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Treatment of inflammatory diseases of the central nervous system in dogs. Inflammatory diseases of the nervous system in dogs

Author: Georgina Child, BVSc, DACVIM (Neurology) / Specialized clinic for small animals, 1 Richardson Pl, North Ryde NSW 2113

Inflammatory diseases The central nervous system affects the brain, meninges, and/or spinal cord. Most pathological processes that cause meningitis also lead to concomitant encephalitis and/or myelitis. In dogs, noninfectious and (presumably) immune-mediated forms of meningoencephalomyelitis are much more common than infectious forms.

The causes of most immune-mediated disorders are unknown.

Immune-mediated diseases are believed to include meningoencephalitis that responds to corticosteroid therapy, granulomatous meningoencephalomyelitis (GME), necrotizing vasculitis, necrotizing meningoencephalitis (NME) in certain breeds (pug, Maltese, Chihuahua), and necrotizing leukoencephalitis (in Yorkshire Terriers).

The final diagnosis is made based on the results histological examination; in most cases, it is not possible to make a lifetime diagnosis without histological examination, since clinical signs and results laboratory research often nonspecific and indistinguishable from signs of infectious meningoencephalomyelitis, vascular diseases and some CNS tumors. Differences in histologic appearance in noninflammatory meningoencephalitis may or may not reflect different causes or immunologic mechanisms.

Meningitis responding to corticosteroid therapy (polyarteritis, necrotizing vasculitis, beagle pain syndrome)

Meningitis that responds to steroid therapy occurs predominantly in young large breed dogs ( average age 1 year), although it also occurs in smaller breeds (for example, polyarteritis in beagles (also called beagle pain syndrome), Nova Scotia retrievers and Italian greyhounds, noted recently).

Symptoms characteristic of meningitis include back pain, unnatural posture, stiff gait, lethargy and lethargy. Fever is common, and a general clinical blood test may reveal leukocytosis. Clinical signs range from acute and severe to episodic. Neurological disorders (paresis/paralysis) are rare, but are possible with damage to the spinal or, in in rare cases, brain. Cases of necrotizing vasculitis of the vessels of the soft and arachnoid membranes have been described. spinal cord in young beagles, German shorthaired pointers and Bernese mountain dogs, sometimes found in other breeds.

Clinical signs are similar to those seen in meningitis that responds to steroid therapy, but symptoms of multiple or focal spinal cord lesions may be present.

Treatment is similar to that used for meningitis, but the prognosis depends on the degree of damage to the spinal cord.

The CSF usually shows marked pleocytosis with neutrophils >10,000/μL. Between episodes, CSF results may be normal. There are no microorganisms in the CSF, and culture results are negative. Some animals develop concomitant polyarthritis. Treatment consists of a long course of corticosteroids at an initial dose of 2–4 mg/kg per day, which is gradually reduced over 3–6 months.

Animals with only symptoms of meningitis have a good prognosis, although relapses are common. If corticosteroids do not work or the animal does not tolerate side effects, azathioprine can be used.

Meningitis that responds to steroid therapy occasionally occurs in cats.

To more accurately designate the diagnosis, the term “meningoencephalitis (or meningoencephalomyelitis) of unknown etiology (or origin)” (MNE or MNP) has been proposed. Other proposed or previous terms include non-pathogenic meningoencephalomyelitis, non-infectious inflammatory disease of the central nervous system, non-suppurative meningoencephalitis, reticulosis, etc.

In this paper, the term GME will be used to describe all non-infectious inflammatory diseases of the central nervous system (even if this is incorrect), since it is generally accepted. These diseases are widespread throughout the world and may account for up to 25% of all cases of CNS disease in dogs.

GME is most widespread in dwarf and small breeds, especially Maltese dogs, miniature poodles and all terriers (including Staffordshire and Airedale). However, it can develop in dogs of any breed, including large dogs, as well as mixed breeds. Most often, middle-aged dogs get sick (less commonly, dogs<2 лет или >10 years). The disease occurs in both sexes, but it is possible that females are affected more often.

The diagnosis of non-infectious inflammatory disease of the central nervous system is based on clinical signs and exceptions infectious causes– often based on the results of serological testing, CSF analysis and brain imaging studies. However, in many cases, a presumptive diagnosis is made based on the best guess based on breed, age, history, and clinical signs. Typically for an inflammatory disease of the central nervous system acute development symptoms of multiple lesions of the central nervous system (brain or spinal cord) and/or hyperesthesia (in the cervical or lumbar-thoracic region). Clinical signs include lesion symptoms forebrain(change in mental state, obsessive circling, convulsions) and/or caudal fossa (ataxia, vestibular disorders, cranial nerve disorders) and/or spinal cord lesions (at any level). In many cases, it is difficult to determine the anatomical location of the lesion. However, the disease is chronic and progressive and in some cases appears episodic, with a significant number of dogs exhibiting focal neurological signs. Animals with meningitis often suffer from severe neck pain, a hunched posture, reluctance to move, and a stiff, stilted gait. Many owners of small dogs note that the animal hides, whines or screams without apparent reason when trying to pick him up. Back pain of uncertain localization is common. However, signs of back pain are not observed in all cases.

Possible symptoms of focal damage to the spinal cord (any part, but most often the cervical), including paresis or paralysis. A form of GME accompanied by optic neuritis has been described, but it is rare. Clinical signs may be acute and rapidly progressing, or subtle and progressing slowly over weeks or months.

In general, GME can have any history, be accompanied by any neurological symptoms, and develop in dogs of any age and breed!

Attempts have been made to classify forms of GME as disseminated, focal, or occurring with damage to the optic nerve. This is very difficult to do intravitally and is not always important for diagnosis, treatment and prognosis. Pedigree necrotizing meningoencephalitis (pugs, Maltese, Chihuahuas and Yorkshire terriers) can develop at a young age (<1 года, особенно у мальтийских болонок и мопсов), но встречается и у собак старше (особенно у чихуахуа). Обычно такой энцефалит развивается остро с симптомами тяжелого поражения переднего мозга, включая судороги. Неврологические нарушения часто быстро прогрессируют. Эти заболевания у разных пород классифицируются в зависимости от поражения оболочек, преимущественного поражения белого вещества и локализации (большие полушария или ствол мозга, или обе части). Такие различия могут отражать разные патологические процессы либо различия иммунного ответа, возможно, генетические.

Usually a clinical examination, clinical and biochemical analysis blood of dogs with any form of non-infectious inflammatory diseases of the central nervous system does not show abnormalities. Fever is possible but rare.

CSF analysis usually shows mild to mild pleocytosis. moderate degree with a predominance of mononuclear cells and varying degrees of increased protein concentration. The total leukocyte concentration varies from<10 до >5000 cells. Protein concentration can range from normal to 4 g/l. Neutrophils typically make up less than 50% of all cells detected. Sometimes macrophages and single eosinophils are found. In some dogs (sometimes more than 10%), CSF analysis shows no abnormalities. Changes in the composition of the CSF may indicate inflammation, which serves as a basis for suspecting GME, however, a similar picture of the CSF is possible in other diseases, including infectious, vascular (infarction) and neoplasms. In most cases, CSF analysis is not sufficient to make a definitive diagnosis, but can provide clarifying information in the search for a probable diagnosis in cases of spinal cord or brain lesions. CSF analysis can detect inflammation, but only if the inflammation involves the meninges, ependymal lining, or tissues close to the CSF circulation pathways. Nonspecific changes in the CSF are often observed in vascular, traumatic, degenerative, tumor and inflammatory diseases of the central nervous system.

In animals with increased intracranial pressure (ICP), CSF sampling is associated with significant risks and can lead to consequences such as the formation of a brain herniation at the cerebellar notch of the cerebellar tentorium or a cerebellar herniation at the foramen magnum. CSF collection is also risky when serious illnesses brain, including without increased intracranial pressure, where changes in cerebral perfusion and a reduced ability of the brain to self-regulate can lead to further deterioration of neurological status.

Unfortunately, it is in these animals that CSF analysis often provides the most valuable diagnostic information. To clinical signs increased ICP include a stunned state, stupor, shortness of breath, the desire to rest the head on objects, bradycardia and an increase in total blood pressure. Some animals with increased intracranial pressure do not have obvious clinical signs.

Withdrawal of CSF from the cistern also carries the risk of structural damage nervous system(spinal or medulla oblongata), especially in small animals or in animals with obstruction of CSF flow at the level of the cerebellomedullary cistern.

Most dogs with GME are small breeds, some of which are predisposed to craniocervical junction malformations, such as Chiari malformations.

I do not routinely collect CSF from dogs with high probability GME, especially in the presence of neurological disorders indicating brain damage. CSF analysis is useful in the evaluation of animals with spinal cord lesions or meninges(I usually use a lumbar puncture).

Changes characteristic of an inflammatory disease can also be identified using visual methods of studying the brain; MRI is considered the method of choice for GME. Magnetic resonance imaging (MRI) is the most sensitive technology for visual diagnosis of diseases of the brain and spinal cord. MRI units with powerful 1.0 T and 1.5 T magnets allow better visualization of inflammatory lesions than units with weak magnets. However, there is no “typical” MRI pattern, and changes may be indistinguishable from those seen in infectious, vascular, or tumor diseases. Singles or multiple lesions can be found anywhere in the central nervous system and may be hypointense on T1-weighted images and hyperintense on T2-weighted and FLAIR images. The degree of contrast enhancement varies. It is possible to enhance the contrast of the meninges. However, multifocal lesions are most typical. Imaging also helps rule out other causes of brain or spinal cord lesions, such as neoplasms or vascular disorders, although focal granulomas with GME can give a picture very similar to neoplasms and infarctions, since the inflammation sometimes looks very similar to vascular disorders due to other causes.

With necrotizing encephalitis in Chihuahuas, pugs, Maltese dogs, etc., characteristic multiple lesions are found in the cerebral hemispheres with an erased boundary between gray and white matter and zones of hyperintensity on T2-weighted / hypointensity on T1-weighted images, corresponding to zones of necrosis.

