On separating the magnocellular from the parvocellular: Responses to two statements by Goodhew et al.

Goodhew et al. (Attention Perception & Psychophysics, 79, 1147-1164, 2017) claim we (Skottun & Skoyles) hold: (1) that it is not possible to separate contributions from the magno- and parvocellular systems to psychophysical tasks, and (2) that there are no differences between magno- and parvocellular cells. Neither of these claims is correct.

Subjective criteria and illusions in visual testing: some methodological limitations.

It is argued that illusions cannot generally be investigated with criterion-independent methods. This limits the value of the data obtained from them. This is particularly important when the results are compared between groups of subjects, for example, between dyslexic readers and controls, since it is possible that the differences between the groups reflect differences with regard to criteria rather than real perceptual differences.

The time course of visual backward masking deficits in schizophrenia.

Schizophrenia, it has been hypothesized, is linked to a deficiency in the magnocellular portion of the visual system. Abnormal backward masking has been invoked as support for this hypothesis. The rationale for linking backward masking to the magnocellular system is the hypothesis that fast responses in the magnocellular systems catches up with, and then inhibits slower responses in the parvocellular system. However, the latency difference between the magno- and parvocellular systems is at most 20 ms. Magnocellular abnormalities as a result would be expected to manifest themselves only at relatively short stimulus onset asynchronies (SOAs) or interstimulus intervals (ISIs). The present study examines this implication. It is found that a substantial number of investigations have uncovered abnormal masking at SOAs or ISIs of 300 ms or larger, and some even at ISIs as large as 700 ms. It is difficult to reconcile abnormalities at these SOAs and ISIs with magno-parvocellular latency differences of 20 ms or less. It is concluded that the abnormal masking does not support the existence of a magnocellular deficiency in schizophrenia.

On identifying magnocellular and parvocellular responses on the basis of contrast-response functions.

It has been proposed that magnocellular and parvocellular sensitivity in schizophrenic individuals can be assessed using steady-state visually evoked potentials (VEPs) to either low-contrast stimuli or stimuli whose contrast is modulated around a high contrast "pedestal" (Green MF, Butler PD, Chen Y, et al. Schizophr Bull. 2009;35:163-181). This suggestion faces 2 difficulties: (1) To use low-contrast stimuli to activate the magnocellular system is inconsistent with lesion studies that have shown that under many conditions, the parvocellular system responds to the lowest contrasts and (2) To rely on contrast-response relationships to identify magnocellular and parvocellular responses is difficult because other neurons exist in the visual system that have contrast-response relationships similar to those of magnocellular and parvocellular cells.

Autism, context/noncontext information processing, and atypical development.

Autism has been attributed to a deficit in contextual information processing. Attempts to understand autism in terms of such a defect, however, do not include more recent computational work upon context. This work has identified that context information processing depends upon the extraction and use of the information hidden in higher-order (or indirect) associations. Higher-order associations underlie the cognition of context rather than that of situations. This paper starts by examining the differences between higher-order and first-order (or direct) associations. Higher-order associations link entities not directly (as with first-order ones) but indirectly through all the connections they have via other entities. Extracting this information requires the processing of past episodes as a totality. As a result, this extraction depends upon specialised extraction processes separate from cognition. This information is then consolidated. Due to this difference, the extraction/consolidation of higher-order information can be impaired whilst cognition remains intact. Although not directly impaired, cognition will be indirectly impaired by knock on effects such as cognition compensating for absent higher-order information with information extracted from first-order associations. This paper discusses the implications of this for the inflexible, literal/immediate, and inappropriate information processing of autistic individuals.

Temporal order judgment in dyslexia--task difficulty or temporal processing deficiency?

Dyslexia has been widely held to be associated with deficient temporal processing. It is, however, not established that the slower visual processing of dyslexic readers is not a secondary effect of task difficulty. To illustrate this we re-analyze data from Liddle et al. (2009) who studied temporal order judgment in dyslexia and plotted the results as d' as a function of Stimulus Onset Asynchrony (SOA). These data make it possible to compare the results of dyslexic readers and controls both in terms of d' which is related closely to task difficulty and in terms of time (i.e. SOA). It is found that the difference between the groups is about equally well accounted for in terms of d' as in terms of temporal factors. This suggests that the results of Liddle et al. (2009) may be equally well accounted for in terms of general task difficulty as temporal factors.

L- and M-cone ratios and magnocellular sensitivity in reading.

It has been proposed that magnocellular deficits cause the reading problems in dyslexia. However, how magnocellular deficiencies are supposed to cause these problems is unclear. Recently it has been proposed that reading performance is limited by the L-/M-cone inputs to the magnocellular system. However, as explained in this review, this is problematic for a number of reasons. Particularly difficult is the linking of L- and M-cone sensitivity specifically to the magnocellular system.

On using Vernier acuity to assess magnocellular sensitivity.

A recent study [Keri, S., & Benedek, G. (2009). Visual pathway deficit in female fragile x premutation carriers: A potential endophenotype. Brain and Cognition, 69, 291-295] has found Vernier acuity deficiencies together with contrast sensitivity defects consistent with a magnocellular deficit in female fragile x premutation carriers. This may appear to support the notion that Vernier acuity may serve as a test of magnocellular sensitivity. However, Vernier acuity deficiencies have been reported in other conditions (e.g., schizophrenia, amblyopia and cortical visual impairment) where there is little evidence for magnocellular deficits. The observation that Vernier acuity deficiencies can occur without magnocellular deficits indicates that Vernier acuity is not a reliable test of magnocellular sensitivity.

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

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.

Are masking abnormalities in schizophrenia limited to backward masking?

Schizophrenia, it has been proposed, is associated with deficits in the magnocellular part of the visual system. In support of this suggestion, it has been claimed that schizophrenic subjects have abnormal backward masking. However, if this abnormality is to be linked specifically to magnocellular defects, then it must be specific to backward masking, and not, also effect, for example, forward masking. We examined this issue by reviewing the studies of masking in schizophrenic subjects. We find: (i) Most studies (56 out of 67) of backward masking have researched only backward masking. This makes it impossible to determine if the abnormalities found in these studies are exclusively confined to backward masking. (ii) Of those studies (11) that have included both forward and backward masking conditions, the majority found some degree of abnormality under both forward and backward masking conditions. It is concluded that the evidence for linking the abnormalities found in those with schizophrenia specifically to backward masking, rather than masking in general, or more general visual impairments, is at present relatively weak. Given the rationale for using backward masking as a test of magnocellular sensitivity, research in this area does not point to a deficit specific to the magnocellular system.