My older German Shepherd Dog seems to be getting weak in its hindquarters

This article outlines a genetic disorder that mainly German Shepherd dogs are prone to. There are other breeds affected by this condition too like Chesapeake Bay Retrievers, Corgis, Boxers, Wirehaired Fox Terriers and Rhodesian Ridgebacks, however, the disease is mostly seen in German Shepherds.

If one breaks down the name of the disease it describes what happens with the disease. Degeneration refers to a breaking down or deterioration of something. That “something” in this case is myelin which is the insulating sheath around neurons in the spinal cord. Neurons are the “electrical wires” of the nervous system and one can compare myelin to the insulating plastic around the wires, almost like one would find with an electrical cord. Whenever a term is followed by “pathy” it refers to a disease or disorder in a certain part of the body. In this case the spinal cord.

Degenerative Myelopathy is a debilitating condition for which there is no cure but only the potential to slow down the progress.

The occurs typically in older German Shepherd Dogs. The average age at which clinical signs start and progress is from 8 to 12 years of age. This is not a condition with rapid onset but instead is slowly progressive with clinical signs worsening with time. Degenerative myelopathy starts out as a very slowly progressive hind limb weakness and loss of function of the back legs called paresis. It is commonly confused with hip pain because the symptoms can mimic hip dysplasia, another debilitating condition with a high incidence in German Shepherds.

The condition is the result of a demyelination (loss of protective cover) and nerve degeneration of the spinal cord in the region of the mid to hind back. This degeneration is something referred to as an ascending lesion meaning that it starts at the tail end of the spinal cord and works its way towards the head. The underlying cause of the disease is thought to be a genetic mutation (change) of the SOD1 gene. This gene is responsible for the protection of cells against certain particles that damage the DNA of cells. The name given to the damaging particles are free radicles. Under normal circumstances the SOD1 gene produces a free radicle scavenger i.e. it helps to clean up the system and prevents damage to the sheath surrounding the nerves.

The way in which the defect is inherited determines whether a particular dog is at a high risk of getting the disease or if they are a carrier of the genetic mutation without showing clinical signs. An individual dog has to carry 2 copies of the mutation in the genes of the cells of their bodies for it to cause the disease. There is no sex predilection, so male or female dogs may be affected equally. What is interesting about the disease is that even if an individual dog has both copies of the mutated gene and they are at very high risk of developing the disease, there are still other factors that influence whether or not they do contract the disease and to what extent they do.  

As mentioned previously this a slowly progressive condition that has a time frame of about 3 years before severe debilitating disease sets in. The clinical signs noticed in dogs include the following:

After 6 to 12 months of contracting the disease, you will notice weakness and partial loss of function of the back legs. Your dog may seem weak and wobbly on the back legs and they may struggle to get up or be slower to get up that what they used to be. When they run, their back legs may sway abnormally.

After 9 to 18 months on contracting the disease, the back legs start to get even weaker and collapse under the dog from time to time. If one assesses the reflexes in the back legs like the patella reflex, you will find that they are abnormal and weakened.

After 12 to 24 months of contracting the disease, the front legs start to become affected and you may notice that your dog starts losing their normal co-ordination and function. By this point, the hind legs are very weak and your dog may struggle to stand and use their legs correctly. Unfortunately, the nerve degeneration also influences bladder and bowel control and they will start to urinate and defecate involuntarily. This is known as urine and faecal incontinence.

After 24 to 36 month of contracting the disease, and if the dog was able to come this far and still cope with the disease, they develop tetraplegia or quadriplegia which is a paralysis that causes partial or total loss of use of all their limbs and body. The loss is usually sensory and motor, which means that both sensation and control are lost, or put a different way, the dog does not know where its legs are and even if they did, they do not have the ability to correct it. Clearly a very unhappy situation.

The way in which this condition is diagnosed by the vet is through a number of tests as well as the typical clinical signs and also the breed of your dog. These, together with the thorough history of the condition, should provide the veterinarian with some very important clues to what is going on with your dog. The important diseases or differential diagnoses to rule out are spinal disc disease (like a slipped disc) and conditions affecting the lower part of the spine where the hips meet the spine, like hip dysplasia or joint disease. The biggest difference with degenerative myelopathy and the other conditions is that degenerative myelopathy is painless because it is the loss of sensation and function which underlies this disease. Special tests such as MRI’s may be done to visualise the damage within the spinal cord and there is also a DNA test available to check if your dog has the genetic mutation discussed earlier.

Unfortunately, there is no specific treatment available. Certain supplements can be used in an attempt to slow down the condition, such as vitamin E and aminocaproic acid. The vitamin E is an essential vitamin which helps various systems in the body to protect it from these damaging free radicles. The aminocaproic acid is an agent used to prevent the breakdown of clots in the bloodstream. The reasoning behind using this is that it is believed that the spinal cord may be indirectly attacked by the body’s own immune system. Antibodies in the bloodstream attach to the foreign material within the bloodstream forming complexes and these stimulate a response from the immune system. These complexes are usually removed by the liver and spleen. Sometimes they can stick to the walls of blood vessels, damage the walls and stimulate the formation of blood clots. The breakdown of these clots are associated with inflammation and this may result in damage to the surrounding tissues, so-called collateral damage. If this happens in the sensitive tissues of the spinal cord, the damage is devastating because the nervous tissue is not able to regenerate and repair itself. The thinking behind using aminocaproic acid is to inhibit clot breakdown in these delicate tissues.

Lastly and most importantly, the most effective treatment for this condition and the only one proven to actually slow down the progress is the use of physiotherapy and hydrotherapy. Another key factor is, the sooner the dog is diagnosed and treatment started, the better the progress of the disease can be slowed, and the more time the vet can give you with your dog. Unfortunately, the sad truth is that eventually, the disease will lead to complete paralysis and eventually, in most cases, euthanasia.

Genetic disorders like degenerative myelopathy can only be prevented by not breeding with animals where there is a family history of the disease. Make sure if you buy a puppy, that you get references on a breeder before you buy.

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