Myelopathy due to fibrocartilaginous embolism and spinal cord infarction (SCI). Valery Shubin, veterinarian. Balakovo. Treatment and prognosis

Fibrocartilaginous embolism (FCE) is a disease with an abrupt onset, which is characterized by sudden thrombosis of blood vessels in the small area spinal cord. A fibrocartilaginous embolus acts as a thrombus.

Main symptoms and causes of FCE

Clinical signs vary depending on what level of the spinal cord the injury occurs. Both dogs and cats are susceptible to the disease, but young dogs are most often affected by FCE.

Clinical signs appear suddenly and do not progress:

• Symptoms are often painless, although some dogs may experience pain early in the disease.
• As a rule, the signs are asymmetrical, i.e. extend to one side.
• manifestations of the disease can vary: from minor sensory disturbances and weakness to complete paralysis.

The true cause of the disease has not been fully established. It is now known that in a certain area of ​​the spinal cord the blood vessels are thrombosed by a fragment of a substance that apparently originates from the nucleus of the intervertebral disc. It is assumed that with minimal trauma, a small fragment of the nucleus pulposus of the disc enters a blood vessel and causes an embolism. As a result, a spinal cord infarction develops in this location. However, due to the presence large quantity collateral vessels, brain tissue is restored quite quickly, which explains fast recovery patients with this pathology.

How is fibrocartilaginous embolism diagnosed and treated?

Fibrocartilaginous embolism is diagnosed based on neurological examination, the severity of the onset of the disease and the progression of symptoms. The final diagnosis is made by a veterinary neurologist based on MRI results.

FCE is a pathology that does not require surgical intervention. Therefore, MRI is decisive in making a diagnosis. The main treatment method is physiotherapy and maintenance general health patient.

What's the prognosis?

The prognosis for fibrocartilaginous embolism depends on how deeply the spinal cord is damaged. Recovery can take from several days to several months.

Despite the fact that the pathogenesis of PCE is not fully understood, in animals that have suffered from this disease, the risk of relapse is minimal.

Fibrous-cartilaginous embolism (FCE) is an acute infarction and ischemic necrosis of the spinal cord parenchyma, which develops during embolization of small arteries and veins supplying the spinal cord parenchyma and membranes with a substance similar to that of the nucleus pulposus of intervertebral discs. Vascular embolization during fibrocartilaginous embolism leads to the development of hyperacute non-progressive signs of dysfunction of any area of ​​the spinal cord, and all this is accompanied by paresis and paralysis. The mechanism of penetration of the substance of the nucleus pulposus into the vessels of the spinal cord, as well as the exact causes of the development of PCE, have not been determined.

Clinical signs

Fibrocartilaginous embolism can develop in dogs of any breed and age, as well as in cats, but FCE is most commonly seen in medium to large breed dogs between 3 and 7 years of age, but has been described in a few dogs less than 1 year of age. In small dogs, FCE occurs more often in breeds such as the Miniature Schnauzer, Sheltie, and Yorkshire Terrier. An interesting fact is that fibrocartilaginous embolism is more often observed in non-chondrodystrophic breeds; chondrodystrophic dog breeds are extremely rarely affected. Descriptions of fibrocartilaginous embolism in cats are rare.

The formation of blood clots with PCE is most often observed in the lumbar and cervical region, but the lesion can develop in any part of the spinal cord. The lesion is often asymmetrical (predominance on one side), but symmetry of neurological disorders may also be noted.

The key feature of fibrocartilaginous embolism is its sudden development, non-progressive course and asymmetric paresis. Fibrous-cartilaginous embolism is characterized by acute or hyperacute development of clinical manifestations; about half of the cases of onset of FCE are noted during a walk during a period of minor trauma or excitement. The onset of the disease is characterized acute pain and vocalization on the part of the animal, the pain goes away very quickly and most dogs do not experience discomfort at the veterinary clinic, even during manipulations in the back.

The results of a neurological examination depend on the zone and extent of the ischemic area. Chest lesions lumbar region with fibrocartilaginous embolism, it develops most often and causes signs of damage to the upper motor neuron in the hind limbs; with damage to the lumbar region, signs of damage to the lower motor neuron develop in the hind limbs. Damage to the cervical spine is the least common, but this type of lesion in FCE is most common in small breeds of animals. The severity of neurological disorders ranges from moderate to severe; when examining animals with FCE, asymmetry of lesions is characteristic (eg, the difference between right and left reflexes).

Diagnosis and differential diagnosis

In fibrocartilaginous embolism, a presumptive diagnosis of high probability is based on characteristic clinical signs and the exclusion of other diseases that can give a similar clinical picture. A radiographic examination is carried out to exclude pathologies such as fracture/dislocation of the vertebral body, lytic lesions of the vertebrae due to neoplasms and diseases of the intervertebral discs. Myelography and computed tomography help exclude compression causes neurological dysfunction. The study of cerebrospinal fluid in fibrocartilaginous embolism is poorly informative. Magnetic resonance imaging can detect focal areas of increased density, but weak degree lesions - changes are not identified. The final diagnosis of FCE is established posthumously, after pathological examination of the affected spinal cord tissue.

Treatment and prognosis

Treatment of fibrocartilaginous embolism consists of supportive care and physical therapy. Of all the methods of treating fibrocartilaginous embolism, the most significant place is given to early implementation full physical therapy. Due to the fact that most dogs with FCE are large and giant breeds, carrying out this type of treatment can cause some difficulties. When an animal asks for help veterinary clinic in the first 6 hours after the development of clinical signs - a single dose of high-dose methylprednisolone may be beneficial, but there is no definitive evidence that this type of treatment improves the prognosis of fibrocartilaginous embolism.

Prognosis depends on the extent and location of the lesion; in general, with fibrocartilaginous embolism, especially in small breed dogs, there is a satisfactory recovery of neurological function, and the decision to euthanasia should never be rushed. In animals with functional improvement of neurological deficits during the first two weeks, the prognosis is closer to favorable, but complete restoration of neurological functions takes weeks (6-8 weeks). signs of complete paralysis and loss of deep pain sensitivity(HBC) worsen the prognosis. If there is no improvement in neurological status within 3 weeks, return normal function nervous system is unlikely.

Valery Shubin, veterinarian. Balakovo

Fibrous-

cartilaginous

embolism

Fibrous-cartilaginous embolism in dogs - increased physical activity and increased levels of fats and proteins in the blood predispose to the development of this disease

Fibrous-cartilaginous embolism in dogs is an acute death of the spinal cord associated with blockage of the supply vessels by a fibrocartilaginous embolus.

Causes of cartilage embolism:The intervertebral disc, or rather its substance, is considered as a possible source of the embolus. The exact causes of embolus formation are unknown. This element clogs the vessels of the spinal cord. As a rule, the lesion in fibrocartilaginous embolism concerns the nervous system.Giant and large breeds of dogs are most often affected by this disease. Also, the breed's tendency to pathology is characteristic of the Scottish Shepherd and Miniature Schnauzer. It is worth noting that these breeds have increased viscosity blood, which causes possible death of the spinal cord even without the formation of fibrocartilaginous embolism and fibrocystic mastopathy fcm. In most cases, the disease occurs at the age of 4 years. Males are more often affected.Increased physical activity and increased levels of fats and proteins in the blood predispose dogs to the development of this disease.