In some cases of inflammatory diseases of the central nervous system, MRI shows no changes.

CT scan(CT) is a less sensitive method, especially when examining lesions in the caudal fossa (an artifact of increased fascicle stiffness). Displacement of the falx cerebri or a change in its normal anatomy as a result of compression by a space-occupying neoplasm may or may not be visible on CT or MRI images.

A definitive diagnosis of GME is only possible based on the results of a histological examination of the brain - which is obviously difficult to do in vivo. Microscopically, GME is characterized by tissue infiltration along the vessels with lymphocytes and/or macrophages. Such lesions can merge into granulomas, visible macroscopically.

A presumptive diagnosis of GME is often made by exclusion of other causes (by serology/CSF culture in some circumstances) and, in many cases, by outcome of treatment. To exclude infectious causes of meningoencephalitis, serum can be examined to determine titers of cryptococcal antigen, antibodies to toxoplasma gondii and neospora caninum (in some cases, CSF is also examined). CSF cultures are often negative, even for bacterial and fungal infections.

If the animal has severe neurological symptoms the benefits of diagnostic testing, especially CSF, must be weighed against the risks of the procedure.

The causes of GME are unknown - most likely it is autoimmune process, which is based on T-cell-mediated hypersensitivity.

It's difficult to make a forecast. GME can be an acute, rapidly progressive and fatal disease despite treatment, but in many cases of suspected GME, treatment will good result and animals remain in remission for months or years. In most published sources, the prognosis for GME is indicated as unfavorable or hopeless, but in practice there are cases successful treatment. Since the diagnosis is made based on the results of histological examination, the authors of published works usually rely on cases of confirmed diagnosis (ie, post-mortem).

The prognosis does not depend on the severity of clinical symptoms on admission, as well as on the severity of changes in CSF analysis or visual examination of the brain.

The mainstay of treatment remains corticosteroids (mainly prednisolone) in immunosuppressive doses. In many cases (for financial reasons and/or due to the risk of further diagnostic testing), treatment is prescribed empirically without further confirmation of the diagnosis.

Initial dose of prednisolone 1–2 mg/kg every 12 hours. Small dogs (<12 кг) следует давать 2 мг/кг каждые 12 ч. Собакам с весом <2,5 кг следует давать такую же дозу, как для собак весом 2,5 кг, а с весом <5 кг – такую же, как для собак весом 5 кг. Доза для более крупных собак (>40 kg) corresponds to the dose for dogs weighing 40 kg, in general I would not recommend giving more than 40 mg every 12 hours long time. Response to corticosteroid therapy may take several days to occur.

The dose of prednisolone is gradually reduced over at least 6 months depending on the clinical response. For the first time, the dose is reduced after 2–4 weeks. After achieving remission, a maintenance dose of prednisolone is used (0.5–1 mg/kg every other day or 2–3 times a week) for 1–2 years. Determining whether an animal is “cured” is difficult. If a dog receiving low dose prednisolone 2-3 times per week has no neurological symptoms for >6 months, treatment can be discontinued. However, side effects of corticosteroids, especially in large dogs, can cause significant problems in the long term. Long-term use corticosteroids leads to iatrogenic hyperadrenocorticism, accompanied by significant wasting muscle mass and calcification of the skin. In addition, treatment predisposes to gastrointestinal ulceration, pancreatitis, diabetes mellitus, infections (especially urinary tract), ligament and tendon injuries.

Small dogs often tolerate it well high doses However, animals that have relapsed neurological symptoms during corticosteroid therapy, require high doses of corticosteroids (>1 mg/kg) over a long period of time to relieve neurological symptoms, or have significant adverse events, should consider the use of other immunosuppressive agents.

Large dogs Timely administration of additional medications is recommended, since many animals do not tolerate high doses of corticosteroids. All dogs with pronounced neurological disorders associated with spinal cord lesions should be prescribed additional therapy, for example cytarabine, on early stage treatment. The addition of other immunosuppressants can reduce the dose of prednisolone, but the need for a certain dose of prednisolone remains in most animals.

Azathioprine (imuran) – an immunosuppressant that suppresses T-cell function. In healthy dogs, it does not cross the blood-brain barrier. Although this drug may be effective for meningitis that responds to steroid therapy, especially in young large breed dogs, in my opinion it is not useful for GME. However, other clinicians recommend Imuran and describe cases of successful use of azathioprine in combination with prednisone, which made it possible to reduce the dose of the latter. This drug causes almost no side effects, the main problem at high doses is bone marrow suppression. The recommended dose is 0.5–1.0 mg/kg every 48 hours. In the first 5–7 days, it can be given at a dose of 2 mg/kg every 24 hours.

Cytosine arabinoside (cytarabine, ara-C) – a drug used as an antitumor agent for dogs and humans, for example for the treatment of central nervous system lymphoma. The mechanism of its action is unknown. Since this drug crosses the blood-brain barrier and is an immunosuppressant, it was proposed approximately 6 years ago as a possible remedy GME treatment. Most authors recommend using it at a dose of 50 mg/m2 subcutaneously twice daily for 2 consecutive days, repeating this cycle every 3 weeks. This dose is lower than usual dose during chemotherapy of neoplasms. The number of side effects of cytarabine is small. Suppression of bone marrow activity has been reported (usually 10–14 days after initiation of treatment), but does not usually lead to clinical impairment. It is recommended to do it periodically general analysis blood, but not necessarily every cycle. Vomiting, diarrhea and/or loss of appetite may occur after treatment. Cytarabine is inexpensive (when purchased in 10 ml bottles) and is suitable for outpatient treatment however, you must wear protective gloves when administering this drug and when handling/disposing of urine and feces. Cytarabine is used in combination with prednisolone; If the animal's neurological status remains stable, I typically taper the prednisone dose every 2 cycles of cytarabine. Cytarabine can be used indefinitely.

Leflunomide (Arava) – an immunosuppressant used in medicine primarily for the treatment of rheumatoid arthritis. Successful use in the treatment of dogs has been described, first in combination with corticosteroids and then alone (for uncontrolled adverse reactions for corticosteroids). The initial dose is 2 mg/kg per day. In my practice, animals relapsed or their condition did not improve. This drug does not cause any significant side effects and is given orally. Can be combined with prednisone.

Cyclosporine - has also been proposed for the treatment of GME due to the presumed autoimmune T-cell nature of the latter. Cyclosporine is a powerful immunosuppressant that suppresses T-cell immune reactions. In healthy animals, the permeability of the blood-brain barrier to cyclosporine is low. However, since GME occurs with tissue damage around the vessels and possible disruption of the blood-brain barrier, it is assumed that the concentration of cyclosporine in the affected areas of the central nervous system may be higher. My experience with this drug is limited, and two dogs that failed to respond to prednisolone and cytarabine were ineffective.

Procarbazine – antitumor agent, soluble in lipids and easily penetrates the blood-brain barrier; used primarily in medicine to treat lymphoma. The recommended dose is 25–50 mg/m2 per day. Procarbazine frequently causes side effects, including bone marrow suppression (30%), hemorrhagic gastroenteritis (15%), nausea, vomiting, and liver dysfunction. I have no experience with this drug and its effectiveness has not been proven. Side effects and low availability limit the possibilities of its use.

Lomustine (CCNU) – an antitumor alkylating drug of the nitrosourea class, highly soluble in lipids and penetrating the blood-brain barrier. The doses used to treat GME are relatively arbitrary, but high doses are not recommended. Treatment with lomustine is associated with significant, in some cases life-threatening, bone marrow suppression, ulceration gastrointestinal tract and hepatotoxicity. The frequency of side effects increases with increasing dose, but such events sometimes occur with an initial relatively low dose. A significant risk factor for bone marrow suppression is sepsis. Toxicity is unpredictable and I do not recommend routine use of this drug for primary treatment.

For seizures, anticonvulsants are needed.

Sick animals should not be vaccinated unless absolutely necessary. Vaccination may lead to recurrence of clinical symptoms. In addition, a low-fat diet is recommended.

Response to therapy is usually assessed by the weakening or disappearance of clinical symptoms. Repeated CSF analysis is usually not recommended, since the severity of changes (or lack thereof) poorly correlates with the severity of CNS inflammation.

In my experience, at least 60% of dogs with suspected GME or noninfectious meningoencephalitis responsive to steroid therapy respond well to corticosteroid monotherapy and can ultimately be tapered off without further relapse. However, relapse may occur days, weeks, months, or years after the first appearance of clinical signs. If neurological symptoms persist despite high doses of corticosteroids and/or prednisone, and if the dose is reduced<2 мг/кг в сутки после нескольких месяцев терапии наступает рецидив, долговременный прогноз менее благоприятный.

In animals that require high doses of corticosteroids over a long period of time to reduce neurological symptoms, cytarabine can be added; this will allow you to reduce the dose of prednisolone and achieve an acceptable quality of life for several months and even >1 year.

Other types of idiopathic meningoencephalitis have been described in several small breeds, including encephalitis in pugs, necrotizing encephalitis in Yorkshire terriers (necrotizing leukoencephalitis), Chihuahuas, and Maltese dogs (necrotizing meningoencephalitis).

Necrotizing encephalitis also occurs in others dwarf breeds.

Histological sections reveal extensive inflammation and predominant necrosis of the cerebral cortex. Often these breed inflammatory diseases are characterized by a pattern of necrosis and cavity formation in the brain parenchyma, while meningeal lesions may or may not be present, and changes on MRI images closely correspond to the lesions found after necropsy. Forecast in all similar cases very careful.
Treatment is the same as for GME, although the response to treatment is often poorer.

Most brain diseases are not of an infectious nature and are associated with the effects of excessively high temperatures on the vessels of this organ. On a hot day, a dog owner should protect his pet from hyperthermia and sunstroke. All of these conditions are accompanied by similar symptoms, but are caused by for various reasons and require different treatments.

