The Brain and the Eye – How They Work Together

The Brain and the Eye

The eye works like a camera. The iris and the pupil control how much light to let into the back of the eye, much like the shutter of a camera. When it is very dark, our pupils get bigger, letting in more light; when it is very bright our irises constrict, letting in very little light.

The lens of the eye, like the lens of a camera, helps us to focus. But just as a camera uses mirrors and other mechanical devices to focus, we rely on eyeglasses and contact lenses to help us to see more clearly.

The focus light rays are then directed to the back of the eye, on to the retina, which acts like the film in a camera. The cells in the retina absorb and convert the light to electrochemical impulses which are transferred along the optic nerve to the brain. The brain is instrumental in helping us see as it translates the image into something we can understand.

The Brain and the Eye

The eye may be small, but it is one of the most amazing parts of your body. To better understand it, it helps to understand the different parts and what they do.

Choroid
A layer with blood vessels that lines the back of the eye and is between the retina (the inner light-sensitive layer that acts like film) and the sclera (the outer white part of the eyeball).

Ciliary Body
The muscle structure behind the iris, which focuses the lens.

Cornea
The very front of the eye that is clear to help focus light into the eye. Corrective laser surgery reshapes the cornea, changing the focus to increase sharpness and/or clarity.

Fovea
The center of the macula which provides the sharp vision.

Iris
The colored part of the eye used to regulate the amount of light entering the eye. Lens focuses light rays onto the retina at the back of the eye. The lens is transparent, and can deteriorate as we age, resulting in the need for reading glasses. Intraocular lenses are used to replace lenses clouded by cataracts.

Macula
The area in the center of retina that contains special light-sensitive cells, allowing us to see fine details clearly in the center of our visual field. The deterioration of the macula can be common as we age, resulting in age related macular degeneration.

Optic Nerve
A bundle of more than a million nerve fibers carrying visual messages from the retina to the brain. Your brain actually controls what you see, since it combines images. Also the images focused on the retina are upside down, so the brain turns images right side up. This reversal of the images Is a lot like what a mirror does in a camera. Glaucoma can result when increase pressure in the eye restricts the flow of impulses to the brain, causing optic nerve damage and makes it difficult to see.

Pupil
The dark center opening in the middle of the iris changes size to adjust for the amount of light available to focus on the retina.

Retina
The nerve layer lining the back of the eye that senses light and creates electrical impulses that are sent through the optic nerve to the brain.

Sclera
The white outer coating of the eyeball.

Vitreous Humor
The clear, gelatinous substance filling the central cavity of the eye.

3/3/16

Susan DeRemerSusan DeRemer, CFRE
Vice President of Development
Discovery Eye Foundation

Pink Eye Tips and Prevention

pink eye
Pink eye is an inflammation or infection of the thin, clear covering of the white of your eyeball (the conjunctiva) and the inside of your eyelids. When the small blood vessels in the conjunctiva become inflamed they are more visible making the whites of your eye to appear pink. Also called conjunctivitis, it can affect one or both eyes.

Common symptoms of pink eye include:

  • Redness in the white of the eyeball(s) and or inner eye lid(s)
  • Increased tearing or discharge
  • Slightly blurred vision from discharge
  • Crusting of the eyelashes from the discharge that may prevent eyes from opening after sleep
  • Mild eyelid swelling
  • Itching or burning sensation
  • Increased sensitivity to light
  • Irritation or gritty feeling in your eye(s)

Make an appointment with your eye doctor if you notice and of the symptoms of pink eye. Some forms are highly contagious for as long as two weeks, so an early diagnosis could protect those around you from contacting the disease. If you were contact lenses, stop using them until directed by your doctor.

There are four general types of pink eye.

Allergic Conjunctivitis
This form is caused by eye irritants such as pollen, dust, animal dander and other environmental factors. It is not contagious. Treatment often includes applying a cool compress to your eyes and using allergy eye drops and artificial tears. In severe cases non-steroidal and anti-inflammatory medications may be prescribed.

Bacterial Conjunctivitis
This type is most often caused by staphylococcal or streptococcal bacteria, is highly contagious and can cause serious damage to the eye if left untreated. This is treated with antibiotic eye drops or ointments to speed up the healing process that can take one to two weeks. While you may see improvement after three to four days, the entire course of treatment needs to be used to prevent a recurrence.

Because this is so highly contagious here are a few things to remember so you don’t spread it to others or re-infect yourself:

  • Don’t touch your eye with your hands
  • Wash your hands frequently and thoroughly
  • Change towels and washcloths daily – and don’t share them
  • Change pillowcases often
  • Get rid of all eye cosmetics and personal care items such as eye creams – and don’t share them
  • Avoid swimming
  • Don’t reuse tissues when wiping your eyes, and throw them out immediately
  • Follow your eye doctor’s instructions related to your contact lens usage and care

Viral Conjunctivitis
This is the same type of virus associated with the common cold. Antibiotics will not work on a viral infection. Like a cold, the infection just needs to run its course which could take anywhere from a few days up to 2-3 weeks. It is also contagious like a cold, so follow the same instructions as listed above to not spread the infection.

Chemical Conjunctivitis
This can be caused by irritants like air pollutions, chorine in swimming pools or exposure to noxious chemicals. To treat this type of pink eye requires a doctor to carefully flush your eyes with saline and may require topical steroids. Acute chemical injuries are very serious and need prompt medical attention to avoid corneal scarring, intraocular damage, vision loss or the loss of an eye.

