Are masking abnormalities in schizophrenia specific to type-B masking?

Abstract

The abnormal visual masking in those with schizophrenia, it has been proposed, arises from a deficiency in their magnocellular system. Two kinds of masking exist: Type-A and Type-B. Type-A masking is characterized by the masking being strongest when target and mask are presented simultaneously. Type-B masking is characterized by a non-monotonic masking curve, i.e. the masking is largest when the mask is presented at some time after the target. The proposed link between masking and magnocellular activity applies mainly to Type-B masking. Thus, a magnocellular deficiency, if it exists, should effect Type-B masking more prominently than Type-A masking. Here we review the relevant literature. The majority of studies of masking in those with schizophrenia, it is found, have examined only Type-A masking. These find substantial evidence for abnormal masking. Where Type-B masking has been obtained, evidence also exists for abnormalities. However, the abnormal masking in these cases is largely unrelated to the defining characteristic of Type-B masking (i.e. to the non-monotonic masking function). It is concluded that the evidence for linking masking abnormalities in schizophrenia specifically to Type-B masking is weak. This undermines the proposal that masking abnormalities in schizophrenia have a magnocellular origin.

Is vision in schizophrenia characterized by a generalized reduction?

“…Likewise, many of the reported cases of abnormal visual masking linked to schizophrenia can be described by a general reduction (see, e.g., Rassovsky et al, 2004). Also this is hard to reconcile with a magnocellular deficit since, according to the theory, such a deficit would have been expected to cause a reduction that was related specifically to the U-shaped Type-B masking function (Skottun and Skoyles, 2009). These observations prompt the question of whether or not other differences between schizophrenic subjects and controls that have been attributed to magnocellular deficiencies can also be accounted by a general reduction in sensitivity or response.…”