Hyperthermia occurs when the body as a whole overheats. In addition to the brain, hyperthermia disrupts the functions of all organs and systems. Most often, hyperthermia occurs in dogs locked in a car or other stuffy, easily heated room on a hot day. The risk group includes dogs of brachycephalic breeds, aging or obese animals and animals with diseases of the cardiovascular and respiratory systems.

Hyperthermia occurs when the external temperature is close to the dog’s body temperature; humid air and lack of drinking water increase the risk of developing hyperthermia. This is a very life-threatening condition for the dog, requiring immediate assistance to the injured animal.

In the most typical cases, body temperature rises to 42-44 degrees. The dog is depressed, breathing and heart rate are rapid, mucous membranes are white or bluish, vomiting, constriction or dilation of the pupils is possible. The dog cannot move, gets up with difficulty and immediately lies down again, shortness of breath increases, possibly falling into a coma and death.

Sunstroke occurs after being or active training in the open air, the midday sun is especially dangerous. Unlike hyperthermia, body temperature may remain normal, especially if the dog has been sunstroke not during training, but in a calm state. Sunstroke is characterized by unsteadiness of gait, alternating slowing and rapid breathing, protruding eyes, and severe convulsions. Sometimes death occurs suddenly in a clinically healthy dog.

Practical recommendations: The dog should be moved to a cool place, cooled with a douche or cold compresses, and given an enema with cold water. Injections of cardiac medications are necessary; if breathing stops, lobeline is given; in any situation, diphenhydramine is administered.

For pulmonary edema, intravenous injections of 40% glucose and calcium chloride are given.

During the recovery period, solutions of sodium chloride and ringer-lock are administered intravenously.

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Disturbance of cerebral vessels

Poor blood circulation in the brain is associated with insufficient blood flow (anemia) or congestion of blood vessels (hyperemia). The latter can be active, caused by increased blood flow, and passive, manifested as a result of impaired blood outflow.

Active hyperemia occurs during active work in the heat, fear, physical or emotional stress, as well as during transportation of dogs that are not accustomed to it by various types of transport. The dog quickly becomes agitated, becomes restless, irritable and abnormally fearful, reacts inadequately to external stimuli and can cause injury to itself or others. The dog barks, squeals, grabs air with its teeth, tries to run away, and sometimes vomits. Body temperature remains normal or slightly increased. But the temperature in the head area increases noticeably.

Congestive hyperemia most often it is a complication of heart disease, less often it occurs due to compression of blood vessels by tight collars or a growing tumor. Symptoms appear slowly, the dog is drowsy, apathetic, reflexes are weakened, and pain sensitivity is reduced. The dog is indifferent to everything, stands with his head bowed low, his appetite is reduced, his skin and mucous membranes are bluish in color. Body temperature remains normal. As congestive hyperemia progresses, the dog falls into a coma.

Anemia of the brain may result from severe blood loss, thrombosis, embolism, atherosclerosis or arteriosclerosis of the vessels supplying the brain, as well as compression of the vessels by a tumor or rope during an attempt to suffocate. In addition, brain anemia can be caused by various blood diseases and heart diseases accompanied by acute cardiovascular failure.

In the acute course of the disease, there is a sudden loss of coordination of movements, the gait becomes unsteady, and the dog may suddenly faint. The pulse becomes thread-like, breathing is intermittent, muscle tremors, sometimes cramps and convulsions occur. Mucous membranes are pale, scalp is cold. Possible vomiting and sweating of paw pads.

Chronic anemia is manifested by weakness, fatigue, decreased vision and hearing. With any physical activity, shortness of breath, muscle tremors, and increased heart rate occur.

Practical advice: You should choose the right collar, prevent the dog from overtiring and promptly treat all diseases of the cardiovascular system. Early diagnosis and timely therapy are the key to success in cerebral circulatory disorders.

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Inflammation of the brain and spinal cord and their membranes

Meningitis– inflammation of the membranes of the brain and spinal cord. Accompanied by increased intracranial pressure, dilated pupils, impaired coordination of movements, and tension in the neck muscles. Sometimes strabismus, paresis and paralysis of the limbs develop.

Encephalitis– inflammation of brain tissue. Characteristic symptoms are vomiting, photophobia, seizures similar to epileptic ones, drowsiness, paresis of the limbs, coma may develop.

Myelitis- inflammation of the spinal cord. Symptoms depend on where the spinal cord is affected, in the lumbar region, thoracic or cervical vertebrae. In any case, myelitis is accompanied by general signs of an infectious process: increased body temperature and impaired sensitivity in the paw pads.

Lumbar myelitis is characterized by paralysis of both pelvic limbs, with the absence of tendon reflexes and spontaneous release of feces and urine. Myelitis of the thoracic region is accompanied by spastic paralysis of the limbs, absence of abdominal reflexes and delayed defecation and urination, subsequently followed by incontinence. Myelitis cervical region causes respiratory distress and often leads to the death of the dog.

The inflammatory process can spread from one part of the central nervous system to others, in which case meningoencephalitis, encephalomyelitis or meningomyelitis is observed. These conditions are characterized by even more severe disturbances of the nervous system and more severe symptoms.

Practical recommendations: at the first signs of a dog’s behavior disorder, a full examination should be carried out to identify inflammation at an early stage. The most reliable treatment procedure is MRI, and to select the most effective treatment, a biopsy of the cerebrospinal fluid for bacteriological examination is required.

Bacterial inflammatory processes in the central nervous system are treated with antibiotics. All cases require the use of anti-inflammatory (metipred) and diuretics (mannitol, furosemide). For inflammatory processes in the central nervous system, antihistamines are prescribed. The use of immunostimulants is contraindicated, since the process of phagocytosis of infected nerve tissue cells leads to a worsening of the dog’s clinical condition.

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About the gentle canine psyche

Anyone who believes that there is no place for neuroses and stress in a dog’s life is seriously mistaken. The complexity of the psyche of a person’s first friends allows them to receive serious mental trauma, followed by one or another disorder of nervous activity.

TO neuroses Sports and service dogs are predisposed to serious violations during training. Often neurosis is caused by beating the dog, frequent blood taking, or prolonged absence of the owner. It is especially difficult for dogs to tolerate a change of owner or area of ​​use, for example, the transfer of a hunting dog to guard duty, on a chain.

Symptoms: Persistent loss of appetite, agitation and aggression, followed by depression, fearfulness and an attempt to hide. Urination becomes more frequent, unconditioned reflexes become stronger and conditioned ones become distorted. For example, a dog in a state of neurosis is characterized by an inadequate reaction to well-known commands. The pulse becomes rapid and arrhythmic.

Stress, disadaptation syndrome differs from neurosis in its chronic course and arises from prolonged exposure to strong stimuli on the psyche. Most often, dogs experience transport and emotional-pain stress. Transport stress manifests itself immediately or 2-3 days after transporting the dog and is accompanied by agitation, intestinal dysfunction (more often diarrhea than constipation), and sometimes convulsions.

Emotional-painful stress is characterized by a successive change of stages: 1) the anxiety stage with decreased performance and increased restlessness, 2) the adaptation stage, during which the dog looks completely healthy, and 3) the disadaptation stage, accompanied by depression and intestinal dysfunction, less often pneumonia.

Practical recommendations: It should be remembered that the dog’s body takes quite a long time to recover from a strong impact on the nervous system: in mild cases, 7 days, in severe cases, more than 20 days. With severe stress syndrome, the development of coma and death of the dog is possible, especially puppies of dwarf breeds are susceptible to this.

A dog in a state of neurosis or stress should be kept calm and well fed. An important condition for recovery is the elimination of the traumatic factor. They use sedatives and, if necessary, anticonvulsants, glucose, vitamins and adaptogens, such as Leuzea extract, ginseng and Schisandra chinensis.

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About epilepsy and other seizure conditions

True epilepsy is rare. This is a hereditary imbalance between the processes of excitation and inhibition in the cerebral cortex. The disease is chronic and manifests itself as periodically occurring convulsive activity with loss of consciousness and reflexes.

True epilepsy is incurable; helping a dog with this disease involves the use of anticonvulsants and sedatives.

The situation is complicated by numerous diseases accompanied by attacks that are clinically no different from epileptic ones. These are the consequences of bruises and concussions, damage to the integrity of the eardrum caused by ear mites, and severe intoxication.

The cause of seizures can be a lack of calcium, magnesium and glucose, as well as a different sodium content in the blood than normal. It is not uncommon for seizures to occur due to a tumor, dropsy, abscess or inflammation of the brain. Conditions similar to epileptic seizures may be accompanied by carnivore plague, lack of oxygen caused by heart or lung diseases, acute hepatitis, chronic kidney disease, poisoning with organophosphorus compounds and other household chemicals.

Symptoms: The most typical is a suddenly occurring convulsive seizure; less often, before the seizure, a change in the dog’s behavior is noted: aimless walking, increased fearfulness, causeless anxiety. During an attack, the dog falls to the ground, the pupils dilate, the head is thrown back, the muscles of the head, neck, limbs and back tense and twitch, and consciousness is lost. Foamy saliva comes out of the mouth, the dog convulsively opens and closes its mouth. Breathing becomes hoarse, and involuntary release of urine and feces is observed. The mucus is bluish. The convulsions become violent and last 2-3 minutes.

Practical recommendations: Any seizure should not be considered a manifestation of epilepsy; it is necessary to examine the dog and find out the real cause painful condition. Many causes can be eliminated, allowing your dog to live a calm life without life-threatening seizures. Corvalol can be used as a first aid remedy for a convulsive attack.

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Eclampsia is a disease of lactating dogs

Eclampsia– these are attacks of convulsions that occur in dogs in the first 2 weeks after birth, less often during pregnancy or after the end of lactation. Sometimes eclampsia is observed in puppies in early milk age.

