Home Orthopedics Degenerative myelopathy. Degenerative Myelopathy in Dogs: Symptoms, Causes and Treatment - Dog Health Has anyone restored a dog with degenerative myelopathy?

Orthopedics

Degenerative myelopathy. Degenerative Myelopathy in Dogs: Symptoms, Causes and Treatment - Dog Health Has anyone restored a dog with degenerative myelopathy?

Degenerative myelopathy dogs (DM)– a severe progressive neurodegenerative disease that leads to paralysis of the lower limbs.

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

Canine DM was first described more than 35 years ago as a spontaneously occurring disease of the spinal cord in adults. It was thought to be unique to the German Shepherd breed, which is why it was also called German Shepherd Myelopathy. Later, DM was identified in a number of breeds - Pembroke Welsh Corgi, Boxer, Rhodesian Ridgeback, Chesapeake Bay Retriever.

The first signs of the disease appear in adult dogs, most at the age of 8-14 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. On late stages myelopathy, the dog has virtually no reflexes in the hind limbs, and paralysis occurs. Then the defeat spreads to upper limbs. In this case, signs of damage to the upper motor neurons appear, which leads to ascending paresis of all extremities and general muscle atrophy. Complete paralysis of the dog's limbs occurs.

Degenerative myelopathy is characterized by an autosomal recessive pattern of inheritance.

Because many spinal cord diseases may have similar Clinical signs, without DNA testing, the final diagnosis of degenerative myelopathy can only be made posthumously after a histological examination.

The main cause of 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).

There is no cure for DM. Since this serious disease It manifests itself only in adult dogs; a preliminary diagnosis can only be made using genetic research.

DIAGNOSTICS

To diagnose DM, a genetic test has been developed that can be performed at any age. A DNA test can identify a defective (mutant) copy of a gene and a normal copy of a gene. The test result is the definition genotype, according to which animals can be divided into three groups: healthy (homozygous for a normal copy of the gene, NN), carriers (heterozygotes, N.M.) and patients (homozygous for the mutation, MM).

Carrying out a DNA test will reduce the frequency of births of sick dogs. The test is recommended for dogs of all breeds.

Degenerative myelopathy in dogs, also known as chronic degenerative radiculomyelopathy and German Shepherd herpetic myelopathy, is hereditary disease, which causes fibers in the brain, spinal cord and nerves to break down over time. It usually appears in dogs around the age of seven 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. There is no cure for the condition, and treatment focuses on keeping dogs comfortable for as long as possible. If you see signs of degenerative myelopathy in your dog, consult with your veterinarian so they can advise you of your options and provide any help possible. Here's what you need to 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 the age of seven, but can appear as early as five years of age. They gradually worsen over time, and it may take years before the front and back legs are completely paralyzed. Fortunately, most dogs do not suffer 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 within a few months, while others survive with the condition for three or more years. Here are the common symptoms of degenerative myelopathy in dogs.

Dragging of hind legs or rolling of joints
Ulcers or chafed nails on hind feet
Stickiness or lameness in the hind legs that gradually moves toward the front legs
Difficulty, walking, jumping or moving
Loss of balance and coordination
Amyotrophy
Increased hind leg paralysis (general paralysis usually occurs within 6-12 months of initial symptoms)
incontinence
Bedsores
Weight gain
Urinary retention
Urinary tract infection
Skin lesions from urine burn
Increased paralysis of the front legs (usually generalized paralysis for several years after initial symptoms)
Difficulty chewing and swallowing
Labored breathing

Causes of degenerative myelopathy in dogs

Degenerative myelopathy in dogs is caused by a genetic mutation, specifically 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 Cardigan Welsh Corgis, Collies, Retrievers, Rhodesian Ridgebacks, Siberian Huskies, Weimaraners and Wolfdog Guides.

Treatment of degenerative myelopathy in dogs

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

Treatment for canine degenerative myelopathy focuses on providing support and comfort to affected animals to maintain quality of life, as there is no way to cure the condition or stop its progression. Certain exercises 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 proper areas and activities that can help your dog maintain muscle strength and the ability to balance and walk over time. Aquatic exercise and hydrotherapy may also be helpful.

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

New treatments and treatments are still being researched, although none have yet been proven to reduce the impact of degenerative myelopathy in dogs. Your veterinarian will be able to give you best recommendations to continue treatment and care for your dog's individual needs.

Degenerative myelopathy is a progressive lesion of the spinal cord experienced by aging dogs. The development of this disease is gradual. The first clinical symptoms of the 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.

Degenerative myelopathy primarily affects the thoracic spinal cord. Pathological examination helps to identify destruction of the white matter of the spinal cord. This structure contains fibers through which the command for movement is transmitted. Destruction is accompanied by the destruction of the myelin sheaths of the nerves and the loss of the nerve fibers themselves. 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 dog's gait takes on a wobbling appearance. The back of the animal is noted to waddle from side to side. Decreased control over the hind limbs and pelvis leads to the dog touching objects and frequent injuries 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, there is weakness in the limbs and difficulty standing. Increasing weakness leads to the inability of the animal to move. In most cases, degenerative myelopathy in dogs results in complete paralysis. As a rule, 6-12 months pass from the development of the disease to the appearance of paralysis.

The disease can also manifest itself as a violation of the separation of urine and feces. This is due to a disorder of innervation Bladder and intestines. It is worth noting that the development of pain is not typical for this pathology.

Diagnosis of the disease

Note that degenerative myelopathy in dogs is a diagnosis of exclusion. In this regard, it is necessary to exclude other diseases with a similar clinical picture. To identify this pathology, myelography is indicated. computed tomography, magnetic resonance imaging. The only way to make a definitive diagnosis is to examine the animal's spinal cord during autopsy. In this case, characteristic destructive changes are detected.

Differential diagnosis

Many diseases that damage a dog's spinal cord can cause loss of coordination and weakness in the limbs. Since the treatment of some of these pathologies appears to be successful, timely necessary tests and research. Most often, weakness of the pelvic limbs develops as a result of herniated intervertebral discs. To identify this disease, myelography, spinal radiography, 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 the disease occurring may lead to a solution to this problem. It is worth remembering that some activities contribute to a significant improvement in the animal’s quality of life:
1. Adequate care.
2. Rehabilitation of the animal through physical activity.
3. Prevention of the development of bedsores and urinary tract infections.

