**3. Vision physiology, symptom, and sign analysis**

*Binocular motion physiology*: In **Figure 3a** we have "F" as the fixation point in the visual field, as projected onto the fovea of the respective eyes. "I," the point of interest in the lateral visual field, has its projections on the nasal and temporal retinas of the respective ipsilateral and contralateral eyes. "M," the movable fixation point, maintains its projections on the fovea of the respective eyes as it moves along

**Figure 3.**

*Two possibilities of eye movements. (a) Eye shift in the right visual field. (b) Eye shift in the left visual field.*

#### *Intraocular Forced Convection Mechanism Defect as Probable Cause of Normal-Tension… DOI: http://dx.doi.org/10.5772/intechopen.89934*

an visual field surface imaginary line, when the eyes travel the smallest angular displacement between the "F" and "I" points.

When the ocular direction shifts from point "F" to point "I," point "M," the contralateral eye visual axis intersection with the surface of the visual field (initially coincides with point "F"), is shifted to point "I." The "M" point moves across an imaginary line on the surface of the lateral visual field with the smallest angular displacement of the axial axis of the contralateral eye. In this trajectory, the contralateral eye maintains its focus at the "M" point because the ciliary accommodation time constant, τC, is much less than the ocular displacement time constant, τR (rectus muscles). Therefore, relative to the visual field laterality, the image projected on the contralateral ocular temporal retina is the primary image because it is the image used by the brain to control eye movement. The image projected on the nasal retina of the ipsilateral eye is the secondary image, because it is the image used by the brain to control the cornea accommodation movement, a slower movement, due to the time constant of the cornea accommodation, τS (superior oblique muscle), which is much longer than the ocular displacement time constant, τR (rectus muscles). Therefore, in this eye movement, the dominant eye is contralateral to the laterality of the "I" point visual field, and the auxiliary eye is ipsilateral because its movement depends on the fusion of the images to keep the projection onto its fovea, the "M" point.

On the return trajectory, **Figure 3b**, the current fixation point "F" is the previous "I" point, and the current interest point "I" is the previous "F" point; hence the current movable fixation point "M" will have an ipsilateral trajectory to the anterior trajectory of "M." Then, the dominant and auxiliary eyes will be contralateral in the anterior trajectory, so eye dominance is circumstantial.

*Refraction error*: Eyesight adaptation to dark is the common pathological symptom that precedes refractive error (see [3]). In 1619 Scheiner, *apud* [12], proved in his experiments, made with holes in a card, that an object is seen in each direction at a different distance. You can reproduce the effects perceived by Scheiner, by fixing the gaze on a distant object, through a pinhole in a paper pressed against the eyelid. When you move the paper without removing it from the eyelid, you can perceive the image of the object jumping from one position to another or moving its shape. The jump indicates the same pathology observed by Scheiner, and the change in form is another presentation of the same pathology [2]. This pathology can be acquired by the dehydrated accumulation of intraocular metabolic residues agglutinated in the form of drops. These drops form lenses that can produce overlapping images (causing blurred vision, floaters, monocular polyopia, and photopsia with and without photochromatic dispersion) and, depending on their transparency, make light transmission difficult. In the postoperative period of cataract surgery, patients report having a clearer view through the operated eye (greater light transmission in the artificial lens). Patients may report blurred vision and secretions released from the anterior surface of the cornea (corneal accommodation variation) and floaters (the metabolic mass stored in the lens prevented their viewing). In Ref. [2] the different symptoms of myopia, hypermetropia, astigmatism, and presbyopia are shown as visual disturbances of the same origin, the intraocular accumulation of dehydrated metabolic secretions.

*Ocular hypertension*: This can be caused by an imbalance in the production, concentration, and drainage of eye movable mass. Increased mass transfer resistance across the trabecular meshwork is an important impediment to aqueous humor drainage. Corneal accommodation movement failure hinders its mass transfer movement, thus being the major factor in the metabolic residue storage in the cornea [5]. The cornea stored metabolic residue elimination process consists in the movement of its curvature, in order to recover its healthy accommodation. In this process, the residues leave the two surfaces and are eliminated by dilution or suspension. On the anterior

surface, the lacrimal fluid drags the residues, and on the posterior surface, the residues are dragged by the aqueous humor. If an important tear drag occurs when the patient is sleeping in the supine position, it may cause nostril obstruction, throat irritation, and hoarseness. Drainage of aqueous humor with suspended residues can impregnate the trabecular meshwork with the residues and increase resistance to outflow causing ocular hypertension. In the postoperative period of cataract surgery, the patient eliminates metabolic residues on both cornea surfaces, due to fusion of images and corneal accommodation; thus metabolic residues may impregnate the trabecular meshwork and cause ocular hypertension. It is possible, by a natural process, for the intraocular pressure return to its previous value.