Cause: Postpartum hypocalcemia also occurs in dogs that receive large amounts of calcium during pregnancy. Consequently, the lack of this mineral in food is not the only cause of the development of the disease. It has been revealed that eclampsia accompanies any disorder of calcium metabolism, with its excess or insufficient intake from food. With an excess of calcium, the activity of the parathyroid glands is suppressed and the production of parathyroid hormone, necessary for the absorption of calcium, is inhibited.

Symptoms: Early signs are increased excitability and rapid breathing. If left untreated, increased drooling, stiffness of gait, impaired coordination of movements and convulsions occur. Seizures recur after 10-30 minutes. The calcium level in the blood is low. Aspiration pneumonia is a common complication of the disease. In severe cases of eclampsia, the dog may die from pulmonary edema.

Practical recommendations: It is necessary to balance the dog’s diet with calcium, magnesium and phosphorus. To relieve a convulsive attack, a 10% solution of calcium gluconate is administered intravenously. The injection should be done very slowly and stopped at the first sign of a slow heartbeat or arrhythmia.

After normalization of heart function, calcium administration continues. To prevent recurrences of seizures, calcium borogluconate is administered subcutaneously at a dosage of 0.5 ml per kilogram of the dog’s weight 3 times a day for 1-2 days. The dog is prescribed vitamin preparations, with special attention paid to vitamin D. If, despite treatment, seizures occur again, it is recommended to remove the puppies from the dog and feed them artificially.

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Vestibular disorders

Violation of the vestibular apparatus is manifested by a complex of symptoms: head tilt, trembling of the eyeballs and impaired coordination of movements while maintaining muscle tone. There are quite a few diseases accompanied by such a clinical picture, so it is very important to establish an accurate diagnosis.

It is especially important to distinguish between disorders of the vestibular apparatus caused by damage to the central nervous system (cerebellum and nerve centers) and caused by damage to the peripheral part of the vestibular apparatus (structures of the middle ear). The latter can be successfully treated, in contrast to lesions of the central nervous system, in which the chances of success are much less.

Causes of damage to the peripheral part of the vestibular apparatus:
- Inflammation of the middle ear due to prolonged external otitis or pharyngeal infection.
- Neoplasm of the middle ear.
- Head injury, palpation is accompanied by severe pain.
- Pedigree dogs (German Shepherd, Cocker Spaniel, Doberman Pinscher, Akita Inu) may have congenital disorders of the vestibular apparatus. Symptoms appear from birth to 3 months of age, but examination shows the absence of organic damage in the middle ear area.
- Degenerative changes in the vestibular apparatus caused by long-term use of antibiotics in excessively high doses. The most dangerous are aminoglycosides (gentamicin, kanamycin).

Causes of damage to the central part of the vestibular apparatus:
- Inflammation of the brain and its membranes. Most often, meningoencephalitis complicates infections: canine distemper, granulomatous meningoencephalitis, cryptococcosis, toxoplasmosis, rickettsiosis.
- Brain tumors. Most often they affect dogs over 5 years of age, but meduloblastomas and choroid plexus papillomas can also occur in young dogs.
- Thiamine deficiency. Most often it occurs when fish or low-quality industrial food predominates in the dog’s diet.
- Skull injuries with bone fractures and indentation of their fragments.
- Congenital enzymatic deficiency, leading to disruption of fat metabolism and accumulation of substances toxic to the nervous system. Symptoms appear around one year of age. In addition to disorders of the vestibular system, there is growth retardation, liver enlargement and curvature of the hip joints.

Symptoms: The dog walks with an unsteady gait, bent over, and may fall on the side of the injury. Her head is tilted to the same side, and sometimes her spine is curved. With more severe injuries, movement in a circle in the direction of tilting the head and vomiting are observed. In the first week after damage to the vestibular apparatus, rhythmic trembling of the eyeballs (nystagmus) occurs, which subsequently compensates by itself.

With a bilateral lesion, the dog prefers to sit, and an attempt to move ends in falling on one side or the other. There is no head tilt or nystagmus, and deafness is possible.

The diagnosis is made after a neurological examination, radiography of the skull, and taking fluid from the middle ear cavity and spinal cerebrospinal fluid for bacteriological culture.

Practical recommendations: You should take ear inflammation seriously and not self-medicate. Do not use aminoglycosides unless absolutely necessary; if there is no other option, treatment should be carried out under the supervision of a physician. Adequate feeding, regular vaccination, and timely removal of tumors of the auricle will protect the dog from the main causes leading to disorders of the vestibular apparatus.

* * * * * * * *

Non-inflammatory spinal cord injuries

Most often, owners of dachshunds encounter myelopathies, but disruption of innervation and paralysis of the pelvic limbs can develop in any dog. The fact is that there are quite a few reasons leading to the same result - narrowing of the spinal canal and compression of the spinal cord or its roots.

Degenerative changes in intervertebral discs. This age-related changes structures of cartilage tissue characteristic of large breed dogs. The intervertebral discs of older dogs become harder, no longer cushion, and become deformed over time, which can lead to cartilage embedding into the spinal canal.

Symptoms: The disease is chronic, at first there is slight stiffness in movements, then the pain increases, and the dog increasingly loses its mobility. From the moment the disc substance is inserted into the spinal canal, the dog begins to shuffle with its paws, erasing the outer surface of the fingers, sometimes it becomes completely impossible to move.

Treatment: In the early stages, the development of the disease can be stopped by changing the diet, proper physical activity and physiotherapeutic techniques. In later stages, only surgical intervention. But even this gives only a temporary effect, since pathological changes affect the entire spine and can appear at any time in another area.

Chondroid metaplasia of the nucleus pulposus is the transformation of the liquid substance of the intervertebral disc into hyaline cartilage, which is squeezed into the spinal canal and disrupts the blood supply to the spinal cord. There are breeds that are predisposed to such changes - these are dachshunds, poodles, French bulldogs and pugs. Contrary to popular belief, an elongated body shape has nothing to do with this disease. For example, beagles do not suffer from chondroid metaplasia.

Symptoms: The dog is in severe pain, dragging its motionless pelvic limbs behind it. The speed of assistance is of great importance - the compressed nerve endings die and the later the problem is eliminated, the less chance there is for the dog to fully recover.

Treatment depends on the degree of damage: if the sensitivity of the limbs is preserved, and the dog does not have paralysis, but only a lack of coordination of movements, conservative therapy is possible (immobilization, rest, metipred), and if paralysis is observed, the damaged area is localized using MRI and carried out surgery. If there is no sensitivity in the pelvic limbs for more than 48 hours, then even surgical treatment will most likely not help, since irreversible changes have occurred in the nervous tissue.

Compression of the spinal cord by a vertebral fragment due to injury or a growing tumor. These conditions require surgical treatment in a specialized clinic.

Symptoms depend on the nature of the damage and in which part it is localized:
Damage in the cervical region is accompanied by muscle stiffness, pulsation of the anus and involuntary movements of the tail, in the thoracic region there are no reflexes of the thoracic limbs, in the lumbar region the dog sits with its hind legs stretched forward along the body. Reflexes on the forelimbs are preserved, but on the hind limbs they are enhanced. The most typical damage to the vertebrae is in the lumbosacral region - the front part of the body moves normally, the entire back part is paralyzed, the tail hangs down, the anus gapes, defecation occurs involuntarily.

Spinal cord ischemia. A relatively rarely diagnosed pathology associated with blockage of the vessels supplying the spinal cord with particles of fat. It is observed in dogs with increased concentrations of cholesterol in the blood and disorders of fat metabolism. A breed predisposition to this disease has been identified in miniature schnauzers.

Symptoms: A painful swelling forms in the area of ​​the damaged area of ​​the spine, the sensitivity of the skin and muscles of the underlying areas of the body is impaired, as well as coordination of movement. Depending on the degree of damage, either a complete recovery or the death of the dog is possible.

Treatment is conservative and involves eliminating the cause and restoring blood vessels. Surgery is not required because the spinal cord is not compressed. But to make an accurate diagnosis, an MRI should be performed to make sure there are no other causes.

Practical recommendations: Any conservative treatment of diseases associated with spinal cord damage without making an accurate diagnosis is a gamble, which can result in disability or death of the dog. You should not be afraid of diagnostic tests under anesthesia (MRI) and surgery - his life depends on how wisely you approach the treatment of your pet.

The material was specially prepared
website for dog breeders portal
veterinarian Kalashnikova O.V.

Articles on the topic.

Inflammatory diseases of the central nervous system affect the brain, meninges and/or spinal cord. Most pathological processes that cause meningitis also lead to concomitant encephalitis and/or myelitis. In dogs, noninfectious and (presumably) immune-mediated forms of meningoencephalomyelitis are much more common than infectious forms. The causes of most immune-mediated disorders are unknown. Immune-mediated diseases are believed to include meningoencephalitis responsive to corticosteroid therapy, granulomatous meningoencephalomyelitis (GME), necrotizing vasculitis, necrotizing meningoencephalitis (NME) in certain breeds (Pug, Maltese, Chihuahua) and necrotizing leukoencephalitis (Yorkie). ski terriers). The final diagnosis is made based on the results of histological examination; in most cases, it is not possible to make a lifetime diagnosis without histological examination, since clinical signs and laboratory results are often nonspecific and indistinguishable from the signs of infectious meningoencephalomyelitis, vascular diseases and some tumors of the central nervous system. Differences in histologic appearance in noninflammatory meningoencephalitis may or may not reflect different causes or immunologic mechanisms.

Meningitis responding to corticosteroid therapy (polyarteritis, necrotizing vasculitis, beagle pain syndrome)

Meningitis that responds to steroid therapy occurs predominantly in young dogs of large breeds (average age 1 year), although it also occurs in smaller breeds (for example, polyarteritis in beagles (also called beagle pain syndrome), Nova Scotia retrievers and Italian greyhounds, most recently noted time). Symptoms characteristic of meningitis include back pain, unnatural posture, stiff gait, lethargy and lethargy. Fever is common, and a general clinical blood test may reveal leukocytosis. Clinical signs range from acute and severe to episodic. Neurological disorders (paresis/paralysis) are rare, but are possible with damage to the spinal cord or, in rare cases, the brain. Cases of necrotizing vasculitis of the vessels of the soft and arachnoid membranes of the spinal cord have been described in young beagles, German shorthaired pointers and Bernese mountain dogs, sometimes occurring in other breeds. Clinical signs are similar to those seen in meningitis that responds to steroid therapy, but symptoms of multiple or focal spinal cord lesions may be present. Treatment is similar to that used for meningitis, but the prognosis depends on the degree of damage to the spinal cord.