Old dogs, just like old people, are susceptible to numerous age-related diseases. One of the most severe is degenerative myelopathy: in dogs, this pathology leads to severe consequences, disability, and the “vegetable” state of the animal.

Degenerative myelopathy is a specific disease of old dogs, characterized by the destruction of the white matter of the spinal cord. Typically, the first symptoms appear between eight and fourteen years of age. It all starts with loss of coordination () and weakness of the hind limbs. A sick dog will sway when walking, sometimes it will simply fall or sit down on its hindquarters. In 70% of cases, only one limb is affected at first. The disease progresses quite quickly, and soon the sick pet cannot walk normally at all.

From the first symptoms to complete paralysis of the hind limbs it can take from six months to a year. If the process develops over a longer period of time, then weakness of the forelimbs gradually develops, and the animal will also have an unpleasant tendency to spontaneous defecation and urination. It is important to note that the pet does not experience any pain.

What causes the disease?

Degenerative myelopathy begins in the thoracic spinal cord. If you look at a section of the affected organ under a microscope, degeneration of the white matter is clearly visible. It contains fibers that transmit motor (motor) commands from the brain to the limbs. When the white matter begins to break down, signals either do not reach the limbs at all, or go to the extremities in a blurred state. This explains the ataxia and somewhat inappropriate behavior.

Read also: The dog has a dry nose: we understand the causes and additional symptoms

In addition, there may be a pathological mixing of signals from the spinal cord and brain, as a result of which the animal eventually completely loses control over its body. Several years ago, geneticists identified a special gene that is found only in predisposed animals. Simply put, degenerative myelopathy is a disease that runs in families.

Diagnosis and differential diagnosis

Unfortunately, a truly effective test for degenerative myelopathy has not yet been developed. Most often, diagnosis consists of consistent exclusion other diseases that may give a similar clinical picture. If all of them are excluded, then only this pathology remains. The only one exact way disease detection - post-mortem diagnosis, carried out through histological examination of the spinal cord of a dead animal. Of course, this will not help the deceased dog in any way, but it will make it possible to find out the circle of predisposed dogs (offspring, parents).

Any disease that affects a dog's spinal cord can cause signs of loss of coordination and weakness. Since many of these diseases can be cured, it is important to use all existing diagnostic methods to distinguish them from myelopathy. X-rays will especially not hurt and ultrasonography spine. For example, degenerative processes in intervertebral discs are detected. This pathology is much more common than the disease we describe.

Homeopathic treatment of cats and dogs Hamilton Don

Degenerative myelopathy

Degenerative myelopathy syndrome is observed mainly in large breed dogs. This disease was first described in German shepherds, but degenerative myelopathy now occurs in dogs of all large breeds. The main symptom is progressive paralysis of the hind limbs; As the disease progresses, control over the activity of the bladder and rectum is also lost.

With this disease, degenerative changes gradually develop in the spinal cord, which leads to disruption of its functions. There is no sensation of pain due to impaired conduction of nerve impulses along the spinal cord. It is this symptom that helps in differentiating degenerative myelopathy from other diseases of the spinal cord and hind limbs, in which their weakness and gait disturbance are combined with pain (for example, slipped intervertebral discs, hip dysplasia or different kinds arthritis of the hind limbs).

The cause of degenerative myelopathy is still unclear, but the autoimmune nature of this disease is beyond doubt. It is possible that the cause or trigger of this disease is vaccination. When I was in veterinary school, degenerative myelopathy was only seen in older dogs, but cases are now seen in young dogs and even (rarely) cats.

If you suspect this disease in your dog, you should definitely contact your veterinarian for appropriate examination and diagnosis. It is not an emergency indication for contacting a veterinary hospital and, in general, does not threaten the life of your pet. However, try to collect as much information as possible before deciding on a treatment option.

Features of observation and treatment for degenerative myelopathy

Allopathic treatment methods for this disease have not been developed; As far as I know, even holistic treatment methods have minimal effect. However, some homeopathic remedies help slow the progression of the disease and can sometimes help reverse the development of symptoms. Of course, it is best to seek help from a homeopathic veterinarian. If this is not possible, then for self-treatment For your pet, you can try one of the remedies listed in this section. Antioxidants help to minimize damage to spinal cord cells, but when they are used, a reversal of symptoms is hardly possible, just like complete cure diseases. I would suggest that you give your pet vitamin C (5-10 mg/lb animal weight 2-3 times daily), vitamin E (5-20 mg/lb animal weight once daily) and vitamin A (75-100 IU/ POUND of weight 1 Time per day). Coenzyme Q10 (Coenzyme Q10, 1–2 mg/lb body weight 1–2 times daily), Superoxide dismutase (2000 IU or 125 mcg/10 lb body weight daily), and Pycnogenol (1–2 times daily) also have good antioxidant effects. 2 mg/lb body weight 2 times daily). You can use one or two of these products in addition to antioxidant vitamins. Lecithin has the ability to improve the passage of impulses along nerve trunks; Lecithin is usually administered at one-half or full teaspoon per 10 pounds of animal weight daily.

Homeopathic remedies for degenerative myelopathy

Aluminum takes part in the development of many diseases, including diseases of the nervous system. The homeopathic remedy Alumina is useful for paralysis, especially in combination with constipation and weakness. Animals showing symptoms of this drug have a weak urge to defecate; feces are usually dry. Dryness and severe flaking of the skin under the fur are also noted. Improvement followed by deterioration can be observed within one day.

Argentum nitricum

The homeopathic remedy Argentum nitricum is prepared from silver nitrate. The administration of this medicine is useful in paralysis of the hind limbs, especially in shaking paralysis. Animals with Argentum nitricum symptoms often have diarrhea with a lot of gas. These animals love sweets and candies, but after eating sweets, the symptoms of the disease often intensify. Animals with Argentum nitricum symptoms tend to feel anxious and fearful, so they often choose to stay at home rather than go for a walk. They like cool, fresh air and do not like to be in a warm room. One of the symptoms of the disease in animals of this type is impaired tongue movement, so food may fall out of the mouth while eating.

