Correspondence

Defective Visual Pathway in Reading-Disabled Children

N Engl J Med 1993; 329:579August 19, 1993

Article

To the Editor:

Lehmkuhle and coworkers (April 8 issue)1 describe abnormalities of the visual evoked potential in children with reading disability. I disagree with the authors' interpretation of their findings as evidence of a selective abnormality of the magnicellular visual pathway.

Their key observation is that transient visual evoked potentials in normal readers and subjects with reading disability are affected differently by a 12-Hz flicker in the background stimuli surrounding a target stimulus. In principle, if a 12-Hz field selectively depressed the sensitivity of magnicellular neurons, these data would suggest that a fast magnicellular pathway participated in the normal visual evoked potential but not in the potential of subjects with reading disability. A 12-Hz flicker, however, provides a strong stimulus for both magnicellular and parvicellular neurons2. Thus, there is no reason to believe that the surrounding 12-Hz flickering field selectively desensitizes the magnicellular system.

Other investigators have reported abnormalities in the visual evoked potential that are associated with reading disability. Livingstone et al.3 reported an abnormality in the transient and steady-state visual evoked potential that might have been consistent with a magnicellular deficit, but the findings were not reproduced in a larger study4. May et al.5 also found abnormalities under low-spatial-frequency conditions, but in this study the visual evoked potentials of subjects with reading disability had a shorter latency than those of normal readers, particularly at the disappearance of the stimulus. In the study by Lehmkuhle et al.,1 the equalization in the responses of normal readers and reading-disabled subjects with the addition of the flickering background reflects not only an increase in response latency in normal subjects but also a (not statistically significant) shortening of response latency in reading-disabled subjects. This finding1,5 defies a simple interpretation in terms of a loss of magnicellular input.

Interpretation of the available data on visual evoked potentials as evidence of magnicellular dysfunction requires the denial of a body of experimental evidence in primates (in addition to that summarized by Kaplan et al.2) as well as selective attention to the data. Other possibilities need to be considered. These include differences in foveal and extrafoveal vision; fixation and accommodative behavior; lateral interactions, masking at retinal and cortical levels, or both; magnicellular-parvicellular interactions in striate and extrastriate cortex; the geometry of the cortical generators of the visual evoked potential; and extrastriate function.

Jonathan D. Victor, M.D., Ph.D.
Cornell University Medical College, New York, NY 10021

5 References

1. 1

   Lehmkuhle S, Garzia RP, Turner L, Hash T, Baro JA. A defective visual pathway in children with reading disability. N Engl J Med 1993;328:989-996
   Full Text | Web of Science | Medline

2. 2

   Kaplan E, Lee BB, Shapley RM. New views of primate retinal function. Prog Retinal Res 1990;9:273-336
   CrossRef

3. 3

   Livingstone MS, Rosen GD, Drislane FW, Galaburda AM. Physiological and anatomical evidence for a magnocellular defect in developmental dyslexia. Proc Natl Acad Sci U S A 1991;88:7943-7947
   CrossRef | Web of Science | Medline

4. 4

   Victor JD, Conte MM, Burton L, Nass RD. Visual evoked potentials in dyslexics and normals: failure to find a difference in transient or steady-state responses. Vis Neurosci (in press).
   

5. 5

   May JG, Lovegrove WJ, Martin F, Nelson P. Pattern-elicited visual evoked potentials in good and poor readers. Clin Vision Sci 1991;6:131-136
   

Author/Editor Response

The authors reply:

To the Editor: Although both the magnicellular and the parvicellular pathways respond to a field that flickers at 12 Hz, this does not invalidate the use of a flickering background to isolate the response of each pathway. The use of such backgrounds is an established psychophysical technique to study parallel visual pathways1. An electrophysiologic variant of this technique was used in our study of reading-disabled children. When a field that flickers at 12 Hz surrounds a target stimulus, the noise level is assumed to be higher in the magnicellular than in the parvicellular pathway. This assumption is based on the results of studies of selected lesions, which demonstrated that the magnicellular pathway is about 10 times more responsive to stimulation at 12 Hz2. The combination of the flickering background and rapid and brief low-contrast target stimuli permits an assessment of the effects of different amounts of noise in each pathway on the processing of different types of visual information.

The response to a rapid, low-contrast, low-spatial-frequency stimulus is dominated by the magnicellular pathway,2 which is more effectively masked by a 12-Hz flickering background. The response to a stimulus with a higher spatial frequency will be dominated by the parvicellular pathway,2 which is not effectively masked by the flickering background. This is the pattern of results observed in both psychophysical experiments and those using visual evoked potentials1.

Flickering backgrounds also increase the latency of visual evoked potentials produced by low-spatial-frequency stimuli. Since the response of the magnicellular pathway is attenuated by the flickering field, the composite response to a low-spatial-frequency stimulus is dominated by the slower, parvicellular pathway, which results in a delay of the evoked potential. Indeed, the delay (of approximately 10 msec) observed in the evoked potential is consistent with the delay observed in the visual latencies of cells in primate striate cortex with selected lesions of the magnicellular pathway3.

The technique, in which the subjects each serve as their own controls, is sensitive to subtle differences in visual processing that might otherwise be overlooked because of the inherent variability of visual evoked potentials. Finally, although other models may explain changes in the visual evoked potential, there is a multitude of psychophysical, electrophysiologic, and anatomical findings that are consistent with a defective magnicellular pathway in reading-disabled children4.

Stephen Lehmkuhle, Ph.D.
Ralph P. Garzia, O.D.
University of Missouri-St. Louis, St. Louis, MO 63121

4 References

1. 1

   Bassi CJ, Lehmkuhle S. Clinical implications of parallel visual pathways. J Am Optom Assoc 1990;61:98-110
   Medline

2. 2

   Merigan WH, Maunsell JHR. How parallel are the primate visual pathways? Annu Rev Neurosci 1993;16:369-402
   CrossRef | Web of Science | Medline

3. 3

   Maunsell JHR, Gibson JR. Visual response latencies in striate cortex of the macaque monkey. J Neurophysiol 1992;68:1332-1344
   Web of Science | Medline

4. 4

   Willows D, Corcos E, Kruk R, eds. Visual processes in reading and spelling. Hillsdale, N.J.: L. Erlbaum, 1993.