How many of you have struggled with different eye disorders? Did you ever think that they could be related to Obstructive Sleep Apnea (OSA)? A multitude of symptoms are associated with OSA, as we have discussed in the past. This month we will focus on the side effects that relate to your eyes. There are many reasons for eye-related headache, and many of them can be directly or indirectly associated with the structures connected to the temporomandibular joint or as a result of its dysfunction. The Sphenomandibularis is an important muscle that borders 1) the lateral and medial tendons of the temporalis, 2) the mandibular head of origin of the superior pharyngeal constrictor, and 3) the zygo mandibularis muscle—all of which have the potential to cause similar pain symptoms from within the mouth. Dr. Janet Travell documented 50 years ago that trigger points in the Trapezius muscle may often refer pain above the eye on the ipsilateral side. All of the structures mentioned above can, and often do, stimulate or refer headache pain near the orbit of the eye.
Facies temporalis ridge on sphenoid bone representing origin site for sphenomandibularis muscle:
The Sphenomandibularis muscle was discovered at the University of Maryland by Dunn, Hack, Robbins and Koritzer in 1995 and reported in 1996 in the Journal of Craniomandibular Practice. I originally read of this muscle prior to its publication in the Journal. It was mentioned in the Wall Street Journal. Upon reading this I called Dr Gary Hack and discussed his research findings and that very day provided a Marcaine injection at the mandibular attachment of the Sphenomandibularis in a patient with retro-orbital pain and noted that within 20 minutes of the procedure… the retro-orbital pain had ameliorated. This protocol has been successfully provided for the past 20 years in my practice and when initially provided in the 1990’s was denied by IME doctors who stated that I was making it up and documented that I should not be paid for injecting a non-existing muscle.
A few other common ophthalmic conditions associated with OSA include the following:
- Floppy Eyelid Syndrome (FES)
- Keratoconus (KC)
- Retinal Vein Occlusion (RVO)
- Central Serous Chorioretinopathy (CSC)
- Nonarteritic Anterior Ischemic Optic Neuropathy (NAION)
Floppy Eyelid Syndrome
Floppy eyelid syndrome (FES) is a condition where the upper eyelids essentially turn inside out. This leaves the eye vulnerable to pain and/or discomfort, and also visual symptoms and/or disturbances.
Studies suggest that most patients with FES suffer from OSA, however, only between 2% – 5% of patients with OSA have FES as well. FES in patients with OSA signifies a greater severity of the disease. Another interesting fact is patients with FES often experience symptoms on the side on which they sleep.
Doctors who are treating patients with possible OSA may identify FES by asking about symptoms of pain in/around the eyes, visual disturbances, blurred vision, excessive watering, etc. Patients with dry eyes sometimes experience excessive tearing, which is the body’s response to underlying dryness. Doctors who already specialize in treating OSA typically know to ask about any eye-related symptoms.
Airway collapse in patients with OSA occurs due to connective tissue compromise in direct relation to neck thickness, and patients with FES display tissue redundancy and exhibit a connective tissue weakness as well.
Believe it or not, Glaucoma is the 2nd leading cause of blindness worldwide. There are several different types of Glaucoma including the following:
-Open Angle Glaucoma (OAG)
-Normal Tension Glaucoma (NTG)
-Angle-Closure Glaucoma (ACG)
Glaucoma is a chronic, progressive visual condition associated with high pressure and visual deficits. While the exact cause is not clear, many theories propose nerve damage and vascular mechanisms. Intraocular pressure (IOP) compresses the optic nerve, which causes the damage to the eye.
One of the biggest challenges for Ophthalmologists is to pinpoint Glaucoma in asymptomatic patients. Initially, the visual discrepancies may be hard (if not impossible) to identify. Once the symptoms finally are detected, it may be too late. Sometimes irreversible nerve damage has already occurred.
Because of this increased risk, patients who have been diagnosed with OSA can benefit from a referral to the eye doctor from their Sleep Medicine Physician. Obviously, everyone should still maintain a regularly scheduled (yearly) eye exam even if you don’t have OSA.
Papilledema is a bilateral swelling of the optic disc (the raised disc on the retina and point of entry for the optic nerve) caused by elevated intracranial pressure. It is associated with increased blood flow and interrupted breathing as well. If untreated, complete vision loss can occur.
