also explain the apparent decrease in the phoria of our patient which re-

mained stable from day to day.

Horizontal fusional amplitude training was probably effective in decreas-

ing the patient’s symptoms in two ways. First, therapy reinforced both the

sensory and motor aspects of the vergence system by stimulating the fast

reflexive fusional response to eliminate the initial large retinal image dispar-

ity and resultant diplopia. Second, either removal or reduction of the fu-

sional vergence demand increased adaptation of the slow fusional vergence

system via its internal adaptive loop.20

One may argue that the patient would have improved in time without any

treatment. This seems unlikely for several reasons. First, prior to the initia-

tion of orthoptic therapy, the patient’s oculomotor status, in particular the

divergence palsy, had remained stable for the previous six months. Second,

orthoptic therapy resulted in large and immediate improvement, with smaller

but consistent successive gains (Fig. 2). Third, and most importantly, re-

peated alternate occlusion increased the deviation from 7^ to the original de-

viation of 40^ esotropia. Thus, orthoptic therapy promoted the development

of slow vergence adaptation which reduced the phoria/tropia, and concur-

rently developed a robust fast reflexive fusional vergence response to com-

pensate for any residual, dynamically-changing oculomotor deviation not

eliminated by slow vergence.

There has only been one report in the literature involving objectively re-

corded dynamics of eye movements in patients with GBS4. The recordings

were obtained within the first two months of symptom onset, and a variety

of intra- and post-saccadic fatigue-like effects were documented, including

slowed saccades. None of these abnormalities were found in the present

case, which was recorded late in the disease and after therapeutic interven-

tion. In addition, the saccadic amplitudes used in the present study (io de-

grees) were considerably smaller than those used by Feldon et al. (20 to 30

degrees). Thus any relatively modest velocity deficit, being proportional to

saccadic amplitude, may not be evident in our patient. In addition to tradi-

tional medical/hospital care, our patient received an extended period of in-

tensive and successful office and home orthoptic therapy.

Residual eye movement deficits included square-wave jerks and a moder-

ate degree of intermittent saccadic dysmetria. Square-wave jerks are found

in a variety of pathological and non-pathological conditions, and thus may

not be of pathognomonic significance.2’ However, the intermittent occur-

rence of the high frequency bursts suggest residual abnormal neural control

of fixation. Further, the intermittent saccadic dysmetria may represent subtle

residual deficits in peripheral neuromuscular conduction. However, this does

not preclude coexisting central involvement, as both square-wave jerks and

ocular dysmetria are also commonly found in such cases.22 Lastly, the near

vergence tracking results confirm and extend the successful clinical orthop-

tic picture. The vergence findings clearly demonstrate that under naturalistic

conditions, in which the full complement of vergence stimuli were present23

(e.g., disparity, blur and proximity), appropriate and full changes in ver-

gence response dynamics occurred.24

Guillain-Barré syndrome

255