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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.
Dr. Butler et al. (1) suggested that magnocellular dysfunction is not related to attentional impairment. However, the sharp separation of early-stage vision and attention is somewhat artificial. The dorsal system, which receives its major input from magnocellular pathways, plays an important role in the attentional regulation of very early perceptual processes and is believed to participate in the integration of domain-specific information mediated by the ventral system (6). Therefore, the magnocellular deficit they measured can be a crucial aspect of attentional problems rather than an independent phenomenon.
This possibility may conceptually lead to the authors’ final question for further research: What is the relationship between early visual dysfunctions and higher-level visuocognitive anomalies? We recently demonstrated that nonmedicated schizophrenia patients with spared magnocellular function exhibited dysfunction in a visual backward-masking task in which the spatial location of letters must be detected (a function of the dorsal stream) (7). Therefore, it seems that higher-level visual anomalies cannot be fully explained by a pure magnocellular deficit, which is likely to show a great degree of heterogeneity among patients with schizophrenia.
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