In this chapter, we show the refractive error treatment result of a patient, the first author, who restarted in 2000, after a 4-year break, at the study start. According to previous publications, the treatment consists of rehydration and elimination of agglutinated, dehydrated and deposited metabolic residues in the cornea, the trabecular meshwork, the crystalline lens and the retina, as a consequence of the failure in the mechanism of intraocular mass transfer by forced convection. However, the forced movement of the metabolic mass to rehydrate one region can cause dehydration in another region. Therefore, the patient developed posterior and capsular cataract in their respective eyes, right and left. This dehydration, during the treatment, increases the difficulties for the success of the treatment. The first part is a chronological record of the most important components of the treatment. Then, the research method and the material used are discussed. The main symptoms and signs are analyzed and correlated with the failure of the mass transfer process and the accumulation of metabolic residues. The anatomy of binocular vision is analyzed as a part of the forced convection mechanism, and in conclusion, the report shows the main oculomotor functions, topographic mapping of corneas over an interval of 17 months.

This paper describes several pathologies associated with pathological movements that can cause physical effort on the optic nerve and damage to vision. The accumulation of intraocular metabolic residues increases ocular globe mass and can change its position in the orbit, as well as increase the cornea and crystalline, accommodation resistance, in addition to being able to increase the aqueous humor output resistance. A series of discreet pathologies may result in optic nerve impairment: cyclotorsion and saccadic movement, position in the orbit, and increased intraocular pressure. The cyclotorsion movements can be stimulated by the superior visual field restriction, due to the metabolic residue accumulation in the light transmission regions of this visual field, preventing correct fusion of the images.

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The metabolic secretions produced by the cells inside the human eye are accumulated simultaneously in all of its parts; subject only to their origin. However, the symptomatology is well characterized by the location of accumulation. Genetic factors are directly related to how the clumps of metabolic secretions occur and the form of accumulation is very specific to the movement of the eyes based on the activities performed by the patient, so any outcome is unpredictable. The outer retinal layers are avascular and are supplied by diffusion from the choriocapillatis. Abnormalities of retinal blood circulation and drainage of metabolic secretions are key indicators to retinal dysfunction and may point to perturbations of systemic circulation. The weakening of the cornea bending mechanism results in the loss of variation of intraocular pressure. Consequently, due to the increase of its work activities, the weakening of the forced convection mechanism of the metabolic secretions produced in the retina initiates the accumulation of these secretions without uniformity in the retina, causing gradual obstruction of its system of mass transport, nutrients and metabolic secretions. This accumulation is readily observed by pressing ones hands for several minutes on closed eyes, subsequently, there is the perception of light in one without a region of uniformity. This work analyzes the anatomic structure and biophysics, depicted in the scientific literature, along with the symptoms of the presbyopia treatment of the first author of this paper, to understand that the accumulation of metabolic secretions causes an agglutination and dehydration process by decanting that triggers the loss of flexibility of the fibrous coat, vascular coat (uveal tissue) and nervous coat (retina) and consequently the gradual obstruction of the system of mass transport in the retina, compromising its nutrition and obstructing the drainage of its metabolic secretion.