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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 prismatic 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, random-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
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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. Proximal gain inputs to both systems.
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Guillain-Barré syndrome
251
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