Eye rubbing: a sine qua non for keratoconus? D Gatinel. Int K Kerat Ect Horn say, 2016; 5 (1): 6-12
(Link to the original article here)
Eye rubbing have the root cause of keratoconus?
Keratoconus has been labelled "dystrophy of unknown origin", and I have long been fascinated by this mysterious disease. A large proportion of my clinical practice is dedicated to the diagnosis, management and prevention of keratoconus, and for many years I have been intrigued by how structural changes and deformation of the corneal wall are so pronounced in keratoconus, yet paradoxically, few detectable genetic and molecular tail exist in this condition.
Eye rubbing has long been acknowledged as a risk factor for keratoconus, but I believe its role in the pathogenesis of keratoconus has not been accorded sufficient prominence. I have thus undertaken the task to pen year article to suggest to readers a pathophysiological concept of keratoconus that I am increasingly convinced of: that eye rubbing is the root cause or sine qua non for keratoconus (download article). As such, eye rubbing is not a "risk factor", as often coined in medical literature, but the direct cause of a syndrome marked by a corneal deformation labeled 'keratoconus.
In this article, I have put forth the theory that keratoconus is not a dystrophy of unknown genetics and biomolecular substratum, but rather a syndrome caused by eye rubbing. i.e. what has been called "keratoconus" is in essence the direct consequence of mechanical trauma to the cornea by chronic and constant eye rubbing, resulting in the progressive deformation and thinning of the corneal wall which are hallmarks of the disease. Eye rubbing is the main character of the "mechanical" hypothesis as the etiology of keratoconus:
The Molecular Hypothesis vs. the Mechanical Hypothesis illustrated in a schematic diagram. The Mechanical Hypothesis states that keratoconus is primarily caused by eye rubbing. Eye rubbing is mainly triggered by atopy, air pollution, and extended computer screen viewing. In contrast to the Molecular Hypothesis where genetics, environmental and other unknown general factors are keys to the appearance of the disease, the Mechanical Hypothesis simply states that the corneal structural changes and deformation are initiated and aggravated by a mechanical cause: eye rubbing. Additional mechanical factors, such as corneal refractive surgery gold night compression of the cornea (by pressure of the hand or pillow) may also accelerate the corneal distortion. The prolonged contact between the eye and eyelids with the pillow of mattress can cause local irritation and contamination. This, in turn, leads to local itchness, and triggers eye rubbing, expecially in the morning. "This explains the striking correspondence between the' head side" on which sleep and the topographic features evocative of keratoconus patients.
Eye rubbing can cause inflammation. The effect of the mechanical stress (distension) is further accentuated by the release of proteinases in the stroma, explaining the progressive thinning of the cornea, which in turn makes it more vulnerable to the trauma caused by rubbing. LASIK cause eye dryness, and this can in turn trigger eye rubbing, we have more vulnetable (thinned by the refractive surgery procedure).
In the Mechanical Hypothesis, keratoconus cannot occur without a repeated mechanical injury such as eye rubbing. When the duration and frequency of eye rubbing exceed the native structural and biomechanical resistance capacity of the cornea, the mechanical imbalance causes the cornea to deform, leading to characteristic topographical patterns, encompassing minor forms of deformation (keratoconus 'unpolished form') to the end stage KC. In my experience, the latter is always encountered in patients who rub the affected eye vigorously and frequently.
As Keratoconus has primary mechanical disease
Just as excessive extension can cause ligament was sprained ankle, chronic eye rubbing can cause the corneal collagen fibers to lose part of their biomechanical resistance, resulting in macroscopically obvious structural deformation. This biomechanical mechanism could also better explain the frequent disparity in the degree of distress between the right and left eyes (patients frequently rub one eye more often and more vigorously than the other) and the focal nature of keratoconus, which has been recently evidence.
