Diseases of the nervous system of dogs: symptoms, manifestations, treatment.

Concussion in a dog

The dog's brain is firmly protected by the skull from possible damage. But sometimes with strong impacts, falls from great heights, as a result of transport accidents and in other cases, a concussion occurs. It is accompanied by disruption of brain function.

The dog becomes dizzy, loses balance, squints, and vomits. After two to three days of rest, a mild concussion usually goes away. But if a blood vessel bursts during a concussion, this leads to hemorrhage in the brain, which, depending on the size and nature of the brain damage, can be dangerous or even fatal for the animal. Therefore, a dog with a concussion must be seen by a veterinarian.

Treatment of inflammatory diseases of the central nervous system in dogs

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 sometimes occurs in cats.

Some dogs exhibit predominantly eosinophilic pleocytosis (eosinophilic meningitis), but the most common cause of eosinophilic pleocytosis on the east coast of Australia is parasitic meningoencephalomyelitis due to infestation by larvae of angiostrongylus cantonensis (rat lung nematode).

The term GME is often used to refer to all other non-infectious inflammatory diseases of the central nervous system (excluding meningitis that responds to steroid therapy), although the pathological physiology may vary.

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, 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 seen 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 prednisolone.

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.

Epilepsy in dogs

The symptoms of this disease are very characteristic. The dog suddenly gets scared, its gaze becomes motionless, after one or two steps its hind legs give way, the dog falls to the side, twitching all four paws in the air. At the same time, her head is thrown back, and abundant foam appears on her lips due to the convulsive movement of the masticatory muscles. Gradually the convulsions stop, the dog calms down and gets up as if nothing had happened.

The attack can last from ten seconds to several minutes at most, but to those who saw it for the first time, it seems that the attack lasted much longer. Some dogs, after such a seizure, circle around helplessly for some time, stumbling over obstacles. Such seizures can occur with long intervals, sometimes several years, and sometimes follow in whole series. In such a situation, the dog often dies from suffocation or heart failure.

Most specialist doctors believe that in dogs, unlike in humans, seizures only resemble epilepsy. The reasons for them are often very difficult to establish.

Only a thorough examination and comprehensive processing of all possible data about a sick patient allows a veterinarian to determine the possible causes of the disease in each specific case and carry out treatment in accordance with the diagnosis.

Neurological diseases in dogs and cats. Interview with a neurologist

Many people notice that dogs often “adopt” the behavior of their owners and are distinguished by extremely wide manifestations of individuality in their character. These differences are mainly due to different types of nervous activity, and sometimes the causes of deviations are diseases of the nervous system in domestic dogs.

In order to understand the reasons for certain manifestations of an animal’s behavior, it is necessary to know the causes of the condition, be able to identify the disease in the early stages and understand when individuality ends and the disease begins. Basic knowledge will help you detect the disease at the very beginning and quickly cure your beloved dog.

Types of nervous activity in dogs

Classification by types of behavior has existed for a very long time and can be correlated with similar observations of human behavior. Based on character traits, it is customary to distinguish the following types:

Sanguines.
Cholerics.
Melancholic people.
Phlegmatic people.

This division, accepted for people, is also suitable for dogs. Scientific research in the field of nervous activity was carried out by Academician Pavlov. He introduced the concept of reflexes and derived three main properties of nervous processes:

force;
equilibrium;
mobility.

All types of reflexes were divided into unconditioned and conditioned. Unconditioned reflexes are also called innate, they are caused by the reaction of the nervous system to environmental conditions. Conditioned reflexes are developed in response to certain influences, persist for as long as they are in demand, and fade away when the need for them ceases.

Not genetically transmitted. Conditioned reflexes are very important for dog training. The easier it is for an animal to develop a conditioned reflex, the easier and faster it can be trained.

According to the strength of nervous activity, dogs can be weak or strong, and this applies to both the stimulation of activity and its inhibition. This is a very important criterion, especially for service breed dogs. They must react quickly to changing situations and calm down just as quickly.

Mobility ensures quick transition from one activity to another. Nervous processes of this type can be reactive and inert.

