also explain the apparent decrease in the phoria of our patient which remained stable from day to day.

Horizontal fusional amplitude training was probably effective in decreasing 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 disparity and resultant diplopia. Second, either removal or reduction of the fusional 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 initiation 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, repeated alternate occlusion increased the deviation from 7^ to the original deviation 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 compensate for any residual, dynamically-changing oculomotor deviation not eliminated by slow vergence.

There has only been one report in the literature involving objectively recorded 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 intervention. In addition, the saccadic amplitudes used in the present study (io degrees) 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 traditional medical/hospital care, our patient received an extended period of intensive 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 occurrence 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 vergence response dynamics occurred.24