D=I8.5 pd BO=I.25 pd BD, OS -3.50D=I8.5 pd BO=I.25 BU with a near add of

+1 .75D. The prescription was fabricated in a high index, plastic progressive

lens with a small 45mrn eye size to minimize thickness and weight. The pris-

matic correction consisted of the least amount of prism required to maintain

bifoveal alignment at all fixation distances. In addition, he was advised and

highly motivated to begin an orthoptic treatment program despite the

guarded prognosis. The patient refused surgical intervention or Botulinum

toxin injections.

Active orthoptic therapy was begun with the goal of increasing both fast

reflexive fusional divergence amplitudes and slow vergence adaptation57

(Fig. i). Stimulus presentation was consistent with an approach previously

described by Kertesz and Kertesz,8 and Cooper.9 10 Fusional targets were

initially large (45 degrees), spatially-complex stimuli presented with a slow,

constant velocity (ramp) divergence demand of o.25^/sec. In addition, ran-

dom-dot stereograms were used in an operant conditioning paradigm to

eliminate the possibility of responses based solely upon monocular cues, as

well as to provide positive reinforcement to the patient.’1 These targets were

presented on the commercially available video-based Computer Orthopter

VTS3 system (RC Instruments). Office therapy also incorporated use of

prism bars, stereoscopes (Keystone) and variable disparity vectograms

(Bernell). In-office therapy was supplemented with daily home therapy for

reinforcement, which included a variety of fusional and anti-suppression

procedures.

As soon as divergence amplitudes improved by more than 7^, the amount

of prism in the spectacles was decreased by 10^ to foster increased fusional

effort and slow vergence adaptation.12 As fusional divergence amplitudes

Fig. i. Model of static accommo-

dation, vergence, and their inter-

actions. The upper negative visual

feedback path is for disparity or

fusional vergence, whereas the lower

negative visual feedback path is for

blur-driven accommodation. Each

path contains (from left to right): (i)

the initial input stimulus value, with

VS = vergence stimulus (retinal

disparity), PS = proximal stimulus

(apparent target distance), and AS =

accommodative stimulus (blur), (2)

the summing junctions for the initial

stimulus inputs and the negative

visual feedback pathways; this

difference represents the updated or

new system error, (3) the fast reflex

controllers; they respond to the initial

or transient aspect of the new error

signal; this gain term multiplies the

error signal and thus derives the

initial system neural signal, (4) the

slow adaptation loops; their input

from the controller is converted to an

output signal that then acts to modify

the controller’s dynamics (i.e.,

transiently increase its decay time

constant); the adaptive ioops function

to sustain the motor response, (5) the

crosslink gain terms which reflect

accommodative convergence to

accommodation (ACA ratio) and

convergence accommodation to

convergence (CAC ratio), (6) tonic

bias inputs that reflect midbrain

baseline neural innervation and add

non-linearly to the controller signal,

(7) second summing junctions, (8) the

peripheral neuroanatomical aspects of

the controlled system, namely the

extraocular muscle complex (EOM)

and crystalline lens complex (LENS),

(9) the system motor response,

namely the vergence response (VR)

and the accommodative response

(AR), and, lastly, (io) higher-level

voluntary vergence control driving

the fusional vergence system. Proxi-

mal gain inputs to both systems.

Guillain-Barré syndrome 251