Eye rubbing: the root cause of Keratoconus?
The sine qua non of keratoconus: the eye rubbing
The repeated eye rubbing have been recognized for a long time as a risk factor for the Keratoconus, but I am convinced that their role in the pathogenesis of Keratoconus has been largely underestimated. I started to write an article to explain to interested readers the pathophysiological concept originally from Keratoconus which I am convinced: 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")
Read the articles: Are the eye rubbing the sine qua non of Keratoconus D Gatinel cause
Keratoconus: the necessary and sufficient condition eye rubbing? Realities OPH September 2016
See also: (original article in English)
Visit the site and see many illustrated clinical case and examples of keratoconus: https://defeatkeratoconus.com/
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 was intrigued by the importance of structural changes and the deformation of the corneal wall in the Keratoconus. Paradoxically, few genetic or molecular anomalies have been detected in this condition, whose consequences on the regularity and transparency of the cornea can, however, be spectacular.
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. Drought, eye irritation, pollution, night work and on screen, where under special conditions (irritating particle, dust, mites introduced by a Sleep position with deep support of the head against the pillow) are all factors that can cause eye itching and the desire to rub your eyes. How many ophthalmological consultations are motivated by "itchy eyes"?
"So, what was called" Keratoconus "could just be the direct consequence of the mechanical trauma of the cornea caused by chronic and constant eye rubbingcausing 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 the etiology of Keratoconus.
The mechanical hypothesis argues that Keratoconus is caused by the eye rubbing. These can themselves be induced by atopy, pollution, labor extended on screen... Unlike the molecular hypothesis where of supposed genetic, environmental or unidentified factors would play a key role in the appearance of Keratoconus, the mechanical hypothesis States simply that the structural changes and the 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 threshold of biomechanical resistance of the cornea, it deforms gradually, which causes the appearance of the characteristic topographic anomalies ranging from crude said forms to the most proven forms of Keratoconus. In my experience, the most advanced forms of Keratoconus with stromal opacities, still meet in the patient who rub the eyes of particularly strong way.
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 rubbing, or that control the thickness and resistance of the cornea. These conditions include diseases as various as Trisomy 21 and atopy (source of eye pruritus). Sleep apnea has been associated with Keratoconus; the lack of quality sleep provides chronic fatigue and fatigue is likely to drive patients to rub their eyes. I saw the case of patients who had a Keratoconus of installation late (after 30 years), due to a schedule change (night work) causing chronic fatigue, and the repetitive urge to rub their eyes. A sex ratio slightly biased in favor of men was reported recently for Keratoconus. In my experience, women who wear makeup tend to less rubbing the eyes than men. However, these rub sometimes eye after removal of make-up. Dry eye increases during pregnancy, due to certain hormonal changes: drought-induced irritation can cause the urge to rub their eyes. This could explain the progression of Keratoconus during pregnancy, and the fact that it has been identified as a risk factor for ectasia post LASIK. Ocular rosacea is also source of discomfort and eye pruritus, where prescribed massages of the eyelids. I met a case of bilateral Keratoconus triggered by bad maneuvers of hygiene of eyelids, leading the patient to rub your eyes every day, leading to the appearance of a characteristic distortion in a few months.
It is all case easier to explain the significant disparity of age, hit between the eyes, and the wide range of phenotypic expression by eye rubbing repeated by a corneal degeneration genetics and the unidentified molecular mechanisms. Fortunately, all patients who rub their eyes do not develop 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 degree of pollution and dryness of the air, combined with poor environmental conditions or work may explain the increased prevalence of Keratoconus in certain ethnic 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 condition, which the main features of the corneal expression flow from a biomechanical weakening of the corneal collagen. Yet, strain typically encountered during Marfan syndrome is not really like what is observed in Keratoconus.
Marfan syndrome is a genetic disease that affects the connective tissue first. It is caused by the mutation of a gene that controls the production of a protein called fibrilline-1, which is widely held within the connective tissue, particularly at the level of the collagen fibrils. This syndrome affects many organs, including the eye. It can lead to the appearance of an aneurysm of the aorta, due to the weakening of the wall of it, subject to the pressure of blood flow. The ectopy (displacement) of the lens is a classic manifestation of Marfan syndrome, as constituting the cristallinien ligament fibers weaken and eventually break.
Marfan syndrome is a perfect counterexample to emphasize failure have current theories to explain the pathophysiology of Keratoconus. These theories link the origin of Keratoconus with unknown collagen dystrophy associated with environmental, cellular and genetic factors. The combination of these factors would be at the origin of the corneal degeneration, we know well what would be the common denominator for triggering the process of al wall corneal ectasia. However, Marfan syndrome responds perfectly to this type of Pathology; a genetic mutation has been identified, and the mutated protein (fibrilline-1) causes the decrease in the resistance of collagen of the eye tissue, including the corneal stroma. However, despite all these favorable characteristics to the outbreak of a corneal distortion, there is no occurrence of an ectasia or Keratoconus in Marfan syndrome. The corneas of patients certainly 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. Ocular distension causes also the increase in ocular axial length, and as a result, the majority of patients with Marfan syndrome are short-sighted. The presence of axile myopia associated with a flattening of the cornea are two eye criteria for positive diagnosis of Marfan syndrome.
An association between Keratoconus and Marfan syndrome has been reported; It is not contradictory with the mechanical theory of Keratoconus. The cornea is more fragile in this syndrome, she is more likely to deform quickly under the effect of eye rubbing.
Contrary to what is observed for Marfan syndrome, patients with Keratoconus the cornea is more arched and asymmetrical, and has thinning of focal nature, central or lower central para. 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 reached in biomechanical terms, there is a reduction of its curvature (global Flattening). Moreover, it is interesting to observe that corneal disorders caused by inflammatory mechanisms are characterized also by a reduction of the curvature. Scars post infectious or interesticielles keratitis or interface (after LASIK) are usually accompanied by a decrease in the keratometry central or paracentrale, and this trend is evidemement opposite to that of 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 to raise it, defend it, but also to publicize the deleterious effects of the eye rubbing the impact of Keratoconus. Whatever the primitive mechanism originally of Keratoconus, emphasise the causal role of friction can only initially reduce the impact, and to stop the progression.
The assumption of friction as the cause sine qua non the Keratoconus defies the widely accepted concept of corneal dystrophy of unknown origin. It will appear simplistic or provocative for sure, and would have even raised my scepticism even 6 or 7 years ago. This scepticism is however today dispelled by the accumulation of clinical observations that confirm one by one the central role of the eye rubbing as a factor triggering of Keratoconus. In the end,. I think even the mechanical theory of friction is able to raise the mystery of the mystery that surrounds 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 the eye rubbing could eradicate the Keratoconus and reduce the risk of ectasia corneal LASIK post, from a point of view practice, this goal is probably unattainable. It is very likely that some patients cannot resist the judged urge to rub their eyes when they "scrape". When the diagnosis of Keratoconus has been laid, to the occaseion of the balance sheet of a decline in vision, it is however necessary to carry out a survey to become aware of the friction, identify their cause to better treat.
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 Keratoconus, and this objectively, comparing topographic surveys at each visit and by subtractive maps. The prospective collection of topographic data in 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.
(Comments are welcome)