Cocculus

Animals with Cocculus symptoms are characterized by severe trembling and spasms of the limbs. They have a history of episodes of motion sickness when traveling in a car. After such trips, paralysis of the hind limbs often worsens in Cocculus animals. Abdominal pain in combination with flatulence and nausea at the sight and smell of food are also characteristic. Dogs showing symptoms of this remedy are usually somewhat lethargic and lethargic; For some, similar mental symptoms appear as the disease progresses.

Conium maculatum

This remedy is prepared from spotted hemlock (hemlock) - it was this poison that caused the death of Socrates. The characteristic symptom of this remedy is a painless ascending paralysis, which in a person begins in the lower extremities and gradually moves upward, involving the upper extremities and respiratory muscles. Death occurs from cardiac arrest and paralysis respiratory muscles. In animals with Conium symptoms, the development of paralysis occurs in the same way - at the beginning of the disease there is weakness of the hind limbs and a slow gradual movement of symptoms to the forelimbs. Severe nausea is also characteristic, which occurs when lying down (in Conium animals all symptoms are worse when resting). The use of this particular drug should be considered first of all for degenerative myelopathy in old animals.

Gelsemium

Gelsemium is characterized by a feeling of weakness, lethargy, heaviness and fatigue various parts bodies. Dogs with symptoms of this remedy sometimes have difficulty even lifting their eyelids. Mental retardation combined with anxiety is noted. Gelsemium dogs are often afraid to leave the house and prefer to be alone; fear often causes

Weakness of the hind limbs often appears after attacks of physical illness or grief.

Lathyrus

Lathyrus is almost specific means for polio in humans. The development of deep painless paralysis is characteristic, but with an increase in tendon reflexes, animals develop a spastic gait. This medicine is prescribed mainly to males. The condition typically worsens in cold, damp weather.

Oleander

When poisoned by this poisonous plant, animals experience paralysis of the hind limbs. Accordingly, the homeopathic remedy Oleander, with a similar pattern of symptoms, can significantly improve the course of paralysis. Characteristic severe weakness and decreased skin temperature of the extremities, as well as trembling of the front paws, especially while eating. Dogs are very hungry, but they eat somehow slowly; flatulence and diarrhea with the release of undigested food debris are often observed. In some cases, when gases pass, involuntary bowel movements occur.

Piricum acidum

The symptoms of this remedy in the form of ascending paralysis resemble those of Conium, but the paralysis progresses much more rapidly. Extreme exhaustion of dogs during any physical effort is typical. The left hind limb is significantly weaker than the right, however, in cases where paralysis reaches the front legs, the opposite picture is observed - the right fore limb is weaker than the left. In some cases, against the background of paralysis, a constant (sometimes painful) erection of the penis occurs.

Plumbum metallicum

This homeopathic remedy is prepared from metal lead. Typical symptoms of lead poisoning include anemia, colicky abdominal pain, and extensor paralysis. Dogs with Plumbum symptoms usually have floppy, weak legs. Unlike typical cases of degenerative myelopathy, dogs of this type experience pain in the extremities; however, the absence of pain does not exclude the possibility of prescribing Plumbum. Typically dogs with symptoms of this remedy are skinny and sickly looking. Feces have yellow, soft consistency and often extremely foul odor.

Thuja occidentalis

Dogs with symptoms of this remedy are extremely cold on the skin and usually have many warts or other growths. The hind legs are generally clumsy and stiff - it is possible that dogs with Thuja symptoms, like people with Thuja symptoms, may have a stiff feeling in the limb area. Weakness, lethargy and even flabbiness of the whole body are also characteristic. Thuja animals do not tolerate cold and dampness well, reacting to them by deteriorating their condition.

Doctor of Science Kozlov, N.A., Zakharova, A.A.

Introduction

Degenerative myelopathy (DM) is a slowly progressive, incurable degenerative disease of the central nervous system of adult medium to large breed dogs that affects both upper and lower motor neurons, resulting in paralysis and subsequent muscle wasting. Averill first described DM in dogs in 1973. In 1975 Griffiths and Duncan published the series clinical cases with signs of hyporeflexia involving the nerve roots and called this disease degenerative radiculomyelopathy. Although most of the dogs in those early studies were German Shepherds, other breeds were also represented. 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 Soft Coated Wheaten Terrier and Pug .

Research results and discussion

The clinical picture of DM typically consists of a slowly progressive, non-painful Th3–L3 myelopathy in older large breed dogs. Degenerative myelopathy manifests at age five or more, but the average age of onset is neurological symptoms The age is considered to be nine years for large dog breeds and 11 years for Welsh Corgis. At the initial stages of the disease, degenerative proprioceptive ataxia and asymmetric spastic paraparesis are noted, with preservation of spinal reflexes. Tremor of the pelvic extremities may occur when supporting 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. 10% to 20% of affected dogs have a reduced or absent knee reflex in one or both limbs. In the presence of normal or increased pelvic limb tone and no 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; perhaps it is part of the pathological process and reflects lesions in the L4-L5 segments of the spinal cord or age-related neuropathy not associated with DM. Paraplegia and moderate loss of muscle mass and decreased or absent 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 move independently. As the disease progresses, the thoracic limbs (paraplegia, paraparesis) are involved in the pathological process, and on the pelvic limbs heavy losses muscle mass, the dog loses the ability to hold urine and feces. In the later stages of the disease, tetraplegia and signs of damage to the brain stem are observed. Difficulty swallowing, tongue movement, lack of ability to bark; decreased or absent 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 nutritional, oxidative stress, excitoxicity (pathological process leading to death nerve cells under the influence 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 related to disorders immune system in dogs suffering from this disease, however, they were unproven. This is not an inflammatory disease of the spinal cord. Attempts to isolate the retrovirus from lesions were unsuccessful. Treatment of dogs with DM with glucocorticosteroids, vitamins E and B12 (often used because of their role in the treatment of other degenerative neurological disorders), and aminocaproic acid has not been shown to slow the progression of the disease. Many other treatments have been used, but none of the procedures has made a noticeable difference in the development of this disease. The long-term prognosis is not favorable and many owners decide on euthanasia.

The uniformity of clinical signs, histopathology, 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 origin of the word amyotrophy means “muscle without nutrition.” The lateral location of axonal disease and sclerosis in the spinal cord means that axons are damaged and replaced by sclerotic or “scar” tissue. Canine DM is considered a spontaneous model of human ALS. A DNA test based on the SOD1 mutation is currently available for dogs. Canine degenerative myelopathy is believed to have an autosomal recessive pattern of inheritance. Dogs homozygous for the mutation are at risk of developing DM and will pass on one chromosome with the mutant allele to all of their offspring. Some dogs are found to be recessive homozygotes by DNA testing 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 pathohistologically confirmed DM identified 118 recessive homozygotes for the mutation and 8 heterozygotes among them.

