AIM: Changes in saccade velocity/amplitude characteristics (main sequence) and attenuation of distance esotropia in response to botulinum toxin (BTX-A) chemodenervation of the antagonist medial rectus were studied in a group of nine patients with chronic lateral rectus palsy. METHODS: Serial measurements of ocular deviation and infrared oculograms of saccadic eye movements to targets at 5 degrees-20 degrees of lateral gaze were made before injection and at 2, 4, 8, 16, and 20 weeks after injection. RESULTS: At 2 weeks after injection, the ocular deviation changed by a mean of 34.5 prism dioptres and the 5 degrees and 10 degrees adduction saccades were significantly slowed (p < 0.02 Wilcoxon signed rank test). By the second examination, however, the adducting saccade peak velocity had returned to normal while the mean ocular deviation remained significantly changed (p = 0.01 Wilcoxon matched pairs). By 20 weeks the mean ocular deviation was not significantly different from that before injection (p = 0.14 matched pairs). CONCLUSIONS: The ocular realignment caused by BTX-A may persist after saccadic function has been restored. This may be because toxin may have a more profound and long lasting effect on the orbital singly innervated fibres which are active tonically at rest to hold gaze whereas there is relative sparing of the additional motor units recruited during fast eye movements.
AIM: Changes in saccade velocity/amplitude characteristics (main sequence) and attenuation of distance esotropia in response to botulinum toxin (BTX-A) chemodenervation of the antagonist medial rectus were studied in a group of nine patients with chronic lateral rectus palsy. METHODS: Serial measurements of ocular deviation and infrared oculograms of saccadic eye movements to targets at 5 degrees-20 degrees of lateral gaze were made before injection and at 2, 4, 8, 16, and 20 weeks after injection. RESULTS: At 2 weeks after injection, the ocular deviation changed by a mean of 34.5 prism dioptres and the 5 degrees and 10 degrees adduction saccades were significantly slowed (p < 0.02 Wilcoxon signed rank test). By the second examination, however, the adducting saccade peak velocity had returned to normal while the mean ocular deviation remained significantly changed (p = 0.01 Wilcoxon matched pairs). By 20 weeks the mean ocular deviation was not significantly different from that before injection (p = 0.14 matched pairs). CONCLUSIONS: The ocular realignment caused by BTX-A may persist after saccadic function has been restored. This may be because toxin may have a more profound and long lasting effect on the orbital singly innervated fibres which are active tonically at rest to hold gaze whereas there is relative sparing of the additional motor units recruited during fast eye movements.