It’s an argument as old as the hills. As basic as nature vs. nurture. Does function alter struture or does structure alter function? Much as we’ve accepted that the environment can influence how our genes are expressed – that epigenetic factors can change genes – it’s time to move on from outmoded idea that structure somehow dictates function. The fact that function alters structure is at the center of thoughts about neuroplasticity.
I’m in Portland this weekend, a city as old as the hills, but one that breathes with an air of renewal. It’s a perfect setting for a set of lectures I’m giving tomorrow on three of my favorite topics: Amblyopia, Stereoscoic 3D, and the Binocular/Disease Masquerade. While all three have elements of structure vs. function, the one I’ll lead with tomorrow and is Amblyopia. It’s been on my mind since last weekend, as a registrant for CE at the Annual Meeting of our State Association in Atlantic City, New Jersey. I attended a lecture on Age-Related Macular Degeneration or AMD, an area that has led the way in Optometry’s interest in the rule of nutrition in vision. The hot topic in AMD seems to be MPOD, or Macular Pigment Optical Density testing. While the purpose of new devices to measure macular pigment appear to revolve around dietary recommendations and supplementation, it brought me back to an old instrument we still use for vision therapy purposes in amblyopia therapy, the MIT. Not to be confused with the venerable technology house of education in Boston, this MIT is the Macular Integrity Tester.
The original purpose of the MIT was not for therapy purposes, but to assess the structural integrity of the macula. The goal was to tease out those patients from therapy who had a malfunctioning macula and therefore likely to be experiencing an organic or structural cause for reduced acuity rather than a functional one that could be “trained”. This is actually the same purpose underlying the motivation for testing MPOD, and the same biological principles are being invoked. The basis for the MIT was the optical neurobiological properties of the macula, and particularly its center, the foveal pit. This region is of interest in amblyopia because it is the retinal area responsible for highest resolution or central visual acuity. The integrity of the macula was inferred by the patient being able to subjectively report the appearance of the Haidinger Brush.
The Haidinger Brush, it’s appearance more like a propellor, gets its name from the fact that the yellow pigment of the macula (xanthophyll) has blue-blocking properties to protect it from oxidative stress. If you have the patient look through a blue filter, and rotate the light through a polarizer, the patient will detect the brush-like pattern shown here. The black portion is seen due to blue and yellow being opponent colors canceling one another, in much the same way as red cancels with green.
What intrigued me, after reviewing information on MPOD, is that the Haidinger Brush phenomenon is typically seen differently by the two eyes even when the patient does not have amblyopia. A beautiful paper by Le Floch and colleagues in Vision Research (including our old acquaintance, Jay Enoch) notes, regarding the perception of the Haidinger Brush: “We have also found that, surprisingly, the rotating pattern is more regular and symmetrical with one of our two eyes around a more circular blue cone-free area, the dominant eye.”
Is this surprising, or is the dominant eye dominant at least in part because it has richer central sighting properties? Wouldn’t it be wild if amblyopia resuted in part from structural properties of the fovea that differed between the two eyes that were due to congenital differences in MPOD? More provocatively, if vision therapy entices the brain to process more foveally with the amblyopic eye, might there be enough neuroplasticity for the foveal region to create or restore blue-free properties that it lacked or lost? If so, this would be a very elegant example of function altering structure. Somehow, that would no longer surprise me.