Conclusion

A lifetime diagnosis of DM is made based on 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 that must be distinguished from DM. It is important to remember that older dogs may simultaneously suffer from degenerative myelopathy and also have one (or more) moderate disc herniations. Neoplasia is also a diagnosis that needs to be differentiated by MRI from DM. Analysis cerebrospinal fluid may help rule out meningitis. The definitive diagnosis of DM is made 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,

First aid is the complete immobilization of the animal, if a spinal fracture is suspected, before arriving at the clinic, where surgery can be performed. It is not recommended to use sedatives and painkillers, as the use of painkillers will increase the animal’s activity, which can lead to even greater displacement of the vertebrae.

Forecast

The prognosis for restoration of limb function in this disease depends on the following factors:

1. Can the animal move independently on its pelvic limbs or not? If so, then the prognosis is favorable.

2. Feeling pain. The absence of deep pain sensitivity indicates that deeper pathways have been damaged, and the lesion is extensive. The lack of ability to move independently on the pelvic limbs, with the persistence of pain in them, leaves a chance for restoration of motor function of the limbs.

3. Time. If deep pain sensitivity and the ability to move in the pelvic limbs are absent for more than 48 hours, then the prognosis is unfavorable: the nerve cells have died, and the restoration of the conduction pathways, and therefore the animal’s ability to move on the pelvic limbs, independently empty the bladder, and control the act of defecation, are completely lost. The longer the time passed from the moment of injury to the visit to the veterinarian and the more intense the primary spinal cord lesions were (the five categories of symptoms listed above), the worse the prognosis.

Diagnostics

1. General radiography of the spine

X-rays should not be performed under general sedation unless you are prepared to operate on the animal within the next hour or 30 minutes. During general sedation, muscles relax, which can lead to increased vertebral displacement and worsen the degree of neurological disorders.

2.Myelography

A contrast agent is injected into the subarachnoid space

Complications during myelography

Convulsive twitching

4. CSF analysis

Myelopathy

Myelopathy - chronic non-inflammatory diseases of the spinal cord

1. Degenerative diseases - degenerative myelopathy, spondylosis, disease intervertebral disc according to type II

2. Anomalies - spina bifida - (Maine Coons, dogs with curled tails), underdevelopment of the vertebra - cauda equina syndrome, spinal instability in the cervical region

3. Tumor – tumors of the spine

4. Infectious discospondylitis

5. Traumatic (acute) – fracture, dislocation, subluxation, type I intervertebral disc disease

6. Vascular – embolism of the fibrocartilaginous ring

TO inflammatory diseases of the spinal cord Granulomatous meningoencephalitis includes:

1. Therapy of long-term degenerative diseases

a) radiculomyelopathy (German shepherds):

- Glucocorticoids

- Nootropic drugs (Tanakan)

- Phospholipids

- Angioprotectors.

b) Spondylosis:

When making a diagnosis, it is necessary to determine whether there is pinching using MRI. If the animal does not have pinching, pain and is not bothered by anything, surgery and corticosteroid therapy are not required.

2. Anomalies- chronic progressive or non-progressive diseases - spina bifida, lumbosacral stenosis, underdevelopment of half a vertebra, spinal instability in the cervical region. - Surgery

3. Tumors- Chemotherapy is ineffective. An X-ray of the chest cavity is necessary, and surgery is possible.

4. Therapy for discospondylitis

Discospondylitis is infection, which is most often caused by staphylococci, streptococci and brucella. Diagnosis of this disease requires puncture of the disc substance and blood culture. In the meantime, they are treated with antibiotics. Surgical decompression may be needed.

- Antibiotic therapy for discospondylitis of unknown etiology: 3-4 generation cephalosporins, fluoroquinolones, lincosamines, carbopenems.

- Immunocorrection (roncoleukin, betaleukin, immunofan)

- Preparations that restore cartilage and bone tissue(calcium preparations, structum, sodium thiosulfate, retabolil)

5. Spinal cord injuries. Over 8 hours, soluble corticosteroids are administered intravenously - methylprednisolone sodium succinate, at a dose of 30 mg/kg every 6 hours on the first day or 30 mg/kg initially, then 5.4 mg/kg every hour for the next 23 hours) Then proceed to oral dexamethasone 0.1 mg/kg 2 times a day for 3 days with associated inflammation and bleeding. Stabilization and decompression may be required.

6. Vascular disorders. Fibrocartilaginous embolism (acute/painless) Methylprednisolone for 8 hours - the condition improves rapidly within 6 weeks. If there is no improvement after 7-10 days, the prognosis is unfavorable - signs of damage to the LMN (lower motor neuron)

Therapy for GME (Granulomatous meningoencephalitis)

It is assumed that the pathology is based on immunological disorders, since almost all animals respond to treatment with immunosuppressive doses of glucocorticoids. When analyzing the CSF, neutrophilic leukocytosis and increased protein content are revealed (pressure is increased due to impaired fluid outflow).

Three factors complicate the procedure for obtaining CSF in such patients.

1. Anesthesia, the implementation of which is always associated with a certain risk, in this case increases it, since there is already a violation of consciousness and damage to the midbrain involving the respiratory center is possible.

2. Patients with encephalitis almost always develop cerebral edema. When part of the CSF is removed, the swelling sometimes increases, which leads to compression of the midbrain and brain stem (tentorial hernia).

3. Changes in the dynamics of CSF outflow can lead to the spread of infection.

Preparations: antibiotics that penetrate well through the blood-brain barrier (chloramphenicol, metronidazole, rifampin). Medications with moderate permeability (amoxicillin, ampicillin, penicillin G) can be prescribed, since their penetration into the central nervous system increases during inflammation. It is not recommended to use antibiotics with low permeability: cephalosporins and aminoglycosides.

Therapy of myelitis (from the Greek myel?s spinal cord), inflammation of the spinal cord when affected by neurotropic viruses:

- 1-2 degree of neurological disorders: non-steroidal anti-inflammatory drugs in combination with ranitidine or cimetidine to prevent the formation of ulcers in the gastrointestinal tract. Additionally - vasodilators.