Of course the best way to deal with pink eye is not to get it. Here are some ways to protect yourself and others.
pink eye

2/24/16

Susan DeRemerSusan DeRemer, CFRE
Vice President of Development
Discovery Eye Foundation

Layers of the Retina

The retina at the back of the eye is essential for all vision. Each layer of cells in this tissue serves a specific purpose. As we prepare for Age-Related Macular Degeneration Awareness Month in February, a closer look at the layers of the retina and their function.

layers of the retina

Layers of the Retina

Choroid – This is made up of a layer of blood vessels that supply oxygen and nutrients to the retina. Defect in the CHM gene can cause choroideremia, leaky blood vessels can expand in the retina causing wet age-related macular degeneration (AMD) and diabetic retinopathy.

Retinal pigment epithelium – This is a single layer of cells that provide essential nutrition and waste removal for the photoreceptor cells. Accumulation of waste can lead to AMD and Stargardt disease.

Photorecptors – This is where the rods and cones are located that convert light into electrical signals. Rods help you with night and peripheral vision. Cones are more concentrated in the macula (the central part of the retina) and proved central and color vision. Death of the rods can cause vision loss called retinitis pigmentosa, while AMD is the loss of central vision.

Horizontal cells – These cells are connect to the photoreceptors that surround the bipolar connected photoreceptor cells and help the help integrate and regulate the input from multiple photoreceptor cells, increasing your visual acuity.

Bipolar cells – The dependence of each layer of the retina on each other is exemplified here. These cells take the electrical information from the photoreceptor cells and pass it along to other retinal cells.

Ganglion cells – These cells extend to form an optic nerve that conveys information to the brain and take the electrical information from the bipolar cells and process it to determine shapes, contrast and color. Glaucoma vision loss results from high intraocular pressure that affects the optic nerve, interrupting the signals to the brain.

 

Top 10 Articles of 2015

eye facts and eye disease
In looking at the many articles we shared with you in 2015, we found that your interests were varied. From the science of vision, eye facts and eye disease to helpful suggestions to help your vision.

Here is the list of the top 10 articles you read last year. Do you have a favorite that is not on the list? Share it in the comments section below.

    1. Rods and Cones Give Us Color, Detail and Night Vision
    2. 20 Facts About the Amazing Eye
    3. Understanding and Treating Corneal Scratches and Abrasions
    4. 32 Facts About Animal Eyes
    5. 20 Facts About Eye Color and Blinking
    6. When You See Things That Aren’t There
    7. Posterior Vitreous Detachment
    8. Can Keratoconus Progression Be Predicted?
    9. Winter Weather and Your Eyes
    10. Coffee and Glaucoma: “1-2 cups of coffee is probably fine, but…”

Do you have any topics you would like to see discussed in the blog? Please leave any suggestions you might have in the comments below.

1/7/16


Susan DeRemerSusan DeRemer, CFRE
Vice President of Development
Discovery Eye Foundation

Tear Film Health is Essential for People with Keratoconus

People afflicted with keratoconus (KC) are often obligated to wear contact lenses in order to obtain functional vision. Unfortunately, wearing contact lenses can have detrimental effects on the ocular surface and tear film layers over the course of decades, ultimately reducing lens tolerance. Therefore, any intervention prolonging the comfortable wear time of contact lenses should be aggressively pursued. The tear film covers the surface of the eye, provides lubrication and is the primary defense against foreign bodies and infection. Without a robust and healthy tear film, safe and comfortable contact lens wear is not possible. This article will describe the structure of the tear film and review simple remedies that can keep it healthy throughout life.

Tear Film Layers

The tear film is a complex, triple layered structure comprised of mucus, water and oil. The surface of the cornea and conjunctiva contain cells specialized to secrete a sticky mucoid substance. These so called goblet cells produce the mucin layer of the tears, which creates a “Velcro” type interface and allows the overlying watery component to stick to the ocular surface without washing away.

The bulk of the tear film is comprised of the watery, or “aqueous” layer which is secreted primarily by the lacrimal gland. This specialized structure is located near the eyebrow. This gland continuously releases small amounts of watery fluid that also contains enzymes and antibodies to help fight infection and wash away contaminants.

The lipid layer is the final, outermost layer of the tears. If the tear film is the first line of defense for the ocular surface, then the lipid layer is the first line of defense for the entire tear film and the ocular surface combined. Because of that role, it is extremely important and helps stabilize the tear film by preventing evaporation. This thin, lipid based layer is released by the meibomian glands, which are modified sebaceous glands that reside in the upper and lower lids. In each lid there are 20-30 glands. These glands open up onto the lid margin and through the action of a complete blink, release the lipid secretion to ocular surface which gets spread with the upward motion of the upper eyelid.

Each one of these layers contributes to the structure of the tear film, and a problem with any one of these structures (goblet cells, lacrimal gland or meibomian glands) will negatively impact the corresponding tear layer.

Tear Film
Image 1 -Layers of the tear film across the ocular surface & Meibomian glands of the eyelids. (Picture courtesy of TearScience™)

Tear Film Issues

Because the tear film is so thin, each individual component is necessary to maintain the integrity of the tears as a whole. When any layer of the tear film is deficient, the tear film becomes unstable and the ocular surface becomes irritated and can progress to developing classic symptoms of dry eye. This includes burning, stinging, redness, tearing, fatigue and contact lens intolerance.

