eye rubbing: THE primitive cause of the keratoconus.
The cause sine qua non of the keratoconus: the eye rubbing
The repeated eye rubbing have been recognized for a long time as a risk factor for the Keratoconusbut I am convinced that their role in keratoconus pathogenesis has been greatly underestimated. Once is not customary, which is often presented as a correlation (eye rubbing and keratoconus) actually masks a direct causal link; keratoconus is caused by the repetition of eye rubbingexcessive intensity, duration and frequency.
I wrote an article to explain this physiopathological concept behind the keratoconus: The chronic and repeated eye rubbing are the primitive, necessary and sufficient cause, i.e. the condition prerequisite not for Keratoconus: no frictions, no Keratoconus ("no rub, no cone")
Keratoconus is classically defined as dystrophy of origin unknown, responsible for a deterioration of vision. This is due to the deformation of the corneal dome, that causes a astigmatism Irregularity and myopia. Many clinical examples of keratoconus are gathered on the site dedicated to the fight against the Keratoconus https://defeatkeratoconus.com/portfolio-filtersearch/. I have always been captivated by this disease whose origin remains mysterious; a large part of my clinical practice is dedicated to the diagnosis, management and prevention of keratoconus, and for many years I have been intrigued by the importance of structural changes and corneal wall deformation in the keratoconus. Paradoxically, few genetic or molecular abnormalities have been detected in this condition, yet the consequences on the regularity and transparency of the cornea can be dramatic.
In this article, I propose the theory that Keratoconus is not unknown to genetics and Biomolecular bedrock dystrophy, but rather a syndrome of mechanical origin originally caused by the rubbing of the eyes. Dryness, eye irritation, pollution, night and screen work, or under special conditions (irritating particles, dust, mites introduced by a Sleep position with deep support of the head against the pillow) are all factors that can cause eye pruritus and the desire to rub your eyes. How many ophthalmological consultations are motivated by "itchy eyes"?
Thus, what has been called "keratoconus" may be only the direct consequence of the mechanical trauma of the cornea caused by the chronic and incessant friction of the eyescausing the deformation and thinning progressive corneal wall, which are characteristic of the disease. The eye rubbing are at the heart of this «» "mechanical" hypothesis as a primitive etiology of the keratoconus.
The mechanical hypothesis argues that Keratoconus is caused by the eye rubbing. These can themselves be induced by atopy, pollution, prolonged work on the screen... Contrary to the molecular hypothesis where supposed genetic, environmental or unidentified factors would play a key role in the appearance of the keratoconus, the mechanical hypothesis simply stipulates that structural modifications and deformation of the cornea are initiated and exacerbated by a mechanical cause : eye rubbing. Other factors of mechanical origin, such as the corneal refractive surgery, or the night extended compression of the cornea (pillow, hand or forearm) are likely to accelerate the deformation of the cornea. The eye rubbing can cause local inflammation with release of pro-inflammatory molecules. The effect of mechanical stress (distension) can be potentiated by the secretion of proteinases in the corneal stroma, which could explain the progressive thinning of the cornea, and make it even more vulnerable to the effects of friction. In the mechanical hypothesis, Keratoconus can occur without the repeated mechanical trauma that are rubbing. When the duration and intensity of these exceed the biomechanical resistance threshold of the cornea, it gradually deforms, causing the appearance of characteristic topographical anomalies ranging from the so-called rough forms to more proven forms of keratoconus. In my experience, the most advanced forms of keratoconus, with stromal opacity, are always found in patients who rub their eyes particularly vigorously.
Keratoconus: a mechanical pathology
Just as an excessive distension of the ligament of the ankle can cause a sprain, chronic eye rubbing can reduce the biomechanical resistance of the mesh of collagen fibers in the corneal dome, and lead to the distortion of it. This biomechanical mechanism is more likely to account for the disparity between the achievement of the right eye and left (patients rub often more one look than the other), and the focal nature of Keratoconus, which has recently been highlighted.
