Clinical presentation of myelopathy in dogs. Myelopathy in a dog is treated at home. Degenerative myelopathy in dogs Rehabilitation for dogs degenerative myelopathy

Degenerative myelopathy is a slowly progressive disease of the spinal cord and lower motor neurons with a predominant lesion of the thoracolumbar region. It has been known in German Shepherds for many years and various theories have been put forward about its etiology over the years. The recent discovery of genetic predisposition has changed the perception and understanding of this disease; the disease is associated with the appearance of a functional mutation in the superoxide dismutase gene. The mode of inheritance appears to be autosomal recessive, so affected dogs have two copies of the mutated gene. Superoxide dismutase gene mutations are present in a small percentage of people with amyotrophic lateral sclerosis (ALS).

Clinical signs

Degenerative myelopathy is now known to affect many dog breeds, but it is most common in German Shepherds, Pembroke Welsh Corgi, Chesapeake Retrievers, and Boxers. Bernese Mountain Dogs are also affected, but they develop a different mutation in the same gene. Affected dogs are usually elderly and typically present with signs of pelvic limb weakness and ataxia, which are often asymmetrical at first. Manifestations are initially localized in the T3-L3 segments of the spinal cord. Over time, the weakness progresses to paralysis, and the chest limbs are affected. If the patient's life is then supported, the symptoms progress to generalized damage to the lower motor neurons with loss of spinal reflexes and muscle atrophy and damage to the cranial nerves.

Diagnostics

Diagnosis is based on excluding compression or inflammatory disease using MRI or myelography and CSF analysis. Affected dogs test positive for a superoxide dismutase gene mutation test performed at OFFA. It is very important to understand that other diseases should be ruled out first, since the test demonstrates a genetic predisposition, but does not confirm the disease state. A complicating factor is that many older dogs have type 2 chronic disc disease and other comorbidities that can impair their gait, so a thorough and complete clinical and diagnostic evaluation should be done in combination with genetic testing.

Treatment

Currently, treatment is focused on providing a balanced diet rich in antioxidants and maintaining the mobility of the animal. Optimal rehabilitation programs are currently lacking, however, it is known that rehabilitation plays an important role in the treatment of people with ALS, however, too much physical activity can be harmful. New treatments will inevitably emerge, but prevention is better than cure, and judicious use of genetic testing in breeding decisions can help eliminate or at least reduce the incidence of this neurodegenerative disease.

Links:

Awano T, Johnson GS, Wade CM, Katz ML, Johnson GC, Taylor JF et al (2009) Genome Wide association analysis reveals a SOD1 mutation in canine degenerative myelopathy that resembles amyotrophic lateral sclerosis. Proceedings of the National Academy of Sciences of the United States of America 106, 2794R 2799.
Wininger FA, Zeng R, Johnson GS, Katz ML, Johnson GC, Bush WW, Jarboe JM, Coates JR. Degenerative myelopathy in a Bernese Mountain Dog with a novel SOD1 missense mutation. J Vet Intern Med. 2011 SepROct; 25 (5): 1166R70.
Coates JR, Wininger FA. Canine degenerative myelopathy. Vet Clin North Am Small Anim Pract. 2010 Sep; 40 (5): 929R50.

Degenerative myelopathy in dogs is a progressively progressive spinal cord pathology with lower motoneutrons, in which the thoracolumbar regions are primarily affected. The disease has been monitored in German shepherds for many years. Recent studies have shown that it is genetic predisposition that plays a major role in the development of the disease. The disease is associated with the manifestation of a functional mutation in the superoxide dismutase gene. An autosomal recessive mode of inheritance is suggested, in which affected dogs have two copies of the gene with signs of mutation.

Symptomatic picture

The disease manifests itself at about 8-14 years old. The first sign is a violation of the coordination of the pelvic limbs. The gait of the animal becomes wobbly, "drunk", the rear part falls in different directions when moving. Reduced control of the pelvic limbs and trunk leads to the fact that the dog is constantly touching objects. It drifts, often hits various obstacles and door edges. The dog makes support on the back of the fingers, dragging them and sometimes erasing the horny part to the bone with the formation of ulcers.

The degree of manifestation of signs may vary depending on the duration, localization of degenerative processes. As the disease progresses, the limbs weaken, making the dog difficult to stand. The weakness increases gradually until the animal loses the ability to walk.

The clinical picture can develop over 6-12 months, and sometimes longer, before complete paralysis develops. A significant manifestation is also a violation of the separation of urine, feces, since paralysis affects not only the musculoskeletal system, but also the urinary system and intestines. This is manifested by fecal and urinary incontinence.

Important! This disease is not accompanied by pain, unless there are other pathologies.

At the moment, it became known that degenerative myelopathy affects not only German shepherds, but also many other dog breeds: Pembroke Welsh Corgi, Boxers, Chesapeake Retrievers, and so on. In Bernese Mountain Dogs, the mutation in the superoxide dismutase gene manifests itself in a slightly different way. Not insured against the manifestation of the disease and mestizo. In general, the disease usually manifests itself in older dogs (over 8 years old) as follows:

The support ability of the hind limbs of the animal is impaired;
Inability to maintain one pose;
Lost muscle mass;
Decreases the skin sensitivity of the pelvic limbs;
Controlled urination and defecation are impaired;
Gradually, complete or partial paralysis develops, spreading to other parts, in particular - the chest.

Signs of degenerative myelopathy in dogs, despite their striking manifestations, can also be the result of other inflammatory processes in the body. Therefore, the diagnosis must be carried out at the first sign in order to exclude or confirm those diseases that are treatable.

How does degenerative myelopathy progress?

The disease begins almost always in the thoracic spinal cord. In the process of studying this pathology, destruction of the white matter in this section was noted. It contains those tissues that transmit movement commands to the limbs from the brain, and also provide sensory feedback from the limbs to the brain. As a result of the destruction of these fibers, the connection between the brain and the limbs is disrupted.

The picture of the development of pathology is as follows: the dog develops signs of weakness of the pelvic limbs, followed by ataxia (in which the coordination of movement of various muscle groups is disrupted). Moreover, at the very beginning, they can make themselves felt asymmetrically. The main manifestations concern the T3-L3 section of the spinal cord. Gradually, weakness progresses and paralysis develops, which spreads to the chest limbs. The dog can no longer control urination.

Provided that the life of the animal is maintained, the signs continue to progress until the lower motoneutrons are involved in degenerative processes, in which spinal reflexes are lost. Cranial nerve damage and muscle atrophy develop. The disease becomes generalized, that is, it has spread to significant areas of organ and tissue systems. Degenerative myelopathy, when spreading to the chest, destroys not only the myelin sheaths of nerve tissues, but also the nerve fiber itself.

Reasons for development

The reasons for this pathology have not been identified. Even despite the fact that there is a clear relationship between genetic predisposition and the development of the disease, it was not possible to prove and predict the development of the disease due to the presence of gene mutations. The disease can manifest itself even in those dogs that were bred from two completely healthy parents who were carriers of the SOD1 () gene.

