PURPOSE: Infantile strabismus in humans and the monkey is associated with maldevelopment of visual motion responsiveness, one manifestation of which is directionally asymmetric motion visual evoked potentials (motion VEPs). Early repair of strabismus in infant monkeys has been shown to restore normal development of motion responsiveness for pursuit and optokinetic eye movements (optokinetic nystagmus [OKN]). The purpose of this study was to determine how early versus delayed repair of strabismus influences the development or maldevelopment of motion VEPs. METHODS: Optical strabismus was created in infant macaques by fitting them with prism goggles on day 1 of life. The Early Repair group wore the goggles for a period of 3 weeks (the equivalent of 3 months before surgical repair in humans), whereas the Delayed Repair group wore the goggles for a period of 3 to 6 months (the equivalent of 12-24 months before surgical repair in humans). Several months after the removal of the goggles, motion VEPs to horizontally oscillating grating stimuli were recorded during monocular viewing. An asymmetry index (AI) was measured for each animal by extracting an asymmetric (F1) and symmetric (F2) frequency component from the motion VEP. The AIs of the infant monkeys with Early versus Delayed Repair were also compared with that of a group of adult monkeys, who had unrepaired, natural strabismus. RESULTS: When tested with a 1-cyc/deg, 6-Hz stimulus, both control and Early Repair monkeys exhibited symmetric motion VEPs (AI < 0.25). Mean AI was 0.15 +/- 0.09 in control and 0.16 +/- 0.13 in Early Repair monkeys. In contrast, both Delayed Repair and naturally strabismic monkeys had asymmetric motion VEP responses: AI = 0.57 +/- 0.22 in the Delayed Repair and 0.49 +/- 0.17 in the naturally strabismic monkeys (P < 0.01). Delayed Repair and naturally strabismic monkeys also had motion VEP asymmetries of equivalent magnitude when tested using stimuli at higher (3 cyc/deg/11 Hz) spatial-temporal frequencies. The concordance between motion VEP symmetry and normal fusional vergence was significant (P < 0.01). CONCLUSIONS: Early repair of optical strabismus in primates restores normal development of visual motion pathways in the cerebral cortex, measured as symmetric motion VEPs. Delayed repair causes permanent motion VEP maldevelopment. These results provide additional evidence that early strabismus repair is beneficial for brain development in infant primates.
PURPOSE: Infantile strabismus in humans and the monkey is associated with maldevelopment of visual motion responsiveness, one manifestation of which is directionally asymmetric motion visual evoked potentials (motion VEPs). Early repair of strabismus in infant monkeys has been shown to restore normal development of motion responsiveness for pursuit and optokinetic eye movements (optokinetic nystagmus [OKN]). The purpose of this study was to determine how early versus delayed repair of strabismus influences the development or maldevelopment of motion VEPs. METHODS: Optical strabismus was created in infant macaques by fitting them with prism goggles on day 1 of life. The Early Repair group wore the goggles for a period of 3 weeks (the equivalent of 3 months before surgical repair in humans), whereas the Delayed Repair group wore the goggles for a period of 3 to 6 months (the equivalent of 12-24 months before surgical repair in humans). Several months after the removal of the goggles, motion VEPs to horizontally oscillating grating stimuli were recorded during monocular viewing. An asymmetry index (AI) was measured for each animal by extracting an asymmetric (F1) and symmetric (F2) frequency component from the motion VEP. The AIs of the infant monkeys with Early versus Delayed Repair were also compared with that of a group of adult monkeys, who had unrepaired, natural strabismus. RESULTS: When tested with a 1-cyc/deg, 6-Hz stimulus, both control and Early Repair monkeys exhibited symmetric motion VEPs (AI < 0.25). Mean AI was 0.15 +/- 0.09 in control and 0.16 +/- 0.13 in Early Repair monkeys. In contrast, both Delayed Repair and naturally strabismic monkeys had asymmetric motion VEP responses: AI = 0.57 +/- 0.22 in the Delayed Repair and 0.49 +/- 0.17 in the naturally strabismic monkeys (P < 0.01). Delayed Repair and naturally strabismic monkeys also had motion VEP asymmetries of equivalent magnitude when tested using stimuli at higher (3 cyc/deg/11 Hz) spatial-temporal frequencies. The concordance between motion VEP symmetry and normal fusional vergence was significant (P < 0.01). CONCLUSIONS: Early repair of optical strabismus in primates restores normal development of visual motion pathways in the cerebral cortex, measured as symmetric motion VEPs. Delayed repair causes permanent motion VEP maldevelopment. These results provide additional evidence that early strabismus repair is beneficial for brain development in infant primates.
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