Other symptoms associated with Papilledema include headaches, nausea and/or vomiting, vertigo, and tinnitus.
MRI or CT evaluation of the brain and/or spine is typically done to identify papilledema.
The Papilledema Grading System is as follows:
Stage 0 – Normal Optic Disc – blurred vision can occur
Stage 1 – Very Early Papilledema – disruption of the nerve fiber layers & subtle gray halo
Stage 2 – Early Papilledema – all borders are obscured; complete peripapillary halo
Stage 3 – Moderate Papilledema – increased diameter of optic nerve; obscured blood vessels
Stage 4 – Marked Papilledema – nerve head is completely elevated; peripapillary halo
Stage 5 – Severe Papilledema – dome-shaped protrusions; optic cup is destroyed
Keratoconus (KC) is another eye disorder in which the cornea becomes thinned over time. The cornea is the dome-shaped “window” at the front part of the eye. This disorder makes the cornea bulge outward like a cone. Usually both eyes are affected simultaneously.
This can result in double vision, blurred vision, astigmatism, nearsightedness, and photophobia (light sensitivity). The cause of this is thought to be a combination of genetic, hormonal and environmental influences.
For most people, this will stabilize after a few years if treated accordingly. Usually special contacts are prescribed.
Retinal Vein Occlusion
OSA-related hypoxia (deficiency in oxygen reaching tissues) can be a major cause of RVO, or, retinal vein occlusion (blockage in artery of vein). This means that the retina is not getting enough oxygen. Just as arteries and veins carry blood to and from the heart, if a retinal vein is blocked, it cannot drain blood from the retina. This leads to leaking fluids and bleeding. RVO is the second most common cause of blindness from vascular disease in the retina.
The main symptoms of RVO include vision loss (central or peripheral) and/or blurred vision. Patients with severe OSA are more at risk for developing RVO.
There are 2 types of retinal vein occlusion (RVO):
-CRVO – central retinal vein occlusion – blockage of main retinal vein
-BRVO – branch retinal vein occlusion – blockage of smaller branch veins
In a study of 40 patients having been treated for RVO, 37% of these patients demonstrated sleep-disordered breathing as measured by nocturnal pulse oximetry. In another series of patients with RVO, OSA prevalence was found to be 77% among patients selected for screening based on nighttime symptoms. (Ocular Manifestations of OSA – J Clin Sleep Med)
Central Serous Chorioretinopathy
This eye disorder is referred to as CSC, and is a condition where fluids accumulate beneath the retina. CSC causes a fluid-filled (serous) detachment, in addition to loss of vision. Objects can appear distorted, blurry or dim, and depth perception is diminished.
Risk factors for developing CSC include high stress levels and increased levels of cortisol. Patients with OSA have increased levels of epinephrine and norepinephrine, which are both also risk factors for CSC.
Sometimes, CSC can show no signs or symptoms, it all depends on the location and amount of subretinal fluid.
Studies suggest that patients being treated for OSA can simultaneously accelerate the treatment time and recovery period for CSC.
Nonarteritic Anterior Ischemic Optic Neuropathy
Nonarteritic anterior ischemic optic neuropathy (NAION) is a sudden, painless, irreversible loss of vision. A loss of blood flow to the optic nerve occurs, which the optic nerve is essentially the “lifeline” between the eye and the brain.
Patients who are on multiple medications for hypertension are at high risk for developing this disorder. Physicians caring for patients with OSA may clarify a history of NAION by asking about any instances of abrupt visual loss upon waking. Most often this disorder occurs first thing in the morning upon the patient awakening from sleep.
It is hypothesized that OSA can possibly cause NAION as a result of increased blood pressure, hypoxemia or intracranial pressure, leading to nerve edema.
A meta-analysis found that patients with NAION had a five-fold increased odds of having OSA. (Ocular Manifestations of OSA – J Clin Sleep Med)
Early diagnosis and management of OSA is critical in reducing or eliminating the risk of visual dysfunction. Because OSA has so many ocular side effects, it is important that the right intake questions are asked during the consultation appointment. Usually, if you don’t specifically ask your patients about their sleep history, they won’t bring it up on their own. If you are concerned about eye pain or have patients with OSA related eye problems, I hope this information was helpful.
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