The most susceptible breeds of this pathology are the German Shepherd, Collie, Pembroke, Boxer, Cardigan Welsh Corgi, Irish Setter, Chesapeake Bay Retriever, Poodle and Rhodesian Ridgeback. But this does not mean that this pathology cannot develop in other breeds. It has been proven that large breeds of dogs are most often among sick animals.

Important! No cure has been invented for this disease, and therefore there is no chance of recovery. The disease will progress anyway.

Diagnostics

Mainly differential diagnostics is carried out, in which inflammatory and compression diseases are excluded. It is performed using MRI or myelography (depending on the equipment of the veterinary center), as well as CSF analysis. Affected animals respond positively to a genetic test that detects a gene mutation. The test is carried out primarily at OFFA. In general, the following activities are carried out:

Laboratory tests for pathogens;
The functionality of the thyroid gland is checked;
MRI and CT scan to identify foci of spinal cord injury.

You need to understand that in this case, diagnosis is needed precisely to exclude other pathologies. The test will only reflect the genetic predisposition, but not the very disease state of the dog. The diagnostic process is also complicated by the fact that many elderly animals in parallel can have diseases of the intervertebral discs, other diseases that also have a gait disorder and other similar symptoms in symptoms. That is why the diagnosis must still be carried out in parallel with the genetic test. In general, the following pathologies can be identified, which, unlike degenerative myelopathy, are treatable:

Type II intervertebral disc disease;
Orthopedic diseases, expressed in the pathology of joints, muscles or the skeleton as a whole;
Pathology of bone development or dysplasia of the hip joint;
Tumors;
Cysts;
Trauma;
Spinal cord infections;
Lumbosacral stenosis accompanied by narrowing of the lower spine or pelvic bone.

Degenerative myelopathy, in contrast to these pathologies, is not treated, and the symptoms are practically not relieved. It is possible to fully diagnose an animal with 100% certainty only posthumously at autopsy. This is why illness is defined by the method of exclusion. What is help to a sick animal with such a pathology?

Myelopathy treatment

The current focus of treatment for degenerative myelopathy in dogs is to provide the animal with a balanced diet that is enriched with antioxidants. It is also necessary to maintain the mobility of the animal. Any rehabilitation programs that will give positive dynamics in the course of the disease have not yet been developed.

Genetic testing should be used as a preventive measure for the further spread of the disease to dog owners who are on the list of the greatest risk of developing the disease. It will show the animal's predisposition to pathology. Therefore, only after such an analysis can a decision be made on further dilution. This approach allows not only to eliminate, but to reduce the incidence of this degenerative disease.

What can be said about those animals that are already sick. In this case, only supportive therapy is offered. Exercises to delay limb and spinal cord atrophy can help. It is also important to monitor the weight of the animal, which, due to lack of movement, can gain excess weight and thus further aggravate its condition with additional load on the spine.

Important! It is worth noting that it is possible and necessary to maintain the mobility of the animal, but there are cases when, due to excessive load, the disease progressed even faster.

Pathology develops quite quickly - in just 6-9 months after diagnosis. Therefore, constant monitoring of the condition of the animal, frequent examinations by a neuropathologist, urine tests for an infectious disease are mandatory.

Gradually, the animal will lose the ability to move independently. Therefore, you need to provide the dog with a special pillow, the position of which must be constantly changed. This will prevent pressure ulcers from developing. It is worthwhile to separately consult with your veterinarian regarding the prevention of the development of a urinary tract infection.

It is recommended that long-haired dogs be shaved to reduce the likelihood of skin damage. The mobility of the dog can also be ensured with the help of a specially equipped trolley. A lying animal suffers not only from incontinence of feces, urine, but also from the limitation of the possibility of self-hygiene. You can apply the following methods and means to maintain the normal life of the animal:

The owners wash the dog quite often - literally twice a week. With proper hair and skin care, pressure sores can be prevented. It will also help get rid of unpleasant odors, prevent infection of the animal and skin. Frequent washing uses moisturizers for the animal's skin to prevent dryness.

If we talk about preventing disease, then the answer is unequivocal. There is no need to talk about preventive measures, since degenerative myelopathy cannot be prevented. Veterinarians recommend euthanasia for dogs that have developed paralysis. Thus, the animal will not suffer from pathological degenerative processes spreading through the body, which cannot be stopped.

Degenerative myelopathy is a progressive disease of the spinal cord in aging dogs. The disease develops gradually and becomes clinically significant between the ages of 8 and 14 years. The first sign of the onset of the development of the disease is the deterioration of coordination (ataxia) of the pelvic limbs. The gait of the dog becomes wobbly, the back of the dog falls from side to side. Reducing control over the pelvic torso and limbs leads to the fact that the dog can touch objects, it can skid, and can also hit the edges of doors and other obstacles. When supported, the dog can lean on the back of the fingers, drag them, sometimes erasing the claws to ulcers and bones. The degree of manifestation of certain signs is different and depends on the degree of duration and localization of the lesion. As the disease progresses, the limbs become weak and the dog begins to struggle to stand. The weakness gradually increases until the dog stops walking completely. Clinical development can vary from 6 months to 1 year, sometimes more than a year, before complete paralysis occurs. A significant symptom is also a violation of the separation of feces and urine, since destructive processes affect not only the work of the limbs, but also the work of the intestines and bladder. This can be manifested by urinary incontinence and even fecal incontinence. It is important to know that this disease is not accompanied by pain, if there are no concomitant painful other pathologies, that is, the dog does not experience pain.

What Happens With Degenerative Myelopathy?

Degenerative myelopathy usually begins in the thoracic spinal cord. Pathomorphological examination reveals the destruction of the white matter of the spinal cord. White matter contains those fibers that carry motor commands from the brain to the limbs and sensory information from the limbs to the brain.

The essence of tissue destruction is demyelination (destruction of the myelin sheaths of uneven fibers), as well as loss of axons (loss of the fiber itself). These processes lead to disruption of communication between the brain and limbs. Recent studies have identified a gene responsible for the onset of the disease, the presence of which significantly increases the risk of developing the disease.

How is degenerative myelopathy diagnosed?

Degenerative myelopathy is a diagnosis of exclusion. This means that it is required to exclude other diseases that could lead to a similar condition and, excluding them, we diagnose a degenerative process. For such a diagnosis, diagnostic tests such as myelography and MRI, CT are used. The only way to make a definitive diagnosis is by examining the spinal cord itself at autopsy, if performed. There are destructive changes in the spinal cord characteristic of degenerative myelopathy and not typical for other diseases of the spinal cord.

What diseases can manifest in the same way as degenerative myelopathy?

Any condition that affects the dog's spinal cord can cause symptoms such as loss of coordination and weakness in the limbs. Because many of these conditions can be effectively treated, it is important to do the necessary tests and research to make sure your dog does not have any of these conditions. The most common cause of pelvic limb weakness is herniated discs. With hernias of the first and second types, paresis or paralysis of the pelvic limbs can be observed. A herniated disc can usually be detected with spinal x-rays and myelography, or with more advanced imaging such as CT or MRI. Diseases such as tumors, cysts, infections, trauma, and stroke should be considered. Similar diagnostic procedures will help diagnose most of these diseases.

