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.

A few words on differentiating magno- and parvocellular contributions to vision on the basis of temporal frequency.

A number of authors have proposed that changes in temporal frequency within the range of 0-30Hz may be used to differentiate contributions from the magno- and parvocellular systems. The present analyses estimate the percentage of active magnocellular cells as a function of frequency based on published cut-off values for magno- and parvocellular cells. These analyses indicate that varying the temporal frequency over the range of 0-30Hz has little effect upon the percentage of active magnocellular cells. The analyses were also carried out for a series of hypothetical cut-off frequencies and standard deviations of these frequencies for magnocellular cells. The results of these simulations indicate that even large alterations in these values do not alter the above conclusion to a noteworthy extent.

A few remarks on the utility of visual motion perception to assess the integrity of the magnocellular system or the dorsal stream.

It has been proposed that visual motion perception may be used to assess magnocellular or dorsal stream integrity. It is here pointed out, based on recently published data from dyslexic readers, that it is possible for deficient motion perception to exist without there being deficiencies in neither the magnocellular system nor in the dorsal stream. This makes it difficult to rely upon tests of motion perception to assess the integrity of these structures.

On the use of spatial frequency to isolate contributions from the magnocellular and parvocellular systems and the dorsal and ventral cortical streams.

Many authors have claimed that suprathreshold achromatic stimuli of low and high spatial frequency can be used to separate responses from different entities in the visual system. Most prominently, it has been proposed that such stimuli can differentiate responses from the magnocellular and parvocellular systems. As is reviewed here, investigators who have examined stimulus specificity of neurons in these systems have found little difference between magno- and parvocellular cells. It has also been proposed that spatial frequency can be used to selectively activate the "magnocellular-dorsal stream". The present review indicates that cells in Area MT of the dorsal stream do prefer very low spatial frequencies. However, the review also shows that cells in Area V4 of the ventral stream respond, not only to relatively high spatial frequencies, but also to low frequency stimuli. Thus, low spatial frequencies cannot be relied upon to selectively activate the dorsal stream.

The need to differentiate the magnocellular system from the dorsal stream in connection with dyslexia.

A number of authors have postulated a "magnocellular-dorsal stream" deficit in dyslexia. Combining the magnocellular system and the dorsal stream into a single entity in this context faces the problem that contrast sensitivity data do not point to a magnocellular deficiency linked to dyslexia, while, on the other hand, motion perception data are largely consistent with a dorsal stream dysfunction. Thus, there are data both for and against a "magnocellular-dorsal stream" deficit in connection with dyslexia. It is here pointed out that this inconsistency is abolished once it is recognized that the magnocellular system and the dorsal stream are separate entities.

A few observations on linking VEP responses to the magno- and parvocellular systems by way of contrast-response functions.

It has been proposed that magno- and parvocellular contributions to Visually Evoked Potentials (VEPs) can be isolated, or differentiated, by noting the contrast-response relationships of the responses. This suggestion is examined quantitatively by determining the similarity between various sets of VEP data that have been attributed to the magno- and parvocellular systems and previously reported contrast-response functions for different kinds of neurons (magno- and parvocellular neurons and V1, V4, and MT cells) and combinations of the contrast-response functions for these neurons. It is found that other neurons, or combinations of other neurons, typically give better fits to the data than do magno- and parvocellular cells. Thus, to attribute VEP responses to the magno- or parvocellular systems based on contrast-responses properties faces difficulties.

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.

On using very high temporal frequencies to isolate magnocellular contributions to psychophysical tasks.

In connection with dyslexia several authors have sought to employ stimuli of very high temporal frequency to isolate magnocellular contributions to visual tasks. It is here pointed out that considerable evidence indicate that the ability to see the very highest temporal frequencies is limited by cortical mechanisms. This suggests that variations and abnormalities in this ability may reflect cortical factors rather than magnocellular ones. It is therefore difficult to rely upon very high temporal frequency stimuli to isolate contributions from the magnocellular system.

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.

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.