Clinical picture of fibrous embolism

The onset of the disease is sudden. There is a strong whining of the animal. Signs of paralysis or paresis may develop within a short time. As a rule, the condition stabilizes within 2 days.Often neurological symptoms are detected on only one side of the dog's body.

Most a common symptom Pain syndrome is considered pathology. However, at the time of the examination this symptom there may not be. Spinal cord damage is affected by the location of the embolus. It is possible that such clinical manifestations such as a slight disturbance of gait, paralysis of the body, lack of deep lateral sensitivity, etc. If symptoms persist for more than 2 days, it is necessary to exclude other diseases with similar symptoms.This disease can be complicated by disturbances in the processes of defecation and urination, infection of the urinary tract, the appearance of ulcers and bedsores.Diseases and recommendations for the Rottweiler

Diagnosis of the disease fibrous embolism

Myelography helps to identify intracerebral swelling in the area of ​​the embolus. However, such a sign is detected only in the acute stage. It is also possible that areas of spinal cord atrophy may appear. The results of cerebrospinal fluid analysis are not always objective. To confirm the diagnosis, a histological examination is performed.Fibrocartilaginous embolism in dogs must be distinguished from the following pathologies:

1. Damage to intervertebral discs, tumors and spinal cord injuries. To exclude data pathological conditions X-ray and myelography are indicated.
2. Hemorrhagic diathesis. It is recommended to perform a coagulogram.
3. Focal inflammation of the spinal cord. A cerebrospinal fluid analysis is performed.

Treatment

The main drug used to treat fibrocartilaginous embolism is methylprednisolone. It is administered intravenously. The duration of such treatment should not exceed 2 days. It's connected with high frequency development of side effects. To prevent their occurrence, the animal is fed foods with a high fibrin content. The animal is subject to an aseptic neurological examination during the first day of the disease. In case of urination disorder, a urine test, cultural examination and subsequent antibacterial treatment are indicated.If pain sensitivity is maintained, the prognosis is favorable. Loss of pain reflexes contributes to a significant worsening of the prognosis.

Neurological disease is a unique condition in which physical therapy is critical to maintaining and restoring function. Dysfunction of the nervous system can lead to impaired motor and autonomic function, as well as a range of sensory disturbances, including loss of sensation (analgesia), abnormal sensation (paresthesia), and increased sensitivity to stimuli (hyperesthesia). The secondary effects of these disorders can be as severe and disabling as the initial injury. For example, animals with peripheral neuropathy may develop muscle contractures that prevent any possibility of restoration of function, and the effects of prolonged lying, such as pressure ulcers and aspiration pneumonia, can be fatal.

A proper rehabilitation program should be an important component of the treatment plan for an animal with a neurological condition. Such a program should be planned in conjunction with treatment of the underlying disease, taking into account the cause of the neurological disorder (eg, central (CNS) or peripheral (PNS) nervous system disorder, central or peripheral motor neuron disease), severity of symptoms, expected progression, and the needs of the owner and animal. This article describes the pathological physiology of damage and recovery of the central nervous system and PNS, assessment of the condition of a neurological patient, data on the prognosis and expected course of recovery in a number of cases. various diseases, as well as rehabilitation exercises suitable for neurological patients.

Acute spinal cord injury

Pathological physiology

The most common causes of acute spinal cord injuries in dogs and cats are acute type 1 disc disease, trauma (vertebral fractures, dislocations, and hyperextension injuries), and vascular events such as fibrocartilaginous embolism (FCE). Types of spinal cord injuries include concussion, compression, rupture, and ischemia (Table 1). Primary injury, mechanical or vascular, initiates a cascade of events causing a progressive decrease in perfusion and neuronal necrosis. Most of these secondary tissue injuries occur within 48 hours of injury. Most acute spinal cord injuries are self-limiting (eg, fibrocartilaginous embolism) or amenable to surgical treatment (eg, decompression by removing bulging disc material).

The goal of treatment is to maximize the restoration of function due to the preserved nerve tissue. Restoration of central nervous system function does not occur due to the regeneration of nervous tissue, but due to the fact that the surviving tissue takes over the functions of damaged axons. So-called “complete” injuries that physically cut the spinal cord usually cause complete paralysis, but recovery is possible if some tissue remains at the site of injury connecting the two parts. This functional plasticity can be enhanced with appropriate rehabilitation exercises. To make a prognosis for recovery and plan the most appropriate rehabilitation program, it is necessary to differentiate the types of damaged nerve tissue.

Vascular and purely contusional injuries often result in the most severe damage to the gray matter of the spinal cord due to the death of neuronal cell bodies. If this occurs at the site of the passage of motor neurons that perform an important function (for example, the 4th and 5th segments of the spinal cord, which give rise to the femoral nerve), the consequences are devastating. If the injury occurs at the level of the thoracolumbar junction, where the motor neurons innervating the abdominal wall pass, the functional consequences are negligible. With extensive vascular injury or concussion, the surrounding tracts in the white matter are also affected, but the axons at the periphery, located under soft shell, are often saved. This is important when assessing the prognosis.

Animals with vascular spinal cord injuries often experience sudden and dramatic improvement in the first week. At first, the area of ​​edema surrounding the area of ​​spinal cord infarction prevents the conduction of action potentials. This swelling quickly subsides, so the function of the affected areas is restored.

Table 1. Tissue injuries associated with common neurological disorders in dogs

Abbreviations: FCE – Fibrocartilaginous embolism; IVD – intervertebral disc.

In contrast, compression injuries are more likely to damage the tract. white matter by damaging myelin, deforming ion channels, obstructing blood flow, and ultimately destroying axons. If axonal death and myelin damage are minor, surgical decompression of the spinal cord can quickly resolve clinical symptoms. Damaged myelin takes time to repair, but remyelination of CNS axons and restoration of function is possible. When axons are destroyed, which often occurs in chronic compression injuries, the chances of restoring function are reduced.

Acute intervertebral disc disease results in varying degrees of compression and concussion of the spinal cord, causing mixed damage to the white and gray matter. The degree of damage varies from minor loss of active nerve tissue, in which complete recovery can be expected, to extremely severe, with complete transection of the spinal cord.

Ruptures, most often observed in injuries, have more serious consequences, since in this case there is an actual violation of the integrity of the nervous tissue, that is, a truly complete injury. The prognosis for functional recovery from injuries of this type in animals with complete functional dysfunction of the spinal cord is more cautious. In some cases, surgical treatment of the underlying disease is not feasible due to financial limitations of the owner or other medical conditions. For example, after an injury that causes a spinal fracture, the animal may develop severe arrhythmia that prevents long-term anesthesia, or the owner may not be able to afford surgical stabilization. In such cases, recovery from rehabilitation is still possible as long as there is no further damage. The underlying mechanisms of subsequent injury include instability leading to repeated concussion and spinal cord compression, and ongoing severe spinal cord compression. However, spinal instability can be managed with simple external splints and treatment, but the physiotherapist should always be aware of the risk of further injury. In addition, the effect of ongoing compression of the nerve roots at their exit from the intervertebral foramina should always be considered. Nerve root compression can cause severe pain and be a limiting factor in the treatment of such cases.

