Changes in the size of a mapped blind spot after any type of treatment (manipulation included) would be due to either a change in the anatomical size of the optic disc or a change in the brain representation of it. Since manipulation does not do anything to the size of the optic disc it would be illogical to promote an argument that it did. The brain representation of the blind spot is well known and understood by today’s brain scientists. It is more appropriate to suggest that the changes in the size of the blind spot are due to changes in brain function than a change in anatomical dimensions (which do not change with manipulation).
Although there is no retinal input within the blind spot, it is filled with the same visual attributes as its surround. Earlier studies have shown that neural responses are evoked at the retinotopic (eye) representation of the blind spot in the primary visual cortex (V1-brain) when perceptual filling-in of a surface or completion of a bar occurs.
Neurons in the V1 (primary visual cortex-brain) region representing the blind spot encode information essential for perceptual filling-in at the blind spot. Although no visual inputs arise from the blind spot, the same visual attribute there as in the visual field surrounding the blind spot is perceived because of this remarkable perceptual filling-in a hole corresponding to the blind spot is not perceived, even when one eye is closed due to brain function.
Those of us that are involved in brain research realize that the blind spot is perceived in the brain and we utilize a variety of techniques to visualize it.
The brain does not objectively reflect outer reality, but rather what is necessary in order to survive and adapt to the environment such that the eye's blind spot reflects the brain's capacity to invent information producing occurrences which in reality have never happened, in such a way that, for the brain, convenient reality and objective reality are two very different things.
Measurement of the blind spot may depict objective measurements dependant upon the convenient reality of brain perception. The sizes of the blind spot are expected to be different when measured and subjected to mathematical analysis. Dichoptic lateral interactions occur in the region of the visual field of one eye that corresponds to the physiological blind spot in the other eye. The presence of these dichoptic interactions in a region lacking direct retinal afferents from one eye is consistent with the proposition that long-range horizontal connections of the primary visual cortex mediate these interactions.
Since the blind spot changes in size and neck manipulation does not have a probability of affecting the size of the optic disc, the changes are most probably explained by brain functional perception. The size of the blind spot is a component of a greater or lesser filling in effect.
When we refer to functional plasticity we are talking about the changes that occur in brain function as a consequence of a variety of events. The relationship between the thalamus and the visual cortex are well known.
The effects of spinal manual therapy (SMT) results in a combination of findings supporting the proposal that SMT may, at least initially, exert part of its influence via activation of structures in the mesencephalon (top of the brainstem associated with vision). The feedback effect on the cervical spine is also recognized in visual disorders and especially when vision is decreased such as in darkness.
Absent retinopathy, the most probable cause of asymmetrical blind spots would be due to brain dysfunction. There are a plethora of reasons for brain dysfunction. A comprehensive neurological examination is required to rule in or rule out various causes of brain dysfunction. Once the brain dysfunction is identified, specific use of the musculoskeletal system as a portal of entry to the Central Nervous System can be utilized to make changes in brain function. Various non-constant modalities such as: light; sound; vibration can also be utilized to affect changes in brain function.
In general terms, if you consistently measure a larger blind spot on the right side, as an example - absent retinopathy -the most probable cause of this is brain dysfunction of the left brain.
Afferentation from the right side of the body will have a probability of increasing left brain function. With increased left brain function, the right blind spot should decrease in size.
Try it. If you apply a treatment and the larger blind spot increased in size, then you should re-think the modality or the side of the body to which you applied it.
Follow the following links for additional studies confirming dynamic sizes of the physiologic blind spot.
Go to: http://www.essaytown.com/blind_spot.html to read how the authors, using the pen and paper method of mapping blind spots, found non-athletes to have statistically significantly larger blind spots. The authors could not explain it but found it.
Read about how other authors found varying sizes of the physiologic blind spot, go to: Conclusions: Semi automated kinetic perimetry can determine the size of the physiological blind spot with good repeatability in young, normal subjects. Determination of each individual's speed of response and inclusion of this variable in the calculations reduced variance of the measure significantly. This study confirmed the presence of considerable interindividual differences in the size of the physiological blind spot.