Vision is Oscillating and Accelerating

People don’t realize that vision is an oscillating system under constant acceleration. We continuously have saccades that drive the sensory stimulation of our vision. This is easily demonstrated by visually dark adapting to a dark room, then keeping your eyes still and not moving (stopping the acceleration), your vision will begin to darken. Move your eyes again and the vision will return.

Too much focus on the optics points and retina/scleral structure clouds the view and potential of myopia control. However, understand vision is an oscillating dynamic system and apply our physiological basics learning both undergrad and optometry school to this, we then can begin to move to higher potential.

Understand positive feedback loops and negative feedback loops. I propose thar visual oscillations is a non-cognitive process meaning subcortical areas of the brain drive this oscillation.

When animal studies with either lens or occlusion induced peripheral form deprivation is the interruption of a physiological loop. When the visual stimulation stops via deprivation in these key areas, so does the visual oscillation. There is going to be a response from other sensory inputs such as CN V and CN VII and and the vision will respond accordingly. Then spasticity and rigidity can ensue. Then scleral and optics changes follow.

The opposite case is the positive feedback loop. In the animal models, the optic nerve is resected, but no form deprivation, emmotropization does not move forward keeping the animals highly hyperopic. The oscillation isn’t going, is therefore never reinforced. We see this in amblyopia and some other disorders. Get the system oscillating and it will feed itself to continue.

Active inhibition oscillation can give us a different results than from mere lack of stimulation of the oscillation.

Habituated Top-down neurocognitive inhibition of this oscillation can act as a form deprivation and therefore a negative feedback loop of the oscillation generating further form deprivation.

An example of this would be “lead of accommodation.” Neurocognitively this can occur even in pseudophakia. Just like brain actively still goes off when a person moves a missing limb, or visualizes a limb moving but not yet moved. There is a neurocognitive neurovisual effect to visual oscillation and can be actively suppressed. When an individual is doing just this, distract their mind with something and get the vision oscillating.

If for some reason, as in amblyopia and other cases, where the vision just simply is not responding as indicated by a high with-motion on retinoscopy, positive feedback loop at that baby and get the system oscillating.

Either way, get the system oscillating.

How? Another post for another day. I’m about out of space.

I certainly wish this would be accounted for in the glaucoma research too. Glaucoma patients don’t oscillate. Is there feedback loop on neurological apoptosis, meaning the less activity equals more apoptosis of the ganglion cell layer?

Can oscillation act as a negative feedback loop for apoptotic ganglion cell layer in glaucoma thereby aiding to prevent visual loss?

That’s a question for researchers to explore.