Grade

When assessing a patient's condition, several important questions must be answered:

• It is necessary to examine all systems and identify all diseases, including existing orthopedic disorders.
• It is necessary to accurately determine the location of damage to the nervous system with an accuracy of one (or more, in the case of injury) of the four sections of the spinal cord: from the first cervical segment to the fifth; from the sixth cervical segment to the second thoracic; from the third thoracic segment to the third lumbar and from the fourth lumbar to the third sacral segments (Table 2).
• It is necessary to assess the severity of the lesion. Specific assessment parameters for different damage locations to obtain the necessary information are listed in Table 3.
• The degree of hyperesthesia and the possible source of pain (eg, postoperative pain, muscle spasticity, compression of nerve roots).

Table 2. Determining the location of spinal cord injuries in dogs

Table 3. Assessing the severity of spinal cord injuries in dogs

Assessment is necessary; - not necessary.
and animals usually survive unless there is severe damage to C1-5 with loss of deep pain sensitivity.

Specific components of assessment, forecasting and planning suitable program rehabilitation are described in the following sections.

Movement

The animal's ability to move is assessed as preserved or absent, or paresis (tetra-, para-, mono- or hemiparesis). If an animal is unable to move, for prognostic purposes it is necessary to differentiate complete paralysis (plegia) from paresis with loss of the ability to move. Scales have been developed to assess the severity of pelvic limb paresis. According to the most common scale for prognosis at the time of injury, the condition is assessed in points from 0 to 5, with 0 corresponding to normal, 1 - only hyperesthesia, 2 - paresthesia and ataxia, 3 - paraplegia, 4 - paraplegia with urinary incontinence and 5 - paraplegia with loss of deep pain sensitivity. A more detailed scale has also been developed to assess the degree of recovery in order to compare the effectiveness of different types of treatment.

Deep pain sensitivity

Assessing deep pain sensitivity is of primary importance when examining animals with paraplegia. This assessment is carried out with the animal lying on its side, or while holding it suspended in a position that is comfortable for it.

Using a hemostatic clamp, gently squeeze the fingers to the bone, first to evoke a withdrawal reflex, and then increase the pressure (the goal is to irritate the periosteum) until a conscious reaction occurs. It is believed that deep pain sensitivity is mediated by polysynaptic diffuse pathways of small diameter in the spinothalamic and propriospinal tracts, which lie deep in the white matter. Thus, significant damage must occur for conscious pain perception to be impaired. During acute injury, loss of deep pain sensation indicates functional transection of the spinal cord. However, this does not involve anatomical transection, so long-term loss of deep pain sensation does not necessarily imply complete damage to the spinal cord. Tetraplegia with loss of deep pain sensation is an uncommon presentation because spinal cord injuries severe enough to cause loss of deep pain sensation also cause paralysis of the respiratory muscles and loss of sympathetic tone to the heart, so most patients die before reaching the veterinary clinic. Exceptions include severe damage to the gray matter of the cervical enlargement (usually as a result of PCE), which can cause loss of deep pain sensation in one or both thoracic limbs while maintaining sensation in the pelvic limbs.

Respiratory function

Injuries to the cervical spine, causing tetraplegia with impaired respiratory function, are among the most severe and life-threatening. In animals with tetraplegia, it is absolutely essential to assess respiratory function and identify hypoventilation or other impairment. respiratory system(eg, aspiration pneumonia) before prescribing therapeutic exercises that may worsen the problem. For example, the weight of the water in a hydrotherapy bath can lead to decompensation due to hypoventilation.

Forecast and recovery

If measures are taken to treat the underlying spinal cord pathology and the problem is corrected, restoration of function is potentially possible in any animal with preserved deep pain sensitivity in the affected limbs.

Paraparesis

For animals with paraplegia, the best prognostic indicator is the presence of deep pain sensitivity. A significant amount of information has been accumulated on the prognosis and likelihood of recovery in animals with acute disc herniation in the thoracolumbar region. One study showed a direct relationship between recovery rates and body weight and age. Alternatively, a high percentage of dogs that recovered from paraplegia with loss of deep pain sensation had persistent mild urinary (32%) or fecal incontinence (41%). The same study examined the recovery of dogs with disc herniation that did not regain deep pain sensation, with long period observations. Approximately 40% of these dogs regained voluntary motor function and the ability to wag their tail, although deep pain sensitivity and incontinence remained. Average recovery time motor function was just over 9 months, and in one dog - 18 months. In most cases, restoration of the ability to wag the tail preceded the restoration of motor function of the pelvic limbs, that is, it served as a reliable prognostic indicator. It is hypothesized that motor function is mediated by surviving axons beneath the pia mater.

There is less reliable information about the recovery of dogs after FCE or injury. The most accurate prognostic indicator for both types of injuries is the presence of deep pain sensitivity. All dogs with preserved deep pain sensitivity recovered from injury, provided there was no further damage. For example, if a dog with a spinal fracture remains unstable, its condition may worsen to paraplegia with loss of deep pain sensation. There have been some studies on the prognosis of dogs with vertebral fractures and loss of deep pain sensation. If the vertebrae are displaced at the time of injury, restoration of function is extremely unlikely. If the vertebrae are not displaced, the chances of restoring function are increased, although they do not reach 50% for intervertebral disc diseases. Recovery after PCE is notable for the fact that in the first 7–10 days after the injury, rapid improvement. This observation may reflect the fact that the center of the affected area is often located in the gray matter, and the area of ​​surrounding edema involves the white matter.

Active discussions have arisen around the phenomenon of "spinal gait". This phenomenon has been observed in rodents and cats after surgical transection of the spinal cord and is thought to be possible in dogs. However, in the experience of one of the authors (NJO), dogs with spinal cord injuries with significant vertebral displacement and loss of deep pain sensitivity (i.e., indicating anatomical transection of the spinal cord) do not recover motor function, despite prolonged attempts at rehabilitation , although sometimes pronounced reflex movements of the pelvic limbs appear. In a group of dogs, motor function was restored (although it remained disconnected and insufficient) without restoration of deep pain sensitivity. All of these dogs had disc disease and would wag their tail randomly (for example, when they saw their owner). It is likely that these dogs retain some intact axons crossing the site of injury and that the dogs are more similar to humans in that they do not develop a spinal gait that could be exploited.

Tetraparesis

Information about the recovery rate of dogs with tetraparesis from different types of injuries is much less objective. In general, involvement of all four limbs complicates rehabilitation; therefore, recovery may be delayed. As noted earlier, it is extremely unlikely to encounter a patient with acute trauma, tetraplegia, and loss of deep pain sensation in all four extremities. In this case, the probability of survival of the animal is low. Hypoventilation as a result of trauma always indicates a poor prognosis unless artificial ventilation is provided.