How is degenerative myelopathy treated?

Unfortunately, there is no effective treatment for this pathology that would clearly show the ability to stop or slow down the progression of degenerative myelopathy. The discovery of a gene that determines the risk of developing degenerative myelopathy in dogs may open the way for future solutions to the problem. Meanwhile, the affected dog's quality of life can be improved through measures such as good grooming, physical rehabilitation, pressure sore prevention, urinary infection monitoring, and ways to increase mobility through the use of trolleys whenever possible.

Canine degenerative myelopathy (DM)- Degenerative Myelopathy (DM) - a severe progressive neurodegenerative disease that leads to paralysis of the lower limbs.

The disease is caused by impaired conduction of spinal cord motor neurons due to degeneration of nerve endings.

Canine DM was first described over 35 years ago as a spontaneously occurring disease of the spinal cord in adults. It was believed to be specific only to the German Shepherd breed, which is why it was also called German Shepherd myelopathy. On July 15, 2008, the mutated gene responsible for DM was found in 43 breeds, including the Rhodesian Ridgeback.

The first signs of the disease appear already in adult dogs, in the majority at the age of 7-14 years. In the initial stages, the animal experiences a loss of coordination, then ataxia of the lower extremities develops. The duration of the disease in most cases does not exceed three years. In the last stages of myelopathy, the dog has practically no hind limb reflexes, paralysis sets in. Then the lesion spreads to the forelimbs. In this case, signs of damage to the upper motor neurons appear, which leads to ascending paresis of all limbs and general muscular atrophy. Complete paralysis of the dog's limbs sets in.

Degenerative myelopathy is characterized by an autosomal recessive inheritance pattern.

Due to the fact that many diseases of the spinal cord can have similar clinical signs, without DNA testing, the final diagnosis of degenerative myelopathy can only be made posthumously after a histological examination.

The main reason for the development of DM is a mutation in the superoxide dismutase 1 (SOD1) gene, leading to a change in the protein sequence (amino acid substitution E40K).

Carriers of DM (having 1 copy of the mutation) will not show symptoms; however, it should be borne in mind that such a dog will pass on the “diseased” gene to its offspring, so only a clean partner should be selected.

A special danger lies in the fact that when two carriers of Degenerative myelopathy are mated, there is a very high probability of giving birth to puppies affected by myelopathy (M / M), up to 25% of the offspring will be sick, and 80% of them manifest this disease clinically.

There is no cure for DM. Since this serious disease only occurs in adult dogs, a preliminary diagnosis can only be made through genetic testing.

Diagnostics

For the diagnosis of DM, a genetic test has been developed that can be performed at any age. A DNA test will reduce the frequency of sick dogs being born. The test is recommended for dogs of all breeds.

A DNA test detects a defective (mutant) copy of a gene and a normal copy of a gene. Test result is definition genotype, according to which animals can be divided into three groups: healthy (clear, homozygotes for a normal copy of the gene, NN), carriers (carrier, heterozygotes, NM) and patients (affected, mutation homozygotes, MM).

DNA test for Degenerative myelopathy can be passed

in Moscow, the test can be taken in the Laboratory "Chance-bio", in St. Petersburg in the Zoogen Laboratory. Take blood or buccal epithelium (from the cheek). Results are ready in 45 days.

D.V.N. Kozlov, N.A., Zakharova, A., A.

Introduction

Degenerative myelopathy (DM) is a slowly progressive, incurable degenerative disease of the central nervous system of medium to large breed adult dogs in which both upper and lower motor neurons are affected, resulting in paralysis with subsequent muscle atrophy. Averill first described DM in dogs in 1973. In 1975, Griffiths and Duncan published a series of clinical cases with signs of hyporephrexia involving nerve roots and called the disease degenerative radiculomyelopathy. Although most of the dogs in those early studies were German Shepherds, other breeds were also introduced. However, for many years DM was considered a disease of German Shepherds. Some breeds have histologically confirmed DM: German Shepherd, Siberian Husky, Small and Large Poodle, Boxer, Pembroke and Cardigan Welsh Corgi, Chepasik Bay Retriever, Bernese Mountain Dog, Kerry Blue Terrier, Golden Retriever, American Eskimo Dog, Irish Wheat Terrier ...

Research results and their discussion

The clinical picture of DM typically consists of slowly progressive, non-painful Th3 – L3 myelopathy in older large dog breeds. Degenerative myelopathy manifests at five or more years of age, but the average age for onset of neurological symptoms is considered to be nine years for large breeds of dogs and 11 years for Welsh Corgi. At the initial stages of the development of the disease, degenerative proprioceptive ataxia and asymmetric spastic paraparesis are noted, with spinal reflexes preserved. Tremors of the pelvic limbs may occur while maintaining weight. The initial clinical signs of spinal cord dysfunction are often mistaken for hip dysplasia, which may also be present in a patient with this spinal cord disorder. In 10% -20% of affected dogs, the knee reflex on one or both limbs is reduced or absent. In the presence of normal or increased tone of the pelvic limbs and the absence of atrophy of the quadriceps femoris muscle, this loss of the knee reflex reflects dysfunction of the sensory components of the reflex arc. What this has to do with axonopathy in DM is unknown, it may be part of a pathological process and reflects lesions in the L4-L5 segments of the spinal cord or age-related neuropathy not associated with DM. Subsequently, paraplegia develops, a moderate loss of muscle mass and a decrease or absence of spinal reflexes in the pelvic limbs. The disease usually progresses over 6-12 months (longer in small dogs than in large dogs) and many owners choose euthanasia due to the patient's inability to walk on their own. As the disease progresses, the thoracic limbs (paraplegia, paraparesis) are involved in the pathological process, severe loss of muscle mass on the pelvic limbs, the dog loses the ability to retain urine and feces. In the later stages of the development of the disease, tetraplegia and signs of damage to the brain stem are observed. Difficulty swallowing, moving the tongue, lack of ability to bark; decrease or absence of skin reflexes; severe loss of muscle mass; urinary and fecal incontinence.

The etiology of degenerative myelopathy has been studied by many scientists. Immunological, metabolic or alimentary, oxidative stress, excitotoxicity (a pathological process leading to the death of nerve cells under the action of neurotransmitters capable of hyperactivating NMDA and AMPA receptors) and the genetic mechanism have been investigated as the pathogenesis of degenerative myelopathy. Several scientific papers have been linked to impaired immune systems in affected dogs, but these have been found to be unsubstantiated. It is not an inflammatory disease of the spinal cord. Attempts to isolate the retrovirus in the lesions were unsuccessful. Treatment of dogs with DM glucocorticosteroids, vitamins E and B 12 (often used for their role in the treatment of other degenerative neurological disorders), and aminocaproic acid have not been shown to delay disease progression. Many other therapies have been used, but none of the procedures have made any noticeable difference in the development of this disease. The long-term prognosis is not favorable and many owners decide to euthanize.