- 2-3 degree: methylprednisolone sodium succinate 30 mg/kg IV, then 15 mg/kg every 6 hours. It is effective when used early (the first 18 hours) as it prevents the development of the pathological process (necrosis of the spinal cord).

Treatment of spinal cord infarctions and strokes:

Correction of bleeding disorders

Blood transfusion, plasma transfusion.

For thrombus formation, fibrinolysin, heparins, streptokinase.

Coagulopathies (proteolysis inhibitors, etamsylate)

Vasodilators in maximum doses. Phospholipids.

Nootropics.

Degenerative diseases of the intervertebral disc in dogs (DISCOPATHIES)

Type I disc protrusion in chondrodystrophic dog breeds.

Treatment

If signs are acute and the animal is immobile, administer steroids as for acute spinal injuries and immediately perform surgical decompression

Type II disc protrusion- in large breeds of dogs.

In type 2, surgical decompression is usually indicated because animals are not brought in until they have developed significant myelopathy.

I would like to note that after 48 hours in dogs with loss of pain sensitivity and the ability to move, the operation is meaningless and is only diagnostic in nature.

Administration of glucocorticoids.

It must be remembered that the supply of corticosteroids in animals is significantly less than in humans and in cases of fairly massive injury state of shock leads to their rapid depletion. Therefore, when treating severe injuries, the administration of steroids is mandatory.

Properties of methylprednisolone:

Normalizes vascular tone;

Stabilizes lysosomal and cellular membranes, prevents the release of lysosomal enzymes;

Inhibits lipid peroxidation and lipid hydrolysis due to inhibition of prostaglandins;

Reduces capillary permeability under hypoxic conditions;

Improves the excretion of Ca from cells;

Reduces spasm and resistance of peripheral capillaries;

Inhibits the activity of polymorphonuclear leukocytes and their blockage of the microvascular bed;

Strengthens the excitation of neurons and the conduction of impulses;

Prevents the development of post-traumatic tissue ischemia;

Supports aerobic energy metabolism.

Use following diagrams:

Doctor of Science Kozlov, N.A., Zakharova, A.A.

Introduction

Degenerative myelopathy (DM) is a slowly progressive, incurable degenerative disease of the central nervous system of adult medium to large breed dogs that affects both upper and lower motor neurons, resulting in paralysis and subsequent muscle wasting. Averill first described DM in dogs in 1973. In 1975, Griffiths and Duncan published a case series of hyporephrexia involving nerve roots and named the disease degenerative radiculomyelopathy. Although most of the dogs in those early studies were German Shepherds, other breeds were also represented. 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 Soft Coated Wheaten Terrier and Pug .

Research results and discussion

The clinical picture of DM typically consists of a slowly progressive, non-painful Th3–L3 myelopathy in older large breed dogs. Degenerative myelopathy begins at age five or older, but the average age for onset of neurological symptoms is nine years for large breed dogs and 11 years for Welsh Corgis. At the initial stages of the disease, degenerative proprioceptive ataxia and asymmetric spastic paraparesis are noted, with preservation of spinal reflexes. Tremor of the pelvic extremities may occur when supporting 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. 10% to 20% of affected dogs have a reduced or absent knee reflex in one or both limbs. In the presence of normal or increased pelvic limb tone and no 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; perhaps it is part of the 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, 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 move independently. As the disease progresses, the pathological process involves the thoracic limbs (paraplegia, paraparesis), severe loss of muscle mass on the pelvic limbs, and the dog loses the ability to hold urine and feces. In the later stages of the disease, tetraplegia and signs of damage to the brain stem are observed. Difficulty swallowing, tongue movement, lack of ability to bark; decreased or absent 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 nutritional, oxidative stress, excitoxicity (a pathological process leading to the death of nerve cells under the influence of neurotransmitters capable of hyperactivating NMDA and AMPA receptors) and genetic mechanisms have been investigated as the pathogenesis of degenerative myelopathy. Several scientific papers have been linked to immune system abnormalities in dogs suffering from this disease, but they have been unproven. This is not an inflammatory disease of the spinal cord. Attempts to isolate the retrovirus from lesions were unsuccessful. Treatment of dogs with DM with glucocorticosteroids, vitamins E and B12 (often used because of their role in the treatment of other degenerative neurological disorders), and aminocaproic acid has not been shown to slow the progression of the disease. Many other treatments have been used, but none of the procedures has made a noticeable difference in the development of this disease. The long-term prognosis is not favorable and many owners decide on euthanasia.

Conclusion

A lifetime diagnosis of DM is made based on 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 that must be distinguished from DM. It is worth remembering that older dogs can simultaneously suffer from degenerative myelopathy and also have one (or more) moderate disc herniation. Neoplasia is also a diagnosis that needs to be differentiated by MRI from DM. A cerebrospinal fluid test can help rule out meningitis. The definitive diagnosis of DM is made 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,

Myelopathy in German Shepherds

This disease is a slowly progressive neurological disorder characterized by slowly progressive weakness or paralysis of the hind limbs and an unsteady, shuffling gait over 2–8 months. The back muscles weaken and ataxia occurs. Damage in German Shepherds with myelopathy is concentrated in the cervical and lumbar regions spinal cord and also in the brain stem.

Sick dogs have leukopenia, and the more severe the myelopathy, the more pronounced it is.

If this disease is genetic in nature, then its inheritance is unlikely to be simple and may be associated with breed selection.

From the book Central Asian Shepherd Dog author Ermakova Svetlana Evgenievna

From the book Caucasian Shepherd Dog author Kuropatkina Marina Vladimirovna

Peculiarities of education and training of Central Asian Shepherds Despite the growing popularity among Central Asian Shepherd breeders, it is rare to see this dog on a training ground. This is due to the fact that: firstly, there are no officially recognized

From the book Training of Domestic Wolfhounds author Vysotsky Valery Borisovich

Special training Central Asian Shepherd Dogs When a person gets a large breed dog like the Central Asian Shepherd Dog, he usually has in mind the protection of his person and property. That is, the dog must be trained to perform protective guard duty.

