Contrast Detection in Schizophrenia

In their study, Chen et al¹ presented new data concerning motion perception disturbances in schizophrenia. Using contrast sensitivity measurements in different experimental paradigms, the authors demonstrated that patients with schizophrenia displayed a specific deficit of motion perception, whereas other visual functions, such as orientation and contrast detection, were preserved. However, the question of medication was not addressed in this study, which makes the final interpretation difficult.

It is well established that dopaminergic deficiency in the visual system dominantly and specifically disrupts spatiotemporal contrast sensitivity functions.² There is some evidence that this impairment is most pronounced for the transient visual channels, which are related to the processing of stimuli with low-spatial and high-temporal frequencies.³ Therefore, studies investigating contrast-sensitivity functions in patients with schizophrenia can be specifically confounded by uncontrolled antidopaminergic medication effects.

For example, Slaghuis⁴ found impaired contrast sensitivity in patients given medication when no motion discrimination was included. In contrast, in a preliminary study, we demonstrated abnormally elevated contrast-sensitivity values at low-spatial frequencies (<2 cycles per degree) in patients who were never medicated.⁵ This effect was more pronounced when the sinusoidal gratings were modulated at higher temporal frequencies. These results are consistent with the theory of overactive motion-sensitive transient channels in schizophrenia. Longitudinal studies in these patients also revealed that antipsychotic medication normalized this hyperactivity. Moreover, in the case of higher doses a parkinsonian hypofunction of transient channels could be detected (S.K. and A.A., unpublished data, 1998).

In the study by Chen et al, contrast sensitivity for a low–spatial frequency stimulus (0.5 cycles per degree) was altered only when the two-alternative, forced-choice paradigm included velocity discrimination, but not when there was a simple contrast detection task.¹ According to the aforementioned data, it is possible that the antipsychotic medication normalized contrast-detection functions in these patients. The impairment of more refined velocity discrimination may reflect a less-pronounced dysfunction of motion-sensitive visual areas or an abnormal interaction between basic mechanisms of contrast and speed detection. In addition, our calculations of motion gain (the ratio of contrast sensitivities obtained for temporally modulated [10 degrees per second] and stationary [0 degrees per second] stimuli in the contrast detection task) from the data shown in the Table revealed a higher value in the schizophrenia group (mean, 2.21[484/219]) than in the control group (mean, 1.73 [502/291]). This may show relative overreactivity of transient channels since, in spite of the applied dopaminergic blockade, the patients with schizophrenia benefited more from the temporal modulation of stimuli than the controls. However, the hypoactivity of these mechanisms may become apparent when higher antipsychotic doses are administered, disrupting simple contrast detection without velocity discrimination. In this respect, it would be interesting to know how the 3 patients receiving no antidopaminergic drugs differed from the other subjects receiving antipsychotic medication.

In the future, studies including patients who were not receiving medication should explore basic spatiotemporal visual dysfunction in schizophrenia.