Ataxia in dogs: symptoms, treatment for puppies and adults

Ataxia in dogs is a disease that gives the animal virtually no chance if the owner does not notice alarming symptoms in time and does not seek help from a veterinarian. The disease is associated with dysfunction of the cerebellum, the main part of the brain. With severe ataxia, the dog loses the ability to coordinate its movements and maintain balance. This disease can be congenital, genetic, or acquired. Today we will talk about the causes of ataxia in dogs, its symptoms and treatment.

Ataxia in dogs: symptoms and treatment

Types of ataxia

Depending on the location of the lesion, ataxia exists in three forms: general proprioceptive (sensitive), vestibular and cerebellar ataxia in dogs - the cerebellar form.

Cerebellar

Cerebellar ataxia in dogs can be characterized by either a sudden onset or a chronic course, be congenital or occur for a number of reasons, progress or remain stable.

As the main coordinator of movements and balance regulator, the cerebellum also controls the animal’s muscle strength and ensures the rhythm and balance of these movements. Because of this, the affected cerebellar hemispheres lead to dynamic ataxia of the limbs, and dysfunction of the cerebellar vermis results in the dog’s inability to maintain body balance and maintain a certain posture (static subtype).

Congenital pathology is caused by autosomal recessive inheritance. The dog receives from each parent 2 defective copies of the mutated gene, affected by ataxia. In this case, the pathology is considered as an isolated disease. The congenital form may not progress throughout the dog’s life.

Acquired cerebellar ataxia in some cases develops as a result of the following pathologies:

tumors in the brain;
falling from height;
autoimmune diseases (systemic lupus);
brain infections and severe inflammation;
collision with a car;
anomalies in the development of cerebellar structures and the structure of the skull;
degenerative processes in cerebellar cells;
metronidazole intoxication;
acute thiamine deficiency;
ischemic infarction in older dogs;
helminthic intoxication.

In most cases, characteristic signs of the disease begin to appear after 3 or even 5 years.

Ataxia is manifested by the dog's awkwardness, which is unusual for the owner, and a gait with widely spaced paws, which is initially most noticeable after the animal has woken up and is trying to get up. After a certain time, strange swaying of the body and a clear inability to maintain balance become more and more obvious.

Read Removing the fifth toe from a puppy and an adult dog: 3 stages

Male dogs begin to lose balance when urinating. The dog moves either too fast with goose steps, or, on the contrary, slow, taking too wide a step. Freezes unpredictably from time to time. When driving in a straight line it goes almost exactly, but gets very lost when turning.

Muscle tremors are present both when the dog tries to maintain a specific position (postural) and when moving (dynamic). There is no threat reflex: the animal does not reflexively close its eyelids when hands or objects approach the eyes, and over time, nystagmus develops - frequent involuntary rotations of the eyes. The pupils of the left and right eyes are of different sizes - anisocoria. Hypertonicity of the forelimbs and occipital muscles manifests itself in paroxysms. The dog often throws its head back.

The progressive form leads to stable weight loss, because it becomes increasingly difficult for the dog to eat. She often hits her face on the food in her bowl. In especially severe cases, the animal ceases to recognize the owner and long-familiar, familiar places. Quite often, owners mistake the clinical manifestations of the disease for a stroke or epilepsy.

Hereditary cerebellar ataxia particularly affects Staffordshire terriers, American and English cocker spaniels, Kerry blue terriers, hairless Chinese crested dogs, Scottish terriers and shepherd dogs.

Sensitive

Sensitive (proprioceptive) ataxia develops in animals in the case of a number of spinal cord pathologies. Often these are damages in the systems of ascending SC fibers that lead to the cerebral cortex, which are responsible for awareness of the position of the body in space. In medicine, these systems are called Gaulle and Burdach bundles. And the second root cause is compression (compression) of the spinal cord due to narrowing of the spinal canal, all kinds of injuries, arterial blockages, cysts, tumors, intervertebral hernias, infections and degenerative processes in the spinal tissues.