The uniformity of clinical signs, histopathologies, age and breed predisposition of dogs suggests a hereditary nature of the disease. Recently, DM has been associated with mutations in the superoxide dismurtase 1 (SOD1) gene. A mutation in the SOD1 gene is known to cause amyotrophic lateral sclerosis (ALS) in humans, which is also known as Lou Gehrig's disease. The Greek word for amyotrophy means muscle without nutrition. Lateral location in the spinal cord of axonal disease and sclerosis means damage to axons and their replacement by sclerotic or "scar" tissue. Dog DM is considered a spontaneous model of ALS in humans. A DNA test based on the SOD1 mutation is currently available for dogs. Canine degenerative myelopathy is thought to be inherited in an autosomal recessive manner. Dogs homozygous for the mutation are at risk of developing DM and will donate one chromosome with the mutant allele to all of their offspring. Some dogs are recessive homozygous on DNA tests and have two mutant alleles, but are free of clinical signs, indicating age-related incomplete penetrance. Heterozygotes are considered only carriers of DM and are capable of passing on a mutation in the SOD1 gene to half of their puppies. However, studies conducted by Zeng R. et al. On 126 dogs with histologically confirmed DM identified 118 recessive mutation homozygotes and 8 heterozygotes among them.

Conclusion

The lifetime diagnosis of DM is based on the recognition of the progression of clinical signs, followed by a system of diagnostic measures aimed at excluding other diseases of the spinal cord. Intervertebral extrusion or disc protrusion is by far the most significant clinical disorder to be distinguished from DM. It should be remembered that older dogs may simultaneously suffer from degenerative myelopathy as well as one (or more) mild disc herniation. Neoplasia is also a diagnosis that needs to be differentiated by MRI from DM. Cerebrospinal fluid analysis can help rule out meningitis. The definitive diagnosis of DM is based on the characteristic histopathological abnormalities in the spinal cord at autopsy.

Literature

Handbook of Veterinary Neurology, 5th Edition by Michael D. Lorenz, BS, DVM, DACVIM, Joan Coates, BS, DVM, MS, DACVIM and Marc Kent, DVM, BA, DACVIM, 2011.
Practical Guide to Canine and Feline Neurology, 3rd edition, by Curtis W. Dewey and Ronaldo C. da Costa, 2015.
Veterinary Neuroanatomy and Clinical Neurology, 3rd Edition
By Alexander de Lahunta, Eric N. Glass, MS, DVM, DACVIM (Neurology) and Marc Kent, DVM, BA, DACVIM, 2009.
Accumulation and aggregate formation of mutant superoxide dismutase 1 in canine degenerativemyelopathy. Nakamae S., Kobatake Y.,Suzuki R, Tsukui T, Kato S, Yamato O, Sakai H, Urushitani M, Maeda S, Kamishina H. 2015
Breed distribution of SOD1 alleles previously associated with canine degenerative myelopathy. Zeng R, Coates JR, Johnson GC, Hansen L, Awano T, Kolicheski A, Ivansson E, Perloski M, Lindblad-Toh K, O'Brien DP, Guo J, Katz ML, Johnson GS. 2014. Journal of Veterinary Internal Medicine published by Wiley Periodicals.

Degenerative myelopathy in dogs, also known as chronic degenerative radiculomyelopathy and herpetic myelopathy in the German shepherd, is an inherited disorder that causes fibers in the brain, spinal cord, and nerves to break down over time. It usually appears in dogs as young as seven years of age and is more common in some breeds. Canine degenerative myelopathy usually results in weakness and loss of coordination at first, and as the disease progresses, it causes complete paralysis and usually death. The condition is not curable and treatment focuses on keeping the dogs comfortable for as long as possible. If you see signs of degenerative myelopathy in your dog, check with your veterinarian so they can advise you of your options and provide any possible assistance. Here's what you should know about the symptoms, causes, and treatment of degenerative myelopathy in dogs.

Symptoms of degenerative myelopathy in dogs

Symptoms of degenerative myelopathy in dogs usually appear after age seven, but may appear as early as age five. They gradually deteriorate over time, and it can take years before the front and back legs are completely paralyzed. Fortunately, most dogs do not suffer from the pain associated with the condition, although their quality of life can be severely affected and the condition is usually fatal. However, the time it takes for the disease to progress can vary greatly. Some dogs are completely paralyzed for several months, while others survive with the condition for three or more years. Here are the common symptoms of degenerative myelopathy in dogs.

Dragging the hind legs or rolling the joints
Sores or frayed toenails on the hind feet
Stickiness or lameness in the hind legs that gradually move towards the front legs
Difficulty walking, jumping or moving
Loss of balance and coordination
Amyotrophy
Increased paralysis of the hind legs (usually general paralysis occurs within 6-12 months after the initial symptoms)
incontinence
Bedsores
Weight gain
Retention of urine
Urinary tract infection
Skin lesions from urine burns
Increased paralysis of the forelegs (usually generalized paralysis for several years after the initial symptoms)
Difficulty chewing and swallowing
Labored breathing

Causes of degenerative myelopathy in dogs

Degenerative myelopathy in dogs is caused by a genetic mutation, especially in the superoxide dismutase 1 (SOD1) gene, which is the same gene that is associated with Lou Gehrig's disease in humans. This mutation is almost certainly passed on to puppies as a recessive trait, as it is more common in some purebred dogs.

Degenerative myelopathy is most common in German Shepherds, Boxers, and Pembroke Welsh Corgis. Several other breeds are capable of inheriting the disease, including the Cardigan Welsh Cordis, Collie, Retriever, Rhodesian Ridgebacks, Siberian Huskies, Weimaraners, and Volkodar guides.

Treatment of degenerative myelopathy in dogs

(Picture Credit: Jeff Greenberg / UIG via Getty Images)

Treatment for degenerative myelopathy in dogs focuses on providing support and comfort for affected animals to maintain quality of life as there is no way to cure the condition or stop its progression. Certain exercise and physical therapy can reduce muscle damage and help maintain some mobility for as long as possible. If your dog is diagnosed with degenerative myelopathy, your veterinarian can instruct you on the right sites and actions that can help your dog maintain muscle strength and the ability to balance and walk for some time. Aquatic exercise and hydrotherapy can also be helpful.

Dogs can move for a longer time using a wheelchair, but as the condition progresses, they become more bedridden. It is important to provide dogs with soft, clean bedding that must be changed frequently to prevent sores from developing. Dogs may need to go on a diet to prevent weight gain.

New therapies and treatments are still being investigated, although none have yet been shown to reduce the effects of degenerative myelopathy in dogs. Your veterinarian will be able to give you the best advice for continuing treatment and care for your individual dog's needs.

