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Crazy Friday Science: New “Dua’s Layer” Discovered in Human Eyes, Ophthalmology Changed Forever

From May 28, 2013 onward, the study of the human eye will forever be changed.  A doctor named Harminder S. Dua, Professor of Ophthalmology and Visual Sciences at the University of Nottingham has discovered a new layer of cells that lies just above Descemet’s Layer of the cornea and the corneal stroma.  Like so:

duas-layer

“Now hold on there cowboy, what’s the cornea?!”

The cornea is the covering for the iris, pupil, and the anterior chamber  – basically the spot in front of the eye’s lens.  It’s one of the body’s most nerve-filled tissues, and it’s filled with fluid for light transmission.  Check this out, it’s an excellent visual description of the cornea, anterior and vitreous chambers — for reference, Dua’s Layer is right between the rear edge of the cornea (closest to the iris) and the middle of the cornea:

Three_Main_Layers_of_the_Eye

 

What Dr. Dua has discovered is a layer within the cornea that seems to have something to do with failures in the cornea where misshaping takes place.  These kinds of diseases are thought to be caused by water becoming waterlogged within the cornea itself, perhaps caused by a tear in this new Dua’s Layer.  They give the person afflicted a cone-shaped cornea that can be corrected with glasses, contacts, or in extreme cases, corneal surgery.  I’ve never seen anything quite like this before, so I’m guessing you haven’t either:

Keratoconus_eye

keratoconus-eye

from http://thesclerallenscenter.com/wp-content/uploads/2010/10/IMG_8964.jpg

Dua’s Layer is the new tissue discovery that is thought to cause things like this crazy degenerative keratoconus, which looks very annoying and painful to me.  Keratoconus causes pretty awful headaches and eye strain for people afflicted, which nobody wants.  But, this discovery is being heralded as a potential game changer for corneal diseases and degenerative conditions.  From Sci News:

“This is a major discovery that will mean that ophthalmology textbooks will literally need to be re-written. Having identified this new and distinct layer deep in the tissue of the cornea, we can now exploit its presence to make operations much safer and simpler for patients,” said Dr Harminder Dua, Professor of Ophthalmology and Visual Sciences at the University of Nottingham and lead author of a paper published in the journal Ophthalmology.

“From a clinical perspective, there are many diseases that affect the back of the cornea which clinicians across the world are already beginning to relate to the presence, absence or tear in this layer.”

The human cornea is the clear protective lens on the front of the eye through which light enters the eye. Scientists previously believed the cornea to be comprised of five layers, from front to back, the corneal epithelium, Bowman’s layer, the corneal stroma, Descemet’s membrane and the corneal endothelium.

…and from Science Daily:

The scientists proved the existence of the layer by simulating human corneal transplants and grafts on eyes donated for research purposes to eye banks located in Bristol and Manchester.

During this surgery, tiny bubbles of air were injected into the cornea to gently separate the different layers. The scientists then subjected the separated layers to electron microscopy, allowing them to study them at many thousand times their actual size.

Understanding the properties and location of the new Dua’s layer could help surgeons to better identify where in the cornea these bubbles are occurring and take appropriate measures during the operation. If they are able to inject a bubble next to the Dua’s layer, its strength means that it is less prone to tearing, meaning a better outcome for the patient.

The discovery will have an impact on advancing understanding of a number of diseases of the cornea, including acute hydrops, Descematocele and pre-Descemet’s dystrophies.

The scientists now believe that corneal hydrops, a bulging of the cornea caused by fluid build up that occurs in patients with keratoconus (conical deformity of the cornea), is caused by a tear in the Dua layer, through which water from inside the eye rushes in and causes waterlogging.

This is the first time I am ever researching Keratoconus — I have a good friend who has Retinitis Pigmentosa, another degenerative disease of the eye (in that case the retina), but the conical cornea is quite an odd phenomena.  Have you ever had or know anyone who has had this disease?  I found some information at WebMD on Keratoconus on diagnosis and treatment:

Keratoconus changes vision in two ways:

  • As the cornea changes from a ball shape to a cone shape, the smooth surface becomes slightly wavy. This is called irregular astigmatism.
  • As the front of the cornea expands, vision becomes more nearsighted. That is, only nearby objects can be seen clearly. Anything too far away will look like a blur.

An eye doctor may notice symptoms during an eye exam. You may also mention symptoms that could be caused by keratoconus. These include:

  • Sudden change of vision in just one eye
  • Double vision when looking with just one eye
  • Objects both near and far looking distorted
  • Bright lights looking like they have halos around them
  • Lights streaking
  • Seeing triple ghost images

To be sure you have keratoconus, your doctor needs to measure the curvature of the. cornea. There are several different ways this can be done.

One instrument, called a keratometer, shines a pattern of light onto the cornea. The shape of the reflection tells the doctor how the eye is curved. There are also computerized instruments that make three-dimensional “maps” of the cornea.

How Is Keratoconus Treated?
Treatment usually starts with new eyeglasses. If eyeglasses don’t provide adequate vision, then contact lenses may be recommended.  With mild cases, new eyeglasses can usually make vision clear again. Eventually, though, it will probably be necessary to use contact lenses or seek other treatments to strengthen the cornea and improve vision.