Deficiencies in the mucin layer are uncommon, and are typically the result of chemical or thermal insult, or scarring. An aqueous deficiency, primarily from a lacrimal gland related etiology, is also relatively uncommon, and can arise from autoimmune and inflammatory causes such as Sjögren’s Syndrome. The most common reason for a poor tear film is linked with excessive evaporation of our tears due to a lack of sufficient lipid secretions from non-functioning or obstructed meibomian glands. It is understood that many factors contribute to why these glands stop performing optimally.

One factor has been linked to our habitual working environments. The compressive force exerted by the muscles of our eyelids that control blinking are essential for lipid secretion. However, the use of computers or wearing contact lenses has been shown to negatively impact our blinking habits, both by reducing the number of blinks and making blinks less complete. With an incomplete blink, the upper and lower lids do not make contact. The negative consequences of this are 1) the meibomian glands do not release their lipid contents, 2) the lower part of the eye is chronically exposed to the air, increasing evaporative stress and 3) dead skin cells accumulate on the lid margin which can clog the meibomian gland openings.

When increased evaporation of the tear film occurs chronically, the integrity of the entire ocular system becomes compromised over time and problems to the health of the eye become permanent attributes. This condition is known as Meibomian Gland Dysfunction or MGD and is linked with 86% of all dry eye sufferers.

Image 2 - Histology slide of a Meibomian gland with a terminal duct blockage
Image 2 – Histology slide of a Meibomian gland with a terminal duct blockage
Contact lenses have been shown in multiple studies to have a negative impact on the integrity of the tear film. To begin with, placement of a lens onto the eye divides the tears into two sections, referred to as the “post” (behind) and “pre” (in front) lens tear films.

The characteristics of the post lens tear film can differ depending on the type of lens that is worn. For example, soft lenses and scleral lenses have very little turnover of this post-lens tear film. This can cause issues related to the build up of toxic waste and bacterial elements that ultimately aggravate the corneal surface. Conversely, rigid gas permeable lenses are designed to have substantial tear turnover behind the contact lens with every blink.

The pre-lens tear film is also greatly affected by the type of lens material, as well as the interaction between the lid and the contact lens surfaces. Eye doctors know that without a healthy tear film, chances for contact lens intolerance increases. The rate of contact lens intolerance substantially increases as patients enter their fourth decade of life, primarily because of MGD caused by years of poor blinking habits.

Tear Film Care

Fortunately, simple interventions can prevent and/or limit the severity of MGD altogether or help to manage it once it occurs. Just like brushing and flossing one’s teeth can prevent gum disease, attention to complete blinking and lid margin hygiene can improve the tear film and prevent contact lens intolerance problems.

Because partial blinking is strongly linked with developing MGD, it is vitally important that the two lids touch when blinking. It is best to practice this several times throughout the day as well as when you are reading or using the computer.

Akin to flossing the teeth, it is also important to clean the lid margins with a Q-tip soaked in saline solution or a bit of mineral oil by gently brushing the Q-tip across the lid margin 10-20 times each night. It is easiest to get the lower lid.

Finally, performing warm compresses daily can provide heat to the Meibomian glands to soften the hardened oil that can plug the meibomian gland ducts. Warm compresses need to be done continuously for at least 10 minutes with consistent heat in order to attain a temperature that is sufficient to melt the oil that clogs the glands. We recommend folding 5-6 small towels or facecloths into a rectangular shape and wrapped together into a circular bundle, similar to the appearance of a cinnamon roll. The towels should be damp and moist, placed in a microwaveable safe dish with a lid and heated for approximately 1 minute and 50 seconds. After removal, wait a minute or two and then proceed to use the outermost cloth and cover the rest. Replace the first cloth after two minutes and grab the next outer most towel from the bundle, continuing this until all towels are used. In this way, the temperature can be adequately maintained for the full 10 minutes. The high temperatures applied to the lid are transferred to the cornea and very often cause temporary deformation, a phenomenon characterized by transient visual blur immediately following compress application. Therefore, it is vitally important, especially for patients with keratoconus, that pressure never be exerted onto the globe of the eye with a compress or massage administered to the lids of closed eyes after a compress.

It is becoming apparent that MGD is developing in patients at earlier ages. Because of this, the condition has likely been present for decades by the time the patient becomes symptomatic. It may take significant time and effort to rehabilitate not only the glands themselves, but also to reduce the resulting inflammation of the ocular surface.

Meibography is the technique used to image Meibomian glands. In chronic cases of MGD, we see abnormal changes to gland structure, in the form of atrophy or loss of gland tissue and/or dilation of glands where obstructed material causes glands to become widened. In severe cases, the prognosis for recovery is guarded.

The visual clarity that contact lenses provide for patients with keratoconus is incredibly important. But the ability to comfortably wear contact lenses is reliant on our body’s ability to provide a sufficiently thick protective tear film. Taking a small amount of time daily to attend to the lipid producing Meibomian glands by proper blinking habits, exfoliation of the lid margin with a Q-tip and warm compresses will help to extend the number of hours, and ultimately the number of years, that contact lenses can be safely and comfortably worn.