The clinical picture.
Based on clinical symptoms, 6 neurological syndromes (stages) are distinguished, corresponding to the degrees of myelopathy (compression of the spinal cord and, as a result, impaired conduction function):
1. Pain syndrome: the animal cannot jump onto towering objects, is inactive, lethargic, restrained. One of the main signs of a hernia in the thoracolumbar region is hyperesthesia, hypertonicity of the muscles of the back and abdominal wall, hunched back (forced kyphosis). And in the cervical spine - an unusual forced position of the neck (head in a semi-lowered position) and sharp pains with squealing;
2. Decreased proprioceptive sensitivity, ataxia, dysmetria, paresis, but the animal can stand up and move independently. May present with or without soreness;
3. Paresis is pronounced, the animal cannot stand up and move on its own, however, the sensitivity is completely preserved;
4. Paralysis - voluntary movements are absent, superficial pain reactions are reduced or absent, a conscious reaction to deep pain is preserved. Possible "seal" setting of the limbs;
5. Severe paralysis (plegia) - superficial and deep pain reactions are absent. "Seal" setting of the limbs;
6. After the dog reaches the 5th degree of neurological disorders, the process of myelomalacia begins to progress.
If animals have a 4-5 degree of neurological deficit, an urgent examination and subsequent (according to the results of the examination) surgical intervention is necessary, because the time passes for minutes, and the faster we decompress the SM (surgical decompression), the more chances for the restoration of the neurological status.
Myelomalacia (necrosis of the compressed area of the CM) is quite rare (2-5% of cases) and is irreversible. Myelomalacia is local and generalized. Local myelomalacia can become generalized. Local myelomalacia occurs with significant compression, bruising, axonal rupture of the CM site by hernia elements (detritus). Local myelomalacia can turn into generalized, when all compensatory mechanisms are exhausted, the pressure on the SM and membranes increases with the development of the inflammatory process, the vascularization of the SM in a long section is reduced to zero. In the overwhelming majority of cases (up to 90%), myelomalacia occurs in sequestered hernias with a large volume of sequestration that migrated (spread) along the CM canal to 3 or more vertebrae (vertebral segments). The larger the contact area of the CM surface with sequestration elements (blood with detritus), the more voluminous the inflammatory process will be. This process occurs in cascade, as in any closed system. In order to remove the cascade of reactions leading to an even stronger compression of the CM due to inflammation (edema), we prescribe steroid anti-inflammatory drugs in high dosages (metipred, dexamethasone, prednisolone, etc.). Generalized myelomalacia is characterized by the following clinical syndromes: sudden onset of progressive paresis, turning into paralysis (from 30 minutes to 3-4 days). The animal's condition is rapidly deteriorating, paraplegia turns into tetraplegia and ends with the death of the animal, caused by ascending necrosis of the spinal cord and brain.
Note: generalized local myelomalacia can be easily provoked by iatrogenic factors:
myelography (injection of a contrast agent into the subarachnoid space of the CM) with already begun local myelomalacia,
non-observance of the rules of asepsis and antiseptics during punctures of the subarachnoid space or surgical interventions on the spine;
inept puncture and unacceptable use of conventional injection needles instead of spinal needles. This leads to the ingress (especially with lumbar punctures) of elements of the skin, muscle tissue, bone tissue, yellow ligament in the parenchyma of the CM and the subarachnoid space;
surgical intervention with significant trauma to the venous sinuses and vessels of the SM roots (especially in several adjacent vertebral segments), as well as incomplete decompression of the SM, when part of the hernia (sequestration) or the whole hernia is not removed.

Photo No. 9a. Intraoperative photo of the thoracolumbar spine of a Dachshund dog. Anamnesis of the disease (anamnesis morbi): the age of the animal is 4 years old, a sudden onset of paraparesis with a grade 3 deficit within a day has passed to grade 4. Conservative treatment (hormones, vit. Group B) did not lead to any improvement. On the 4th day, this animal was admitted to us for examination. According to the owners, yesterday evening the dog had a deep pain sensitivity. However, in the morning, the dog's condition began to deteriorate: deep pain sensitivity disappeared, severe pains and inappropriate behavior of the dog appeared (according to the owners - the dog throws its head up). After a neurological examination, the diagnosis was made: neurological deficit of 5-6 degrees, decreased reflexes of the cranial nerves, complete areflexia of the muscles of the lumbar region and abdominal wall, progressive ascending generalized myelomalacia. The owners were warned of an unfavorable prognosis, but insisted on examination and surgery. Based on the results of CT examination, the diagnosis was made: sequestered prolapse of the L3-L4 disc (Hansen 1), bilateral hernia with predominant localization on the right (at 14 and 20 hours), fresh, encircling, with stenosis of the CM channel of about 1/2 and migration of sequestration up to 1 / 2 bodies L6 caudally and up to 1/2 body L2 cranially (by 5 vertebrae). Hemilaminectomy on the right was performed to visualize the CM. After opening the dura mater (dura mater), the diagnosis was confirmed - generalized ascending myelomalacia.

Photo number 9b... It's an animal. The photo shows the place where the dura mater was opened with tweezers. At the site of the defect, we visualize a structureless mass of necrotic SM, which has gone beyond the dura mater at the L1-L2 level, i.e. much more cranial (above) the herniation site (L3-L4).

Photo number 9c. Sagittal tomogram (soft tissue window) of the lumbosacral spine of a 9-year-old West Highland White Terrier dog. On the tomogram, we see a generalized increase in the densitometric parameters of the spinal cord (up to 150 HV, with a norm of 34 ± 10), the absence of epidural spaces (fat). The dog underwent myelography the day before the CT scan. Diffuse spread of contrast (omnipak 350) in the lumen of the CM channel indicates complete destruction of the spinal cord and membranes. Conclusion: ascending generalized myelomalacia.

Photo No. 9g. Axial tomogram of the same animal (soft tissue window). Density CM 147 HV.

Pathogenesis of the onset of neurological deficiency syndrome (myelopathy).

Disc prolapse is accompanied by the release of a certain amount of detritus into the CM channel in a short period of time. It can be sequestered (prolapse with sequestration) and non-sequestered (prolapse). It depends on the volume and consistency of detritus and on the location of the rupture of the annulus fibrosus relative to the mid-sagittal plane of the disc. If the rupture of the annulus fibrosus occurs paramedially or laterally, then the venous sinus is injured and detritus, mixing with venous blood, spreads cranially and caudadally along the epidural space, filling and infiltrating the epidural fat and foraminal spaces. In the cervical region, due to anatomical features (IVDs rise above the venous sinuses. See photo No. 8a) disc prolapses in 95% - 100% have a compact mushroom shape (non-sequestered), and in the thoracolumbar region, prolapses are observed in about 70 - 80% of cases with sequestration (See photo # 8b). In some cases, the sequestration elements are squeezed out extraforaminally (outside the CM canal) (see photo No. 5 f).

