Wed, 05/26/2021 - 8:53am

Unusual Eye Diseases

Watch our for this trio of acronyms

What is SARDS?

Sudden Acquired Retinal Degeneration Syndrome (SARDS) is a poorly understood condition that affects the function of the retinal tissue of the eye. The retina contains millions of light-sensitive cells (rods and cones) as well as other nerve cells that receive and organize visual information. The retina sends this information to the brain through the optic nerve, enabling the eye to see.

The symptoms of SARDS seem to develop overnight. Affected dogs will experience a sudden onset of blindness as well as dilation of the pupils. Along with the loss of vision, many dogs show other signs such as increased appetite, increased thirst and urination, and a rapid, recent weight gain. Owners report that their dogs are bumping into walls or furniture. The dogs may become anxious and begin barking or panting excessively. These symptoms are similar to hyperadrenocorticism, or Cushing’s disease, but many dogs with SARDS have normal adrenal function.

SARDS can be diagnosed in any breed, but Miniature Schnauzers, Beagles, Dachshunds and Pugs seem at higher risk. I diagnosed SARDS in a Bichon Frise last month. The average age of onset is seven to 10 years.

To confirm a diagnosis of SARDS, referral to a veterinary ophthalmologist for electroretinography is recommended. Electroretinography tests the electrical function of the retina. Dogs with SARDS will have no electrical response from the retina.

SARDS is caused by a widespread loss of function of the light receptors in the retina, but researchers have been unable to discover what causes this loss. Most feel it is an autoimmune disease. Unfortunately, there is no treatment at this time for SARDS.

Dogs affected with SARDS adapt to their blindness over a period of six to eight weeks. Avoid moving furniture in order to give your dog the opportunity to learn to navigate without vision. Outside, dogs should be walked on a leash or confined to a small fenced area to avoid injury. Once the dogs have had sufficient time to adjust to their loss of vision, more than 75 percent of owners report their dogs have an excellent quality of life.


What is NAD?

NAD stands for neuroaxonal dystrophy, which is a rare, inherited neurodegenerative disease. It has been seen in mammals all over the world, including dogs, humans, sheep, cattle, horses and cats. Dog breeds that are predisposed to NAD Include Papillons, Rottweilers, Collies, German Shepherds, Jack Russell Terriers, and Spanish Water Dogs.

The first symptoms appear in puppies at around three months of age. There can be loss of coordination, head tremors, inability to stand, as well as partial or complete paralysis of the legs. After six months of age, the dog may develop further neurologic symptoms, such as blindness, difficulty swallowing and shrinking of the brain.

NAD is a neurodegenerative disease, which means the nerves break down over a period of time. Each neuron, or nerve cell, has one long cable that snakes away from the main part of the cell. This cable is several times thinner than a hair. Called an axon, it is where electrical impulses from the neuron travel away to be received by other neurons. On autopsy, dogs affected with NAD show severely swollen axons, which prevents transmission of the neurons’ electrical impulses.

The disease is caused by a mutation in the gene that is involved in the correct metabolism of phospholipids, which are the main components in cell membranes. NAD is a recessively inherited disease. The disease develops in dogs that inherit the mutated gene from each parent. These dogs are designated as P/P (positive/positive). The carriers of the mutated gene are designated N/P (negative/positive). The carriers inherited the mutated gene from only one parent and do not show any clinical signs. However, they pass the possibility of the disease to their offspring.

When mating heterozygotes (N/P), there theoretically 25 percent of the offspring will be clear, 50 percent of the offspring will be carriers, and 25 percent of the offspring will inherit the mutated gene from both parents and develop the neurodegenerative disease NAD. Mating one healthy dog (N/N) with a carrier of this mutation (N/P) should produce 50 percent carriers and 50 percent healthy offspring. If a carrier (N/P) is mated with an affected dog (P/P), there will be, on average, 50 percent carriers and 50 percent affected dogs.

There is no cure for NAD in dogs. Some dogs respond to prednisone, which is a corticosteroid and acts as an anti-inflammatory. Some veterinarians may prescribe methocarbamol, a muscle relaxant, to help the muscles relax and stop spasms. Dogs with a slow progression of NAD can live comfortable lives with medical treatment. Puppies born with severe neuroaxonal dystrophy are usually humanely euthanized. All breeds with the potential for NAD should be tested before being used in a breeding program.


What is PPM?

PPM is the abbreviation for Persistent Pupillary Membrane. These are strands of tissue inside the eyeball. Pupillary membranes are blood vessels that supply nutrients to the developing lens of the eye before birth. Normally, they go away by four or five weeks of age. Persistent pupillary membranes are remnants of these vessels that fail to disappear as the dog grows.

You can see the PPMS as tiny strands inside the eye crossing the pupil. In many dogs, these tissue remnants cause no problems. Depending upon the location and extent of the strands, they may interfere with vision. When they bridge from iris to iris across the pupil or from the iris to the cornea, they cause white spots to develop on the cornea. Multiple membranes may form sheets of tissue with a spider web appearance in the forward chamber of the eye. There are also free-floating PPMs visible in the eye liquid in front of the pupil and iris.

Diagnosis of PPM usually requires the expertise of a veterinary ophthalmologist. Using drops to dilate the eye enables the veterinary specialist to examine the interior of the eye. PPMs are not a serious concern in puppies. Minor developmental delays can result in the pupillary membranes remaining in place longer than normal. A puppy with a PPM should be rechecked in six months to a year. If the PPM has resolved by one year of age, it is nothing to worry about.

The American College of Veterinary Ophthalmologists does not consider iris-to-iris PPMs to be significant, and they will pass a screening examination with a notation. However, the PPMs that attach to the lens or cornea can cause blind spots. These types of PPMs will not pass a CERF exam.

There is no treatment for the membranes themselves. If there is significant swelling, or bluish tint, to the cornea, eyedrops may help. Surgery may be required if there are extensive cataracts.

PPMS are found in many breeds of dogs. Studies to determine the mode of inheritance are so far inconclusive. However, it is recommended that dogs with PPMs that attach to the lens or cornea be removed from any breeding program. Dogs with less serious types of PPMS should not be linebred closely or to mates that have a recent history of PPM.




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