Discussion This is the first case report describing the use of orthoptic therapy to improve oculomotor vergence control in a patient with acquired bilateral sixth nerve paralysis. One may argue that the strabismic deviation was a result of a divergence paralysis, since the velocities of the horizontal saccades were equal and normal for both left and right gaze, and the deviation was not significantly greater at distance.’3 However, there are several findings which suggest that the origin of his esotropia was a bilateral sixth nerve palsy. First, he had a total ophthalmoplegia, which by definition includes a sixth nerve palsy; second, the deviation at distance was equal to the sum of the individual lateral rectus palsies, i.e., 2O ^ from each eye (diver gence paralysis would have a much smaller deviation). Third, it is possible that the initial presentation of a similarly-sized deviation at distance and near was masked by the wearing of prisms and the resultant motor slow vergence (prism) adaptation. And, lastly, GBS is thought to be a disease of peripheral nerve involvement.

Recently, Chiba et al.14 demonstrated that patients with either Miller Fisher syndrome (MFS) or GBS with an associated ophthalmoplegia have the same specific serum anti-GQ1 6 IgG antibody. They also reported that none of the controls with various neurological conditions had this antibody. In addition, the serum antibodies were only found in peripheral nerves III, IV, and VI. None of the nerve fibers in the spinal cord or brainstem demonstrated serum antibodies. These findings lend credence to the notion that both GBS and MFS are variants of the same disease and mainly affect peripheral nerve function.

Prisms were used to reduce the vergence demand on the fast reflexive fu sional vergence system and to eliminate diplopia at all distances. Concur rently, orthoptic therapy was designed to improve fusional amplitudes with the goal of reducing the amount of prism in the spectacles. Initial reduction in the magnitude of the prism placed a new demand on the fast reflex component of the fusional vergence system. However, through appropriate visual feedback and prolonged visual effort, the patient partially adapted to the prism as evidenced by a decrease in the size of the distance esotropic deviation from 40 ^ to 7^• This resulted in a decreased demand on reflex fusional vergence.’5 The longer the vergence system maintains fusion, the larger is the slow vergence adaptive contribution, and the smaller is the fast reflexive fusional vergence contribution. This results in a decrease in the standard clinically-measured phoria.’6

These findings are similar to those previously reported by Ogle and Pragen,’7 and later by Carter,16 in which vergence adaptation occurred after a patient wore either vertical or horizontal prisms for a considerable period of time. Complete adaptation was demonstrated by similarity of fixation disparity (i.e., small static vergence error), cover test, and fusional amplitude measurements both prior to and while wearing the prisms.’8”9 Removal of an ‘adapted prism’ usually resulted in diplopia with a slow return (e.g., minutes to several hours) to the position of the eyes prior to wearing the prism.’6 Recovery can be significantly accelerated by slowly decreasing the prismatic value via a Risley prism, while allowing fusion to be maintained continuously. Carter16 has shown that vergence adaptation is unaffected by sleep. This non-stimulus mediated ‘memory’ appears to maintain vergence adaptation during non-waking hours, thus preventing the occurrence of diplopia upon initial eye opening. This level of maintained vergence adaptation may