10/20/15

tear filmAmy Nau, OD
Korb and Associates, Boston, MA
Contact lens fitting for keratoconus, other ocular surface disorders and dry eye
 
 
 
 
 
 

tear filmDavid Murakami, MPH, OD, FAAO
Tear Science, Inc.
Researcher, Dry Eye

When Is The Best Time For Cataract Surgery?

As you age, cataracts become a concern prompting the question – when is the best time for cataract surgery?

There are decades worth of old wives tales floating around regarding cataracts that often lead to unnecessary fear and apprehension for many patients. These myths involve concepts such as “ripeness”, having to wear eye patches afterwards, danger in “waiting too long, etc. Just as the techniques of cataract extraction have changed over the decades, so have the indications to proceed to surgery.
best time for cataract surgery - people
Firstly, cataracts are a normal part of the aging process. Patients should not be alarmed if they are told that they are developing cataracts, even as early as their fifties. As we age, the natural clear lens inside the eye becomes progressively harder, darker, and cloudier. This dark, cloudy lens is what is referred to as a cataract. Cataracts develop at different rates for different people, and even between the two eyes of the same person. It typically takes many years for the lens to become cloudy enough to impact the clarity of vision. There are many different types of cataracts depending of what area of the lens becomes cloudy, but the typical cataract related to normal aging results in a relatively uniform cloudiness with a denser central core, and is referred to as “Nuclear Sclerosis”. Other varieties of cataracts tend to grow more quickly, are relatively uncommon, and often result from certain conditions other than typical aging.
best time for cataract surgery
Regardless of what type of cataract the patient has, the treatment is the same: cataract extraction with an implant of an intraocular lens. There have been great advances in lens design over the years, and they now result in excellent, stable, predictable vision for the remainder of the patient’s lifetime and do not typically need to be changed once implanted.

Cataracts result in different symptoms that may be more of less relevant to a specific person’s needs, such as:

  • Glare with bright lights
  • Difficulty with fine print
  • Difficulty following the golf or tennis ball
  • Impairment in night driving
  • Difficulty with seeing street signs
  • Seeing the score or small print on the television
  • Fine visual tasks such as threading a needle, etc.

Although cataract surgery is an incredibly successful procedure with only about a 1-2% risk of complications, it still DOES have some risk. Therefore, cataract surgery should only be undertaken when there is something to gain. In other words, the BENEFITS MUST OUTWEIGH THE RISKS. This means that if your symptoms are mild and are not interfering with your activities of daily living, it is not time to accept the risks of surgery. Once your visual impairment progresses to the point that YOU feel your activities of daily living and enjoyment are impaired, this is the time to proceed to surgery. This threshold is very different between people. Some people feel impaired with vision of 20/25, and others still function within their scope of usual activities until they are 20/100! The best first-step in determining if it is time for your surgery is to get an up-to date refraction. This means a detailed check for new glasses. Often, cataract development will change a person’s glasses prescription, and updating this can improve the visual symptoms for months to years. When a new glasses prescription no longer improves the sight adequately, this is when surgery is indicated.

For the most part, putting off cataract surgery does not impact the final outcome. It will not harm you or your eye to leave the cataract alone until you are ready. There are of course certain exceptions to this rule, such as in Fuchs’ dystrophy, pseudoexfolation, untreated narrow-angle glaucoma, and some others. However, these are relatively rare conditions that your doctor will speak to you about if you have any of these diagnoses.

In summary, the time to proceed to cataract surgery is something that you as the patient determine. YOU assess your lifestyle needs and your vision performance within your scope of activities. When you feel you are impaired in these activities, the benefits will outweigh the risks, and it’s time to take them out. You should not feel any pressure to urgency in this process.

Once you have determined you are ready to have cataract surgery, your surgeon will discuss with you your options for intraocular lens implantation including astigmatism neutralizing lenses, standard distance or near-vision lenses, multiple focal distance lenses, accommodating lenses, and others. The current standard approach for cataract surgery is called “phacoemulsification” and uses ultrasound technology to remove the cataract. There are also laser devices that assist in making the incisions and breaking up the lens, which many surgeons now employ in addition to the phacoemulsification. In general cataract surgery only takes a few minutes, is performed with topical anesthesia, is pain-free, and has a very short recovery time. No pirate-patches are used these days! Most patients are very happy with the results, but this requires adequate discussion with the surgeon prior to the procedure to best assess the needs of the individual patient. A well- informed patient who participates in their care results in the best outcomes!

6/18/15

Sameh Mosaed, MD best time for cataract surgerySameh Mosaed, MD
Director of Glaucoma Services, Gavin Herbert Eye Institute, UC Irvine
Associate Professor, Cataract and Glaucoma Surgery, UC Irvine School of Medicine

Cataract Prevention

The more you know about cataracts, the easier it is to focus on cataract prevention.

What is a cataract?

At birth, with rare exceptions, most of us arrive in the world with a clear crystalline lens within each eye. The pathway of our visual images start with light passing through the cornea (the clear front window of the eye), through the pupil (the opening in the center of the iris, or colored portion of the eye) and through crystalline lens which functions to focus light onto the center of the retina (the film of the eye). cataract preventionThe retina, via the optic nerve, will then transmit visual images to the brain. When the crystalline lens becomes opacified (cloudy), this system becomes disrupted, and vision becomes impaired. Opacification of the crystalline lens is called “cataract”, and there are many variations in appearance and type and many causes and can present at any age. The word cataract originates from the Greek word “cataracta”, which means waterfall. The ancient Greeks used this term as they noticed a similarity in the appearance of the white opaque rushing water of a waterfall and the appearance of a white mature cataract.

