John R. Skoyles

Attention, reading and dyslexia

It has been proposed that magnocellular deficits cause dyslexia through reduced attention. According to one model (Vidyasagar, Clinical and Experimental Optometry 2004; 87: 4–10), attention is shifted from letter to letter during fixations and magnocellular deficits are hypothesised to cause reading problems by interfering with the ability to control the attention. The present report points out several problems in this model.

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.

The use of visual search to assess attention

Background:  Under some conditions, the time required for a visual search increases with the number of elements to be searched. It has been suggested that the overall search time reflects the duration that attention is devoted to each element multiplied by the number of elements. On this basis, it has been proposed that visual search time can be used as a measure of attention capability in dyslexic readers. However, there is evidence to suggest that the search time reflects task difficulty rather than attentional factors. Many dyslexic readers suffer from various sensory deficits. These deficits would effectively increase task difficulty for these readers. Here we use computer simulations to investigate the potential effects of sensory deficits on visual search.

Coherent motion, magnocellular sensitivity and the causation of dyslexia.

The central tenet of the magnocellular deficit theory of dyslexia is that dyslexia is caused by a magnocellular deficit. A number of investigators have found deficiencies in visual coherent motion perception among dyslexic readers. These deficiencies have been attributed to magnocellular deficits, which means that they directly reflect the cause of dyslexia. However, similar perceptual deficiencies have been found in association with autism, Williamss syndrome, hemiplegia, and schizophrenia. These findings appear to undermine at least one of the following claims: (1) that a magnocellular deficit is the cause of dyslexia, and (2) that coherent motion is a reliable test of magnocellular sensitivity.

A few remarks on attention and magnocellular deficits in schizophrenia

In connection with schizophrenia, it has been proposed that the magnocellular system is specifically linked to the guiding of covert visual attention. The argument is that the magnocellular pathway provides input to the dorsal cortical stream which then projects back to area V1. We review problems with this model. (1) It requires that responses in the magnocellular system have a lead time over responses in the parvocellular system. However, measurements indicate that the actual response time difference between the two systems is small or negligible when entering the visual cortex. (2) Attention can be modified by stimuli that do not activate the magnocellular system. And, (3) lesions to area MT in the dorsal stream impair smooth pursuit eye movements, but not saccadic eye movements which are associated with shifts in attention. For these reasons, it is difficult to link attention defects in schizophrenia to potential magnocellular deficits.

The use of phantom contours to isolate magnocellular and parvocellular responses.

In some “flickering” spot stimuli, two kinds of percepts can be seen at different frequencies: phantom contours and “surface characteristics.” It has been proposed that their perception may be used to evaluate the magnocellular and parvocellular systems. This, however, is problematic. First, the difference in temporal frequencies associated with the two percepts is large compared to that between the temporal tuning of magno- and parvocellular neurons. Second, the lack of absolute temporal phase information in the case of surface characteristics does not fit with parvocellular neuron behavior. Third, the low temporal threshold of surface characteristics suggests cortical mechanisms rather than parvocellular ones. And fourth, the relationship between the two percepts and color may reflect parvocellular responses not magno- and parvocellular ones.

YELLOW FILTERS, MAGNOCELLULAR RESPONSES, AND READING

It has been suggested that yellow filters may increase magnocellular responsivity. This suggestion was, in large part, based on the assumption that the S-cones inhibit the magnocellular system. However, the evidence invoked to justify this assumption is only indirect. A previously reported direct electrophysiological investigation of this issue has found that S-cone input to the magnocellular system actually sum with L-and M-cone inputs. Therefore, the notion that yellow filters enhance magnocellular responses by reducing inhibition from S-cones cannot be maintained.

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.

Is vision in schizophrenia characterized by a generalized reduction

How the visual capabilities of those with schizophrenia differ from those of individuals without schizophrenia is a topic of active research. Of special interest is the question of whether or not they might have a magnocellular deficiency. It has been concluded that contrast sensitivity in schizophrenic subjects is characterized by a general reduction in sensitivity, and so does not indicate a magnocellular deficiency (Skottun and Skoyles, 2007). 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. Differences between schizophrenic subjects and nonschizophrenic controls attributed to magnocellular deficiencies have been found using visually evoked potentials (VEP). Butler et al. (2009) obtained VEP data for schizophrenic subjects and controls under two conditions. One condition aimed at predominantly stimulating the magnocellular system, the other the parvocellular system. Butler et al. (2009) found statistically significant reduction in the responses from the schizophrenic subjects, relative to those of controls, under the condition favoring the magnocellular system but not under the parvocellular condition. The authors interpreted this as evidence for a magnocellular deficiency linked to schizophrenia. The present report examines the possibility that these results could reflect instead a general response reduction. The data of Butler et al. (2009) have been re-plotted in Figure ​Figure1.1. The open and filled symbols give the results for the schizophrenic subjects and controls, respectively, while panels A and B give the data obtained under the magno- and parvocellular conditions. A general response reduction was modeled by a simple linear scaling of the response from the control group. The scaling factor was determined by the best fit to the data of the schizophrenic subjects by calculating the smallest sum of squared deviations. Analyses of both magno- and parvocellular data conditions were included, giving a single scaling value of 0.756. (The scaling factors for the magno- and parvocellular data sets computed separately were 0.737 and 0.797, respectively). The scaled data are indicated by the dashed lines in Figure ​Figure1.1. Even though the data for the schizophrenic subjects in the magnocellular condition in some instances are slightly below the dashed line and the data in the parvocellular condition in some cases are slightly above the dashed line, the overall finding is that the scaled data give close fits to the data for the schizophrenic subjects for both conditions. This suggests that Butler et al.s (2009) data for schizophrenic subjects in both the magnocellular and the parvocellular conditions are consistent with scaling by the same factor. This is consistent with a general reduction in the response rather than a difference (as suggested by Butler et al., 2009) between the magnocellular and parvocellular systems. No reason therefore exists to account for these data with a deficiency linked specifically to the magnocellular system. Figure 1 Data re-plotted from Figure 4 of Butler et al. (2009). Open and filled symbols give data for schizophrenic subjects (N = 20) and controls (N = 17), respectively. (A,B) Give results obtained under conditions aimed at stimulating predominately the magno- ... One explanation for the differences between controls and schizophrenic subjects being significant in the magnocellular condition but not in the parvocellular one could be that the response differences were larger in the magnocellular condition. The fact that the responses were larger in this condition would have made the difference between the groups (as a result of scaling by a constant) larger under this condition, and so more likely to result in a statistically significant difference. Further, it is an invalid inference to conclude that a magnocellular deficiency exists solely based on the finding that a magnocellular condition gives statistically significant differences whereas a parvocellular condition does not. To do so would require making an interpretation of the non-significant data—but a statistically non-significant result does not allow any conclusions to be inferred (Gill, 1999). The finding that the difference is statistically significant under the magnocellular condition and not under the parvocellular condition, moreover, is not itself strictly pertinent. What might have been somewhat more relevant would have been if the difference between the data obtained under the two conditions were statistically significant. (It should in this connection be kept in mind that the difference between a statistically significant result and a non-significant result need not itself be statistically significant. Gelman and Stern, 2006). However, it is not clear that even this would have solved the problem since it may be possible for a single factor to have effects that are different under different conditions (as shown in Figure ​Figure1).1). The difference between these effects may, or may not, be statistically significant.

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.