Genetics of Keratoconus is unclear. The frequency of occurrence within members of the same family are not clearly defined and would be slightly less than 20%. In the hypothesis where the friction are essential to the genesis of affection, the genetic factors involved would be rather related to conditions that predispose to the development of the eye rubbingor controlling the thickness and strength of the cornea. These conditions include pathologies as diverse as trisomy 21 and atopy (source of ocular pruritus). Sleep apnea has been associated with keratoconus; lack of quality sleep results in chronic fatigue, and this fatigue is likely to lead patients to rub their eyes. I have observed patients casewho had a late onset keratoconus (after 30 years), following a change in schedule (night work) that caused chronic fatigue, and the repetitive urge to rub their eyes. A slightly biased sex ratio in favour of men has recently been reported for keratoconus. In my experience, women who wear makeup tend to rub their eyes less than men. However, they sometimes rub their eyes after removing makeup. Dry eyes increase during pregnancy due to certain hormonal changes: irritation caused by dryness can lead to a desire to rub your eyes. This could explain the progression of keratoconus during pregnancy, and the fact that pregnancy has been identified as a risk factor for post-partum ectasia LASIK. Ocular rosacea is also a source of eye discomfort and pruritus, where eyelid massages are prescribed. I encountered a casebilateral keratoconus triggered by poor eyelid hygiene maneuvers, which led the patient to rub his eyes every day, leading to the appearance of a characteristic deformity in a few months.It is in all the caseeasiest to explain the significant differences in age, damage between the two eyes, and the wide range of phenotypic expression by eye rubbingrepetition than by corneal degeneration to unidentified genetics and molecular mechanisms. Fortunately, not all patients who rub their eyes develop a keratoconus. For the same intensity and the same amount of friction, the cornea which is less the thickness and resistance may undergo a deformation greater than more strong and thick corneas. Exposure to high levels of air pollution and drought, combined with poor environmental or working conditions, may explain the increased prevalence of keratoconus in some ethnic social groups. The explosion of work on screen and the generalization of the screens led to the emergence of a disease called «» Computer Vision Syndrome "(that can be translated as 'Labour on screen Syndrome'). It includes eye fatigue chronic source of irritation and eye pruritus, which can lead to a repeated eye rubbing and play an important role in the increase in the prevalence of Keratoconus.
Vs Keratoconus Marfan syndrome
The comparison between violations eye, especially corneal of Marfan syndrome, and those observed for Keratoconus is a particularly important point for our argument. All the necessary ingredients for a Keratoconus induction are present in this conditionwhose main features of corneal expression flow from a biomechanical weakening of corneal collagen. However, the deformation typically encountered during Marfan syndrome does not really resemble what is observed in the keratoconus.
Marfan syndrome is a genetic disease that first affects the connective tissue. It is caused by the mutation of a gene that controls the production of a protein called fibrillin-1, which is widely distributed in connective tissue, particularly in collagen fibrils. This syndrome affects many organs, including the eye. It can lead to the appearance of an aortic aneurysm, due to the weakening of the aorta wall, which is subject to blood flow pressure. Ectopy (displacement) of the Crystalline lensis a classic manifestation of Marfan syndrome, as the fibers that make up the crystalline ligament weaken and eventually rupture. Marfan syndrome is a perfect counterexample to emphasize failure have current theories to explain the pathophysiology of Keratoconus. These theories link the origin of the keratoconus to an unknown collagen dystrophy associated with environmental, cellular and genetic factors. The combination of these factors would be at the origin of corneal degeneration, without it being clear what the common denominator would be for the initiation of the corneal wall ectasia process. Marfan syndrome responds perfectly to this type of pathology; a genetic mutation has been identified, and the mutated protein (fibrillin-1) causes a decrease in the collagen resistance of the eye tissues, including the corneal stroma. However, despite all these characteristics favourable to the development of corneal deformation, ectasia or keratoconus do not occur during Marfan syndrome. The corneas of affected patients tend to be thinner, but also flatter, and either assemblies. This reduction of camber is not paradoxical if it is agreed that under physiological conditions, the eye pressure is evenly on the inner surface of the corneal dome. This force, resulting from the distribution of intraocular pressure on the inner wall of the sclera and the posterior face of the corneal, causes a progressive distension of the eyeball, and thus a reduction of the camber of the cornea (by increase of its radius of curvature), as well as its concomitant thinning. Without the input of an external force, the biomechanical weakening of the cornea as in Marfan syndrome leads to flattening of the. Eye distension also causes an increase in the axial length of the eye, and as a result, most patients with Marfan syndrome are myopic. The presence of axial myopia associated with corneal flattening are two of the ocular criteria for the positive diagnosis of Marfan syndrome. An association between keratoconus and Marfan syndrome has been reported; it is not contradictory to the mechanical theory of keratoconus. Since the cornea is more fragile during this syndrome, it is more likely to deform quickly under the effect ofeye rubbing. Unlike Marfan syndrome, the cornea of keratoconus patients is more arched and asymmetric, with a thinning of a focal, central or lower para-central nature. The use of an external force is better able to account for this type of table than an unidentified molecular anomaly who would reach the cornea as a whole, but would save the other tissues of the body. The force exerted by the digital friction, especially the knuckles against the cornea is considerable scale of it. It causes the stretching and the disorganization of the collagen fibers of the cornea. The increase in acute and repeated intraocular pressure can cause a distension of the sclera and an elongation of the eyeball. To corroborate this observation with the induction of a repeated pressure elevation intraocular suites in support of fingers for rubbing, it seems that the average axial length of patients with Keratoconus is slightly higher than that of free patients of Keratoconus.