To understand the different types of cataracts and causes, it is important to understand the anatomy of the lens. Using a metaphor, the lens anatomy can be compared to a Peanut M&M candy™. There is an outer candy coating (the lens capsule), a chocolate layer inside (the lens cortex), and a peanut in the center (the lens nucleus).

The most common cause of a cataract is an age related nuclear clouding which is due to long term accumulation of metabolic and oxidative waste products within the lens and possibly UV-B/Sunlight light exposure. Cortical clouding (within the cortex of the lens), due to similar causes, is also a common cause of an age related cataract.

Cataracts can occur earlier in life with poorly controlled diabetes resulting in cortical and nuclear cataract. Patients who are exposed to steroid medications in any form (orally, topically as eye drops, skin creams etc.) are at an increased risk to develop a posterior subcapsular (PSC) cataract which occurs on the posterior lens capsule. PSC cataracts can have a much more abrupt and earlier onset in life than nuclear or cortical cataract. Smoking has also been known to predispose patients to formation of a PSC cataract. Other less common varieties of cataract can occur with any trauma to the eye or even present at birth as a congenital cataract with a large variety of causes.

What can be done to prevent cataracts?

I often joke with patients that a cataract is such a common occurrence that just like birth, death, and taxes, it is an issue we must all face at some juncture in life (hopefully later than earlier). I am often asked if there are any dietary measures or vitamin supplementation to reduce the formation of a cataract, however this is not as well studied as the use of vitamins in the prevention of macular degeneration. Several scientific epidemiological studies following populations over many decades have shown some merit however that using multivitamins regularly (Vitamin B6 and B12, Vitamin C, beta carotene, antioxidants and possibly lutein and zeaxathin) can reduce the degree of lens opacification over time. As with all medications, you should consult with your physician before deciding to use any vitamin supplementation to clarify if you have any contraindication to using them.

There is conflicting evidence regarding the role of UV-B exposure in sunlight as a causative agent for cataracts. There is some support that using sunglasses on a regular basis to block UV-B light may help to reduce cortical cataract formation. Smoking cessation can also help to reduce the formation of cataract. If a patient is diabetic, strict blood sugar control is also an important measure to reduce the formation of a cataract. If possible, reducing or avoiding the use of steroid medication can reduce the formation of a PSC cataract.

What can be done if a cataract is worsenening and glasses cannot help improve vision significantly?

If you are experiencing gradual painless loss of vision, you should consult with your ophthalmologist as cataract can be a common cause. If you are found to have cataract formation, there is generally a shift in the glasses prescription in the early stage. Having your glasses prescription checked to see if your vision can be improved with glasses is the first step in determining how significant your cataract has become. If glasses are not able to sufficiently improve your vision and your daily activities are affected by the decrease in vision your experience, you may be a candidate to have cataract surgery.

Modern cataract surgery has improved a tremendous degree compared to decades earlier. It is the most common and successful surgery in the world, and is typically performed on an outpatient basis with topical anesthetic and often without any sutures or eye patch. Prior to surgery the pupil is dilated, and once in the operating room, a small self-sealing incision is made on the side of the cornea. The surgeon then makes a circular opening in the anterior lens capsule (the candy coating of the peanut M&M), and uses an ultrasound instrument to emulsify and vacuum out the nucleus (the central peanut), and remove the cortex (the chocolate layer). The inside of the lens capsule is polished and an intraocular lens is folded and introduced into the eye through the corneal incision and seated into the remaining lens capsule to conclude the surgery.

Prior to surgery, measurements are taken to determine the power of lens necessary to achieve the best vision after surgery based on the curvature of the cornea and anterior-posterior length of the eye. Intraocular lenses (IOLs) can potentially have several features depending on a patient’s needs. The most common IOL used is a monofocal lens, which does not typically require an additional out of pocket expense. This lens is chosen to have a point of focus either for distance vision (driving, TV) or near vision (reading), but not both. Typically patients who have the monofocal lens will choose to have distance focus and use reading glasses for near vision. There are multifocal/accommodating IOLs available for patients who are appropriate candidates, to allow the patient a larger range of vision at far, near and intermediate (computer) distance and may allow great independence from glasses. There are still other IOLs which can correct astigmatism (a special type of glasses prescription) at the time of cataract surgery. After discussion of the patient’s needs and preferences, the surgeon can best advise their patient regarding which type of IOL may best suit them.

6/11/15

Anand Bhatt, MD - cataract preventionAnand B. Bhatt, MD
Assistant Professor of Glaucoma and Cataract Surgery, Gavin Herbert Eye Institute
UC Irvine School of Medicine

Fuchs’ Dystrophy: Current Insights

What is Fuchs’ Dystrophy?

Corneal dystrophies are a debilitating group of progressive diseases that can ultimately deprive a person of sight. The cornea, which forms the front of the eye, is a window for vision, and dystrophies due to intrinsic defects in the corneal tissue cause this window to become opaque and hazy. Fuchs’ dystrophy, also known as Fuchs’ corneal endothelial dystrophy (FCED), is amongst the most commonly diagnosed corneal dystrophies requiring corneal transplantation. The ophthalmologist Ernest Fuchs first described the disease in 1910.

