Previous research about the maturation of the smooth pursuit system has been carried out in newborns and in human infants in the first months of life. A lower gain was found with respect to adults (where gain is close to 1), with frequent saccadic intrusions. On the contrary, no data are available about smooth pursuit response in children. To fill this gap, we analyse in this study the level of maturation reached by children over 7 yr old (the minimum age in which a correct test can be done). Using a cosinusoidal stimulation, the smooth pursuit characteristics (velocity and position gains and phases) evaluated in children are compared to the corresponding parameters in adults. Our data show a clear difference between the two groups, in particular for velocity gain values (which are lower in children), and a larger variability in children. Since the influence of fatigue and prediction appears to be small, we conclude that these differences can be justified both by high level psychological or cognitive factors and incomplete maturation of smooth pursuit system in children.
Our findings emphasise the possible role of growth hormone in ocular development, and its interaction with the physiological process of emmetropization.
The age-related trend values and the normal intraocular pressure (IOP) increase curve from birth through the 16th year of life were studied in 460 subjects with a noncontact tonometer (Keeler Pulsair, Keeler, Ltd, Windsor, Berks, UK). Much lower values than in adults were recorded in subjects up to the age of 3 or 4 years. This finding leads us to believe that in the treatment of infantile glaucoma IOP should be kept within the age physiologic levels, in an attempt to prevent visual field loss and optic atrophy.
The aim of this study was to study the influence of growth hormone deficiency (GHD) on emmetropization and to evaluate the effect of growth hormone replacement therapy on eye refraction. Twenty-eight children affected by congenital GHD and undergoing substitutive therapy (group 1), and 28 healthy subjects (group 2), were prospectively studied. All patients had a thorough eye examination, including cycloplegic refraction and axial length measurement (only GHD children). After 2 years, we found in both groups a reduction of the dioptric power of the eye. A t test for paired data showed statistically significant differences in both groups (p < 0.001), but the change of refraction was higher in group 2 (p < 0.01). Axial length showed a statistically significant increase, according to the myopic shift (p < 0.001). The change of the refraction found in GHD children could be related to the somatic growth and partially induced by growth hormone therapy. The difference between the two groups could be explained with the late beginning of the therapy in GHD children. It is possible to form the hypothesis that a correct and well-timed substitutive therapy could permit a normal emmetropization process.
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