Thus, in this clinical model where the cornea is undoubtedly biomechanically affected, there is a reduction in its curvature (overall flattening). In addition, it is interesting to note that corneal diseases caused by inflammatory mechanisms are also characterized by a reduction in curvature. Post-infectious scars, or interestitial or interface keratitis (after LASIK) are usually accompanied by a decrease in central or paracentral keratometry, and this trend is obviously the opposite of that of the keratoconus.
The mechanical hypothesis can naturally generate distrust and skepticism, because it is both simple, provocative, and difficult to demonstrate. However, it would also be, see more difficult to prove that the friction are not the cause of Keratoconus.
The purpose of this article is to raise it, defend it, but also to make the deleterious effects of the eye rubbing the impact of Keratoconus. Whatever the primitive mechanism at the origin of the keratoconus, emphasizing the causal role of friction can only a priori reduce its incidence and stop its progression.
The assumption of friction as the cause sine qua non of the keratoconus challenges the widely accepted concept of corneal dystrophy of unknown origin. It will seem simplistic or provocative to some, and would even have received my scepticism just 6 or 7 years ago. However, this scepticism is now dispelled by the accumulation of clinical observations that confirm one by one the central role of keratoconus eye rubbingas a trigger factor. In the end, I even think that the mechanical theory of friction is able to unravel the mystery of the enigma surrounding the keratoconus, and could close the chapter opened in 1854 by Dr John Nottingham and his treatise on the "conical cornea"..
If the removal of keratoconus eye rubbingcould eradicate keratoconus and reduce the risk of post-LASIK corneal ectasia, from a practical point of view, this goal is probably unattainable. It is very likely that some patients will not be able to resist the irrepressible urge to rub their eyes when they "scratch". When the diagnosis of Keratoconus has been laid, However, when assessing a loss of vision, it is necessary to carry out an investigation to become aware of the friction and identify its cause in order to better treat it.
Nevertheless, the less ambitious goal of reducing the size and frequency of the eye rubbing patients likely to develop Keratoconus, or see their condition progress is an essential issue. Before any patient suffering from Keratoconus, I take time to well conduct interrogations intended to search for the existence of eye rubbing, and insists in a vehement manner on the importance of their strict stop, which is a major point to stop the progression of the disease.
It is important to document the possible progression of Keratoconus in refractive and topographic terms. My experience shows that the judgment of the eye rubbing enough to stop evolution of Keratoconusobjectively, by comparing topographic surveys at each visit and mapssubtracting them. The prospective collection of topographic data from patients followed at the Rothschild Foundation is very encouraging, and confirms that the judgment of friction stops indeed the evolution of Keratoconus. The results of this monitoring should be documented to ensure that stability over the long-term, but if they are confirmed, they will provide a strong argument for sit the mechanical hypothesis and confirm that Keratoconus could never have been a real dystrophy, but be a syndrome which refractive and topographic expression is the result of a mechanical stress of the cornea: the eye rubbing repeated.
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