A last resort is a cornea transplant.  This involves removing the center of the cornea and replacing it with a donor cornea that is stitched into place.

Congratulations to Dr. Harminder Dua and his team at the University of Nottingham for this amazing discovery!
Keep up the excellent game-changing work, good sir!

dr-harminder-dua

Check out the abstract at the journal Ophthalmology.

keratoconus-normal

from http://www.centralohioeyecare.com/user-files/PageImage206991.jpg

Thanks to Wikipedia on Keratoconus, Dua’s Layer, Traffic Shaper!

Second Sight Medical Products Delivers a Kick to the Giftbag for Retinitis Pigmentosa

This is very exciting news for the realm of artificial vision.  I have someone I look up to that suffers from Retinitis Pigmentosa, and it sucks to see this degenerative disease affect this man’s sight.

But:  advances are being made in “bionic” tech all the time that tries to bridge the gap between natural vision and artificially enhanced vision – and since we don’t understand that much about how the brain translates sight into information for the brain, every time there is a breakthrough in technology in this arena, it’s a big deal!

First, what is Retinitis Pigmentosa?  It sounds like something that is not very good, and in fact it is not.  From Wikipedia and the NIH:

Fundus of patient with retinitis pigmentosa, mid stage (Bone spicule-shaped pigment deposits are present in the mid periphery along with retinal atrophy, while the macula is preserved although with a peripheral ring of depigmentation. Retinal vessels are attenuated.) Hamel Orphanet Journal of Rare Diseases 2006

Fundus of patient with retinitis pigmentosa, mid stage (Bone spicule-shaped pigment deposits are present in the mid periphery along with retinal atrophy, while the macula is preserved although with a peripheral ring of depigmentation. Retinal vessels are attenuated.) Hamel Orphanet Journal of Rare Diseases 2006

Retinitis pigmentosa (RP) is an inherited, degenerative eye disease that causes severe vision impairment and often blindness.[1] Sufferers will experience one or more of the following symptoms:

  • Night blindness or nyctalopia;
  • Tunnel vision (no peripheral vision);
  • Peripheral vision (no central vision);
  • Latticework vision;
  • Aversion to glare;
  • Slow adjustment from dark to light environments and vice versa;
  • Blurring of vision;
  • Poor color separation; and
  • Extreme tiredness.

The progress of RP is not consistent. Some people will exhibit symptoms from infancy, others may not notice symptoms until later in life.[2] Generally, the later the onset, the more rapid is the deterioration in sight. Also notice that people who do not have RP have 90 degree peripheral vision, while some people that have RP have less than 90 degree.

A form of retinal dystrophy, RP is caused by abnormalities of the photoreceptors (rods and cones) or the retinal pigment epithelium (RPE) of the retina leading to progressive sight loss. Affected individuals may experience defective light to dark, dark to light adaptation or nyctalopia (night blindness), as the result of the degeneration of the peripheral visual field (known as tunnel vision). Sometimes, central vision is lost first causing the person to look sidelong at objects.

The effect of RP is best illustrated by comparison to a television or computer screen. The pixels of light that form the image on the screen equate to the millions of light receptors on the retina of the eye. The fewer pixels on a screen, the less distinct will be the images it will display. Fewer than 10 percent of the light receptors in the eye receive the colored, high intensity light seen in bright light or daylight conditions. These receptors are located in the center of the circular retina. The remaining 90 percent of light receptors receive gray-scale, low intensity light used for low light and night vision and are located around the periphery of the retina. RP destroys light receptors from the outside inward, from the center outward, or in sporadic patches with a corresponding reduction in the efficiency of the eye to detect light. This degeneration is progressive and has no known cure as of June 2012.

That sucks so much.  However, now you have to meet Second Sight Medical Products’ Argus® II Retinal Prosthesis System, which just got FDA approval for patent this week:

All I can say about this is holy crap.

argus-2-system-overview

From the MedGadget article on the Argus II system:

The bionic eye works by replacing the disease-damaged photoreceptors of the eye with tiny chips that translate light into electrical signals, which in turn stimulate the optic nerve. The normal retina is really not a camera, and the optic nerve does not send pixels, per say, to the brain, but rather a highly processed and optimally encoded representation of the visual scene. The fact that bionic eyes like the Argus II can work at all – and indeed so well – is due more to the brain’s ability to make sense out of whatever relevant signals it receives, than to current understanding of how the retina actually works. As researchers advance their understanding of  the retina, bionic eye technology will continue to advance hand-in-hand to provide new vision to the blind at ever higher resolution.

This is amazing technology.  I hope that the Argus II system can restore vision in those who have lost it due to terrible degenerative diseases like RP.

To my buddy:  hang in there, big man.  I’m always on the lookout.

Side note:  under the Did You Know? section of the Argus II System website:

The Latin word “Argus” refers to a giant in Greek mythology with 100 eyes, Argus Panoptes, who was considered all-seeing. Argus was the servant of Hera, goddess of women and marriage as well as the wife of Zeus. Zeus seduced the nymph Io who was also the priestess of Hera.  In order to hide her from Zeus, Hera transformed her into a white heifer and asked Argus to watch over Io and protect her from Zeus.

Too cool, Second Sight.