Dry eye disease (DED) is a major public health problem.
Dry eye disease has been estimated to impact the lives of 15-30 million people in the U.S. alone. These numbers are growing as are its enormous personal, societal and economic costs. Therefore, it is baffling that despite the seemingly obvious cause and effect and the considerable financial and intellectual resources invested in its research, little of consequence has trickled down to its victims.
This impasse, I believe, is the result of the misplaced reverence that experts in this field have for the current model based on tears. And as I will point out, some of its adherents are so committed to it that they have made unprincipled efforts to prevent the consideration of new ideas that point to a different direction.
What is dry eye disease?
The diagnosis itself implies that the cause of this disorder is the lack of tears despite the fact that many patients whose eyes feel abnormally dry are not dry. Although experts attribute this conundrum to tear films that evaporate too rapidly (which they label as evaporative dry eye), many patients whose chronic dry eye symptoms, despite the presence of adequate tears, contradict this explanation as do others with scanty tears and obstructed Meibomian glands that would be expected to cause excessive dry eye symptoms but don’t.
These findings alone should have questioned the validity of the tears-based model of this disease long ago had there been a better theory to consider. Now that there is, efforts have been made to suppress it.
Dry eye symptoms.
These sensations are a type of pain generated by many of the high concentration of pain-sensitive nerve endings located just under the surface of our corneas (the transparent dome-shaped front surface of our eyes through which our colored iris and pupil are visible).
Pain is our body’s alarm signal of imminent or actual tissue damage. However, that of dry eye differs in that it is designed to warn us that our tear film has thinned excessively and is in danger of breaking up. This information is critical since if the tear film covering our corneas does breakup, our eyesight would become instantly reduced to seeing shadows until the optical tear film is restored. Because it was an existential risk to the survival of our distant ancestors, the dry eye alarm evolved to monitor the thickness of the tear film in real time and trigger the release of fresh tears when it senses that it is in danger of breaking up. However, if the response to the call for more tears isn’t adequate, the alarm escalates to conscious sensations of dry eye pain. The conventional dry eye model assumes that insufficient tear-release is the underlying disease.
I argue that inadequate tears is a secondary issue that has obscured the primary disease.
What is the primary disease of “dry eye disease”? A new theory.
I suggest that the underlying disorder is a malfunctioning dry eye alarm system.
Like a fire alarm with a short circuit that increased the sensitivity of its heat sensors so that it is triggered at room temperatures, the dry eye alarm will be activated prematurely if the sensitivity of its tear evaporation sensors is increased. The result is that the dry eye alarm (dry eye symptoms) is activated prematurely thereby causing false alarms.
In other words, these eyes feel drier than they are and require a thicker than normal tear film to keep the alarm (dry eye symptoms) quiet. This translates to corneal nerve disease (otherwise known as corneal neuropathy) that I believe can begin by increasing the sensitivity of its tear evaporation sensors resulting in false dry eye alarms. Moreover, as every eye doctor knows, as nerve diseases progress they lose their ability to send messages calling for more tears. The eventual result is drier eyes.
If the current dry eye disease theory is so flawed, why is it still used?
The tears-based theory is so deeply entrenched that it has been interpreted as fact. (The wording of its diagnosis leaves no room for considering other options.) Because research programs have focused on studying the effects of drying the corneal surface, expertise in studying the biochemistry of residual tears following evaporation and its effects on the corneal tissues of mice has been greatly advanced. This financially funded momentum has discouraged any incentive to challenge this basic premise.
On the other hand, should this nerve disease model take root it will require a different skill set that is friendlier to neuroscientists.
Centralized eye pain
One highly important and unexpected finding is the existence of a devastating eye pain syndrome that had never before been previously associated with eyes. Known as centralized pain, it is typically associated with normal-looking eyes because, although the disease feels that it originates in around and behind the eyes, it is generated in eye pain centers located in the brain.
It is a form of phantom pain that can also be projected to patients’ head (headaches), ears, face and jaws. When present, dry eye pain is especially severe and can be worsened by exposure to cold. Incapacitating photosensitivity is common as is spontaneous pain that patients describe as hot/burning, sharp, cutting, pins and needle-like, aching, and pressure-like. Its crippling intensity and the contrasting normal appearance of their eyes invite accusations that they are exaggerating or even imagining their symptoms. Some patients have been driven to suicide to find relief.
Why has centralized eye pain been ignored?
We don’t know why certain people are more prone to developing centralized pain. In my experience it can be associated with certain complex diseases such as fibromyalgia and Sjogren’s syndrome and it can follow corneal nerve injuries.
I believe that its existence has been suppressed because it can be a complication of LASIK surgery. I examined 21 patients who developed devastating centralized corneal pain after LASIK. At the time of my initial examination this pain syndrome had been present from 2 to 16 years. I studied the corneal nerves with the laser scanning microscope of every patient and in compiling the data of their histories I discovered that this horrendous pain disease began after the surgical pain had completely resolved in a majority of patients and this delay lasted for years in some patients.
The messages suggested by this data are:
- Devastating centralized corneal neuropathic pain can be caused by LASIK, a procedure that provides no medical benefits,
- the effectiveness of treatments is disappointing at the present time and
- the disease is long-lasting and may be permanent in some people.
I submitted this paper to Ophthalmology, the journal of the American Academy of Ophthalmology, suggesting that the peer reviewers include an authority in neuropathic pain. The paper was rejected and I was given no option for its resubmission. (Although the reviewers are anonymous, their comments suggested that most were LASIK surgeons and none seemed knowledgeable in pain mechanisms.)
I then submitted the paper to the Journal of Cataract and Keratorefractive Surgery, reputed to have significantly lower standards. It was again rejected without recourse and one can infer from the reviewers’ comments that once again most were LASIK surgeons and none were authorities in pain mechanisms.
Is it possible that the reviewers were correct in their assessment that the paper was unworthy of being published and was too flawed to be rehabilitated?
Normally, two rejections is terminal for publishing a medical paper in a peer-reviewed journal. Nevertheless, I decided that it will not be buried and posted it on this website with the commitment that all comments will be published requiring only that the authors reveal their identity.
Despite its label, there are cogent reasons to question the soundness of the tear-based theory of what has been known as dry eye disease. The model based on malfunctions of the nerve architecture of the dry eye alarm system anticipates major features of this diseases that cannot otherwise be explained.
If its validity is proven by scientific studies, assuming that they are permitted, it would seem more logical to refocus much of the limited research financial resources on better understanding the aberrant sensitization process of the corneal pain system that extends from its nerve endings close to the surface of the cornea to the cortex of our brain.