Neurological evidence for dissociation of pursuit and optokinetic systems

Patients with neurological disease were examined for dissociations between the performance capabilities of pursuit, immediate onset passive and active optokinetic responses to determine whether these functions are subserved by separate mechanisms. We found a patient in whom pursuit was intact in the presence of severely impaired optokinetic responses and another in whom optokinetic responses were intact in the presence of severely deranged pursuit. These dissociations suggest that pursuit and immediate onset optokinetic responses are mediated, to some extent, by separate mechanisms as the results are not explicable in terms of a continuum of performance ability related to target size. Another patient, who had virtually no pursuit or passive optokinetic responses, produced high slow phase velocities of active optokinetic response, which demonstrates that the active form of optokinetic response can be more than a linear addition of pursuit and passive optokinetic responses.