Rehabilitation

The goals of rehabilitation programs for acute spinal cord disorders are to reduce postoperative and muscle pain, maintain joint range of motion, reduce muscle atrophy, and restore nerve and muscle function. These goals can be achieved through a rehabilitation program consisting of exercise, functional activity, and therapeutic modalities (Table 4).

Passive exercises are prescribed to neurological patients who have lost the ability to make voluntary movements or are unable to move due to severe proprioceptive impairment.

Passive range of motion

Passive movement of each joint with a normal range of motion helps maintain healthy joints in patients with impaired voluntary motor activity. Passive range of motion (ROM) exercises do not improve muscle strength or mass; for stimulation muscle tissue Active exercises are required to maintain range of motion.

Step 1. Immediately after surgery:

• Applying cold to the seam.
• Exercises to maintain range of motion.
• Massage of the muscles of the limbs.
• Care:

The animal needs soft, voluminous and dry bedding.
Turn the animal over at least once every 4 hours to avoid bedsores, preferably once every 2 hours.
Make sure the animal remains dry and clean.
Water and food must be available to the animal
Monitor your bladder and bowel movements.

• Inspect the paws and bony prominences for ulcers or abrasions; If necessary, safety boots can be used.

Step 2: Ability to support your own weight (without moving your limbs):

• Exercises to maintain the range of passive movements.
• Standing in the water.
• Neuromuscular stimulation.

Step 3. Initial movements of the limbs.

Exercises to maintain the range of passive movements:

• Exercises in a standing position.
• Exercises before walking and exercises with body weight transfer.
• Walking (on a treadmill, dry ground) depending on the degree of assistance required.
• Swimming (with support).
• Neuromuscular stimulation.

Step 4. The animal can move its limbs well. Exercises to maintain the range of passive movements:

• Exercises with getting up from a sitting position.
• Exercises for balance and coordination.
• Walking (on a treadmill, dry ground, sand, snow).
• Swimming (with support).

Step 5: Almost normal gait Balance and coordination exercises:

• Walking (longer duration, up an inclined surface or steps).
• Swimming.

Exercises to maintain APD should be performed with the animal lying on its side on a soft surface. The upper limbs are carefully flexed and extended at each joint to a degree that is comfortable for the patient. Animals with spinal cord injury typically exhibit increased muscle tone or spasticity.

To overcome this tone, you should not place your hands on the lower surface of the animal's paws (which can cause an extensor reflex). Applying differential pressure under the knee joint or to the front of the elbow helps relieve the tone. If there is a strong increase in tone, gentle flexion of the fingers can reduce extensor tone. After 15-20 cycles of movement in each joint, you can move on to rotational movements (as when riding a bicycle) and do another 15-20 repetitions. Then the animal is turned over and the same exercises are performed with opposite limbs.

Exercises should be performed 3-4 times a day until the animal begins to move independently.

Inducing the flexion reflex

In patients with central motor neuron disorders, inducing the thoracic or pelvic limb withdrawal reflex results in active flexion of the elbow and wrist or knee and hock joints, respectively, and increased muscle tone. To perform this exercise, the animal must be laid on its side and the skin between the toes of the thoracic limb should be pinched. Since the reflex causes an active withdrawal of the limb, to create resistance, the doctor gently holds the paw, creating a “tug of war” effect in which the patient pulls harder on the limb to release it from the grip.

This exercise is repeated 3 to 5 times, 3 to 4 times a day.

Inducing the knee (extensor) reflex

Similar to the flexion reflex, the patellar reflex enhances muscle tone and muscle strength in patients with weakened conduction or intact femoral nerves. This exercise should be prescribed to patients with central motor neuron dysfunction to benefit from a normal or enhanced extensor reflex. To stimulate contraction of the quadriceps muscles, the patient is placed in a standing position with the entire surface of the hind paw pads on the floor. Sometimes the animal needs help to maintain this position. The animal's hindquarters are then gently lifted (to lift the toes off the ground) and lowered so that the animal has to support its weight as the hindquarters are lowered to the ground. The patient can be left standing until he begins to fall; at this point the animal is supported and returned to a standing position. Alternatively, you can induce the extensor reflex by placing your hand on the sole and pressing on it. This exercise should be repeated 15 - 20 times 2 - 3 times a day.

Active exercises

These exercises are designed to improve muscle strength, neuromuscular balance, and coordination in patients who still have some ability to move their limbs voluntarily. In patients with acute illness, muscle and nerve dysfunction is more important than muscle atrophy, which influences the choice of rehabilitation measures. In people with spinal cord injuries, starting rehabilitation with resistance training earlier (within 2 weeks of injury) improves motor performance and function.

Seated rise exercises strengthen the knee and knee extensors. hip joints and are indicated for patients whose mobility and muscle strength are sufficiently preserved to stand without or with minimal support. The animal is seated and forced to stand on all four limbs. The exercise is repeated 3 to 5 times, 2 to 3 times a day until movements and gait are restored to an almost normal degree. This exercise can be performed before other active exercises; however, if the patient is too tired, breaks should be taken between exercises.

Walking with support

If some degree of voluntary movement is preserved, several short walks a day will increase muscle strength and improve neuromuscular coordination. If necessary, to support the back of the body, you can use a loop of tape with a soft lining (ready-made or made independently from smooth fabric or Vetrap dressing material). If recovery is expected to be long, a cart or wheeled chair with a counterweight may be used to help the animal move around. Ideally, a non-slip floor covering is needed to improve proprioception and facilitate proper positioning of limbs. You can use commercially available shoes for extra traction. You can also use a treadmill, floor or underwater. Walking on a treadmill has been shown to promote a smooth and symmetrical gait in people with hemiplegia, and buoyancy when exercising on an underwater treadmill or in a pool helps the patient support their body weight. Walking should be slow and last from 2 to 5 minutes, depending on the ability of the patients. It is advisable to stop the exercise before fatigue develops; It is better to perform the exercise briefly several times a day than for a longer period 1-2 times a day.

Walking exercises

Once the patient is able to walk, even with residual proprioceptive impairment, some resistance can be added to strengthen the muscles. To do this, walk up a strong inclined surface; vigorous walking on a treadmill underwater, with elastic exercise bands, on sand or snow. The depth of the water, sand or snow determines the amount of resistance the patient must overcome when walking. For postoperative patients, one of the authors (KVN) recommends starting underwater exercises no earlier than 7–14 days after surgery and only after confirmation of healing of the surgical wound. Like assisted walking, resistance walking should be limited to 2 to 5 minutes depending on the patient's level of fatigue. It can be performed daily or every other day until normal gait is restored.

Swimming

The benefit of aquatic therapy is to minimize the effort required to support weight, which allows the patient to increase the range of motion in the joint, as well as muscle strength. In people with spinal cord injuries, exercise in water has been shown to reduce muscle spasticity and increase muscle strength. Because swimming can be accompanied by strong muscle contractions, one of the authors (KVN) recommends waiting 4 to 6 weeks after surgery to allow the tissue in the laminectomy or pediculectomy area to heal sufficiently. In between, you can schedule walking on a treadmill underwater.

