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D. Newsham, P.C. Knox, R.W. I. Cooke; Increased vergence latency provides further evidence of a frontal lobe deficit in children born preterm. . Invest. Ophthalmol. Vis. Sci. 2004;45(13):3428.
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Purpose: Preterm children (<32 weeks) are at increased risk of cerebral deficits and have increased incidence of binocular control anomalies. To investigate this we extended our previous studies of oculomotor control by examining the binocular control of eye movements during vergence. As the control circuitry for vergence is situated in frontal cortex, we expanded our examination of antisaccade performance, and investigated interactions between performance on the two types of task. Methods: Vergence (and antisaccades) were examined in 7 (and 28) preterm children aged 9–10 years with normal IQ (>85) who were free from major neurological deficits, plus 8 (and 25) full term age matched controls. Subjects viewed a monitor at 57cm with their head stabilised whilst their eye movements were recorded by infrared oculography. Antisaccade targets were randomly interleaved at an amplitude of 5° over 96 trials. The vergence task required a binocular shift of 27°, changing fixation from a midline target at 57cm to a target in the same plane at a distance of 10cm, over 24 trials. Results: The mean vergence latency was significantly longer in the preterm group (Right: 714 ±155ms; Left: 702 ±136ms; mean ±sd) compared to full terms (R: 539 ±93ms; L: 551 ±116ms; R: p=0.022; L: p=0.038). The time from target onset to peak vergence velocity was also longer for the preterms (R: 1055 ±160ms; L: 1148 ±177ms) compared to the full term group (R: 885 ±178ms; L: 923 ±208ms; R: p=0.074; L: p=0.042). No significant difference in peak vergence velocity or vergence angle executed was found between the two groups. On the antisaccade task we confirmed that preterms made significantly more errors (76% ±16) on the antisaccade task compared to the full term controls (58% ±18; p=0.001). A significant positive correlation was present between vergence latency and antisaccade error rate for the preterms (R: r=0.80, L: r=0.82; p<0.05). Conclusions: The increased vergence latency for the preterm children is consistent with a deficit of cortical origin and could involve a cortical area just anterior to the frontal eye fields. Further evidence comes from both the increased antisaccade error rate in preterms and the correlation between the vergence latency and the antisaccade error rate. This suggests that preterm children may be at risk of a diffuse deficit affecting the frontal cortex.
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