The aims of this study were to analyze the relationship between dyslexia and eye movements and to assess whether this method can be added to the workup of dyslexic patients. The sample was comprised of 11 children with a diagnosis of dyslexia and 11 normal between 8 and 13 years of age. All subjects underwent orthoptic evaluation, ophthalmological examinations, and eye movement analysis, specifically, stability analysis on fixating a still target, tracking saccades, analysis of fixation pauses, speed reading, saccades, and regressions through the reading of a text. Stability analysis on fixating a still target showed a significant (p < 0.001) difference between the two groups showing an increased amount of loss of fixation among dyslexic subjects (5.36 ± 2.5 s and 0.82 ± 2.1, respectively). Tracking saccades (left and right horizontal axis) did not show a significant difference. When reading parameters were looked into (number of saccades, number of regressions, reading time through the reading of a text), a significant (p < 0.001) difference was found between the groups. This study supports the belief that the alteration of eye movement does not depend on oculo-motor dysfunction but is secondary to a defect in the visual processing of linguistic material. Inclusion of assessment of this defect might prove beneficial in determining the presence of dyslexia in young children at a younger age, and an earlier intervention could be initiated.

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The possible intragastric nitrosation of ranitidine to genotoxic derivatives has been investigated in rats and mice given, by gavage, high single doses of this histamine H2 receptor antagonist along with NaNO2. Liver DNA fragmentation, as revealed in rats by both DNA alkaline elution and DNA alkaline denaturation followed by hydroxylapatite chromatography, was found to be dependent either on the molar ratio drug/nitrite or on the gastric pH. It occurred only with doses of 175 mg/kg ranitidine HCl + 80 mg/kg NaNO2 (molar ratio 1:2.32) or 350 mg/kg ranitidine HCl + 80 mg/kg NaNO2 (molar ratio 1:1.16) and concurrent reduction of gastric pH from 5.5 to 2-3 (produced by prolonged fasting). A further reduction of pH elicited by histamine injection increased the amount of DNA damage. DNA fragmentation in gastric mucosa showed a similar dependence on both pH and ranitidine/NaNO2 ratio, but was more marked than in liver. Simultaneous administration of ascorbic acid reduced the damage of gastric DNA. Oral administration of 175 mg/kg ranitidine HCl + 80 mg/kg NaNO2 in fasted and histamine-injected mice induced a modest but statistically significant increase in the frequency of sister chromatid exchanges in bone marrow cells.