The exact genetics of keratoconus has yet to be elucidated. The frequency of occurrence in close family members is not clearly defined and is estimated to be less than 20%. In the 'eye rubbing as a sine qua non for keratoconus' hypothesis, the influence of genetics is related to the predisposition to conditions that lead to increased eye rubbing, and to corneal thickness and resistance. Down syndrome and atopy are obviously such conditions. Sleep apnea has also been associated with year increased incidence of keratoconus. The deprivation of good quality sleep causes chronic fatigue, and fatigue can induce patients to rub their eyes more frequently. I have often observed casees of late onset keratoconus (after 30 years of age) in workers who had a disturbance of their biological clock by a shift in their work hours from day to night, causing them to be chronically fatigued, and inducing them to rub their tired eyes frequently. A recent male predominance has been discovered in KC. In my experience, women who wear eye make-up tends to rub their eyes less often and less GamePorts than men. However, some women with keratoconus tends to rub their eyes heavily after make-up removal. Dry eye and ocular irritation are frequent during pregnancy: the occurrence of keratectasia after pregnancy may be explained by increased eye rubbing again. It is easier to explain the variation in the age of presentation, laterality, severity and broad spectrum of phenotypic expression by excessive eye rubbing than has corneal degeneration caused by year unknown genetic disorder or molecular casecade. For the same eye rubbing intensity, duration and frequency, corneas with natively reduced thickness and biomechanical strength may deform more readily and significantly thicker and stronger corneas than. Exposing people with thinner corneas to high level of pollution, dry air, irritating allergic agents and bad gold and/or intensive working conditions may account for the prevalence of keratoconus in some socio-ethnic groups. The recent increase in computer use has been linked to various ocular symptoms gathered together to be called «» Computer Vision Syndrome ", and this includes eye fatigue, which elicits eye rubbing, which may in turn account for the increase in prevalence keratoconus.
Marfan syndrome vs Keratoconus
These and other concepts are explored further in the article, through both scientific and anecdotal evidence. A relevant comparison with the cornea changes in Marfan Syndrome is also made:
Marfan syndrome is a genetic disorder of connective tissue. It is caused by a mutation in the gene controlling a protein called fibrillin-1, which is widely distributed in connective tissue throughout the body, and is a major component of collagen fibrils. In this syndrome, many organs of the body are affected, including the eye. The aorta, which media included broad layers of connective tissue, can progressively weaken and stretch under pressure from within the blood vessel, leading to a bulge in the vessel wall called year "aneurysm". In the eye, Marfan syndrome is associated with a displacement of the crystalline lens (ectopia lentis), due to weakening and loss of resistance of the zonular fibers which attach the lens to the sclera. Thesis zonular fibers are partly made up of fibrillin-1. The lens subluxation caused by the broken gold zonular fibers is typically bilateral, symmetric, and attenuated the superotemporal direction, although it may occur in other directions.
Marfan syndrome represents a perfect counter-example to explain the irrelevance of current theories on the pathogenesis of keratoconuswhich describe keratoconus to be year unknown collagen dystrophy associated with environmental, cellular and genetic factors causing a degenerative changes in the cornea. In fact, based on these assumptions,. Marfan syndrome should perfectly support the theories of keratoconus that attempt to explain the ectatic process. In Marfan syndrome, the gene mutation is identified, and the fibrillin-1 molecule involved in this connective tissue dystrophy is responsible for the reduction of the strength of the collagen present in the ocular tissues, including the corneal stroma. Yet, despite all these features, no. keratoconic gold ectatatic pattern is seen in the corneas of patients with Marfan syndrome. The Marfan corneas are thinner, but tends to be flatter instead of steeper. This surprising topographical feature can be easily accepted in principle if one considers that in normal conditions, the hand force exerted against the cornea is intraocular pressure. Apparatus for measuring pressure within year eye typically include mechanisms to increasingly deform the cornea by applying a progressively increasing force onto it. This force (eg: a puff of air) is responsible of year inward deformation of the corneal surface, which, for the same intraocular pressure, will be easier if the cornea is thinner or weaker biomechanically. Because the force resulting from intraocular pressure is evenly distributed against the posterior surface of the cornea and the inner surface of the sclera, has softer eyeball will undergo a progressive distension of its shell, which causes the local radii of curvature of the cornea to increase (and the corneal curvature to decrease), with concomitant progressive thinning. Hence, in the absence of a localized additional focal gold force or trauma, the biomechanical weakening of Marfan corneas results in a flatter corneal surface. This distension of the eyeball also contributes to its increase in axial length, and most Marfan patients indeed suffer from axial myopia. Abnormally flat corneas and axial myopia both corresponds to the ocular diagnostic criteria for Marfan syndrome.
