To the Editor: We read with interest the excellent contribution of Pamela D. Butler, Ph.D., et al. (1) on the dysfunction of magnocellular visual channels in schizophrenia. We would like to raise some points that merit further clarification and may increase the impact of their contribution. First, the effect of medication on their results should be investigated and discussed in more detail. Although the authors cite a single study in which there was found no acute effects of haloperidol, there is evidence that dopamine receptor antagonists alter both early and late components of visual event-related potentials and that a hypodopaminergic state may predominantly disrupt magnocellular functions (2). More directly, we found that schizophrenia patients receiving higher doses of conventional antipsychotics and exhibiting more severe drug-induced parkinsonism showed poorer magnocellular function (3). This issue is related to the problem of symptom variation. It has been demonstrated with both psychophysics and electrophysiological methods that the presence of different symptoms of schizophrenia is related to distinct patterns of visual information-processing abnormalities (4, 5). These questions should be addressed with correlation/covariance analyses or with the consideration of clinical subtypes, which may help resolve the apparent controversy of the literature correctly outlined, but not targeted, by the authors.