[Pomoland] Background Info: Riley's Eye Condition/Mechanism
Disclaimer: This genetic condition is completely fabricated but has been wrangled through hell and back in order to make it work as best it could within the macro confines of science. By "hell and back" I mean "the filter of classes I took for my BA in neurobiology, of which included a 9hr/week neurophysiology lab and a upperlevel cognitive psychology course." And by "the filter of [...] et cetera" I mean "if you'd like to be an onerous bitch and want to argue the validity of the theory, please go piss off and do your own research." OTL This is honestly the best we could come up with with college textbooks and edumacation; the next step requires something along the lines of finding a research grant, usurping a lab, raising some mice, and start knocking out genes. Else, if you have any other questions of academic nature on the probability/improbability of Riley's Little Problem, you can leave them here.
Pomoland and all its characters belong to kirui & Inaho. Including this fictional condition.
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Condition: Still working on that name, right
Classification: Sex-linked disorder, namely X-chromosome recessive. In a blind/fail stab at layman's terms, this means the defective gene (or group of genes--we're not nitpicking those details yet) is located on the X-chromosome and can only contribute to the physical manifestation (i.e. the phenotype) if it is unmasked by the dominant ("normal" in this case) allele. If the mother is a carrier (heterogeneous genotype Xx, with "x" being an arbitrary genotypic label), only sons who receive the defective allele will be subject to its phenotype. The father cannot be a carrier.
Mechanism: The physical components of Riley's disorder involve at least two sources of origin: his eye, and the neural pathways leading to and making up his visual cortex. The former contributes in the lack of responsive cone cells--either complete absence of or merely an underdevelopment that renders what he does have null. The latter isn't so much a problem with the grey matter itself, but rather with the circuitry that would otherwise allow him to process what his eyes surveys (a connectivity issue, per se).
The state of his cone cells doesn't necessarily make it so that his rod cells are equally out-of-commission, albeit they are typically less sensitive than those found in a normal human eye. Rather, what it actually means is that Riley's still capable of differentiating light intensity and detecting bright/dark gradients to some degree. This is quite essential in allowing him visual acuity (edge sharpness), and, perhaps, some modicum of depth perception, depending on how contrastive the light reflection is around an object of interest.
Now, having established the fact that the majority of his eye is actually in working order, the proverbial searchlight turns to the role in which his brain plays. The fact that Riley does react to movement indicates that the deep tectal cells of the Superior colliculus (see: optic tectum in non-mammals) are still in functional condition and receive a synaptic transmission when unique shapes with delineated edges pass through his visual field. (Note: The more defined the moving edge, the "clearer" Riley can see it.) That he turns his attention to follow the movement proves that the portion of his brain controlling saccadic eye movement is also intact. But that he doesn't seem to be aware of, or perhaps more accurately, is physically incapable of noticing stationary objects, suggests that there's a gap in the wiring somewhere.
So it probably goes something like this: Something moves into or within Riley's visual receptive field; his eye sends a signal that synapses all the way back to the deep tectal cells in the back of his brain; the activation of those cells sets off another cascade of synaptic transmissions to his prefrontal cortex, in effect bringing the object of interest to attention. Meanwhle, non-moving objects do not trigger such a reaction and are thus never actually processed. The source/point of disconnect is thought to lie somewhere between the eyeball and the visual cortex, possibly the optic nerves feeding from the eye.
The paradox of how Riley perceives things visually, of what in his receptive field does his brain choose to process, is exactly that: a separation between what his eyes "see" and what his mind comprehends as him "seeing."
Effects: What constitutes as a landscape from Riley's vision is very bare, two-dimensional even. The concept of prism colors is lost on him, though he is capable of distinguishing between white/black/grey. As is, the canvas of the world may very well be a "sea of white" or any other monochromatic shade (pardon the cliché), depending on the net light amount in any given survey of area. Things in motion are processed as dark shapes and, depending on the light's strength and how it refracts/reflects, may even be depicted with more detailed features.