A flat keratometry is a diagnostic criteria for a Marfan cornea, some association between Marfan syndrome and keratoconus has been reported. This however does not contradict the mechanical theory: the biomechanically weaker corneas of Marfan patients may be more vulnerable to the effects of eye rubbing.
In contrast to the Marfan cornea, the typical topographic pattern of a keratoconus includes steepening and asymmetry of the cornea corneal surface and changes in central corneal thickness, including gold answers accelerated thinning. Invoking year external source of trauma to the cornea (such as eye rubbing) as a pathogenetic event provides a better explanation to these findings than still unraveled processes of molecule changes mysteriously affecting only the cornea and preserving the other tissue of the body components. The force exerted against the corneal shell by the pressure of the fingers, particularly the knuckles, may be considerable. Repetitive force can cause stretching and disorganization of the corneal collagen lamellae. Year acute rise in intraocular pressure from sudden reduction in eye volume from the compression of the globe by the fingers could also stretch the scleral shell and lead to year axial myopic refractive shift. Despite contradicting reports, the axial length of keratoconus patients seems to be slightly but significantly higher than in non-keratoconus patients.
There will understandably be skeptics and naysayers to this theory, especially since the hypothesis may be impossible to prove. However, the primary purpose of this article is to increase the awareness of the potential ill-effects of eye rubbing and its association with keratoconus. Highlighting its causative role may help to dramatically reduce the incidence of keratoconus, and stop its progression in eyes already affected.
It is interesting to note that conditions that are characterized by the presence of corneal inflammation generally induce a reduction in corneal curvature, not year increase in corneal curvature. This also underlines the importance of the mechanical hypothesis to account for the focal steepening which is observed in corneas with keratoconus.
The "eye rubbing as a sine qua non for keratoconus" blatantly defies the widely accepted concept of keratoconus being theory has corneal dystrophy of unknown origin. To many, it may appear provocative in its simplicity, and there are personal level, would have triggered some skepticism 6 or 7 months ago. However, in recent years, after conceiving the hypothesis and applying it to my day to day management of keratoconus patients, the skepticism is waning. The theory is compatible with most of what is known about keratoconus. In fact, day by day, after each patient interview, I am increasingly convinced that This mechanical first hit theory is the answer to the enigma surrounding keratoconus. This opens fascinating perspectives. It could close the chapter of the mystery of the pathogenesis of keratoconus opened by Dr. John Nottingham's 1854 treatise on the conical cornea. In theory, it could also lead to the eradication of the disease if it were possible to prohibit everyone from chronically and incessantly rubbing their eyes. However, from a practical standpoint, this is probably year impossible mission.
A less ambitious but important goal is still attainable, and this involves reducing the incidence and progression of keratoconus by increasing the awareness of patients on the potential dangers of chronic and vigorous eye rubbing, and encouraging them to refrain from it. In the management of my many patients with keratoconus, I religiously counsel them on the dangers of eye rubbing, and tell all of 'em to stop rubbing their eyes. I also routinely perform detailed assessment of their condition, including refraction and subtractive topography maps between each consultation to document disease progression. None of my patients who have completely stopped rubbing their eyes have seen progress in their disease since they kicked the habit. These observations are still ongoing, and will require a longer follow up, goal if they stand the test of time, they will bring forth a strong argument to support the "eye rubbing as a sine qua non for keratoconus' theory, and more importantly, demonstrate its clinical benefits."
Link to the original paper