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.

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 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.

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.

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.

Visual search: magno- and parvocellular systems or color and luminance processes?

It has been found that visual search is slower with isoluminant color stimuli than with luminance stimuli. This has been interpreted to mean that the magnocellular system plays a vitally important role in visual search. We here propose that this observation can be more parsimoniously understood in terms of color and luminance rather than in terms of the magno-and parvocellular systems. According to this interpretation, the slower search under isoluminant condition is a consequence of the fact that visual processing in general is slower, and that spatial vision is poorer, under isoluminant color conditions relative to luminance conditions. We also point out that in order to draw meaningful conclusions with regard to the underlying neural substrate, one needs to equate the luminance and color stimuli for discriminability.

Some remarks on the use of visually evoked potentials to measure magnocellular activity.

It has been claimed that magnocellular activity can be assessed by measuring the second harmonic responses in visually evoked potentials (VEPs) to On/Off flickering stimuli. The empirical support for this claim is examined. It is noted that: (1) there is in some instances a failure to differentiate counterphase flicker from On/Off flicker. (2) The suggestion that magnocellular activity can be assessed from second harmonic VEP responses was based on the assumption that magnocellular and parvocellular responses correspond, respectively, to transient and sustained responses. This assumption has been undermined by recent quantitative research. (3) Second harmonic responses can be obtained with isoluminant color stimuli. (4) The attenuation of second harmonic responses at high temporal frequencies is not specific to chromatic stimulation. (5) Also, VEPs to contrast reversing stimuli show reduced amplitudes in the case of chromatic stimulation. It is therefore difficult to link second harmonic response to On/Off flicker specifically to magnocellular activity. It is concluded that second harmonic responses in VEPs should only be used with caution, if at all, to assess magnocellular activity.

Contrast sensitivity and magnocellular functioning in schizophrenia.

It has been suggested that schizophrenia is associated with a magnocellular deficit. This would predict a loss of contrast sensitivity at low spatial and/or at high temporal frequencies. We here review research that tested contrast sensitivity in individuals with schizophrenia. We find that the results of this research tend to show uniform reductions in contrast sensitivity that are generally not consistent with a magnocellular deficit. While much of this data may be consistent with an attentional deficiency on the part of the schizophrenic individuals, it is difficult to link such an attentional deficiency specifically to the magnocellular system. The conclusion of the present review is that contrast sensitivity data do not indicate the existence of an association between magnocellular deficits and schizophrenia.

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.

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. 1. It requires dissociation of eye movements and attention, which may be problematic within the framework of reading. 2. There is direct evidence to indicate that reading is not carried out in a letter-to-letter manner during fixations. 3. There are aspects of the visual performance of dyslexic readers, which are difficult to attribute to inattention. 4. There are indications that attentional deficiencies of dyslexic readers are not associated with magnocellular deficits. 5. The evidence for linking magnocellular deficits to dyslexia in general is weak.

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.

Interaural time difference discrimination thresholds for single neurons in the inferior colliculus of Guinea pigs.

Sensitivity to changes in the interaural time difference (ITD) of 50 msec tones was measured in single units in the inferior colliculus of urethane-anesthetized guinea pigs. ITD functions were measured with 100 repeats and fine spacing (100 points per cycle). The just noticeable difference (jnd) for ITD was determined using receiver operating characteristic (ROC) analysis of the spike-count distribution at each ITD. The jnd became progressively smaller as the signal frequency increased from 50 to 800 Hz but became unmeasurable above 1 kHz. The lowest jnds (30 microsec) were comparable with human jnds, indicating that there is sufficient information in the firings of individual neurons to permit discrimination without obligatory pooling. ROC analysis requires the choice of a reference ITD from which the jnd may be found by stepping the target ITD through the ITD function. For each neuron the reference was chosen to minimize the jnd. The lowest jnd was usually for ipsilateral leading references, near the minimum of the ITD function where the variance was also low, but where the slope was nearing its steepest. This was despite the peak of the ITD function occurring for contralateral leading stimuli. When the reference ITD was on midline, a jnd could be obtained by looking for firing rates either greater or smaller than the firing rate at midline. The lower jnd was usually obtained by looking for a decrease in firing rate. As duration increased, jnds either decreased or increased, depending on unit type, whereas when level increased, jnds generally increased.

Magnocellular reading and dyslexia.

It is pointed out that the question of the potential role of magnocellular neurons in reading is distinctly separate from the question of whether or not a magnocellular deficit is the cause of dyslexia. These two issues should not be confused. With regard to the second, the data do not at present favor the hypothesis that dyslexia is the result of a magnocellular deficit.

End-stopping in the visual cortex: excitation or inhibition?

In the visual cortex some neurons respond more strongly to short stimuli than to long ones. This is referred to as "end-stopping" and has been generally attributed to inhibition. The role of inhibition, however, has been difficult to demonstrate. Moreover, modeling has shown that end-stopping can be created solely from excitation. The roles of excitation and inhibition were investigated using intracellular recordings (Anderson et al., 2001, J. Neurosci. 21: 2104-2112). The results of that study were interpreted in favor of inhibition. The present report re-examines these results and finds that they may be in good, perhaps even better, agreement with an excitation model of end-stopping.

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.

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.

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.