Who gets it?

The disease is rare, and it is difficult to predict who will get it. We know that it affects women more than men (3:1 ratio), older adults (older than 50 years of age), and those with a family history. There are forms in which there could be up to a 50% chance of transmission to children of parents with Fuchs’ dystrophy. Most cases, however, occur sporadically.

What causes it and how does it progress?

Although the cause of Fuchs’ dystrophy is still being studied, there are characteristic findings associated with it: small outgrowths on Descemet’s membrane called “guttae” or “guttata”, thickening of Descemet’s membrane, and defects in the endothelial cells (Figure 1).

fuchs dystrophy 1
Figure 1: Fuchs’ dystrophy can affect all layers of the cornea. Layers of the cornea from anterior to posterior, or frontside to backside, include (A) epithelial cells where blisters and bullae may form in late-stage disease, (B) Bowman’s layer where scarring can occur in late-stage disease, (C) stroma where corneal swelling occurs early in disease, (D) Descemet’s membrane where guttae form (arrows) and thickening occurs, and (E) endothelial cells that decrease in number and change shape and size with disease progression.

Descemet’s membrane is a thin corneal layer between the endothelial cell and the stromal layers of the cornea. Endothelial cells make up the backside of the cornea and function as a barrier and pump for keeping fluid out of the cornea and maintaining corneal clarity. As guttae accumulate on Descemet’s membrane, patients experience progressive loss and change in endothelial cells. Dysfunction of endothelial cells causes corneal swelling, which distorts vision. First, the back of the cornea swells, and eventually, swelling can reach the epithelial cells at the front of the cornea. Swelling can range from mild moisture accumulation, to painful “bullae”, or blisters. In very late-stage disease, significant corneal scar tissue can form and dramatically reduce vision. The progression to late stage Fuchs’ varies from person to person, but usually takes a couple of decades.

What are signs and symptoms?

A patient may be asymptomatic for years despite having guttae. Initial symptoms, including blurry, hazy, or cloudy vision, are typically due to corneal swelling from dysfunction of the endothelial cell layer. Patients may also experience glare or halos around light in the early stages just from the density of guttae. New studies suggest that patients can get glare and higher order aberrations from guttae without any corneal swelling. Symptoms tend to be worse on awakening, but usually improve throughout the day. This is because the closure of eyelids during sleep results in the accumulation of fluid in the cornea. For the same reason, humid weather can also worsen symptoms. As the disease progresses, poor vision may last longer into the day. There may be associated pain if blisters develop.

How is it diagnosed?

The presence of any of the above signs and symptoms, especially with a family history of Fuchs’, should prompt a consult with an ophthalmologist who will diagnose the disorder and follow its progression with regular checkups. An ophthalmologist will conduct a microscopic slit-lamp examination of the eyes, looking for guttae and Descemet’s membrane thickening (Figure 2).

fuchs dystrophy 2
Figure 2: Slit-lamp examination showing speckling pattern on the backside of the cornea characteristic of guttae in Fuchs’ dystrophy.

Special tests may be done to measure corneal thickness, a marker of swelling, or count endothelial cells to track disease progression (Figure 3 and 4).

fuchs dystrophy 3
Figure 3: Optical Coherence Tomography (OCT) showing (A) a normal, healthy cornea and (B) corneal swelling typical in Fuchs’ dystrophy.
fuchs dystrophy 4
Figure 4: In-vivo slit-lamp scanning confocal microscopy showing (A) normal endothelial cells and (B) guttae causing endothelial cell loss and change in Fuchs’ dystrophy.

How is it managed?

Management can be medical or surgical depending on symptoms. Patients may have mild or slow progression of disease that can be managed medically including over the counter salt solution drops (5% NaCl) to reduce corneal edema.

When there is late-stage disease, a corneal transplant may be necessary to improve vision. A corneal transplant replaces the patient’s corneal tissue with human donor corneal tissue. Donor corneas are readily available via excellent eye banks throughout the United States. The surgery is outpatient surgery with regular follow-up appointments and suture removal during the subsequent months. The postoperative healing of the cornea and vision stabilization can take up to a year.

Great strides have been made in the last decade in corneal transplantation surgery, giving patients better treatment options. Patients used to be limited to penetrating keratoplasty (PK), a full-thickness replacement of the cornea. We now have newer surgeries known as endothelial keratoplasty (EK), which is a partial-thickness transplant that replaces only the damaged part of the cornea (the endothelial layer). The different types of EK are DSEK (Descemet’s-Stripping Endothelial Keratoplasty) and DMEK (Descemet’s Membrane Endothelial Keratoplasty). The techniques vary by thickness of the transplanted tissue. The type of EK most appropriate is determined by the corneal surgeon and is variable on a case to case basis. Both types of EK surgeries provide comparable long-term visual results. In both surgeries, the patient’s diseased Descemet’s membrane and endothelial cells are stripped from the inner layer of their cornea. The thin lamellar donor graft is then inserted into the eye and positioned onto the back of the patient’s cornea via a gas or air bubble. The patient is then instructed to lie in a face up position for several hours post surgery during which time the bubble supports the graft until the new endothelial cell pumps begin to wake up and naturally adhere to the back side of the recipient cornea. Occasionally, the doctor may replace another air bubble into the eye the next day to allow more time for the graft to adhere. Visual recovery is on the order of 1-2 weeks in DMEK and 2-3 months in DSEK surgery. Rejection risk is still a possibility in EK surgery but has a much lower rate than traditional full thickness PK surgery.