When swimming, a patient with a neurological impairment needs support, either manually or using a swimming vest. For small breed dogs, you can use a bathtub filled so that the animal cannot touch the bottom as a swimming pool. For maximum patient comfort during exercise, the water temperature should be from 25 to 30 o C. More large dogs A public or home swimming pool is required (preferably 1.5m wide x 2.5m long x 1.2m deep). In addition, you can use an underwater treadmill with a flow created by a stream of water that allows you to swim. Some patients get tired quickly, so swimming should be limited to 2 to 5 minutes every other day.

There are several exercises that can improve balance and coordination, especially in patients with severe proprioceptive impairment who are capable of voluntary movements. Due to nervous muscle weakness These exercises may require support. A simple coordination exercise involves lifting a limb off the ground from a standing animal. With such a lift, the animal has to redistribute its weight to the remaining limbs. The exercise can be performed with each limb alternately. You can place treats on the floor in front of your pet to encourage him to reach for them, redistributing his weight.

For this purpose, you can use several commercially available or home-made shells.

Balance balls are large-diameter gymnastic balls on which the animal can be placed and supported by rolling the ball to redistribute the load on the front and hind limbs.

A balance board is a rectangular piece of plywood with a narrow rod running along the bottom. When the animal stands on the board, it tilts laterally or cranio-caudally depending on the orientation of the rod.

You can use obstacles in the form of horizontal bars that rise to such a height that the animal has to raise its limbs to step over them. In addition, standing or walking on a mattress filled with porous material is suitable for improving balance and coordination.

Exercises to develop balance and coordination can be included in regular walks. For example, part of the walk can be devoted to walking over horizontal obstacles or on a mattress. These exercises are continued until normal or nearly normal gait is restored.

Therapy methods

Applying cold

Cryotherapy helps relieve pain from acute post-operative inflammation.

In the first 2 days after surgery, a cold pack wrapped in a damp towel can be applied to the surgical incision for 10 to 15 minutes. During inflammation, this procedure can be repeated every 4 hours. If wet towels are used during recovery from anesthesia or sedation, the patient should be carefully monitored (use dry towels for sedated animals). Inflammation (pain, redness, and swelling) in the incision area for more than 48 hours may indicate an infection and requires proper evaluation and treatment.

Ultrasound therapy

The therapeutic effects of ultrasound on soft tissue help relieve pain by improving blood flow to the tissue and promoting healing. Ultrasound may be beneficial for epaxial muscle spasms. Its use is contraindicated when spinal cord tissue is exposed, and continuous ultrasound is not recommended for postoperative neurosurgical patients. For non-surgical patients with acute spinal cord disease and neuromuscular spasms, ultrasound treatment of the epaxial muscles helps relieve pain and spasms.

Neuromuscular stimulation

Electrical stimulation of nerves and muscles in patients with acute spinal cord diseases can improve tissue perfusion, reduce pain, and slow the progression of muscle atrophy due to inactivity. In patients with peripheral motor neuron disease, stimulation of the affected muscle groups slows the development of neurogenic muscle atrophy and reduces its severity. Electrical stimulation is preferable for muscle groups that do not spasm. It is contraindicated in the area of ​​laminectomy or pediculectomy until the tissue has healed sufficiently. Neuromuscular stimulation of muscle groups in the affected limbs should be applied once daily for 15 minutes until ambulation is restored with mild to moderate ataxia.

Chronic spinal cord injuries

Pathological physiology

Chronic spinal cord disease is a common and insidious problem in older dogs of large and small breeds. Usually the result of degenerative changes in the vertebrae and associated soft tissue strictures. Examples include cervical spondylomyelopathy (instability syndrome in all its forms), Hansen type II intervertebral disc disease in the thoracic and cervical regions, spinal malformations (atlantoaxial joint subluxation and stenosis spinal canal), and cystic changes(subarachnoid cysts and syringohydromyelia). Degenerative diseases of the lumbosacral region primarily affect the peripheral nerves of the cauda equina and are discussed in the section on peripheral neuropathies. Tumor diseases also lead to chronic compression and, if the tumor is growing slowly or has been treated, rehabilitation plays an important role in pain relief.

In general, chronic compression diseases cause damage to nerve tissue by compressing it, causing demyelination, deforming axonal membranes and ultimately leading to their death. If the spinal cord is viable and there are no symptoms of acute deterioration, decompression promotes recovery. However, histological examination in chronic compression diseases, such as caudal cervical spondylomyelopathy, shows significant gray matter damage. Such damage may be caused by impaired blood supply to the spinal cord as a result of compression, as well as minor injuries due to concussion during spinal movements caused by hypertrophied soft tissues(eg, annulus fibrosus), or bone (eg, articular surfaces). Strengthening the muscles can have the beneficial effect of minimizing any sudden movements and helping to maintain a normal range of motion in the spine.

Grade

The approach to assessing animals with chronic and acute paresis is identical. It is important to identify other chronic conditions, such as degenerative knee diseases, and to look for long-term secondary effects of neurological disease (chronic urinary tract infections due to impaired urination). Hyperesthesia can become a significant problem in such cases, especially in animals with cervical lesions. The severity and possible causes of hyperesthesia should be established. Additionally, due to the chronic nature of symptoms, any significant muscle atrophy should be noted and taken into account when planning a rehabilitation program.

Forecast and recovery

Recovery expectations and treatment goals are different for chronic and acute spinal cord injuries. First, spinal cord injury is usually caused by some structural abnormality of the spinal cord or spinal column, which often cannot be identified. For example, cervical instability syndrome is thought to result from actual instability, but it is difficult to demonstrate with radiography and biomechanical studies. Surgical decompression and stabilization of the spinal cord does not always correct the disorder that caused the problem, or may change the dynamics of adjacent areas of the spine. Complete cure usually does not occur, and symptoms return relatively often. As discussed in the section on pathological physiology, the role of physical therapy in the treatment of the underlying spinal cord abnormality can be critical and is an area in need of development.

The second problem is that in chronic spinal cord diseases the damage increases gradually, allowing the animal to compensate; therefore, symptoms become apparent only after significant irreversible damage has developed. The predicted recovery is not as rapid or complete compared to acute spinal cord injuries. It is preferable to begin conservative or surgical treatment while the animal is still able to ambulate. Results described surgical treatment cervical spondylomyelopathy with various techniques. In general, even in dogs unable to move, recovery of this ability occurs in 80% of cases, although the relapse rate is at least 20%.

Rehabilitation

The goals of a rehabilitation program for chronic spinal cord diseases are to reduce postoperative and muscle pain, maintain joint range of motion, correct muscle atrophy, and restore nerve and muscle function. To achieve these goals, rehabilitation programs consisting of therapy and exercises are used (see Table 4).

Passive and reflex exercises

Passive exercises should be prescribed to neurological patients who are unable to make voluntary movements or have insufficient muscle strength, as well as in cases where proprioceptive impairment interferes with normal movement. In animals with a chronic disease, the range of motion in the joint is determined by the duration of the process and the severity of neurological disorders. In these patients, baseline joint range of motion should be determined to determine which joints are most affected and require preferential attention.

