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D. Newsham, P.C. Knox, R.W. I. Cooke; A Longitudinal Study of Vergence and Anti–Saccade Performance in Children Born Preterm . Invest. Ophthalmol. Vis. Sci. 2006;47(13):2485.
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Preterm children (<32 weeks; PT) are at increased risk of cerebral deficits and have increased incidence of binocular control anomalies. We have previously demonstrated that, compared to full–term (FT) controls, PTs at 9–10 years of age, have significantly increased anti–saccade directional error rates (PT: 76±16%; FT: 58±18%; mean±sd, p=0.001) and have increased vergence latency (PT: Right: 714±155ms; Left: 702±136ms; FT: Right: 539±93; Left: 550±116ms; mean±sd, R: p=0.022; L: p=0.038). Both of these aspects of oculomotor control have a long developmental period and improve substantially between the age of 8 and 12 years, until maturation at approximately 16 years. Our aim was to determine the longitudinal development in PT children in comparison to FT controls.
Vergence and anti–saccades were re–examined (4 years after initial testing) in 8 PT children aged 13–14 years with normal IQ (>85) who were free from major neurological deficits, and 4 FT age matched controls. In addition we also examined a new cohort comprising of 4 PTs aged 15–16 years and 5 FT age matched controls. Subjects viewed a monitor at 57cm with their head stabilised whilst their eye movements were recorded by infrared oculography. Anti–saccade targets were presented at an amplitude of 5° and the vergence task required a binocular shift of 27°. Data was collected over 96 trials for anti–saccades and 24 trials for vergence.
Compared to 9–10 year olds, vergence latency reduced for both PTs (Right: 542.4±64ms; Left: 554.6±58ms; mean±sd) and FTs (Right: 452.9±85ms; Left: 448.7±90.9) by the age of 13–14 years. The decrease was marked for PTs, reducing the difference between the two groups (R: p=0.09; L: p=0.04). Also both PTs (35.7±13%) and FTs (31.9±6%) made fewer anti–saccade directional errors at 13–14 years (p=0.7). At 15–16 years vergence latencies were similar for both groups (PT: Right: 441.5±61ms; Left: 453.4±56ms; FT: Right: 474.8±91; Left: 451.1±97ms; mean±sd, R: p=0.6; L: p=0.9). Anti–saccade errors also showed further reduction (PT: 21±7%; FT: 17±8%; mean±sd, p=0.6).
Increased vergence latency and anti–saccade error rates in preterms could arise due to a diffuse deficit affecting the frontal cortex or a delay in the maturation. Although our numbers are small, our findings indicate that the deficit found in preterms age 9–10 years is not permanent. Rather, development proceeds in preterms reducing the deficit by 13–14 years and all but eliminating the gap by 15–16 years of age, when maturation of the frontal cortex is thought to be complete.
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