Other surgical considerations depend on the presence of cataracts. Cataract surgery can worsen Fuchs’ dystrophy because of damage to the endothelial cell layer. For this reason, patients with cataracts and Fuchs’ requiring surgical intervention are often recommended to undergo cataract surgery before or at the same time as corneal transplantation to ensure the best outcome for the transplant.

Patients should work with an ophthalmologist to determine the best management plan. Ultimately, vast improvements in treatment options have given many Fuchs’ dystrophy patients the exciting opportunity to regain vision with improved healing times and reduced infection and rejection of the graft.

Citations: Figure 2 and 4 are from Zhang J, Patel DV. The pathophysiology of Fuchs’ endothelial dystrophy—a review of molecular and cellular insights. Exp Eye Res. 2015 Jan

6/4/15

priscilla-thumbnailPriscilla Q. Vu, MS
Medical Student
University of California, Irvine School of Medicine

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Farid 3.6.14Marjan Farid, MD
Director of Cornea, Cataract, and Refractive Surgery
Vice-Chair of Ophthalmic Faculty
Director of the Cornea Fellowship Program
Associate Professor of Ophthalmology
Gavin Herbert Eye Institute, University of California, Irvine

The Optic Nerve And Its Visual Link To The Brain

The optic nerve, a cable–like grouping of nerve fibers, connects and transmits visual information from the eye to the brain. The optic nerve is mainly composed of retinal ganglion cell (RGC) axons. In the human eye, the optic nerve receives light signals from about 125 million photoreceptor cells (known as rods and cones) via two intermediate neuron types, bipolar and amacrine cells. In the brain, the optic nerve transmits vision signals to the lateral geniculate nucleus (LGN), where visual information is relayed to the visual cortex of the brain that converts the image impulses into objects that we see.
Optic Nerve
In the retinal tissues of the eye, more than 23 types of RGCs vary significantly in terms of their morphology, connections, and responses to visual stimulation. Those visual transmitting RGCs are the neuronal cells. They all share the defining properties of:

  1. possessing a cell body (soma) at the inner surface of the retina
  2. having a long axon that extends into the brain via the optic chiasm and the optic tract
  3. synapsing with the LGN. The RGCs form multiple functional pathways within the optic nerve to mediate the visual signal

Human beings can see three primary colors: red, green, and blue. This is due to our having three different kinds of color sensitive cone cells: red cones, green cones, and blue cones.

The RGCs connecting to the red and green cones are midget RGCs. They are mainly located at the center of the retina (known as fovea). A single midget RGC communicates with as few as five photoreceptors. They transmit red-green color signals to the parvocellular layer in the LGN (see Figure). The midget-parvocellular pathway responds to color changes, but has little or no response to contrast change. This pathway has center-surround receptive fields, and slow conduction velocities. Because of this pathway, we can see objects precisely in detail and in full color.
retina and optic nerve
The bistratified RGCs are likely involved in blue color vision. Bistratified cells receive visual information input originally from an intermediate numbers of cones and rods. The bistratified RGCs connect to the koniocellular layers in the LGN (see Figure). The koniocellular neurons form robust layers throughout the visual hemifield and have moderate spatial resolution, moderate conduction velocities, and can respond to moderate-contrast stimuli. They have very large receptive fields that only possess on-center regions (no off-surround regions).

Objects can be seen in the dark with motion and coarse outlines accentuated due to the parasol RGCs. At the periphery of the retina, a single parasol RGC connects to many thousands of photoreceptors (many rods and few cones). The parasol RGCs project their axons to the magnocellular layers of the LGN (see Figure) and are primarily concerned with visual perception. They have fast conduction velocities, can respond to low-contrast stimuli, but are not very sensitive to changes in color.

Finally, humans can see objects in three-dimension courtesy of the crossing over of optic nerve fibers at the optic chiasm. This anatomic structure allows for the human visual cortex to receive the same hemispheric visual field from both eyes (see Figure), thus making it possible for the visual cortex to generate binocular and stereoscopic vision.

Recently, a new type of RGC, called photosensitive RGCs, was discovered. The photosensitive RGCs contribute minimally to our vision, but play a key role in vision regulation. Photosensitive RGCs axons do not have connections to the LGN, but form the retino-hypothalamic tract, and synapse to three other locations in the brain for specific vision regulation functions:

  1. Pretectal nucleus: involved in reflexive eye movements, thereby helping to target what we want to see
  2. Midbrain nuclei: involved in controlling the size of the pupil, thus helping to adjust the brightness of objects; and coordinating movement of the eye for focusing
  3. Suprachiasmatic nucleus: involved in regulating the sleep-wake cycle

A fully functional optic nerve is essential for vision. Obviously, any damage of the optic nerve will sever the precise transmission of visual information between the retina and brain, directly leading to vision distortion and/or vision loss. Damage to the optic nerve can result from:

  1. Direct/indirect physical damage (e.g. ocular trauma)
  2. Acute/sub-acute physiological lesion (e.g. infection or inflammation, or malignancy (cancer))
  3. Chronic neuronal degeneration (e.g. glaucoma, a most common cause of optic nerve damage)

Moreover, the optic nerve is also a very important vivo model for studying central nervous protection and regeneration. At the cell biology level, the RGC axons are covered with myelin produced by oligodendrocytes (rather than Schwann cells of the peripheral nervous system) after exiting the eye on their way to the LGN and thus part of the central nervous system. Scientists have recently acquired more and more evidence that certain types of damage to the optic nerve may be reversible in the future. Therefore, the optic nerve provides a potential window to explore more complicated neuronal degenerative diseases, such as Alzheimer’s disease and Huntington disease.

