of the divergence excess type, Br J Ophthahnol 1982; 66:398-404.
Copyright 1982, BMJ,).
number of X(Y)s. Burian (10) used this principle of occlusion to classify DEX(T) patients into two groups, simulated and true. He defined a simulated DEX(T) as a DEX(T) whose near deviation increased after 30 minutes of occlusion so that the distance and near deviations approximated each other. In other words, the deviation changed from a DEX(T) to a basic X(1) and the calculated distance near AC/A decreased. But in reality monocular occlusion eliminated vergence aftereffects which artificially altered the AC/A.
Burian & Franceschetti (24) reported that the change in deviation with occlusion occurred in approximately 60% of the DEX(T) population. The other 40% who are
unaffected by occlusion are known as true DEX(T), i.e., distance/near relationship is unaffected by occlusion. Thus, distance/near AC/AS are high before and after occlusion in the true DEX(T). Since both objective and gradient AC/As in the true DEX(T) have been shown to be normal, Cooper et al (40) postulated that proximal convergence is responsible for the discrepancy between post occlusion distance/near AC/A and gradient AC/A in true DE The calculated proximal convergence factor for the true DEX(T) is 3.0/D (54), while the normal person has a smaller proximal vergence finding of approximately 1.8/1 ±1.6 (55,56).
Ogle et al also found higher than normal proximal convergence values
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