Passive range of motion

Passive movements in each joint with a normal amplitude help maintain healthy joints in patients with voluntary movement disorders and help restore normal range of motion when it is limited. Methods of exercises to maintain the amplitude of passive movements have been described previously. Passive exercises do not strengthen muscles or increase their mass. Exercises to maintain passive range of motion for chronic patients should be performed 3 to 4 times a day until they begin to move or until the recovery process reaches a plateau.

Stretching

In joints with limited range of motion, passive exercises should be combined with stretching exercises to help restore function to the affected joint. The affected joint and adjacent muscles must be pre-warmed by applying heat or massage, and then performing passive exercises to maintain the range of motion in the joint. After appropriate maximum extension and flexion, the limb should be gently pulled, keeping the joint in a position maximum flexion or extension. For destruction fibrous tissue Careful jerking movements can be made around the joint. If the patient experiences discomfort after stretching, cold may be applied to the joint.

Inducing the flexion and knee (extensor) reflex

The flexion and extension reflexes in patients with chronic neurological disease are evoked in the same way as in patients with acute neurological disease. This exercise is repeated 20 times 2 - 3 times a day.

Active exercises

Active exercises are aimed at increasing muscle strength, neuromuscular balance and coordination in patients who have retained at least some ability for voluntary limb movements. In patients with chronic disease, muscle atrophy may play almost as much a role as neuromuscular dysfunction, and the rehabilitation protocol should address both disorders.

Exercises to get up from a sitting position

As described previously, sit-to-stand exercises strengthen the knee and hip extensors and are indicated for patients with sufficient motor activity and muscle strength to stand up.

Supported and resisted walking, swimming, balance and coordination exercises

These exercises are similar to those described for patients with acute neurological disorders. In chronic diseases, they are especially important, since recovery in such cases can be lengthy.

Therapy methods

For patients with chronic neurological impairment, cold application, ultrasound therapy, and neuromuscular stimulation can be used as previously described for the treatment of patients with acute neurological impairment. Neuromuscular stimulation helps restore muscles that have atrophied due to prolonged inactivity.

Peripheral nerve damage

Pathological physiology

Common causes of damage peripheral nerves include fractures (for example, fractures of the femur with damage to the sciatic nerve), intramuscular injections(usually damaging the sciatic nerve), traumatic avulsion brachial plexus and improper surgical technique. Vascular injuries are also possible, the most common of which are thrombosis iliac artery in cats, leading to distal sciatic neuropathy; in addition, thrombosis of the brachial artery occurs, causing monoparesis of the thoracic limb. The difference between peripheral nerves and their counterparts in the central nervous system lies in their ability to regenerate at a rate of up to 1 mm per day. For regeneration to be possible, nerves must be surrounded by Schwann cells.

Peripheral nerve injuries are classified according to severity into three groups, as described below:

• With neurapraxia, the conduction of impulses along the axon is disrupted without destruction of the axon itself. This is usually caused by compression, temporary ischemia, or blunt trauma. Loss of conduction may result from myelin damage or insufficient energy to maintain the axon's resting potential.
• During axonotmesis, the integrity of the axon is disrupted, but the endoneurium and the Schwann cell sheath in which it is located remain intact, allowing tissue regeneration to the target cell. Successful regeneration is possible, especially if the site of axonal injury is close to the target cell.
• With neurotmesis, the structure of the nerve is completely disrupted. The axon is capable of regenerating, but to do this it must find a sheath from the Schwann cell, which complicates the process. The prognosis for recovery from such injuries is guarded even with surgical treatment.

In case of peripheral nerve injuries, sensitivity and muscle atrophy must be taken into account. Regeneration of peripheral nerves, as well as any disease that causes peripheral neuropathy, can be accompanied by unpleasant abnormal sensations (paresthesia) and hyperesthesia, both of which can lead to self-injury. The consequence of muscle denervation is severe muscle atrophy, which over time can lead to contracture and, in growing animals, to skeletal deformities.

Grade

As with spinal cord injuries, a neurological examination is necessary to determine the exact location of the injury and its severity. You should know the muscles innervated by each nerve. In addition, it is advisable to refer to manuals that show the areas of skin innervation by peripheral nerves. The severity of the lesion is determined by assessing the degree of motor function and deep pain sensitivity.

Electrophysiological assessment of muscles and nerves using electromyography (EMG) and nerve conduction velocity studies allow us to establish in more detail the severity and dynamics of the injury. In completely denervated muscles, spontaneous electrical activity appears at rest, although such changes do not appear until at least a week after denervation. Nerve conduction study results should be interpreted with caution. Immediately after injury, there may be loss of conduction at the site of injury, while conduction in the distal portion of the injured nerve may persist from several hours to several days. As nerves regenerate and innervation of denervated muscles is restored, the size of the motor units increases and, consequently, the magnitude of the motor unit potentials on the EMG increases.

Forecast and recovery

Neurotmesis generally has a poor prognosis unless immediate surgery is performed to repair the damaged nerve. Axonotmesis or neuropraxia has a better prognosis. Neuropraxia usually resolves within 2 weeks of injury, although myelin damage delays recovery by up to 4 to 6 weeks. In axonotmesis, recovery depends on the proximity of the injury site to the innervated muscle, the severity of muscle atrophy, and the presence of contractures. If the damaged area is located far from the target muscle (for example, in the brachial plexus), severe muscle contracture may develop by the time the axon grows, limiting recovery options.

Brachial plexus injuries are more common in the caudal 2/3 (radial, median, ulnar and lateral thoracic nerves, as well as sympathetic innervation of the head) or cover the entire plexus, although damage to the cranial part has been described. When examining animals with damage to the caudal part of the plexus, errors are possible, since the function of the musculocutaneous nerve and elbow flexors is preserved. This function does not play a role in weight bearing ability and should not be used to assess prognosis. Instead, deep pain sensation, especially of the lateral finger, should be assessed. The absence of deep pain sensitivity in this finger indicates severe damage to the radial nerve. If sensation is not restored within 2 weeks after injury, the prognosis for recovery of useful motor function of the limb is guarded.

Rehabilitation

The goals of a rehabilitation program for patients with peripheral motor neuron injury are to restore and maintain joint range of motion, strengthen muscles, restore neuromuscular junction function, and prevent self-injury and injury to the affected limb. The absence of spinal reflexes and corresponding muscle tone in such patients greatly complicates their rehabilitation, in which it is necessary to pay attention Special attention restoration of muscle and joint function.

Passive and reflex exercises

Because of the disruption of the spinal reflex arc in patients with peripheral motor neuron disorders, they require passive exercise until near-normal gait is restored.

Passive exercises to maintain range of motion, stretching

These exercises are used in the same way as for acute and chronic neurological disorders. Stretching the affected and antagonist muscles may be beneficial for peripheral motor neuron dysfunction. Loss of tone of antagonist muscle groups predisposes to the development of joint contractures. Massage of muscle groups with minor contracture can also help restore their function; it is carried out 2 – 3 times a day after pre-warming the area.

Inducing flexion and knee (extensor) reflexes

In animals with impaired sciatic nerve function, it is not always possible to induce a withdrawal reflex. However, it is necessary to monitor progress by periodically assessing the reflex arcs of the spinal reflexes.