From this moment, a cascade of pathological processes begins, which constitute the pathogenesis of myelopathy:
1.prolapse of the disc (loss of detritus in the CM channel);
2. compression (contusion, contusion) of CM with membranes;
3. violation of liquorodynamics, hematodynamics and, as a consequence, trophism and metabolic processes in the compressed section of the CM;
4.inflammatory edema of the CM site, which is compressed and in contact with the hernia elements.

That is, we observe a symptom complex (syndrome) of aseptic inflammation occurring in a closed system (limited by the walls of the CM channel). The cascade of pathological processes in a closed system plays a primary role in the pathogenesis of disturbances in the conductive functions of the SM parenchyma. The degree and intensity of neurological manifestations (see above) corresponds to the degree and intensity of compression (edema) of the CM site and depends on:
1. The volume of material prolapsed (dropped out) into the CM channel (the larger the volume, the stronger the compression);
2. Areas of contact of sequestration elements with dura mater. This is typical for hernias around hernias and sequestered hernias. That is, the larger the surface area of the dura mater is in contact with the sequestration elements, the more intense and voluminous the inflammatory process, which occurs, as a rule, on 2-3 or more CM segments;
3. Compliance (compliance) of the CM parenchyma. Compliance is a set of compensation mechanisms. Compliance is determined by the property of compliance, that is, the ability to adapt to an increase in the volume of the craniospinal system. Compliance is a property of a material (system) characterized by the ratio of elastic displacement to the applied load. An absolutely rigid (non-deformable) body would have zero compliance. Compliance is the reciprocal of the system stiffness.
The first response to the appearance and spread of additional volume (hernia) is to use the reserve of elasticity of the medulla and free spaces within the CM channel. Compliance of the spinal system is provided mainly by the volume of the subarachnoid and epidural spaces, the size of the foraminal openings. It is the displacement of the CM within the CM channel and the filling of the free spaces of the CM channel with sequestrum (hernia) that makes it possible to free up additional spaces for the "swollen" spinal cord, restraining the development of microcirculatory disorders. As these compensatory mechanisms are exhausted, the perfusion pressure of the blood begins to decrease, which is facilitated by an increase in CM edema. Hypoperfusion provokes the formation of new areas of ischemic tissue. In these areas, the extraction of О2 increases, reaching 100%. Due to the involvement of additional sections of the CM parenchyma in the inflammatory process, the volume of ischemic and edematous tissues increases. And this leads to a cascade of pathogenetic mechanisms (edema - ischemia + involvement of additional tissues - edema - ischemia + ..... etc.). This is the cascade of pathogenetic processes in closed systems.

In my opinion, compliance can be divided into two of its constituent elements:
spatial compliance (described above);
parenchymal compliance.
Parenchymal compliance is an individual genetically determined ability of the SM parenchyma (neurons with processes, glia and blood capillaries) to elasticity (elasticity) or the ability to restore its functions after exposure to external or internal pressure. That is, in one animal with disc prolapse (under equal circumstances), after surgical decompression, the functions will be restored, while in the other, a neurological deficit will remain. Let me give you a simple example. With the help of a dynamometer, we measure the force of impact on an area of the skin of one animal and another. The force of the blow is the same. The first animal has a slight edema, while the other has edema + hematoma. Under equal circumstances, we can confidently say that the compliance of the subcutaneous tissue in the first animal is higher than in the second;
4. Spatial localization of the gypsum in the sectors of the spinal canal and parts of the spine (in the cervical and lumbar spine, the CM canal is wider). Quite often, during CT examination, we meet animals with pronounced hyperostosis of the elements of the spinal canal (arches, vertebral legs). This leads to a decrease in spatial compliance due to stenosis of the CM canal and foraminal spaces and holes. This pathology is inherent mainly in brachycephalic breeds of dogs (French bulldogs, pugs, Pekingese), as well as dachshunds with a rough constitution (deep chest, powerful bones);
5. The rate at which prolapse of the nucleus pulposus occurs. The faster this happens, the more intense the inflammatory process;
6. Immunoreactivity of the organism. If hyperergic inflammation occurs in a more reactive organism, the degree of the inflammatory response will be greater. At risk are animals with auto-allergies and sensitized exoallergens.

Diagnostics and treatment. Algorithm of actions in the event of a neurological syndrome caused by IVD hernia.

So, the dog developed a grade 1-3 neurological syndrome (see Clinical Presentation). After a neurological examination, steroid hormones (metipred, dexamethasone, hydrocortisone), group B vitamins and symptomatic treatment (H2-blockers of histamine receptors, laxatives, etc.) in therapeutic doses are prescribed. In case of an increase (progress) of neurological deficit within 12-24 hours, CT, MRI examination is recommended. Further, the sequence of actions depends on the dynamics of the increase or decrease in the degree of neurological deficit during treatment with anti-inflammatory drugs:

1-2 degree of neurological deficit (the animal can move independently):
in case of an increase in neurological deficit up to 3-4-5 degrees within 12-24 hours during therapy, an examination (CT, MRI) is recommended, followed by surgical intervention;
in case of improvement of the neurological state within 12-24 hours against the background of anti-inflammatory therapy, we continue to observe the animal for 5-7 days. Then we cancel anti-inflammatory therapy and conduct a neurological examination in 24-48 hours. If pain syndrome and neurological deficit reappear, we perform CT or MRI examination. Further, based on the classification of hernias, it can be concluded that medical or surgical treatment is necessary. It is especially necessary to pay attention to points 6,7,8 of the classification of IVD hernias.

3 degree of neurological deficit (the animal cannot move independently, however, superficial and deep pain sensitivity is preserved):
in the case of an increase in neurological deficit up to 4-5 degrees within 12-24 hours against the background of therapy or maintaining this degree for 24-48 hours, an examination (CT, MRI) is recommended, followed by surgical intervention;
in case of improvement of the neurological state within 12-24 hours against the background of anti-inflammatory therapy, we continue to observe the animal for 3-5-7 days (depending on the dynamics of recovery). Then we cancel anti-inflammatory therapy and conduct a neurological examination in 24-48 hours. If pain syndrome and neurological deficit reappear, we perform CT or MRI examination followed by surgical intervention;

4-5 degree of neurological deficit (loss of superficial and, or deep sensitivity):

Within 12-24 hours or immediate (grade 5) CT, MRI examination of the animal, followed by surgery.

In conclusion, I would like to bring to your attention an exception to the rule - a giant hernia (Hansen 1) at the T1-T2 level.

Photo # 10a. Mid-sagittal tomogram (soft tissue window) of the cervicothoracic spine of a 7-year-old Dachshund dog. In this animal, this is the second hernia (the first at the T11-T12 level), we operated on 2 years ago. The animal was delivered to the clinic 12-24 hours later after the onset of severe pain, forced neck position, tetraparesis with increasing dynamics of neurological deficit. The sagittal tomogram shows a giant prolapse of the T1-T2 disc, causing secondary stenosis of more than 1/2 (up to 2/3) of the CM of the canal.