From the book Domestic Breeds service dogs Asian descent author Kalinin Vladimir Alexandrovich

Reproduction of Central Asian Shepherds The maintenance and diet of dogs intended for mating should be given increased attention. Approximately 1-1.5 months before the day of the planned mating, you should give Central Asian Shepherd Dogs anthelmintics, which ones to choose correctly

From the book Police Dog Training by Gersbach Robert

Approximate daily diet for 1-2 month old Caucasian Shepherd dogs? Meat – 100–200 g;? milk – 450–500 g;? egg – 1 pc. (yolk);? cottage cheese – 120–150 g;? vegetables – 150 g;? vegetable oil – 10 g;? mineral fertilizing – 10 g;? vitamins - as prescribed

From the author's book

Approximate daily diet for 3-month-old Caucasian Shepherd dogs? Meat – 200–300 g;? milk – 500 g;? egg – 1 pc. (yolk);? cottage cheese – 140–160 g;? vegetables – 170–200 g;? vegetable oil – 10 g;? mineral fertilizing – 10 g;? vitamins - as prescribed

From the author's book

Approximate daily diet for 4-month-old Caucasian Shepherds? Meat – 300–400 g;? milk – 500 g;? egg – 1 pc. (yolk and white);? cottage cheese – 180–200 g;? vegetables – 180–200 g;? vegetable oil – 10 g;? mineral fertilizing – 20 g;? vitamins - as prescribed

From the author's book

Approximate daily diet for 5-month-old Caucasian Shepherds? Meat – 500 g;? milk – 500 g;? egg – 1 pc. (yolk and white);? cottage cheese – 200–210 g;? vegetables – 200 g;? vegetable oil – 25–30 g;? mineral fertilizing – 20 g;? vitamins - as prescribed by the veterinarian. In the daily diet of puppies

From the author's book

Approximate daily diet for 6-month-old Caucasian Shepherds? Meat – 500 g;? milk – 500 g;? egg – 1 pc. (yolk and white);? cottage cheese – 240–250 g;? vegetables – 230–250 g;? vegetable oil – 25–30 g;? mineral fertilizing – 20 g;? vitamins - as prescribed

From the author's book

Approximate daily diet for 7-12 month old Caucasian Shepherd dogs? Meat – 500 g;? egg – 2 pcs. (no more than 2 times a week);? cottage cheese – 250–260 g;? vegetables – 220–250 g;? vegetable oil – 30 g;? mineral fertilizing – 20 g;? vitamins - as prescribed

From the author's book

12. Breeding Caucasian Shepherds Sooner or later, every owner of a Caucasian Shepherd is faced with the question of the offspring of their dog. The owner will have to resolve a number of important issues related to the developmental characteristics of the dog’s body, the search for a healthy partner, etc.

From the author's book

INFANTILISM AS A REGULATOR OF RELATIONS OF DOMESTIC SHEPHERD DOGS IN THE PACK Infantilism - “prolonged childhood” - is habitually perceived by us as something negative. And indeed, with regard to representatives of the species “Homo sapiens” this statement is quite true:

From the author's book

Chapter 1. On the origin of the Central Asian and Caucasian Shepherd Dogs According to modern ideas, the immediate ancestor of domestic dogs is considered to be the wolf, which, along with them, the jackal and the North American coyote, forms a common systematic unit: the genus of dog (Canis), family

From the author's book

Chapter 2. Exterior of the Central Asian and Caucasian Shepherd Dogs Understanding the exterior of the Central Asian and Caucasian Shepherd Dogs is impossible in isolation from the specific conditions in which these breeds were formed. They embodied the wisdom of nature, served certain tasks, living

From the author's book

Distinctive features of “German Shepherds” General overview. - The German Shepherd is slightly taller than average, slightly elongated, robust (strong), muscular, lively and agile, distinguished by its attentiveness and intelligence. As for height, it varies

From the author's book

Some notes about German Shepherds The way they hold their ears. a) Prick ears should sit high and not stick out to the sides like horns. When at rest or in motion, they should be turned more backwards. An attentive dog always alerts its ears in the direction of the sound. b)

Causes and pathogenesis

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

Clinical picture

The disease can also manifest itself as a violation of the separation of urine and feces. This is due to a disorder of the innervation of the bladder and intestines. It is worth noting that the development of pain is not typical for this pathology.

Diagnosis of the disease

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

Differential diagnosis

Many diseases that damage a dog's spinal cord can cause loss of coordination and weakness in the limbs. Since the treatment of some of these pathologies appears to be successful, the necessary tests and studies are carried out in a timely manner. Most often, weakness of the pelvic limbs develops as a result of herniated intervertebral discs. To identify this disease, myelography, spinal radiography, CT or MRI are used. It is also necessary to distinguish degenerative myelopathy from tumors, cysts, infections, trauma and stroke.

Treatment of the disease

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

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

Canine DM was first described more than 35 years ago as a spontaneously occurring disease of the spinal cord in adults. It was thought to be unique to the German Shepherd breed, which is why it was also called German Shepherd Myelopathy. On July 15, 2008, the mutated gene responsible for MD was discovered in 43 breeds, including the Rhodesian Ridgeback.

The first signs of the disease appear in adult dogs, most 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 reflexes in the hind limbs, and paralysis occurs. 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 extremities and general muscle atrophy. Complete paralysis of the dog's limbs occurs.

Degenerative myelopathy is characterized by an autosomal recessive pattern of inheritance.

Because many spinal cord diseases may have similar clinical features, without DNA testing, a definitive diagnosis of degenerative myelopathy can only be made postmortem after histological examination.

The main cause of 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).

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

A particular danger is that when mating two carriers of Degenerative Myelopathy, there is a very high probability of giving birth to puppies affected by myelopathy (M/M), up to 25% of the offspring will be affected, and in 80% of them this disease manifests itself clinically.

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

Diagnostics

To diagnose DM, a genetic test has been developed that can be performed at any age. Carrying out a DNA test will reduce the frequency of births of sick dogs. The test is recommended for dogs of all breeds.

A DNA test can identify a defective (mutant) copy of a gene and a normal copy of a gene. The test result is the 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, N.M.) and sick (affected, homozygous for mutation, MM).

You can take a DNA test for Degenerative Myelopathy

in Moscow the test can be taken at the Laboratory "Chance-bio", in St. Petersburg at the Zoogen Laboratory. They take blood or buccal epithelium (from behind the cheek). The results are ready in 45 days.