The CSF usually shows marked pleocytosis with neutrophils >10,000/μL. Between episodes, CSF results may be normal. There are no microorganisms in the CSF, and culture results are negative. Some animals develop concomitant polyarthritis. Treatment consists of a long course of corticosteroids at an initial dose of 2–4 mg/kg per day, which is gradually reduced over 3–6 months.

Animals with only symptoms of meningitis have a good prognosis, although relapses are common. If corticosteroids do not work or the animal does not tolerate side effects, azathioprine can be used.

Meningitis that responds to steroid therapy occasionally occurs in cats.

The term GME often used to refer to all other non-infectious inflammatory diseases of the central nervous system (excluding steroid-responsive meningitis), although pathological physiology may be different.

To more accurately designate the diagnosis, the term “meningoencephalitis (or meningoencephalomyelitis) of unknown etiology (or origin)” (MNE or MNP) has been proposed. Other proposed or previous terms include non-pathogenic meningoencephalomyelitis, non-infectious inflammatory disease of the central nervous system, non-suppurative meningoencephalitis, reticulosis, etc.

In this paper, the term GME will be used to describe all non-infectious inflammatory diseases of the central nervous system (even if this is incorrect), since it is generally accepted. These diseases are widespread throughout the world and may account for up to 25% of all cases of CNS disease in dogs.

GME is most common in toy and small breeds, especially Maltese dogs, toy poodles and all terriers (including Staffordshire and Airedale terriers). However, it can develop in dogs of any breed, including large dogs, as well as mixed breeds. Most often, middle-aged dogs (less often dogs 10 years old) get sick. The disease occurs in both sexes, but it is possible that females are affected more often.

The diagnosis of non-infectious inflammatory disease of the central nervous system is based on clinical signs and the exclusion of infectious causes - often based on the results of serological testing, CSF analysis and brain imaging. However, in many cases, a presumptive diagnosis is made based on the best guess based on breed, age, history, and clinical signs. An inflammatory disease of the central nervous system is typically characterized by the acute development of symptoms of multiple lesions of the central nervous system (brain or spinal cord) and/or hyperesthesia (in the cervical or lumbar-thoracic region). Clinical signs include symptoms of forebrain (mental state changes, compulsive circling, seizures) and/or caudal fossa lesions (ataxia, vestibular disorders, cranial nerve disorders) and/or spinal cord lesions (at any level). In many cases, it is difficult to determine the anatomical location of the lesion. However, the disease is chronic and progressive and in some cases appears episodic, with a significant number of dogs exhibiting focal neurological signs. Animals with meningitis often suffer from severe neck pain, a hunched posture, a reluctance to move, and a stiff, stilted gait. Many owners of small dogs note that the animal hides, whines or screams for no apparent reason when trying to pick it up. Back pain of uncertain localization is common. However, signs of back pain are not observed in all cases.

Possible symptoms of focal damage to the spinal cord (any part, but most often the cervical), including paresis or paralysis. A form of GME accompanied by optic neuritis has been described, but it is rare. Clinical signs may be acute and rapidly progressing, or subtle and progressing slowly over weeks or months.

In general, GME can have any history, be accompanied by any neurological symptoms, and develop in dogs of any age and breed!

Attempts have been made to classify forms of GME as disseminated, focal, or occurring with damage to the optic nerve. This is very difficult to do intravitally and is not always important for diagnosis, treatment and prognosis. Pedigree necrotizing meningoencephalitis (pugs, Maltese, Chihuahuas and Yorkshire terriers) can develop at a young age (

Typically, a clinical examination, clinical and biochemical blood test of dogs with any form of non-infectious inflammatory diseases of the central nervous system does not show abnormalities. Fever is possible but rare.

CSF analysis usually shows mild to moderate pleocytosis with a predominance of mononuclear cells and varying degrees of increased protein concentration. The total leukocyte concentration varies from 5000 cells. Protein concentration can range from normal to 4 g/l. Neutrophils typically make up less than 50% of all cells detected. Sometimes macrophages and single eosinophils are found. In some dogs (sometimes more than 10%), CSF analysis shows no abnormalities. Changes in the composition of the CSF may indicate inflammation, which serves as a basis for suspecting GME, however, a similar picture of the CSF is possible in other diseases, including infectious, vascular (infarction) and neoplasms. In most cases, CSF analysis is not sufficient to make a definitive diagnosis, but can provide clarifying information in the search for a probable diagnosis in cases of spinal cord or brain lesions. CSF analysis can detect inflammation, but only if the inflammation involves the meninges, ependymal lining, or tissues close to the CSF circulation pathways. Nonspecific changes in the CSF are often observed in vascular, traumatic, degenerative, tumor and inflammatory diseases of the central nervous system.

In animals with increased intracranial pressure (ICP), CSF sampling is associated with significant risks and can lead to consequences such as the formation of a brain herniation at the cerebellar notch of the cerebellar tentorium or a cerebellar herniation at the foramen magnum. CSF sampling is also risky in severe brain disease, including without increased intracranial pressure, where changes in cerebral perfusion and a reduced brain capacity for self-regulation may lead to further deterioration of neurological status.

Unfortunately, it is in these animals that CSF analysis often provides the most valuable diagnostic information. Clinical signs of increased ICP include stupor, stupor, shortness of breath, tendency to rest the head on objects, bradycardia, and increased general blood pressure. Some animals with increased intracranial pressure do not have obvious clinical signs.

Withdrawal of CSF from the cistern also carries the risk of damage to nervous system structures (spinal cord or medulla oblongata), especially in small animals or in animals with obstruction of CSF flow at the level of the cerebellomedullary cistern. Most dogs with GME are small breeds, some of which are predisposed to craniocervical junction malformations, such as Chiari malformations.

I do not routinely collect CSF in dogs with a high likelihood of GME, especially those with neurological deficits suggestive of brain damage. CSF analysis is useful in evaluating animals with spinal cord or meningeal lesions (I usually use lumbar puncture).

Changes characteristic of an inflammatory disease can also be identified using visual methods of studying the brain; MRI is considered the method of choice for GME. Magnetic resonance imaging (MRI) is the most sensitive technology for visual diagnosis of diseases of the brain and spinal cord. MRI units with powerful 1.0 T and 1.5 T magnets allow better visualization of inflammatory lesions than units with weak magnets. However, there is no “typical” MRI pattern, and changes may be indistinguishable from those observed in infectious, vascular, or neoplastic diseases. Single or multiple lesions can be found anywhere in the central nervous system and may be hypointense on T1-weighted images and hyperintense on T2-weighted and FLAIR images. The degree of contrast enhancement varies. It is possible to enhance the contrast of the meninges. However, multifocal lesions are most typical. Imaging also helps rule out other causes of brain or spinal cord lesions, such as neoplasms or vascular disorders, although focal granulomas in GME may present a very similar picture to neoplasms and infarcts, as the inflammation sometimes appears very similar to vascular disorders due to other causes. With necrotizing encephalitis in Chihuahuas, pugs, Maltese dogs, etc., characteristic multiple foci are found in the cerebral hemispheres with an erased boundary between gray and white matter and zones of hyperintensity on T2-weighted/hypointensity on T1-weighted images, corresponding to zones of necrosis.

In some cases of inflammatory diseases of the central nervous system, MRI shows no changes. Computed tomography (CT) is a less sensitive method, especially when examining lesions in the caudal fossa (an artifact of increased fascicular stiffness). Displacement of the falx cerebri or a change in its normal anatomy as a result of compression by a space-occupying neoplasm may or may not be visible on CT or MRI images.

A definitive diagnosis of GME is only possible based on the results of a histological examination of the brain - which is obviously difficult to do in vivo. Microscopically, GME is characterized by tissue infiltration along the vessels with lymphocytes and/or macrophages. Such lesions can merge into granulomas, visible macroscopically.

A presumptive diagnosis of GME is often made by exclusion of other causes (by serology/CSF culture in some circumstances) and, in many cases, by outcome of treatment. To exclude infectious causes of meningoencephalitis, serum can be examined to determine titers of cryptococcal antigen, antibodies to toxoplasma gondii and neospora caninum (in some cases, CSF is also examined). CSF cultures are often negative, even for bacterial and fungal infections.

If an animal has severe neurological symptoms, the benefits of diagnostic testing, especially CSF, must be weighed against the risks of the procedure.

The causes of GME are unknown, but most likely it is an autoimmune process based on T-cell-mediated hypersensitivity.

It's difficult to make a forecast. GME can be an acute, rapidly progressive and fatal disease despite treatment, but in many cases of suspected GME, treatment is successful and animals remain in remission for months or years. In most published sources, the prognosis for GME is indicated as unfavorable or hopeless, but in practice there are cases of successful treatment. Since the diagnosis is made based on the results of histological examination, the authors of published works usually rely on cases of confirmed diagnosis (ie, post-mortem).

The prognosis does not depend on the severity of clinical symptoms on admission, as well as on the severity of changes in CSF analysis or visual examination of the brain.

The mainstay of treatment remains corticosteroids (mainly prednisolone) in immunosuppressive doses. In many cases (for financial reasons and/or due to the risk of further diagnostic testing), treatment is prescribed empirically without further confirmation of the diagnosis.

The starting dose of prednisolone is 1 – 2 mg/kg every 12 hours. For small dogs (40 kg) the dose is equivalent to a dog weighing 40 kg, in general I would not recommend giving more than 40 mg every 12 hours for long periods of time. Response to corticosteroid therapy may take several days to occur.