The dog's gait suddenly becomes "strange." While walking, the animal often looks down carefully and takes very careful steps, as if it is afraid to step on something. The most basic typical sign of this form of the disease is volar flexion - when moving, the dog does not fully raise its paws, but seems to “drag” its toes along the floor or on the ground.

Read 10 symptoms of allergies in dogs and effective ways to treat the disease

The animal looks confused and cannot determine the correct direction of movement for a long time. At the same time, the rest of the dog’s behavior is completely adequate. Severe lesions lead to complete inability to move.

Vestibular

A sluggish, unsteady gait, staggering and periodic “throwing” to the side, which are accompanied by a tilt of the dog’s head to the left or right, are signs of vestibular ataxia. Along with this, spontaneous strabismus and nystagmus are often observed, regardless of head movements. One-sided or bilateral deafness cannot be ruled out. During an examination at the clinic, specialists may detect facial paralysis and Horner's syndrome - pathological constriction of the pupil and drooping of the upper eyelid.

The vestibular system controls muscles that are directly involved in maintaining head position, eye movements, and overall balance. And all incoming information from the outside is used to appropriately coordinate and regulate the movements performed.

The central structures of the vestibular apparatus are located in the brain, and the peripheral structures are located in the inner and middle ear. Damage to these structures in one area or another causes vestibular ataxia. In particular, these are the following pathologies:

congenital vestibular syndrome;
hypothyroidism;
polyneuropathy;
internal and otitis media;
fungal infections;
tumors in the ear or brain;
ototoxic antibiotics;
nerve degeneration.

Special Recommendations

Loving your pet will help you learn to cope with illness!

A sick animal must be protected from injury. To do this, he is given a separate room, in which there is practically no furniture and no sharp corners. The disease gradually progresses, so the risk of injury increases.

The pet's condition can be satisfactory, even if the disease is hereditary. Therefore, you should not panic ahead of time and try to euthanize the animal. Many pets cope well with the disease. The body simply adapts to the lack of coordination.

Of course, it will be noticeable that the dog walks strangely: it places its legs incorrectly or raises its paws too high and lingers on every step. But this is not a reason to get rid of your pet. Good care, good nutrition and love for your pet can work wonders.

Symptoms

Regardless of the location of the initial lesion, some manifestations of ataxia are common to all three forms:

incoordination of movements, which is manifested by staggering, uncertain, careful walking, stumbling, squatting when turning, or rolling onto one side;
it is extremely difficult or even impossible for a dog to climb stairs or jump even on a low surface (for example, on a sofa);
during walks the animal does not show activity towards other dogs;
muscle tremors are noticeable at rest or during movement;
appetite is significantly reduced;
Nystagmus periodically appears: rapid movements of the eyeballs to the sides or up and down.

Each dog has its own quantitative and qualitative symptoms. The intensity of manifestations is always individual. And if one animal has all the symptoms “on the list,” another dog may have only one symptom (balance problems), and the diagnosis for both dogs will be the same. In addition, in some cases there is a mixture of symptoms of cerebellar and sensory ataxia, as well as cerebellar and vestibular. This suggests that the animal has a mixed form of the disease.

Read Etiology of actinomycosis in dogs: signs, therapy and prevention

Prevention

To prevent the development of a terrible pathology in a pet, it is recommended to follow simple preventive measures:

Buy a dog from breeders who do not allow individuals with symptoms of ataxia to be bred;
Treat non-contagious and infectious diseases of the dog in a timely manner;
Feed your pet a balanced diet with vitamin and mineral supplements.

Signs of ataxia in puppies

Mostly, the pathology affects already mature dogs. But in a situation of congenital pathogenesis, ataxia in a puppy manifests itself quite clearly already at the 4th or 5th week. As a rule, the root cause is hypoplasia (underdevelopment) of the cerebellum.

The puppies shake their heads, rise to their paws with great difficulty, and fall onto their sides after only 2-3 steps. Possible nystagmus. In all other respects, the behavior of babies is no different from healthy puppies: they are very active, curious and have a good appetite.

Similar symptoms of cerebellar ataxia can be observed in a puppy against the background of infestation with large helminths.