Clinical picture of myelopathy in dogs

Clinical picture.
Based clinical symptoms There are 6 neurological syndromes (stages), corresponding to the degrees of myelopathy (compression of the spinal cord and, as a consequence, impaired conduction function):
1. Pain syndrome: the animal cannot jump onto elevated objects, is inactive, lethargic, constrained. One of the main signs of the presence of a hernia in the thoracolumbar region is hyperesthesia, hypertonicity of the back muscles and abdominal wall, hunched back (forced kyphosis). And in the cervical region - an unusual forced position of the neck (head in a half-lowered position) and sharp pain with squealing;
2. Decreased proprioceptive sensitivity, ataxia, dysmetria, paresis, but the animal can stand up and move independently. May present with or without pain;
3. Severe paresis, the animal cannot stand up and move independently, but sensitivity is completely preserved;
4. Paralysis - voluntary movements absent, superficial pain reactions are reduced or absent, conscious reaction to deep pain is preserved. A “seal” positioning of the limbs is possible;
5. Severe paralysis (plegia) - there are no superficial and deep pain reactions. "Seal" positioning of the limbs;
6. After the dog reaches stage 5 neurological disorders, the process of myelomalacia begins to progress.
If animals have a 4-5 degree neurological deficit, an emergency examination and subsequent (based on the examination results) surgical intervention is necessary because time passes by minutes, and the faster we decompress the SM (surgical decompression), the greater the chance of restoring the neurological status.
Myelomalacia (necrosis of a compressed area of the SM) is quite rare (2-5% of cases) and it is irreversible. Myelomalacia can be local or generalized. Local myelomalacia can become generalized. Local myelomalacia occurs when there is significant compression, bruise, or axonal rupture of the SC area by elements of the hernia (detritus). Local myelomalacia can become generalized when all compensatory mechanisms are exhausted, the pressure on the spinal mass and membranes increases as the inflammatory process develops, and the vascularization of the spinal mass over a long period is reduced to zero. In the vast majority of cases (up to 90%), myelomalacia occurs with sequestered hernias with a large volume of sequestration that has migrated (spread) along the SC canal to 3 or more vertebrae (vertebral segments). The larger the contact area of the SM surface with sequestration elements (blood with detritus), the more voluminous it will be. inflammatory process. This process occurs in cascade, as in any closed system. In order to remove the cascade of reactions leading to even stronger compression of the spinal cord due to inflammation (edema), we prescribe steroidal anti-inflammatory drugs (metipred, dexamethasone, prednisolone, etc.) in large dosages. 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 quickly deteriorates, paraplegia turns into tetraplegia and ends in the death of the animal, caused by ascending necrosis of the spinal cord and brain.
Note: generalized myelomalacia from local one can be easily provoked by iatrogenic factors:
myelography (introduction of a contrast agent into the subarachnoid space of the SM) with local myelomalacia having already begun,
failure to comply with the rules of asepsis and antisepsis when performing punctures of the subarachnoid space or surgical interventions on the spine;
inept punctures and unacceptable use of conventional injection needles instead of spinal ones. This leads to hits (especially when lumbar punctures) elements of the skin, muscle tissue, bone tissue, ligamentum flavum into the SM parenchyma and subarachnoid space;
surgical intervention with significant trauma to the venous sinuses and vessels of the spinal roots (especially in several adjacent vertebral segments), as well as incomplete decompression of the spinal column, when part of the hernia (sequestrum) or the whole hernia is not removed.

Photo No. 9a. Intraoperative photo of the thoracolumbar spine of a Dachshund dog. History of the disease (anamnesis morbi): the animal is 4 years old, suddenly appeared paraparesis with a deficiency of the 3rd degree within 24 hours passed into the 4th degree. Conservative treatment (hormones, vitamin B) did not lead to any improvement. On the 4th day, this animal was admitted to us for examination. According to the owners, just yesterday evening the dog had a deep sensitivity to pain. However, in the morning the dog’s condition began to deteriorate: deep pain sensitivity disappeared, severe pain and inappropriate behavior of the dog appeared (according to the owners, the dog throws its head up). After a neurological examination, a diagnosis was made: neurological deficit grade 5-6, 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 about the unfavorable prognosis, but insisted on examination and surgical intervention. Based on the results of a CT study, a diagnosis was made: sequestered prolapse of the L3-L4 disc (Hansen 1), a bilateral hernia with a predominant localization on the right (at 14 and 20 o’clock), fresh, encircling, with stenosis of the SM canal of about 1/2 and migration of the sequestrum up to 1 /2 bodies of L6 caudally and up to 1/2 bodies of L2 cranially (for 5 vertebrae). A right hemilaminectomy was performed to visualize the SM. After opening the dura mater (hard meninges) the diagnosis was confirmed - generalized ascending myelomalacia.

Photo No. 9b. It's an animal. In the photo, tweezers indicate the location of the dura mater opening. At the site of the defect, we visualize a structureless mass of necrotic SM, extending beyond the dura mater at the L1-L2 level, i.e. much more cranial (above) the site of herniation (L3-L4).

Photo No. 9c. Midsagittal 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 densitometric parameters of the spinal cord (up to 150 HV, with the norm being 34±10), the absence of epidural spaces (fat). A day before the CT examination, myelography was performed on this dog. Diffuse spread of contrast (omnipaque 350) in the lumen of the spinal canal indicates complete destruction of the spinal cord and meninges. Conclusion: ascending generalized myelomalacia.

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

Pathogenesis of neurological deficit syndrome (myelopathy).

Disc prolapse is accompanied by the loss of a certain amount of detritus into the SC canal over a short period of time. It can be sequestered (prolapse with sequestration) and non-sequestered (prolapse). This depends on the volume and consistency of the debris and on the location of the rupture of the annulus fibrosus relative to the midsagittal plane of the disc. If the rupture of the fibrous ring occurs paramedially or laterally, the venous sinus is injured and the detritus, mixing with venous blood, spreads cranially and caudally 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-shaped shape (non-sequestrated), and in the thoracolumbar region, prolapses with sequestration are observed in approximately 70 - 80% of cases (See photo No. 8b ). In some cases, the sequestration elements are squeezed out extraforamally (outside the SC canal) (see photo No. 5 e).