In patients with weakened or preserved withdrawal reflexes, inducing the flexion reflex improves muscle tone and neuromuscular coordination. Patients with femoral nerve injury require significant assistance to maintain this position. To support the body while slowly lowering the hind legs to the ground, you can use a gymnastic (Swiss) ball. The animal's hindquarters are then carefully lifted (so that the toes are off the ground) and lowered so that the animal is required to support its body weight as the hindquarters are lowered.

Radial nerve stimulation

For mild disorders of the radial nerve function, exercises based on the forelimbs are useful. Patients with complete loss of elbow or wrist extensor function (eg, brachial plexus avulsion) should not perform this exercise until some extensor tone has been restored. To perform the exercise, the animal is positioned with its torso and forelimbs supported. Then the degree of support is gradually reduced, while the animal’s front paws should rest on the ground with their entire surface. When the animal's forelimbs begin to sag, the therapist supports the animal and returns it to a standing position. An exercise ball or custom-made orthotic devices may be used to support the patient. The exercise is repeated 5 times, 2 – 4 times a day.

Active exercises

These exercises are aimed at strengthening muscles, improving neuromuscular balance and coordination in patients who have retained at least some ability for voluntary movements of the limbs. In certain animals with peripheral nerve damage in more than one limb, impaired neuromuscular transmission may interfere with some exercise performance.

Sit-to-stand exercises, assisted and resisted walking, and swimming

Many animals with sciatic nerve dysfunction are able to rise from a sitting position, as this requires active extension in knee joint, but passive flexion at the knee and hock joints.

Balance and coordination exercises

Such exercises are useful for patients with peripheral nerve damage. The correctness of their implementation was described earlier.

Therapy methods

Neuromuscular stimulation

Neuromuscular electrical stimulation in case of peripheral nerve disorders, it helps to slow down the development of neurogenic muscle atrophy and restore the condition of the affected muscles. When the affected muscle is completely denervated, electrical stimulation is considered the method of choice.

Stimulation of the affected muscle groups is carried out once a day for 15 minutes for each.

Neuromuscular diseases

Pathological physiology

Neuromuscular diseases include neuropathies, neuromuscular junction disorders, and myopathies. The most common neuropathies requiring rehabilitation include immune-mediated polyradiculoneuritis (also known as canine coonhound paralysis), infectious neuritis (eg, caused by Neospora caninum), degenerative or toxic neuropathies (breed or developed due to diabetes or insulinoma) and compression neuropathies (for example, in degenerative diseases of the lumbosacral region).

Botulism is the most significant functional impairment requiring rehabilitation. Distinguish Various types myopathies, including infectious/inflammatory (immune-mediated polymyositis and protozoal myositis), degenerative (muscular dystrophy) and metabolic myopathies.

Before planning a rehabilitation program, it is necessary to carefully consider the various possible pathological processes. For example, in animals with X-linked muscular dystrophy, muscle necrosis or myocardial failure may rapidly develop with excessive exercise.

In general, diseases affecting peripheral motor neurons lead to severe and rapid muscle atrophy, and over time, contractures can form that limit joint mobility. In addition, the muscles of the esophagus, pharynx, and larynx may be affected, leading to potentially fatal swallowing disorders and aspiration pneumonia. These disorders may be complicated by hypoventilation, especially in bedridden animals. Myopathy and botulism can cause cardiac damage, another potentially fatal complication.

Grade

Following a routine assessment of a patient with generalized peripheral motor neuron disorder, specific parameters should be assessed, including:

• The severity of symptoms of damage to peripheral motor neurons and the extent of the damage, that is, the differentiation of the ability and inability to move, as well as tetraparesis and tetraplegia with the inability to move.
• Respiratory function for the presence of hypoventilation (partial pressure of carbon dioxide in arterial blood) or aspiration pneumonia
• Function of the esophagus, larynx, and pharynx by carefully questioning the owner about voice changes, cough after eating or drinking, and regurgitation. You should also do x-rays chest to detect megaesophagus.
• Heart function. Ideally, for generalized myopathies, echocardiography should be done.
• The presence and severity of muscle atrophy and range of motion in the joints to establish the initial condition.

Forecast and recovery

Although the prognosis and course of recovery are highly dependent on the underlying disease, the following general statements can be made:

• Dysfunction of the esophagus, pharynx and larynx worsens the prognosis, especially if the animal has aspiration pneumonia. The physical therapist performing exercises on the animal should be aware of this potential complication.
• Hypoventilation to a degree requiring mechanical ventilation significantly worsens the prognosis.
• The more severe the muscle atrophy, the longer the recovery. The appearance of muscle contractures can impede recovery even after the underlying disease has resolved.
• If the underlying disease is incurable (X-linked muscular dystrophy, hereditary neuropathy such as polyneuropathy/laryngeal palsy complex), the role of the physiotherapist is to relieve the animal's symptoms. It is very important to prevent a crisis caused by aspiration pneumonia or an episode of muscle necrosis. In addition, physical therapists can recommend appropriate protective and assistive devices, as well as preventative and posture techniques for caring for the animal at home and for safe transport to the clinic if necessary.

The literature describes the expected course of recovery from some common self-limiting diseases. Recovery from botulism requires the production of new proteins to replace those bound by botulinum toxin, which usually takes about three weeks. If maintenance treatment is successful during this period, the animal should recover. Most dogs with immune-mediated polyradiculoneuritis recover in 3 to 6 weeks. Both diseases require intensive physical therapy and supportive care during the recovery period for the animals to survive.

Rehabilitation

The goals of the rehabilitation program for generalized neuromuscular diseases are determined pathological physiology specific diseases and specific neurological disorders. Because generalized weakness and peripheral motor neuron dysfunction are common clinical features of most neuromuscular disorders, rehabilitation of such patients includes optimizing housing conditions, maintaining joint range of motion, preventing neurogenic muscle atrophy, and restoring muscle and nerve function. These goals can be achieved through a rehabilitation program with exercise and therapy.

Passive and reflex exercises

These exercises are performed in the same way as described earlier.

Active exercises

Exercises with standing up from a sitting position, walking with support and resistance

For dogs with neuromuscular diseases, the active exercises described earlier are used. Walking on a treadmill underwater is especially beneficial for patients with generalized neuromuscular disorders, as buoyancy compensates for their weakened condition. Due to muscle weakness and the risk of drowning, it is important to constantly monitor the animal's head position while it is in the water.

Swimming

When swimming animals with generalized neurological diseases, it is important to provide constant support, manually or using a swimming vest. As with walking on an underwater treadmill, the therapist must constantly monitor head position to avoid drowning or aspiration. Such patients tire easily, so swimming should be limited to 1 to 3 minutes every 2 to 3 days.

Therapy methods

Neuromuscular stimulation

Electrical neuromuscular stimulation for generalized neuromuscular dysfunction helps improve tissue perfusion and minimize neurogenic muscle atrophy. The muscle groups of the affected limbs are stimulated once a day for 15 minutes for each group.

Summary

Rehabilitation of dogs with neurological diseases consists of a combination of active and passive exercises, functional and therapeutic methods. Coordinated involvement of the patient, owner, and physician is key to maximizing the restoration of function.