Examination and diagnosis

Despite the characteristic signs of the disease, an accurate diagnosis can only be made in a veterinary clinic. As a rule, there is only one examination method - the animal undergoes magnetic resonance imaging. This procedure is performed under general anesthesia and allows the doctor to make a conclusion about the functioning of all parts of the brain, including the cerebellum.

During the diagnosis, the veterinarian must also exclude or detect other or concomitant diseases that may give similar symptoms or be the root cause of ataxia in the animal.

How is an MRI of a dog's head performed?

Diagnostics

Based on a number of visual manifestations, detailed complaints from the owner and specific tests, a specialist can easily determine ataxia and its form. But in order to find out the root cause of the pathology, it is necessary to donate blood and undergo an MRI - an extremely informative diagnostic option for suspected ataxia. If the clinic does not have such equipment, use an x-ray.

The symptoms of vestibular ataxia are quite striking. In this case, an additional otoscopy (detailed examination of the ear) is performed, and a CT scan or ultrasound is required if there is no way to undergo an MRI.

There are known cases of hereditary cerebellar ataxia, when by all indicators the results are normal, but the animal dies, and the diagnosis is clearly confirmed after an autopsy.

Causes

An independent specific disease has been described in American Staffordshire Terriers - primary cerebellar ataxia. American Staffordshire Terrier cerebellar ataxia (also known as cerebellar cortical degeneration) is caused by degeneration (progressive tissue change) of the cerebellum. In particular, in the cerebellar cortex, gradual death of Purkinje cells occurs, and the molecular and granular layers of the cerebellum become thinner. This disease is genetic in nature and is hereditary.

Treatment of ataxia in dogs

The treatment regimen is determined by the root cause of ataxia. The most favorable prognosis is for the vestibular and sensitive forms. In this case, it is enough to eliminate the tumor, inflammation or symptoms of intoxication for the recovery process to begin. Whether recovery is complete or only partial depends on the severity of the original lesion. Some irreversible processes often leave residual neurological signs, which still allow the dog to live more or less fully for several more years.

The cerebellar form is the most severe case. Genetic etiology, unfortunately, cannot be treated. But if the disease does not progress, the dog lives a fairly tolerable life, adapting to its “shortcomings.” At the same time, acute cerebellar ataxia, provoked by an ischemic infarction, often allows the animal to fully recover after timely treatment.

To one degree or another, a dog’s life is made easier by sedatives, multivitamin complexes, antispasmodics, anti-inflammatory drugs, antibiotics and painkillers. Each product and its dosage must be prescribed exclusively by a veterinarian. Any experiments on the part of the owner can result in irreversible consequences.

What causes the disease?

As mentioned earlier, the main reason for the development of the disease is heredity, that is, the disease develops when a dog suffering from this disease participated in their mating. Once we have figured out what it is, it is worth discussing other reasons that can trigger the appearance of the disease in a dog. Here are the main ones:

tumors;
serious infectious diseases;
otitis;
neuritis;
serious injuries resulting in damage to the animal’s brain.

Symptoms of the disease

When the symptoms of a disease in dogs are mentioned, this is exactly what should be discussed first, because it is by them that the disease can be identified in the early stages. Let's look at the symptoms that occur most often, here is a list of them:

constant trembling, as well as noticeable nervousness;
lack of coordination of movements, which may give the impression that the dog is drunk;
strange walking, the essence of which is steps of different lengths and constant stops;
constant falls that occurred, it would seem, on a straight road;
severe panic in the dog, which is most often expressed in panic attacks;
the animal’s desire to quickly hide somewhere and not move;
weakness that becomes more pronounced over time;
random rotation of the head or, for example, eyeballs;
lethargy;
decreased appetite (the amount of food eaten decreases);
hearing impairment;
changes in behavior, decreased activity;
constant head tilt, which was not previously characteristic of a particular dog.

It is not necessary that all the symptoms on this list will appear immediately, since the disease manifests itself in different ways. But if there are at least a few signs, it’s worth showing the animal to a specialist, because even if your fears are not confirmed, the dog will still have some problems. You can find out about them from your veterinarian.

