{'fraction_non_alphanumeric': 0.03650442477876106, 'fraction_numerical': 0.01991150442477876, 'mean_word_length': 5.470483005366726, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Letter to the Editor

The early part of the visual system— from the retina to the visual cortex— contains two parallel streams: the magnocellular and parvocellular systems. The most pronounced difference between the two is that some, if not all, neurons in the parvocellular system respond to differences in color, whereas all neurons in the magnocellular system respond only to differences in luminance (for a review, see Shapley & Perry, 1986). Birch and Chase (2004) used four vision tests—contrast sensitivity, sine wave detection, object perception, and reading of spatially filtered text—to assess magnocellular sensitivity. The tests were administered to two groups of individuals: compensated readers with dyslexia (i.e., individuals who have at one point been diagnosed with reading impairment but who do not show severe current reading impairment) and uncompensated readers with dyslexia (i.e., individuals who have received a diagnosis of reading impairment and who currently show such a reading impairment). Contrary to Birch and Chase’s expectations, none of these tests revealed evidence for magnocellular deficits in either the compensated or uncompensated readers with dyslexia. Birch and Chase (2004) proposed a number of possible explanations for this seeming discrepancy: (a) magnocellular deficits may manifest themselves only on some tasks; (b) there may not have been enough frames in the stimulus; (c) the presentation condition may not have been appropriate; (d) there may be individual differences among readers with dyslexia; (e) only certain subtypes of dyslexia display magnocellular deficits; or (f) the parvocellular system may compensate for magnocellular shortcomings. These suggestions are all rather speculative, and none of them are compelling. However, rather astonishingly, Birch and Chase failed to point to the most parsimonious explanation, namely, that dyslexia is not associated with magnocellular deficits. Several other tests have been used in attempts to assess magnocellular sensitivity. However, as we have shown in a series of reports, these tests are problematic or have shortcomings (Skottun, 2001a, 2001b, 2004a, 2004b; Skottun & Skoyles, 2004; see also Skottun, 2000a, for a discussion of the use of motion perception to test magnocellular sensitivity). The most direct psychophysical test of magnocellular functioning is contrast sensitivity. In fact, of the four tests used by Birch and Chase (2004), one is contrast sensitivity and another, sine wave detection, is closely related to contrast sensitivity. One of us (Skottun) reviewed the evidence for magnocellular deficits among readers with dyslexia based on studies of contrast sensitivity (Skottun, 2000a, 2000b). The result of this review was that although some studies have produced results that are more or less consistent with magnocellular deficits, there are larger numbers of studies that either have found no deficits or have found deficits of a nature that is incompatible with a deficiency in the magnocellular system. These results indicate, therefore, that dyslexia is not linked to magnocellular deficits and, consequently, that dyslexia is not caused by a deficiency in the magnocellular system. This conclusion has been further strengthened by additional, subsequent results (Amitay, Ben-Yehudah, Banai, & Ahissar, 2002; Ramus et al., 2003; Spinelli et al., 1997; Stuart, McAnally, & Castles, 2001; Williams, Stuart, Castles, & McAnally, 2003). The fact that Birch and Chase (2004) did not find evidence for magnocellular deficits appears to provide even further support for this conclusion.