Photo number 10b. Axial tomogram (soft tissue window) of the same animal at the IVD T1-T2 level. Medial (paramedial) hernia with predominant localization on the right at its base. Sector localization: at the base at 16-18 hours. The height of the hernia is 4.8 mm, with a mid-sagittal height of the CM of the canal of 7 mm. The hernia causes significant compression of the CM and roots. On the left (black arrows), a zone of increased CM density up to 45-49 HV is visualized, which is explained by the presence of blood (infiltration) in the CM parenchyma. An urgent surgical intervention was performed using the method of right-sided hemilaminectomy. The operation and rehabilitation were successful. After 12 days, neurological examination did not reveal any signs of impairment of the conductive function of the SM.

References:

1. Borzenko E.V. Theory of hernia formation in chondrodystrophic breeds. Ekaterenburg. N. p. Journal "Veterinary Doctor", No. 3, 2012, pp. 26-27;
2. Orel A.M. Development and change of the spine // Bulletin No. 5 of the Moscow professional association of chiropractors. M., 2003; S. 99-101;
3. Ball MU, McGuire JA, Swaim SF, et al. Patterns of occurrence of disk disease among registered dachshunds. J. Am. Vet. Med. Assoc. 1982; 180: 519-522;
4. Bergknut N, Auriemma E, Wijsman S, et al. Evaluation of intervertebral disk degeneration in chondrodystrophic and nonchondrodystrophic dogs by use of Pfirrmann grading of images obtained with lowfield magnetic resonance imaging. Am. J. Vet. Res. 2011; 72: 893-898
5. Braund, K. G., Ghosh. T. F. K., Larsen, L. H .: Morphological studies of the canine intervertebral disc. The assignment of the beagle to the achondroplastic classification. Res. Vet. Sci. 1975; 19: 167-172;
6. Cappello R., Bird J.L, Pfeiffer D, Bayliss M.T, Dudhia J .: Notochordal cell produce and assemble extracellular matrix in a distinct manner, which may be responsible for the maintenance of healthy nucleus pulposus. Spine (Phila Pa 1976). 2006 Apr. 15; 31 (8): 873-82;
7. Jeannette V. Bouw J. Canine intervertebral disc disease: A review of etiologic and predisposing factors, Veterinary Quarterly 1982; 4 (3), 125-134;
8. Shapiro I.M., M. Risbud Transcriptional profiling of the nucleus pulposus: say yes to notochord. Arthritis Res. Ther. 2010; 12 (3): 117;

Degenerative myelopathy refers to the progressive spinal cord injury experienced by aging dogs. The development of this disease is gradual. The first clinical symptoms of pathology appear after eight years of the animal's life.

Causes and pathogenesis

It has been established that this disease develops due to gene mutations.

Primarily, degenerative myelopathy affects the thoracic spinal cord. Pathological examination helps to identify the destruction of the white matter of the spinal cord. This structure contains fibers through which the command to move is transmitted. The destruction is accompanied by the destruction of the myelin sheaths of the nerves and the loss of the actual nerve fibers. As a result, the connection between the limbs and the brain is disrupted.

Clinical picture

As a rule, the initial stages of degenerative myelopathy are characterized by impaired coordination of the hind limbs. The gait of the dogs takes on a wobbly appearance. The rear of the animal rolls from side to side. Decreased control over the hind limbs and pelvis leads to the dog touching objects, frequent damage to the animal against obstacles.

The degree of manifestation of clinical signs of pathology is influenced by the duration and localization of the pathological process. Over time, weakness of the limbs and difficulty in standing is noted. Strengthening weakness leads to the impossibility of movement of the animal. In most cases, degenerative myelopathy in dogs results in complete paralysis. As a rule, it takes 6-12 months from the moment the disease develops to the onset of paralysis.

Also, the disease can manifest itself as a violation of the separation of urine and feces. It is associated with a disorder of the innervation of the bladder and intestines. It should be noted that the development of pain syndrome is uncharacteristic for this pathology.

Diagnosis of the disease

Note that degenerative myelopathies in dogs represent a diagnosis of exclusion. In this regard, the exclusion of other diseases with a similar clinical picture is required. To identify this pathology, myelography, computed tomography, and magnetic resonance imaging are shown. The only way to make a definitive diagnosis is to examine the animal's spinal cord during autopsy. In this case, the detection of characteristic destructive changes occurs.

Differential diagnosis

Many conditions that damage the spinal cord of a dog can cause loss of coordination and weakness in the limbs. Since the treatment of some of these pathologies seems to be successful, the necessary analyzes and studies are provided for in a timely manner. Most often, pelvic limb weakness develops as a result of herniated discs. To detect this disease, myelography, spinal x-ray, CT or MRI are used. It is also necessary to distinguish degenerative myelopathy from tumors, cysts, infections, trauma, and stroke.

Treatment of the disease

There is no effective treatment for degenerative myelopathy in dogs. According to scientists, the discovery of a gene that determines the possibility of a disease may lead to a solution to this problem. It is worth remembering that some activities contribute to a significant improvement in the quality of life of the animal:
1. Adequate care.
2. Rehabilitation of the animal through physical activity.
3. Preventing the development of pressure ulcers and urinary tract infections.

What Happens With Degenerative Myelopathy?

How is degenerative myelopathy diagnosed?

What diseases can manifest in the same way as degenerative myelopathy?

How is degenerative myelopathy treated?

Symptomatic picture

Important! This disease is not accompanied by pain, unless there are other pathologies.

The support ability of the hind limbs of the animal is impaired;
Inability to maintain one pose;
Lost muscle mass;
Decreases the skin sensitivity of the pelvic limbs;
Controlled urination and defecation are impaired;
Gradually, complete or partial paralysis develops, spreading to other parts, in particular - the chest.

How does degenerative myelopathy progress?

Reasons for development

Important! No cure has been invented for this disease, and therefore there is no chance of recovery. The disease will progress anyway.

Diagnostics

Laboratory tests for pathogens;
The functionality of the thyroid gland is checked;
MRI and CT scan to identify foci of spinal cord injury.

Type II intervertebral disc disease;
Orthopedic diseases, expressed in the pathology of joints, muscles or the skeleton as a whole;
Pathology of bone development or dysplasia of the hip joint;
Tumors;
Cysts;
Trauma;
Spinal cord infections;
Lumbosacral stenosis accompanied by narrowing of the lower spine or pelvic bone.

Myelopathy treatment

Important! It is worth noting that it is possible and necessary to maintain the mobility of the animal, but there are cases when, due to excessive load, the disease progressed even faster.

D.V.N. Kozlov, N.A., Zakharova, A., A.