Methionine

Methionine is an essential amino acid, nutrient, lipotropic and urinary acidifier (Connally HE, Thrall MA, Forney SD, et al. Safety and efficacy of 4-methylpyrazole for treatment of suspected or confirmed ethylene glycol intoxication in dogs: 107 cases (1983-1995 J Am Vet Med Assoc 1996;209:1880-1883).

It is used as a food additive for animals. Accidental use may lead to neurological disorders and metabolic acidosis. Methionine's toxicity is partly due to its metabolism (it is converted to ammonia and increases the amount of mercaptan-like substances in the body).

Its toxicity is especially high for dogs predisposed to liver disease.

Clinical signs: excessive salivation, vomiting, ataxia, depression, lethargy, circling, head drooping, aimless walking, aggression, blindness, seizures, stupor and coma.

Treatment is supportive, it is necessary to induce vomiting, give the animal sorbents, saline laxatives, bicarbonate must be included in the infusion therapy.

Rodenticides anticoagulants

Warfarin is the most common anticoagulant used in rodenticides. It is an antagonist of vitamin K, replaces it in the liver, causing a decrease in the synthesis of blood coagulation factors II, VII, IX and X, which leads to coagulopathy and bleeding (March PA, Podell M, Sams RA. Pharmacokinetics and toxicity of bromide following high-dose oral potassium bromide administration in healthy Beagles. J Vet Pharmacol Ther 2002;25:425-432.).

Intracranial or subdural bleeding may cause ataxia, rigidity, and seizures. Diagnosis is based on a study of blood clotting (bleeding time of the buccal mucosa, coagulation rate, prothrombin time, etc.).

Treatment consists of transfusion of frozen plasma (9 ml/kg) or whole blood (20 ml/kg) and oral administration of vitamin K1 at a dose of 2.5 mg/kg over a course of 2-4 weeks.

Barbiturates

Barbiturates prevent the accumulation of calcium in nervous tissue and thus inhibit the release of neurotransmitters (Dorman DC. Neurotoxic drugs in dogs and cats In: Bonagura JD, ed. Kirk's Current Veterinary Therapy XII Small Animal Practice. Philadelphia: WB Saunders Co, 1995; 1140-1145. ). Barbiturates used for anesthesia lead to severe respiratory and central nervous system depression, hypothermia, hypotension, shock, cyanosis and coma.

Side effects of phenobarbital: depression, nystagmus, ataxia, behavioral changes, excitability, polydipsia, polyuria and gluttony (Neer TM. Drug-induced neurological disorders. In: Proceedings of the 9th Annu Meet Vet Med Forum, ACVIM 1991; 261-269.) .

These complications may disappear within a few weeks of treatment as the animal's body adjusts to the dosage. A difficult side effect to correct may be excitability, in which case phenobarbital should be discontinued.

Treatment of patients poisoned by barbiturates involves the use of an emetic, activated carbon or other adsorbents, gastric lavage, artificial pulmonary ventilation (ALV) and infusion therapy.

Neurotoxins can be classified into the following groups:

Metals: lead, mercury. Auto chemicals and auto cosmetics: ethylene glycol. Solvents/detergents: alcohols, chlorhexidine, hexachlorophene. Rodenticides: anticoagulants, bromethalin, strychnine, thallium. Insecticides, molluscicides, repellents: amitraz, chlorinated hydrocarbons, metaldehyde, organophosphates/carbamates, pyrethrins and pyrethroids. Herbicides: (2-methyl-4-chloro)phenoxyacetylic acid. Plant toxins: cyanide, cycad. Bacterial toxins: botulism, tetanus. Animal toxins: causing tick paralysis, toad toxins.

Amitraz

Amitraz is an alpha-adrenergic antagonist and weak monoamine oxidase inhibitor that, when overdosed (for example, when treating demodicosis) or ingested (in the case of a dog chewing a flea collar), can cause symptoms such as weakness, depression, ataxia and muscle weakness ( Neer TM. Drug-induced neurological disorders. In: Proceedings of the 9th Annu Meet Vet Med Forum, ACVIM 1991; 261-269.).