3/12/15

Jun Lin, MD, PhD
Assistant Professor,
Department of Ophthalmology
New York Eye and Ear Infirmary of Mount Sinai
Icahn School of Medicine at Mount Sinai

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James Tsai, MD, MBA
Chair, National Eye Health Education Program Glaucoma
Subcommittee President, New York Eye and Ear Infirmary of Mount Sinai Chair
Department of Ophthalmology
Icahn School of Medicine at Mount Sinai

Understanding and Treating Corneal Scratches and Abrasions

Corneal Scratches and Abrasions

Call it a scratch, an abrasion or erosion; no matter how you describe it or what the cause, damage to the cornea most always causes pain.

So what exactly is the cornea and why can even a small scratch hurt so much? The cornea is the clear dome at the very the front of the eye. Its primary job is to surface the tears and with them, focus light into the eye. It then passes through the crystalline lens and on to the retina where it is transformed into electrical impulses that are ultimately transformed by the brain into sight.

Because vision is so essential for survival and the cornea so critical to seeing, it is among the most richly innervated and exquisitely sensitive of all tissues. Even the smallest piece of dust that finds its way into the eye and touches the cornea can cause significant discomfort, irritation and copious tearing in an attempt to wash it away. A healthy cornea is transparent and consists of several layers that give the cornea its smooth dome like shape. The outermost layer, the epithelium, is designed to break away to protect the delicate deeper layers if scratched or abraded.
cornea layers - corneal scratches and abrasions

Looking For the Cause

The most common causes of corneal scratches are accidents. Tiny infant fingers and fingernails are a common cause of abrasions in young parents, tree branches are a frequent source of abrasions in hikers and lovers of the outdoors, and makeup brushes are a typical cause in women. Scratches can also be caused by foreign objects that get into the eye and then work their way on to the inside of the upper lid – causing a scratch that occurs with each blink. That’s why its important to carefully investigate the cause of every corneal scratch.

A scratch pr abrasion usually produces near instantaneous pain and tearing as the eye tries to wash away the irritant. Light sensitivity soon follows and can be so intense that the eye can involuntarily shut. This is actually nature’s way of “patching” the eye to facilitate healing.

To confirm you have a scratched cornea, a doctor or other health care professional will often apply a wetted fluorescein strip to the inside lid or white of the eye. Fluorescein is a dye that glows bright green when exposed to black light. The dye is absorbed by damaged areas, clearly showing the area if the scratch or abrasion.

Getting On the Mend

The good news is that most scratches will rapidly heal on their own, especially smaller and more superficial ones. The confocal microscope, a high tech device that provides extreme magnification views of living tissue, has been used to observe corneal healing in real time. The video captures are breathtaking as individual corneal cells can be seen literally stretching over each other to mend and seal the corneal surface.

If an abrasion is larger or deeper it may require patching to help healing. The traditional eye patch applied with tape to keep the eye shut has largely been replaced by the bandage contact lens which is far more comfortable and allows some vision and easier observation during follow up examination. It also allows medication to be applied if needed. Because there is a risk of infection whenever the outer boundaries of the body are breached, topical antibiotics are often used as a precaution in treating scratches of the cornea and ocular surface.

Most commonly the cornea heals quickly and completely, but not always. In rare cases damaged areas of the cornea may not heal fully, leaving the outer layers of the cornea susceptible to coming off again for no apparent reason. This is thought to be more common after scratches caused by organic material such as a tree branch. Called recurrent corneal erosions, they often occur during sleep waking the person with a sudden sharp pain and excessive tearing. There are a variety of treatments for recurrent corneal erosion.

Conclusion

Most people will sooner or later experience a scratched cornea. Most scratches will be minor and will resolve with minimal treatment. However, some can be serious and have significant consequences. The best way to avoid problems is to be aware that they can occur and take measures to protect the eyes in situations where the risk of eye trauma is higher. This includes: wearing safety glasses while working with power tools, or sports where eye contact is possible. This includes cycling and sport shooting.

Be aware of active infants with little fingers that seem to have a magnetic attraction of their parents eyes. If you use eye makeup, leave enough time to properly apply it without rushing and potentially scratching your cornea in the process.

Finally, if you experience a scratched cornea and the pain doesn’t rapidly abate, see an eyecare specialist. Urgent care centers are fine for most things, but when it comes to the eyes finding a knowledgeable eye care professional is wise.

2/10/15

AArthur B. Epstein, OD, FAAO
co-founder of Phoenix Eye Care
and the Dry Eye Center of Arizona
Fellow of the American Academy of Optometry
American Board of Certification in Medical Optometry
Chief Medical Editor of Optometric Physician™