Introduction

Research results and their discussion

Conclusion

Literature

Handbook of Veterinary Neurology, 5th Edition by Michael D. Lorenz, BS, DVM, DACVIM, Joan Coates, BS, DVM, MS, DACVIM and Marc Kent, DVM, BA, DACVIM, 2011.
Practical Guide to Canine and Feline Neurology, 3rd edition, by Curtis W. Dewey and Ronaldo C. da Costa, 2015.
Veterinary Neuroanatomy and Clinical Neurology, 3rd Edition
By Alexander de Lahunta, Eric N. Glass, MS, DVM, DACVIM (Neurology) and Marc Kent, DVM, BA, DACVIM, 2009.
Accumulation and aggregate formation of mutant superoxide dismutase 1 in canine degenerativemyelopathy. Nakamae S., Kobatake Y.,Suzuki R, Tsukui T, Kato S, Yamato O, Sakai H, Urushitani M, Maeda S, Kamishina H. 2015
Breed distribution of SOD1 alleles previously associated with canine degenerative myelopathy. Zeng R, Coates JR, Johnson GC, Hansen L, Awano T, Kolicheski A, Ivansson E, Perloski M, Lindblad-Toh K, O'Brien DP, Guo J, Katz ML, Johnson GS. 2014. Journal of Veterinary Internal Medicine published by Wiley Periodicals.

In this section, we will talk with you about the main genetic diseases to which our breeds can be susceptible. The policy of our work is aimed at using the most health-tested dogs in breeding. This moment is not obligatory in the work system of the Russian Kennel Federation, but it is an important moment in the breeding work of many responsible breeders.

DEGENERATIVE MYELOPATHY (DM)

Canine degenerative myelopathy (DM)- A progressive neurodegenerative disease leading to hind limb paralysis is common in some dog breeds. The disease is caused by dysfunction of the spinal cord motor neurons due to degeneration (simplification) of their nerve endings.

Degenerative myelopathy was first described over 35 years ago as a spontaneously occurring disease of the spinal cord in adult dogs. It was believed to be specific only to the German Shepherd breed, which is why it was also called German Shepherd myelopathy. Later, the disease was found in a number of breeds - Welsh Corgi Pembroke, Boxer, Rhodesian Ridgeback, Chesapeake Bay Retriever ...

Symptoms

The first signs of the disease appear already in adult dogs, in the majority at the age of 8-14 years. The earliest manifestation of degenerative myelopathy begins with an almost imperceptible weakness in one or both of the hind limbs. Over time, you can hear the so-called "shuffling" of the claws of the hind legs on the asphalt. The dog has some difficulty getting up from a sitting or lying position.

Loss of balance appears. The dog's tail becomes "inactive", its mobility is lost. If the tail is long, it can get tangled in the dog's legs. Also, in the initial stages, the animal experiences a loss of coordination, after which ataxia of the hind limbs develops. The duration of the disease in most cases does not exceed three years. In the last stages of myelopathy, the dog has practically no hind limb reflexes, paralysis sets in. Then the disease spreads to the forelimbs. In this case, signs of damage to the upper motor neurons appear, which leads to ascending paralysis of all limbs and general muscle atrophy. Complete paralysis of the dog's limbs sets in.

Diagnostics

To diagnose the disease, a genetic test (DNA test) has been developed that can be performed at any age. A DNA test allows you to identify the presence / absence of a mutant (defective) gene copy, leading to a given disease. Since degenerative myelopathy is characterized by an autosomal recessive nature of inheritance, the patients will be animals homozygous for the mutant copy of the gene.

To date, there is no medical or surgical treatment for DM, so it becomes very important to know if a dog carries a mutant copy of the gene. A DNA test will reduce the frequency of sick dogs being born.

Since this serious disease manifests itself only in adult dogs, it is possible to make a preliminary diagnosis by determining the genotype only with the help of genetic research.

Molecular genetics (for specialists)

The main reason for the development of DM is a homozygous mutation in the second exon (exon2) of the superoxide dismutase 1 (SOD1) gene, leading to a change in the sequence of the E40K protein (c.118G> A; p.E40K), as a result of which the construction of defective E40K proteins containing the wrong amino acid sequences (Awano et al., 2009). It should be noted that in T.Awano's study, all test dogs were homozygous. However, some homozygous mutant dogs did not show any signs of degenerative myelopathy, which indicates either incomplete gene penetrance or that the disease may not manifest for another reason (Awano et al., 2009). In 2011, it was discovered that, in addition to the mutation in the coding of the E40K protein in the SOD1 gene, which is common in most dog breeds, a mutation can also occur in the coding of the Thr18Ser protein (c.52A> T; p.Thr18Ser) in the Bernese Mountain Dog ,) (Wininger et al. 2011). Then, in 2014, studies were carried out for this dog breed for both of the above mutations (Pfahler et al. 2014). 408 Bernese Mountain Dog were genotyped. After conducting the study, Pfahler, S. and his colleagues came to the conclusion that individuals with mutant copies of the gene (heterozygotes) for both proteins (p.E40K and p.Thr18Ser) can pose a similar risk of dog disease, as with a homozygous mutation of the p.E40K protein (Pfahler et al. 2014). Recent research in this area has reported variability in SP110-mediated gene transcription that may underlie at least partial development of the disease in the Pembroke Welsh Corgi (Ivansson et al. 2016).

Currently, there are dozens of promising studies of this disease, but so far not a single method for its treatment has been developed.

Degenerative myelopathy. Two exons (DM Ex1, Ex2)

Description

Severe progressive neurodegenerative disease leading to hind limb paralysis. It is caused by impaired conduction of spinal cord motor neurons due to degeneration of nerve endings. The analysis includes the study of two mutations found in the Bernese Mountain Dog breed.

Interpretation of results:

Autosomal recessive inheritance (AR)

MM - there is a likelihood of developing a disease associated with the studied mutation. The animal will pass on the allele to the offspring.

NM - healthy, carrier of the disease allele. The disease associated with the studied mutation will not develop. An animal can transmit the allele to offspring.

NN - healthy, does not carry the disease allele. The disease associated with the studied mutation will not develop. The animal will not pass on the allele to the offspring.

Symptomatic picture

Important! This disease is not accompanied by pain, unless there are other pathologies.

The support ability of the hind limbs of the animal is impaired;
Inability to maintain one pose;
Lost muscle mass;
Decreases the skin sensitivity of the pelvic limbs;
Controlled urination and defecation are impaired;
Gradually, complete or partial paralysis develops, spreading to other parts, in particular - the chest.

How does degenerative myelopathy progress?

Reasons for development

Important! No cure has been invented for this disease, and therefore there is no chance of recovery. The disease will progress anyway.

Diagnostics

Laboratory tests for pathogens;
The functionality of the thyroid gland is checked;
MRI and CT scan to identify foci of spinal cord injury.

Type II intervertebral disc disease;
Orthopedic diseases, expressed in the pathology of joints, muscles or the skeleton as a whole;
Pathology of bone development or dysplasia of the hip joint;
Tumors;
Cysts;
Trauma;
Spinal cord infections;
Lumbosacral stenosis accompanied by narrowing of the lower spine or pelvic bone.

Myelopathy treatment

Important! It is worth noting that it is possible and necessary to maintain the mobility of the animal, but there are cases when, due to excessive load, the disease progressed even faster.

About the author: Anna Alexandrovna Maksimenkova

Practicing veterinarian in a private clinic. Directions: therapy, oncology, surgery. Read more about me in the "About us" section.