From this moment, a cascade of pathological processes begins, which constitute the pathogenesis of myelopathy:
1. disc prolapse (loss of detritus into the SM canal);
2. compression (bruise, contusion) of the spinal column with membranes;
3. disturbance of liquorodynamics, hematodynamics and, as a consequence, trophism and metabolic processes in the compressed area of the SM;
4. inflammatory edema of the area of the SM that is compressed and in contact with the elements of the hernia.

That is, we are observing a symptom complex (syndrome) of aseptic inflammation occurring in a closed system (limited by the walls of the SC canal). The cascade of pathological processes in a closed system plays a primary role in the pathogenesis of disorders of 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 SC area and depends on:
1. The volume of material prolapsed (falling out) into the SC canal (the larger the volume, the stronger the compression);
2. Contact areas of sequester elements with dura mater (dura mater). This is typical for hernias surrounding hernias and sequestered hernias. That is, the larger the surface area of the dura mater is in contact with the elements of the sequestrum, the more intense and extensive the inflammatory process, which usually occurs in 2-3 or more segments of the SM;
3. Compliance (compliance) of the parenchyma of the SM. 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 rigidity of the system.
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 inside the SC canal. The compliance of the spinal system is ensured mainly by the volume of the subarachnoid and epidural spaces and the size of the foraminal openings. It is the displacement of the SC inside the SC canal and the filling of the free spaces of the SC canal with sequestration (hernia) that makes it possible to free up additional spaces for the “swelling” spinal cord, restraining the development of microcirculatory disorders. As these compensatory mechanisms are exhausted, the blood perfusion pressure begins to decrease, which is facilitated by an increase in SM edema. Hypoperfusion provokes the formation of new areas of ischemic tissue. In these areas, O2 extraction increases, reaching 100%. Due to the involvement of additional areas of the SM parenchyma in the inflammatory process, the volume of ischemic and edematous tissue 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 SC parenchyma (neurons with processes, glia and blood capillaries) to elasticity (strength) or the ability to restore its functions after exposure to external or internal pressure. That is, in one animal with disc prolapse (in equal circumstances), after surgical decompression, functions will be restored, while in another, neurological deficits will remain. Let me give you a simple example. Using a dynamometer, we measure the impact force on a skin area of one animal and another. The impact force is the same. The first animal has slight swelling, and the other has swelling + hematoma. Under equal circumstances, we can confidently say that the compliance of subcutaneous tissue in the first animal is higher than in the second;
4. Spatial localization of the hernia in sectors of the spinal canal and parts of the spine (in the cervical and lumbar spine the spinal canal is wider). Quite often, during CT examinations, we encounter animals with severe hyperostosis of the elements of the spinal canal (arches, vertebral pedicles). This leads to a decrease in spatial compliance due to stenosis of the SC canal and foraminal spaces and openings. This pathology is inherent mainly in brachycephalic breeds of dogs (French bulldogs, pugs, Pekingese), as well as dachshunds with a rough constitution (deep rib cage, powerful bones);
5. The speed at which prolapse of the nucleus pulposus occurs. The faster this happens, the more intense the inflammatory process;
6. Immunoreactivity of the body. When hyperergic inflammation occurs in a more reactive organism, the degree inflammatory reaction there will be more. Animals with autoallergy and sensitized by exoallergens are at risk.

Diagnosis and treatment. Algorithm of actions in the event of a neurological syndrome caused by IVD herniation.

So, the dog developed a neurological syndrome of 1-3 degrees (see Clinical picture). After a neurological examination, steroid hormones (metipred, dexamethasone, hydrocortisone), B vitamins and symptomatic treatment(H2-blockers of histamine receptors, laxatives, etc.) in therapeutic doses. In case of intensification (progress) of neurological deficit within 12-24 hours, CT or 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 the case of an increase in neurological deficit to grade 3-4-5 within 12-24 hours during therapy, examination (CT, MRI) followed by surgical intervention is recommended;
If the neurological condition improves within 12-24 hours against the background of anti-inflammatory therapy, we continue to monitor the animal for 5-7 days. Then we cancel anti-inflammatory therapy and conduct a neurological examination after 24-48 hours. If it occurs again pain syndrome and neurological deficit - we perform a CT or MRI examination. Further, based on the classification of hernias, we can conclude about the need for medical or surgical treatment. It is especially necessary to pay attention to points 6,7,8 of the classification of IVD hernias.

3rd degree of neurological deficit (the animal cannot move independently, but superficial and deep pain sensitivity is preserved):
in the case of an increase in neurological deficit to grade 4-5 within 12-24 hours during therapy or persistence of this degree for 24-48 hours, examination (CT, MRI) followed by surgical intervention is recommended;
if the neurological condition improves within 12-24 hours against the background of anti-inflammatory therapy, we continue to monitor the animal for 3-5-7 days (depending on the dynamics of recovery). Then we cancel anti-inflammatory therapy and conduct a neurological examination after 24-48 hours. If pain and neurological deficit reappear, we perform a 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 surgical intervention.

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

Photo No. 10a. Midsagittal tomogram (soft tissue window) of the cervicothoracic spine of a 7-year-old Dachshund dog. This is the second hernia in this animal (the first at the T11-T12 level) we operated on 2 years ago. The animal was delivered to the clinic 12-24 hours after the onset of severe pain, forced neck position, tetraparesis with increasing dynamics of neurological deficit. The midsagittal tomogram shows a giant T1-T2 disc prolapse, causing secondary stenosis of more than 1/2 (up to 2/3) of the cm canal.

Photo No. 10b. Axial tomogram (soft tissue window) of the same animal at the IVD level T1-T2. The hernia is medial (paramedian) with a predominant localization on the right at its base. Sector localization: at the base at 16-18 o’clock. The height of the hernia is 4.8 mm, with a midsagittal height of the CM canal of 7 mm. The hernia causes significant compression of the SC and roots. On the left (black arrows) a zone of increased density of the SC up to 45-49 HV is visualized, which is explained by the presence of blood (infiltration) in the parenchyma of the SC. Emergency surgery was performed using right hemilaminectomy. The operation and rehabilitation were successful. After 12 days, a neurological examination revealed no signs of impaired conduction function of the spinal cord.

References:

1. Borzenko E.V. Theory of hernia formation in chondrodystrophic breeds. Ekatirenburg. 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 chiropractors. M., 2003; pp. 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;