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... so I apologize for my complete inability to not talk like a science-fag (why am I going into Law again? LOLOL). If necessary, I might make a diagram of Riley's visual system, tracing the mechanism's pathway--but only if absolutely necessary. In fact, my profoundest hope at the moment is that everybody who reads this will be so overwhelmed by all the highfalutin terminology that they won't even bother.
Pomoland and all its characters belong to kirui & Inaho. Including this fictional condition.
__________________________________________________
Condition: Still working on that name, right
Classification: Sex-linked disorder, namely X-chromosome recessive. In a blind/fail stab at layman's terms, this means the defective gene (or group of genes--we're not nitpicking those details yet) is located on the X-chromosome and can only contribute to the physical manifestation (i.e. the phenotype) if it is unmasked by the dominant ("normal" in this case) allele. If the mother is a carrier (heterogeneous genotype Xx, with "x" being an arbitrary genotypic label), only sons who receive the defective allele will be subject to its phenotype. The father cannot be a carrier.
Mechanism: The physical components of Riley's disorder involve at least two sources of origin: his eye, and the neural pathways leading to and making up his visual cortex. The former contributes in the lack of responsive cone cells--either complete absence of or merely an underdevelopment that renders what he does have null. The latter isn't so much a problem with the grey matter itself, but rather with the circuitry that would otherwise allow him to process what his eyes surveys (a connectivity issue, per se).
The state of his cone cells doesn't necessarily make it so that his rod cells are equally out-of-commission, albeit they are typically less sensitive than those found in a normal human eye. Rather, what it actually means is that Riley's still capable of differentiating light intensity and detecting bright/dark gradients to some degree. This is quite essential in allowing him visual acuity (edge sharpness), and, perhaps, some modicum of depth perception, depending on how contrastive the light reflection is around an object of interest.
Now, having established the fact that the majority of his eye is actually in working order, the proverbial searchlight turns to the role in which his brain plays. The fact that Riley does react to movement indicates that the deep tectal cells of the Superior colliculus (see: optic tectum in non-mammals) are still in functional condition and receive a synaptic transmission when unique shapes with delineated edges pass through his visual field. (Note: The more defined the moving edge, the "clearer" Riley can see it.) That he turns his attention to follow the movement proves that the portion of his brain controlling saccadic eye movement is also intact. But that he doesn't seem to be aware of, or perhaps more accurately, is physically incapable of noticing stationary objects, suggests that there's a gap in the wiring somewhere.
So it probably goes something like this: Something moves into or within Riley's visual receptive field; his eye sends a signal that synapses all the way back to the deep tectal cells in the back of his brain; the activation of those cells sets off another cascade of synaptic transmissions to his prefrontal cortex, in effect bringing the object of interest to attention. Meanwhle, non-moving objects do not trigger such a reaction and are thus never actually processed. The source/point of disconnect is thought to lie somewhere between the eyeball and the visual cortex, possibly the optic nerves feeding from the eye.
The paradox of how Riley perceives things visually, of what in his receptive field does his brain choose to process, is exactly that: a separation between what his eyes "see" and what his mind comprehends as him "seeing."
Effects: What constitutes as a landscape from Riley's vision is very bare, two-dimensional even. The concept of prism colors is lost on him, though he is capable of distinguishing between white/black/grey. As is, the canvas of the world may very well be a "sea of white" or any other monochromatic shade (pardon the cliché), depending on the net light amount in any given survey of area. Things in motion are processed as dark shapes and, depending on the light's strength and how it refracts/reflects, may even be depicted with more detailed features.
__________________________________________________
... so I apologize for my complete inability to not talk like a science-fag (why am I going into Law again? LOLOL). If necessary, I might make a diagram of Riley's visual system, tracing the mechanism's pathway--but only if absolutely necessary. In fact, my profoundest hope at the moment is that everybody who reads this will be so overwhelmed by all the highfalutin terminology that they won't even bother.