The dose of prednisolone is gradually reduced over at least 6 months depending on the clinical response. For the first time, the dose is reduced after 2-4 weeks. After achieving remission, a maintenance dose of prednisolone is used (0.5 - 1 mg/kg every other day or 2-3 times a week) for 1-2 years. Determining whether an animal is “cured” is difficult. If a dog receiving low dose prednisolone 2-3 times per week has no neurological symptoms for 6 months, treatment can be discontinued. However, side effects of corticosteroids, especially in large dogs, can cause significant problems in the long term. Long-term use of corticosteroids leads to iatrogenic hyperadrenocorticism, accompanied by significant muscle wasting and skin calcification. In addition, treatment predisposes to gastrointestinal ulceration, pancreatitis, diabetes mellitus, infections (especially urinary tract), and ligament and tendon injuries. Small dogs often tolerate high doses well, but animals that have experienced relapse of neurological symptoms during corticosteroid therapy, require high doses of corticosteroids (1 mg/kg) over a long period of time to relieve neurological symptoms, or have significant adverse events should be considered. possibility of using other immunosuppressants. In large dogs, timely administration of additional medications is recommended, as many animals do not tolerate high doses of corticosteroids. All dogs with significant neurological impairment associated with spinal cord lesions should be given additional therapy, such as cytarabine, early in treatment. The addition of other immunosuppressants can reduce the dose of prednisolone, but the need for a certain dose of prednisolone remains in most animals.

Azathioprine (imuran) is an immunosuppressant that suppresses T-cell function. In healthy dogs, it does not cross the blood-brain barrier. Although this drug may be effective for meningitis that responds to steroid therapy, especially in young large breed dogs, in my opinion it is not useful for GME. However, other clinicians recommend Imuran and describe cases of successful use of azathioprine in combination with prednisone, which made it possible to reduce the dose of the latter. This drug causes almost no side effects, the main problem at high doses is bone marrow suppression. The recommended dose is 0.5 – 1.0 mg/kg every 48 hours. In the first 5-7 days it can be given at a dose of 2 mg/kg every 24 hours.

Cytosine arabinoside (cytarabine, ara-C) is a drug used as an anticancer agent in dogs and humans, for example in the treatment of central nervous system lymphoma. The mechanism of its action is unknown. Because this drug crosses the blood-brain barrier and is an immunosuppressant, it was proposed as a possible treatment for GME approximately 6 years ago. Most authors recommend using it at a dose of 50 mg/m2 subcutaneously twice daily for 2 consecutive days, repeating this cycle every 3 weeks. This dose is lower than the usual dose for cancer chemotherapy. The number of side effects of cytarabine is small. Suppression of bone marrow activity has been described (usually 10 to 14 days after the start of treatment), but this does not usually lead to clinical problems. It is recommended to do a complete blood count periodically, but not necessarily every cycle. Vomiting, diarrhea and/or loss of appetite may occur after treatment. Cytarabine is inexpensive (when purchased in 10 ml vials) and is suitable for outpatient treatment, but protective gloves must be worn when administering this drug and when handling/disposing of urine and feces. Cytarabine is used in combination with prednisolone; If the animal's neurological status remains stable, I typically taper the prednisone dose every 2 cycles of cytarabine. Cytarabine can be used indefinitely.

Leflunomide (Arava) is an immunosuppressant used in medicine primarily for the treatment of rheumatoid arthritis. Successful use in dogs has been described, first in combination with corticosteroids and then alone (for uncontrolled adverse reactions to corticosteroids). The initial dose is 2 mg/kg per day. In my practice, animals relapsed or their condition did not improve. This drug does not cause any significant side effects and is given orally. Can be combined with prednisone.

Cyclosporine has also been proposed for the treatment of GME due to the presumed autoimmune T-cell nature of the latter. Cyclosporine is a powerful immunosuppressant that suppresses T-cell immune responses. In healthy animals, the permeability of the blood-brain barrier to cyclosporine is low. However, since GME occurs with tissue damage around the vessels and possible disruption of the blood-brain barrier, it is assumed that the concentration of cyclosporine in the affected areas of the central nervous system may be higher. My experience with this drug is limited, and two dogs that failed to respond to prednisolone and cytarabine were ineffective.

Procarbazine is an antitumor agent that is lipid soluble and easily penetrates the blood-brain barrier; used primarily in medicine to treat lymphoma. The recommended dose is 25 – 50 mg/m2 per day. Procarbazine frequently causes side effects, including bone marrow suppression (30%), hemorrhagic gastroenteritis (15%), nausea, vomiting, and liver dysfunction. I have no experience with this drug and its effectiveness has not been proven. Side effects and low availability limit the possibilities of its use.

Lomustine (CCNU) is an antitumor alkylating drug of the nitrosourea class that is highly lipid soluble and penetrates the blood-brain barrier. The doses used to treat GME are relatively arbitrary, but high doses are not recommended. Treatment with lomustine is associated with significant, in some cases life-threatening, bone marrow suppression, gastrointestinal ulceration, and hepatotoxicity. The frequency of side effects increases with increasing dose, but such events sometimes occur with an initial relatively low dose. A significant risk factor for bone marrow suppression is sepsis. Toxicity is unpredictable and I do not recommend routine use of this drug for primary treatment.

For seizures, anticonvulsants are needed.

Sick animals should not be vaccinated unless absolutely necessary. Vaccination may lead to recurrence of clinical symptoms. In addition, a low-fat diet is recommended.

Response to therapy is usually assessed by the weakening or disappearance of clinical symptoms. Repeated CSF analysis is usually not recommended, since the severity of changes (or lack thereof) poorly correlates with the severity of CNS inflammation.

In my experience, at least 60% of dogs with suspected GME or noninfectious meningoencephalitis responsive to steroid therapy respond well to corticosteroid monotherapy and can ultimately be tapered off without further relapse. However, relapse may occur days, weeks, months, or years after the first appearance of clinical signs. If neurological symptoms persist despite high doses of corticosteroids and/or prednisone, and if the dose is reduced

In animals that require high doses of corticosteroids over a long period of time to reduce neurological symptoms, cytarabine can be added; this will allow you to reduce the dose of prednisolone and achieve an acceptable quality of life for several months and even 1 year.

Other types of idiopathic meningoencephalitis have been described in several small breeds, including encephalitis in pugs, necrotizing encephalitis in Yorkshire terriers (necrotizing leukoencephalitis), Chihuahuas, and Maltese dogs (necrotizing meningoencephalitis). Necrotizing encephalitis also occurs in other toy breeds. Histological sections reveal extensive inflammation and predominant necrosis of the cerebral cortex. Often these breed inflammatory diseases are characterized by a pattern of necrosis and cavity formation in the brain parenchyma, while meningeal lesions may or may not be present, and changes on MRI images closely correspond to the lesions found after necropsy. The prognosis in all such cases is very cautious. Treatment is the same as for GTE, although the response to treatment is often poorer.

A pinched nerve in a dog is a fairly serious disease. It is characterized by an acute onset - piercing shooting pains in the back, hindering movement. Alarming symptoms grow gradually, so the owner has enough time to take action and prevent the disease from moving into the acute phase, painful and difficult to treat.

Pinched spinal nerves are compression of the nerve roots extending from the spinal cord by adjacent vertebrae. The situation is complicated by the fact that the muscles surrounding the spine swell and reflexively spasm. Long-term compression leads to the death of nerve tissue, as a result of which the mobility of the dog’s limbs begins to suffer. Further development of inflammation is fraught with partial or complete paralysis of the animal.

There are several types of pinched spinal nerves. It depends on which part of the spine is involved in the pathological process:

  • pinched nerve of the cervical spine;
  • pinched thoracic nerve;
  • pinched sciatic nerve (sciatica).

Pinching upper sections spine (cervical and thoracic) can cause paralysis of the entire lower part of the dog’s body. Pinching of the sciatic nerve causes severe pain and autonomic disorders in the dog's hind limbs, leading to a gradual loss of sensitivity.

Difficulties in diagnosis

Diagnosis of this disease has its own characteristics. It can be difficult to determine exactly where the pathological process is localized, since the pain is diffuse. Only a competent specialist can identify this. Therefore, if any peculiarities appear in the dog’s behavior, you should immediately contact a veterinary clinic. The owner should be alert to the following points:

  • the dog protects his back and doesn’t let him get close to him;
  • drags his hind legs;
  • whines when changing position;
  • reacts to weather changes;
  • refuses active play during walks;
  • spends a lot of time alone;
  • there is stiffness of movement.

Main causes of the disease

The disease, as a rule, is a consequence of already existing pathologies spine, not diagnosed and not treated on time. Provocateurs of a pinched nerve can be:

  • spondylosis;
  • radiculitis;
  • intervertebral hernia;
  • spinal neoplasms;
  • injuries and damage to the back with displacement of the vertebrae;
  • posture disorders;
  • osteochondrosis;
  • metabolic disorders;
  • hypothermia.

Spondylosis

Spondylosis usually occurs in older dogs as a result of age-related changes in the vertebral segments. It is a degenerative-dystrophic process of the anterior sections of the intervertebral discs. The disorder is accompanied by the appearance of bone growths – osteophytes – on the anterior and lateral parts of the spine. Osteophytes can affect the nerve roots, narrowing the lumen of the spinal canal.

The disease actively progresses with spinal injuries, osteochondrosis, and decreased immunity. The risk group includes dogs with complicated heredity.

Spondylosis can affect the cervical or thoracic region spine, but a particularly common location is the lower back.

The clinical picture of the disease is as follows: the dog’s movements become heavy and slow. She does not allow touching the back, much less using force during the examination. There is a deterioration in health depending on changes in weather conditions.

Spondylosis is diagnosed using x-ray examination spine.

