La majorité des patients schizophrènes présente un trouble de la poursuite oculaire et leurs apparentés ont souvent plus d'anomalies de la poursuite oculaire que la population générale. Le but de cette étude était de rechercher une altération de la poursuite oculaire à la fois chez les patients schizophrènes et leurs parents afin d'avoir une indication quant à l'hypothèse selon laquelle l'altération de la poursuite oculaire serait un marqueur de la vulnérabilité génétique de la schizophrénie. Nous avons inclus 15 patients schizophrènes (selon les critères du DSM IV), 19 apparentés et 2 groupes de sujets témoins appariés aux patients (n = 15) et aux parents (n = 19). Les apparentés étaient les pères ou mères des patients afin d'avoir une population homogène tant au niveau du risque génétique qu'au niveau de l'âge et étaient dénués de troubles du spectre schizophrénique actuels ou passés. Chaque sujet a été évalué avec le paradigme de la poursuite sinusoïdale lente permettant de calculer le gain de poursuite et la fréquence des saccades (« catch-up », « back-up », « square-wave-jerk », saccades anticipatoires). Le gain ne différait pas significativement entre les parents et les sujets témoins, mais les parents avaient un nombre de saccades « catch-up » pendant la poursuite lente significativement plus important que les sujets témoins. Par contre, bien que le gain des patients soit plus faible que celui de leurs sujets témoins, aucune différence significative du gain ou des fréquences des saccades entre les patients schizophrènes et les sujets témoins appariés n'était observée. Nos résultats n'indiquent pas que l'altération de la poursuite oculaire lente pourrait être considérée comme un marqueur de vulnérabilité de la schizophrénie. En effet, s'il existe une altération de la poursuite sinusoïdale lente (saccades « catch-up ») chez les parents de patients schizophrènes, cette altération n'était pas observée chez les patients.

Several studies have confirmed the existence of genetic factors in schizophrenia. However, the genotype predisposing for the disease is not known yet. Nevertheless, those genetic factors in the families of schizophrenic patients urge us to search for genetic vulnerability markers of schizophrenia. Ocular pursuit disorders, in particular, could be one of those vulnerability markers. Eye movements have been often tested in schizophrenia. Most of the schizophrenic patients have eye-tracking disorders and their biological relatives demonstrate an increased prevalence of eye-tracking impairments. The aim of the study was to research if smooth pursuit eye movements could be a vulnerability marker of schizophrenia. In order to have an indication about this hypothesis, impairments of smooth pursuit eye movements were researched in both schizophrenics and their parents. Methods – Fifteen DSM IV schizophrenic patients stabilized at the time of the inclusion and not treated with lithium, benzodiazepines, barbiturates, or chloral hydrate ; 19 parents without history of schizophrenic spectrum disorders (SADS-LA and IPDE), and 2 groups of healthy subjects matched in age and sex with probands and with the parents, were included in the study. Parents only were included (fathers or mothers) in order to have an homogeneous population for the genetic risk and age. The eye-tracking paradigm used was a smooth pursuit task. The stimulus was a sinusoidal wave form moving on a horizontal line, with a frequency of 0.4 Hz and an amplitude of 30. Different parameters were measured : gain (ratio between the eye velocity and the target velocity) and saccades frequencies (catch-up saccades, back-up saccades, anticipatory saccades and square-wave-jerks). For each parameter, analysis of covariance (ANCOVA) with age as covariable was carried out. For the results reaching the significance of 0.05, the Bonferroni correction was applied (level of significance 0.016). The effect size of the parameter was calculated ((the mean of the subjects minus the mean of the matched controls) divided by standard deviation of the two groups). According to Cohen, 0.20 indicates a small effect size, 0.50 indicates a medium effect size and 0.80 indicates a large effect size. Results – Comparison between patients and matched controls : the means of global gain, of gain for the movements to the left and of gain for the movements to the right did not differ significantly between patients and their matched controls. The size effects are 0.31 for the global gain, 0.20 for the movements to the left and 0.41 for the movements to the right. The frequencies of total saccades, catch-up saccades, back-up saccades, anticipatory saccades and square-wave-jerks did not differ significantly between patients and their controls. The size effects for those parameters were 0.09, 0.03, 0.00, 0.39 and 0.63 respectively. Comparison between parents and matched controls : the means of global gain, of gain for the movements to the left and of gain for the movements to the right did not differ significantly between the two groups. The size effects for those parameters were 0.00, 0.05 and 0.17 respectively. The frequency of total saccades did not differ significantly between the groups whereas the size effect was 0.63. The frequency of catch-up saccades was significantly more important in parents than in controls (p = 0.006) and the size effect was 0.80. The other saccadic parameters did not differ significantly between groups, their size effects were 0.24 for the back-up saccades, 0.21 for the anticipatory saccades and 0.00 for the square-wave-jerks. Whereas the gain of the patients had a tendency to be lower than the gain of their controls, no significant difference was observed between patients and their controls. Only a size effect of 0.63 for the frequency of square-wave-jerks was obtained. This large effect size suggests that the difference between patients and controls might be significant in a larger sample. The catch-up saccades frequency between parents and controls was significant. The differences between our study and the previous studies could be due to several factors. The paradigms used were different between the studies and our sample was small (only 15 patients and 19 relatives). Moreover, some patients in the previous studies were treated by lithium, drug well known to modify ocular pursuit and, finally the relatives in the other studies were 10 years older than ours and age is known to alter ocular pursuit. Since an impairment of the smooth pursuit was observed in the relatives of schizophrenic patients but not in the probands, this study does not support the hypothesis that eye-tracking disorders could be considered as a marker of vulnerability of schizophrenia.