May be accompanied by hypertension, mydriasis, hypothermia, bradycardia, hyperglycemia; cause vasoconstriction, hyperperistalsis, vomiting, diarrhea (Nicholson S. Toxicology In: Ettinger S and Feldman E, eds. Textbook of Veterinary Internal Medicine. Philadelphia: WB Saunders Co, 2000; 357-363.; Hugnet C, Buronrosse F, Pineau X , et al. Toxicity and kinetics of amitraz in dogs. Am J Vet Res 1996;57:1506-1510).

Rarely, amitraz poisoning can lead to generalized seizures (Welsh Corgi).

Treatment: Yohimbine 0.1 mg/kg intravenously. Some literature sources suggest normalizing the condition as a treatment using low doses of atipamezole 50 mcg/kg (antisedan)

Ethylene glycol

Ethylene glycol, used as antifreeze, is moderately toxic, but its metabolites, including glycolic acid, are extremely toxic to dogs and cats. About 57% of animals are exposed to ethylene glycol after contact with antifreeze leaking from a car.

According to new data from ongoing studies, the mortality rate from ethylene glycol poisoning is 28% (according to earlier studies - 43%) (Merchant SR, Neer TM, Tedford BL, et al. Ototoxicity assessment of a chlorhexidine otic preparation in dogs. Prog Vet Neurol 1993; 4: 72-75).

A tablespoon of antifreeze is lethal to a cat, but 126 grams is lethal to a 20-pound dog (Nicholson S. Toxicology In: Ettinger S and Feldman E, eds. Textbook of Veterinary Internal Medicine. Philadelphia: WB Saunders Co, 2000; 357-363) .

A few hours after poisoning, depression, vomiting, ataxia and coma are observed. Affected animals may develop hypothermia. The disorder is associated with metabolic acidosis, serum hyperosmolarity and ultimately renal failure, polydipsia, polyuria, calcium monohydride and dihydride crystalluria and isosthenuria (Summers B, Cummings J, de Lahunta A. Veterinary Neuropathology. St Louis: Mosby, 1995; 250 -280).

Glycolic acid is broken down into formic acid, oxalic acid and oxalates. The resulting calcium oxalates are deposited in the renal tubules (mainly in the proximal ones) and in the lumen of the perivascular space of the brain capillaries. Birefringent crystals can be found in cat urine after 3 hours, in dog urine after 5 hours.

Moderate hypercalcemia can be detected in the blood serum.

The ultrasound picture can vary from complete absence of changes to a significant increase in cortical density (Rowland J. Incidence of ethylene glycol intoxication in dogs and cats seen at Colorado State University Veterinary Teaching Hospital. Vet Hum Toxicol 1987; 29: 41-44).

Treatment consists of immediate administration of sodium sorbent sulfate, correction of dehydration and acidosis, and maintenance fluid therapy.

Fomepizole (4-methylpyrazole), an alcohol dehydrogenase inhibitor, is effective in dogs if no more than 8 hours have passed since the poisoning.

Initial dose 20 mg/kg, IV, then 15 mg, 15 mg and 5 mg after 12, 24 and 36 hours.

The use of this drug for cats is not recommended. Instead, cats are prescribed 20% ethanol in saline solution, which is also an inhibitor of ethylene glycol metabolism at a dose of 5 ml per kg, IV and 5% sodium bicarbonate solution at a dose of 6 ml per kg five times every 6 hours, then four times every 8 hours.

For dogs, the dose of ethanol is 5.5 ml/kg, IV and 8 ml/kg bicarbonate, five times every 5 hours, then four times every 6 hours. In severe cases, hemo- or peritoneal dialysis is recommended.

The forecast is cautious. Although dogs whose treatment was started no later than 8 hours after poisoning have a good prognosis. For animals that have increased ultrasound density of the renal cortical layer and anuria, the prognosis is extremely unfavorable.