Radiculitis

A pinched spinal nerve can also cause radiculitis, an inflammatory lesion of the spinal cord roots. Its main symptom is severe pain. The disease can occur as a complication of osteochondrosis, as a result of hypothermia, injuries and infections. Dogs with developmental anomalies are at risk various departments spine. Radiculitis can be chronic or acute form. There is also a complicated form of it – meningoradiculitis. It affects the membranes of the spinal cord.

Intervertebral hernia

Age-related changes in the spine or injury can lead to stretching or rupture of the fibrous ring of the intervertebral disc, which has lost most of its shock-absorbing properties. In this case, the gelatinous disc protrudes beyond its boundaries, compressing the spinal cord or its roots. Intervertebral hernia may be chronic or acute.

Spinal neoplasms

Spinal tumors sometimes cause damage to the spinal cord and major spinal nerves. This condition is irreversible and threatens severe paresis and even complete paralysis of the limbs. In this case, the dog will lose the ability to move independently. There are special wheelchairs for animals that replace the function of their legs and help them lead a fairly active life.

Symptoms of the disease

The severity and nature of the symptoms of the disease are determined by the degree of impairment of the sensitivity of the limbs:

  1. A mild degree of the disease can be judged by moderate pain. The dog's behavior is relatively calm. Sensitivity is not impaired or slightly impaired. The animal is passive. Take care of your back, lie down carefully, avoiding sudden movements. Appetite is not impaired, body temperature is normal.
  2. The average degree of the disease is characterized by fairly severe back pain, which the animal expresses with anxiety and plaintive whining. He rejects an attempt to examine his back with a growl. Muscle spasm is manifested by an unnaturally curved back and a tense abdomen (especially with sciatica).
  3. Severe third degree of the disease is characterized by severe limitation of movements. The sacral spine is most often affected and sciatic nerve. At the same time, a “wooden” gait develops with unnatural tension in the legs. There is no appetite, body temperature may be elevated.

Treatment

A pinched nerve in a dog has painful symptoms, and therefore treatment should be aimed primarily at relieving the pain and only then treating the pinched nerve.

Symptomatic therapy

Basic moments symptomatic therapy are:

  • relief of pain using painkillers;
  • stop inflammatory process in muscles and nerve roots with the help of non-steroidal anti-inflammatory drugs (Quadrisol and Rimadyl);
  • appointment sedatives which will help calm your pet and restore its nervous system;
  • providing the dog with complete rest and limiting movements.

Treatment of a pinched nerve

In order to relieve a pinched nerve in a dog, complex treatment is prescribed:

  1. Vitamin therapy has a good effect. Animals are prescribed vitamins B1, B6, B12, which affect the conduction of nerve impulses.
  2. Neuromuscular conductivity is well restored by the drug “Proserin”.
  3. Homeopathic remedies help stop the destruction of neuromuscular tissue in the early stages of the disease.
  4. To dissolve osteophytes on the vertebral discs, absorbable agents (Lidaza) are prescribed.
  5. Physiotherapeutic procedures (massage and warming up diseased segments of the spine with a blue lamp) help relieve muscle inflammation.
  6. If conservative therapy does not have the desired effect, surgery may be indicated for the sick dog. But you need to know that such interventions are not always successful. The operation is quite traumatic for the spine and surrounding tissues.

Spinal pathologies should be treated exclusively in a veterinary clinic under the supervision of a specialist.

The prognosis of the disease with a mild course is often positive. But, if the course is severe, the prognosis is cautious.

Prevention

Not a single sign of health problems spinal system dogs should not be left unattended by the owner. Every day you need to take care of maintaining the health of your pet and his physical development according to age, namely:

  1. You should exercise your dog regularly to strengthen its muscle corset.
  2. It is imperative to give the animal timely rest. Active games, training and training sessions should be dosed.
  3. It is important to feed your dog properly. The diet must be balanced and enriched with essential nutrients.
  4. It is necessary to avoid hypothermia and colds, and monitor the state of the immune system.

A pinched nerve in a dog is treatable. Huge role in successful therapy plays a role in the attention of the owner and strict adherence to the recommendations of the attending physician. To avoid relapses, it is recommended to periodically conduct courses of maintenance therapy.

Skull fractures are the result of road accidents, very strong blows, or a dog falling from a significant height. They can be open or closed, depressed or linear. Fractures result in various types of brain damage. There are also brain injuries that are not associated with skull fractures - these are bruises, concussions and brain swelling.

A bruise is a minor injury that is not accompanied by loss of consciousness or any manifestations that pose a threat to the dog’s life. Normal health is restored relatively quickly.

A concussion is characterized by more high degree gravity. It is the result of a strong blow and may be accompanied by loss of consciousness.

Swelling and formation of hematomas in the brain tissue pose a great danger to the dog’s life. They arise as a result of damage to the blood vessels of the brain and are characterized by extremely serious condition animal. The dog not only loses consciousness, but may also fall into a coma.

Swelling of the skull bones puts pressure on the brain, which can lead to sudden death dogs. When a hematoma forms, paralysis of one side of the body may occur, and one pupil stops responding to light.

With traumatic brain injuries, symptoms of increased intracranial pressure may appear. Different degrees The severity of the animal’s condition is characterized by various signs.

Within 1 day after the dog is injured, it is necessary to carefully monitor its well-being. The dog may experience unusual drowsiness, lack of reaction to surrounding objects and people, including the owner, and may experience unhealthy agitation. To control general condition body, the animal must be woken up every 2 hours for 1 day.

With a mild degree of compression of the brain, the dog's breathing remains normal, but there is weakness and lethargy on one side of the body and constriction of one pupil, but the reaction to light remains. The animal may be slightly agitated.

At medium degree compression of the brain, the animal breathes heavily, there is general weakness and difficulty moving. The reaction of the pupils to light remains normal.

Severe compression of the brain is characterized by the dog falling into a coma. Heart and respiratory rhythms are disturbed, breathing is very difficult, and there is no reaction of the pupils to light. This degree of compression is especially dangerous, and it is imperative to consult a doctor, since brain damage can lead to serious complications and death of the dog.

In case of traumatic brain injuries, it is important to properly transport the dog to the nearest veterinary clinic. The animal can be wrapped in a blanket and carried so that the dog's head is slightly lower than the body. The animal should not be fed or watered.

Severe damage to the skull bones, as well as the presence of hematomas, may require surgical intervention. For cerebral edema, diuretics and steroids are prescribed, and antibiotics are also used to avoid infection.

The success of treatment depends on the severity of the injury and how timely and qualified the assistance was provided. With duration comatose state over 1 day there is little chance of recovery, but with persistent and constant improvement in the animal’s condition, the animal can be cured. However, in the future it is possible various complications– such as partial loss of vision, changes in head position and recurrent seizures.

Spinal cord injuries occur for the same reasons as traumatic brain injuries - as a result of falls and road accidents. The most common spinal cord injuries are associated with various fractures spine, displacement of the vertebrae and rupture of intervertebral discs.

Symptoms of spinal cord injuries include loss of sensation or even paralysis of the limbs, accompanied by general weakness.

Spinal cord injuries are very dangerous and if they are suspected, you should take your dog to the vet immediately. For mild bruises, a course of drug treatment aimed at relieving swelling is usually sufficient. With more serious injuries Surgical treatment may be required, but not in all cases it completely eliminates all the negative changes that have occurred in the dog’s body. The effects of severe injuries often last a lifetime. Very severe injuries can cause the death of the animal.

Severe injuries often cause the dog to go into a coma. Coma is such a deep loss of consciousness that the animal stops responding to external stimuli. A dog may fall into a coma suddenly (for example, with a strong blow to the head), but a gradual transition from simple fainting to deeper and deeper states of complete insensibility up to coma is also possible.

In addition to injuries, the cause of a coma can be heat or sunstroke, severe hypothermia, certain diseases, as well as poisoning carbon monoxide or other potent poisons.

When a dog falls into a coma, the first thing you should do is check the body’s most important vital signs – pulse and respiration rates. Needs to be cleaned oral cavity from mucus and pull your tongue out. The animal must be laid on a hard surface so that the head is slightly lower than the hind limbs. If there are no signs of life, it is necessary to perform a cardiac massage and artificial respiration. Be sure to call the vet.

With head injuries, as well as with a disease of the central nervous system such as epilepsy, convulsive syndrome. It includes a whole range of symptoms, including involuntary twitching of the limbs, chewing movements, slurping, foaming from the mouth, uncontrolled urination and defecation, and loss of consciousness.

An atypical manifestation of this syndrome may also be observed, which is expressed in increased activity and unexplained aggression. The animal may bark for no reason, lick and bite its own body parts, or lunge at its owner and other people, or the dog may experience hysterical fits and convulsions.

The cause of seizures is usually increased activity certain groups of brain cells, often as a result of injury.

Convulsive syndrome is observed in dogs with reduced content sugar or calcium in the blood, in case of poisoning with various potent toxins, in case of kidney or liver failure, as well as in puppies with helminth infections. There are also a number of conditions similar to convulsive syndrome.

They develop when bitten by certain insects (for example, bees), when a foreign body gets into the throat, as well as from cardiac arrhythmia. In addition, severe anxiety and stress can cause muscle twitching in dogs. In the latter case they give sedatives– “Diazepam”, “Seduxen”, “Relanium”, but these drugs must be prescribed by a veterinarian.

Epilepsy

This disease manifests itself in repeated convulsive seizures. The cause may be either a congenital predisposition to the disease or its later development, for example, after a traumatic brain injury.

Since similar symptoms are observed in many diseases, you need to know that epileptic seizures are characterized by the fact that they all proceed in the same way.

An epileptic seizure consists of 3 phases. The first phase (aura) is a sign of an approaching seizure. At this stage, the animal experiences an increase in the level of anxiety; the dog becomes restless, shakes its head, has involuntary chewing movements, foams at the mouth, and has darting eyes.

The next phase (rigid) is characterized by profuse salivation and cramps. The animal's pupils are dilated and involuntary urination or defecation may occur. After this phase is completed, the dog experiences unsteadiness in its gait, and in the presence of irritating factors, the attack may recur.

