Picking up where we left off in Part 1, there is overwhelming evidence for the theory of magnocelluar deficit in reading disabilities, placing an onus on developing clinical tests and interventions sensitive to developing and integrating dorsal stream function. Ironically two clinical tests diagnostic devices recognized for their utility in probing mangocellular function, FDT (Frequency Doubling Technology) and VEP (Visual Evoked Potential), were introduced not for reading, but for glaucoma management. Let’s look briefly at each.
Pammer and Wheatley published the first study on dyslexics as compared to control readers using FDT. The counterphase flicker of the stimulus pattern results in a target that will appear to flicker or shimmer at various locations in the visual field. When perceived, the patient presses the clicker on their mouse. Loss in sensitivity gives you the typical printout of visual field deficits.
Pammer and Wheatley concluded:
“In general, the results from the current study provide good evidence for magno system involvement in dyslexia that is apparent at the retinal ganglion level of visual processing, with specific dysfunction in M(y)-cell activity. Given the strong correlation of this measure with both higher-order dorsal stream activity and actual reading ability, sensitivity to the frequency doubling illusion could provide a simple and powerful diagnostic tool for the evaluation and identification of dyslexia.”
We are now using the Humphrey Matrix 800, a third generation FDT test for routine visual field testing. Here is their training video, though to get an idea of the patient’s task, you can zoom straight to the 14:00 minute mark.
It has been asserted that loss of sensitivity in magnocelluar function can be detected using the VEP even earlier than the changes detected through FDT perimetry. VEP abnormalities implicating the magnocelluar system have previously been reported in dyslexic children by Romani et al and Brannan et al, though not in the way it is currently done for early glaucoma detection. That is, by directly comparing the VEP response to high contrast (85%) vs. low contrast (15 – 20%) checkerboard patterns (A and B respectively below).
Yadav and Ciuffreda reported that as the check size becomes smaller, the mean VEP latency (P100) increases, although to a modest extent. At 40 minutes of arc the latencies are equal for high and low contrast. At 20 minutes of arc the low contrast is delayed a few milliseconds compared to the high contrast. And at 10 minutes of arc the delay increased to about 12 msec, averaging about 118 msec for high contrast and increasing to 130 msec for low contrast.
We use the Diopsys NOVA Multi Contrast VEP (LX) clinically to compare the high vs. low contrast with patients who have reading difficulties. It is the same system that Diopsys markets for early glaucoma detection. As with magno vs. parvo considerations in glaucoma, we know that the differences in latency are relatively more reliable than the differences in amplitude on repeat measure. We are therefore looking closely at latency differences on the P100 at three different check sizes, which simulate differences between large, medium and small print size when reading. If we get significantly delayed responses at all three check sizes with low contrast, we suspect a magnocellular deficit. We are then interested in changes when re-measuring with low plus lenses added at near and/or prism, and changes over time with therapeutic intervention such as neuro-rehabilitative therapy.