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Restriction in movement for a cat is a serious problem both for him and for the owner. Lack of mobility of the hind legs may result in complete or partial immobilization. Complete immobilization is called paralysis of the limbs, partial - paresis.

Failure of a cat's hind legs: causes and provoking factors

Failure of a cat's hind legs may be due to an ongoing inflammatory process in the spinal cord.

There may be several reasons and all of them associated with serious diseases , which are difficult to treat, or even not treatable at all. Factors may be the following:

• mechanical damage to the spine - trauma;
• inflammatory processes in the spinal cord;
• embolism of a fibrocartilaginous nature;
• arterial thromboembolism;
• consequence of a stroke;
• mite infestation;

Pathologies such as kidney damage, myasthenia gravis, and medications can also lead to a similar phenomenon.

Risk group

There are diseases that are more common to certain breeds of cats that lead to a similar symptom.

In the breed burmese Hypoglycemia is considered such a disease. For and Chartreuse– femoral dysplasia. Cymriks suffer from congenital weakness of their paws. In addition, a lack of foods containing thiamine in the menu can also be a cause of paresis or paralysis.

The Burmese cat breed is at risk for the disease.

Each disease has characteristic signs and causes.

Spinal cord inflammation

This disease is characterized by a disorder of the functions of the substances filling the cavity of the spinal cord.

The cause of the disease can be inflammatory processes in the uterus during the cat’s pregnancy.

Making a diagnosis includes taking an anamnesis, clinical studies, and differentiating infectious pathologies.

Help and treatment

The best help is timely help!

• Help consists of placing the animal in dark room , ensuring peace.
• Procedures in the form of UHF, electrophoresis .
• Carry out paw massage and lumbar region.
• Intravenous glucose infusion and ascorbic acid.
• Recommended injections: thiamine, pyridoxine, cyanocobalamin .
• To prevent muscle atrophy, the following drugs are acceptable: nitrates of strychnine, securin, echinopsis, chilibuha extract, proserin .

To ensure peace for your cat, you need to place it in a dark room.

Fibrocartilaginous embolism

The cause of the disease is blockage of the spinal cord vessels, which leads to tissue necrosis. As a result, the cat may lose the ability to move its hind and front legs.

The cat loses the ability to move its hind legs due to blockage of the spinal cord vessels.

This is for cats rare disease , most often affects dogs. The main symptoms are expressed in sudden pain syndrome, which passes quickly. Then the cat becomes apathetic, lacks sensitivity in the area of ​​the hind legs and lower back, there may be partial loss and then the prognosis is cautious. If the pet does not respond to stimuli - prognosis is unfavorable.

Therapy

At an early stage of the disease, it is permissible to introduce methylprednisolone into the body.

Therapy is supportive. Physiotherapy is provided in full. It is acceptable to administer a large volume at an early stage of manifestation. methylprednisolone , but due to the severe course of the disease and the almost always sad outcome, this measure is doubtful.

Arterial thromboembolism

Arterial thromboembolism complicates the work of the cat’s heart.

Severe tissue ischemia resulting from a thrombus of the aorta or artery is called arterial thromboembolism.

Illness complicates the work of the heart , causing heart failure, as well as as a result of muscle and nervous ischemia, affects the functioning of the nervous system and causes damage to the functioning of the musculoskeletal system.

Symptoms

Diagnostics and femoral pulse.

In addition to restricting movement, it causes severe pain on palpation . There is no femoral pulse, and cyanosis of the paw pads is visible. Decreased temperature in the affected extremities. Maybe cardiopalmus when listening or the presence of heart murmurs. The animal constantly breathes with its mouth wide open, visible weak signs shortness of breath.

When sick, a cat constantly breathes with its mouth open.

Diagnostics

Diagnosed by physical examination, urine samples and general examination. Thoracic radiography is performed to detect fluid in the lungs. Echocardiography and computed tomography are performed.

To diagnose the disease, urine samples are taken from the cat.

Treatment

Treatment is aimed primarily at eliminating pain through the use of opioids.

Infusion therapy is prescribed for treatment.

1. Next, the blood clot is eliminated.
2. Anticoagulants are prescribed, and the use of antioxidant and infusion therapy is recommended.
3. Acceptable solutions are those that promote the resumption of microcirculation and are anti-shock agents.
4. Thrombolytic drugs: streptokinase for three days, urokinase for 24 hours, altepase.
5. It is advisable to use heparin therapy: dalteparin, enoxaparin.
6. It is possible to prescribe aspirin as an antiplatelet agent.

Cardiomyopathy

The pathology is not common among felines, but age takes its toll and the risk of cardiomyopathy increases. In this case, the hind legs are taken away.

A cat loses its hind legs due to cardiomyopathy.

The essence of the disease lies in pathological changes in the structure of cardiac muscle tissue. There are four types of the disease.

Most common species – hypertrophic , which is expressed in the enlargement of the heart itself due to the thickening of its walls. The dilated form also occurs due to an increase in the volume of the heart, but not due to thickening of the walls. The organ itself becomes flabby and weak, which interferes with the normal contraction process and leads to oxygen starvation of the entire body.

Fibrosis of the heart muscle

The presence of fibrosis of the heart muscle is characteristic of the restrictive type. The heart loses its softness, resulting in the same oxygen starvation of the whole body.

With fibrosis of the heart muscle, oxygen starvation of the entire body occurs.

A very rare and almost non-existent form - intermediate , which is characterized by the presence of several types of myocardiopathy at once. The causes are other pathologies: hyperthyroidism, increased arterial pressure, excess growth hormone. Also factors are: congenital anomaly Bull's heart, lymphoma, overdose or misuse of drugs, a genetic predisposition that affects all artificially bred breeds.

Symptoms

At the initial stage of the disease, when listening to a cat, extraneous heart sounds can be heard.

Symptoms at the initial stage almost invisible . Then, when listening to the heart, you can hear noises, an atypical heartbeat rhythm, like a gallop, an irregular pulse - a decrease or increase.

Therapy

Therapy includes the use of Atenolol.

• Therapy involves the use of beta blockers - atenolol, propranolol.
• Calcium channel blocking drugs, in particular diltiazem.
• Ramipril, enalapril as inhibitors.
• But it is also permissible to prescribe pimobendan in parallel, which is capable of dilating blood vessels.
• It is advisable to use diuretics.

Whatever disease causes the failure of a cat’s hind legs, it is recommended that the specific treatment be diluted with additional measures.

In addition to therapeutic measures includes massage of the cat's lumbar region and hind legs.

1. Massage of the limbs and lumbar region is indicated in order to prevent atrophy of the muscle tissue of the hind legs. Should be done every day for about ten minutes.
2. Some kind of gymnastic exercises will be a good help.
3. You need to imitate the walking or running movements of the animal’s limbs. It is possible to imitate primitive walkers, when the fabric supports the cat under the stomach, and the paws move quietly along the floor.
4. Swimming worked well. The pet strains its paws, involuntarily moves them in the water, while the owner supports it under its belly. You can also use a small ball. Place the cat on top and roll it back and forth so that its limbs touch the floor.

Video about failure of a cat's hind legs