Such irritating factors can be loud noise, rough handling, fatigue and overexcited state of the dog, bright lighting and even females in heat.

These two phases pass quite quickly (within 3 minutes), but the subsequent phase gives the impression that the animal is continuing to have convulsions, although in fact the actual epileptic seizure does not last longer than 5 minutes. The pattern of seizures in different dogs can vary greatly, therefore, at an appointment with a veterinarian, it is necessary to describe as accurately as possible all the characteristic symptoms of the animal’s disease, the frequency and similarity of the attacks.

During an epileptic seizure, you should never try to put your fingers into the dog’s mouth, as the animal, being in an uncontrollable state, may bite you.

Some owners' concerns that their dog might swallow its own tongue are unfounded.

The attack passes quickly, but it is necessary to call a veterinarian to examine the animal and prescribe appropriate treatment.

From medicines Phenobarbital and Primidone are used, as well as intravenous injections of Relanium. It was noticed that significant deterioration in health status against the background epileptic seizures Those dogs that develop the disease in adulthood are more susceptible. Treatment does not always give the desired effect, and this is due not only to the characteristics of the disease, but also to the lack of necessary skills among dog owners, so consultation with an experienced doctor is necessary.

Paralysis

Paralysis, that is, damage to the motor nerves, as a result of which the animal completely or partially loses the ability to move, can cause not only injuries, but also some diseases.

One of the causes of paralysis in dogs may be the poison contained in the salivary glands of female forest ticks. The symptoms that develop in a dog in this case are very similar to the symptoms of helminth infection, so it is difficult for a non-professional to understand the cause of the animal’s painful condition. First, the dog experiences severe weakness for several days, then paralysis develops. It is necessary to contact a veterinarian as soon as possible, since the animal may not only lose the ability to move, but even die due to respiratory arrest.

Another cause of paralysis can be bacteria - the causative agents of botulism. The source of infection for this infection is carrion, as well as spoiled food. The symptoms are similar to those above. This disease often leads to fatal outcome, so it is important to contact your veterinarian as soon as possible. Doctors usually use the drug "Anatoxin".

In addition to paralysis, in a number of diseases there is increased weakness of the entire body or limbs of the animal.

With myasthenia gravis, biochemical processes in nerve cells are disrupted, which leads to weakening of the dog’s hind limbs. The movement of a sick animal is difficult, and unsteadiness of gait is observed. Treatment is carried out using special medications under the supervision of a veterinarian.

Brain diseases

Encephalitis, or inflammation of the brain, can be caused by a variety of causes. Encephalitis is often one of the symptoms of an infectious disease.

Inflammation of the brain is provoked by plague, rabies and parvoviruses, as well as some others. In addition, encephalitis can develop as a result of a bacterial or fungal infection.

Symptoms of encephalitis include increased sleepiness or unjustified aggression, impaired coordination of movements, inappropriate reactions to external stimuli, fever, convulsions, fainting and coma.

Bacterial contamination can also cause other heavy defeat brain - meningitis, that is, inflammation of the membranes of the brain and spinal canal.

These diseases should be treated by a veterinarian. It is aimed at identifying the causes of health problems in dogs and eliminating them. For this purpose, antibiotics and corticosteroid drugs are used.

The causes of granulomatous meningoencephalomyelitis in dogs have not yet been precisely established. It is believed that this is an infection unknown to science. Symptoms of the disease include loss of coordination, paralysis, seizures and coma. This disease can manifest itself in different forms. Sometimes the picture of the disease resembles the symptoms observed with the appearance of brain tumors. In rare cases, complete or partial blindness occurs.

No effective treatment has been developed for this disease. The use of certain medications can temporarily alleviate the condition of a sick dog, but complete recovery does not occur.

Brain tumors occur predominantly in dogs with large cranial volumes. For benign tumors, surgical treatment is used, as well as radiation and chemotherapy. When malignant brain tumors form, treatment is ineffective.

Spinal cord diseases

The cause of these diseases is usually various injuries, as well as age-related changes in the dog’s body and the genetic predisposition of some breeds to certain diseases.

Herniated disc

Symptoms of this disease include pain, weakness, unsteadiness of gait and loss of coordination, as well as fainting. Damage to the intervertebral disc can lead to the development of paralysis of the hind limbs, along with which, a violation of the act of urination is often observed.

The causes of this disease are varied, it can develop gradually, or damage occurs unexpectedly as a result of sudden movement of the animal. It has been established that some dog breeds are more predisposed to this disease than others. This primarily applies to Beagles and Pekingese.

There are disc injuries in the lumbar and cervical spine. The latter are less common, and in this case paralysis of the limbs usually does not develop. If a cervical disc is damaged, the dog tries not to move its head, as this causes pain. Because of this, the animal's neck appears shorter than normal.

Surgical intervention for intervertebral disc injuries is usually not required. However, it is necessary to show the dog to the veterinarian, since the doctor will be able to determine the nature of the damage and prescribe treatment. Drugs that have a decongestant effect are used. During the recovery period, stress on the dog's spine and spinal cord should be limited.

Under no circumstances should you try to straighten an intervertebral disc on your own.

Unstable vertebra syndrome

The disease develops as a result of degeneration of the cervical vertebrae and their displacement as a result of sudden head movements. Symptoms include progressively worse coordination of the hind limbs and a wobbling gait. Possible loss of coordination of the forelimbs, as well as partial paralysis.

This syndrome most often affects dogs with long necks (such as Doberman Pinschers and Great Danes). It has not been established exactly what factors influence the development of the disease, but there is an assumption that it is provoked by excess nutrition of puppies.

Treatment should be carried out by a veterinarian. It is mainly aimed at eliminating swelling and inflammation of the spinal cord, for which special drugs are used. If the dog's condition does not improve, surgery is possible.

Cauda equina syndrome

This disease has the following symptoms: hind limb lameness and gait disturbance, tail paralysis, urinary incontinence and uncontrollable bowel movements (which are caused by paralysis Bladder and rectum). The animal may bite and gnaw the anal area, as sensitivity is lost.

The disease is caused by damage to the nerves located at the caudal end of the spine.

Therapeutic treatment methods are successful if the symptoms are mild. In severe cases, surgery is performed. With paralysis of the bladder and rectum, there is usually no noticeable effect from treatment.

Other diseases of the nervous system

Stress, prolonged exposure to solitude, as well as violation of living conditions can cause a dog mental disorders, manifested in changes in the behavior of the animal.

Neuroses

Neuroses in dogs develop for various reasons. The most common cause is severe stress; in addition, the cause of neurosis can be the inattentive attitude of the owner and poor-quality nutrition of the animal, and infectious diseases.

Neurosis can manifest itself in an inhibited or excited type. In the first case, the dog’s activity decreases sharply, the animal does not react (or reacts very slowly) to external stimuli, and stops following the owner’s commands.

In the second case, on the contrary, the animal becomes extremely susceptible to even minor influences external factors, the dog’s activity increases and at the same time it either becomes extremely timid or aggressive.

Neuroses can become a provoking factor in the development of many serious diseases of internal organs, therefore, if the described symptoms appear, it is necessary to take measures to cure the dog.

At mild form neurosis is often enough preventive measures of a general nature so that the animal recovers. Firstly, you should not physically or emotionally overload your dog. Temporarily stop active training. It's better to walk in quiet places, away from highways and crowded streets. You need to treat the animal calmly, avoid rude shouting and punishment - all this will only worsen the problem. neurotic state animal.

The food you give your dog should contain enough essential vitamins and microelements. It is recommended to include more dairy and meat products. Of course, they all must be fresh and of high quality.

If your dog has developed a severe form of neurosis, you should consult your veterinarian regarding the use of medications. You should not give tranquilizers to your animal yourself. You can try the remedies traditional medicine- decoctions of valerian roots, motherwort herbs as a sedative, and for raising vitality– tinctures of Eleutherococcus senticosus, Leuzea safflower, Rhodiola rosea, Schisandra chinensis or ginseng. But we should not forget that both during and after treatment you need to be attentive to your pet, try to protect the dog from strong experiences that can cause not only neuroses, but also other diseases.

Obsessive states

The result severe stress so-called obsessive states may also develop, when the animal regularly repeats the same actions, deprived practical significance, and sometimes even harmful to the dog itself. An animal can lick its fur and bite its own body parts, which leads to the development of skin diseases and the appearance of wounds and ulcers on the skin. Also dogs with the syndrome obsessive states They can try to catch their own tail, chasing it, bark at food, swallow pebbles and dirt. Often observed increased salivation. In addition to the listed symptoms, dogs can experience visual hallucinations - in this case, the animals behave as if they are hunting imaginary prey.

It has been established that this behavior of dogs is an unconscious desire to protect themselves from negative impact stress. However, the actions carried out by dogs with obsessive-compulsive disorder do not reduce the influence of stress factors on the animal’s body.

To overcome the syndrome, it is necessary to pay more attention to the animal. You should walk with your pet more often, train your dog, and also play with it. Obsessive states often appear in those animals that are left alone for a long time and do not walk much, so you need to try to make the dog’s life more interesting and varied. At the same time, you should avoid anything that causes stress in the animal.

If symptoms of obsessive states appear (imaginary hunting, licking, etc.), there is no need to show the dog your concern about its behavior, since the owner’s anxiety is quickly transferred to the animal.

For achievement maximum effect before treatment, you should consult your doctor. A number of effective antidepressants have been developed that will speed up the dog’s recovery process, but they should be taken under the supervision of a specialist.

Hyperkinesis

This disease is characterized by excessive activity of the dog. Along with it, other symptoms associated with disruption of the nervous system appear: increased agitation, involuntary movements of the limbs, increased breathing and heart rate, dilated pupils and redness of the eyes.

Veterinarians usually prescribe the drugs Amphetamine and Ritalin. Besides therapeutic treatment, an animal with this disease needs significant physical activity, so you need to walk your dog as much as possible and train it.