Based on balance, dogs are divided into balanced and unbalanced types.

It cannot be argued that all types of higher nervous activity in domestic dogs appear in their pure form. As with humans, animals with mixed or transitional types of behavior are often found. The most common are dogs of the unrestrained type, which, according to the “human” classification, can be classified as choleric.

These are strong, sometimes even aggressive dogs that easily adapt to changes in the environment, easily form and fix conditioned reflexes, their inhibitory reflexes are difficult and are developed with effort.

If such an animal is overloaded and given too difficult tasks, it becomes susceptible to neuroses. The excitable type of dog must undergo special training in order to develop adequate inhibition processes. Dogs of the sanguine type are strong, energetic, very active, with sharp reactions and excellent sociability.

They easily form conditioned reflexes, just as easily move from strong excitement to concentration, and cope well with difficult tasks that require a quick and error-free choice of solution. Dogs with this type of nervous organization are better suited than others to perform official tasks.

Melancholic people are fearful, suspicious, and have weak processes of excitation and inhibition. Such dogs are always wary; they behave this way even towards their own owner. Developed conditioned reflexes quickly fade away.

Phlegmatic people are even less suitable for the role of a service dog. They react slowly and return to their original state just as sluggishly, poorly assimilate new information and quickly lose previously acquired skills. Rapid transitions from one type of nervous activity to another are practically impossible for them.

The behavior of a dog with abnormalities in nervous health can be pronounced or implicit, hidden.

If a dog not only flinches at the sound of a bunch of keys unexpectedly falling on the tile, but begins to bark hysterically or even rush at people, there are clearly disturbances in the functioning of its nervous system.

A healthy dog with a sanguine temperament will not even turn its ear towards the sound and will not “go crazy” itself.

Signs of a disease of the nervous system include seizures, sudden unmotivated mood changes, unreasonable aggression or complete apathy.

Why does a pinched nerve occur in a dog, and what should be done first?

Inflammation of the nerve (neuritis), nerve plexus (plexitis), and spinal roots (radiculitis) are independent or simultaneous diseases characterized by the development of an inflammatory process in the nervous tissue.

Source: https://arts-family.ru/drugoe/nevrologiya-u-sobak.html

Paralysis

The inability to work one muscle or group of muscles is called paralysis or paresis. It is a consequence of a violation of the nervous connection, which is expressed in the inability to transmit and execute commands of the central nervous system. The cause of this disorder may be associated with disruptions in the activity of both the central and peripheral nervous systems.

When people talk about paralysis, they usually mean paralysis of the limbs, but it can affect any of the dog's organs, such as the lower jaw, ears, tail, facial muscles, bladder or rectal muscles. The affected organ becomes sluggish and atrophies over time.

Central nervous system paralysis mainly affects paired organs, while peripheral paralysis affects only one side or even part of an organ. It is usually caused by injury to nerve tissue. The causes of paralysis are determined by a veterinarian, who also decides on the possibility of treatment, which, as a rule, is long-term and intensive.

Nervous system diseases in dogs

Inflammatory diseases of the nervous system in dogs are a fairly broad group of diseases, which includes meningomyeloencephalitis/meningoencephalitis of varying degrees of causation.

Meningitis is an inflammatory disease of the meningeal membrane of the central nervous system, myelitis is an inflammatory process of the spinal cord, and inflammation of brain tissue is called encephalitis. With meningitis, the subarachnoid space is involved in the inflammatory process. In other words, it is an inflammatory process of tissues that contain nerve cells.

Eclampsia

This is a disease of pregnant and lactating bitches. It is more often observed in small breed dogs; eclampsia is very rare in large dogs. The disease is based on a lack of calcium in the body and reduced function of the parathyroid glands.

Pregnant or lactating bitches suddenly develop anxiety, fear, rapid breathing, accelerated pulse, and increased salivation. The dog tries to walk, coordination of movements is impaired, urination and defecation are delayed. The animal falls, convulses, the pupils stop responding to light, the dog does not respond to calls.

During treatment, the animal requires complete rest and warmth. The dog is prescribed a dairy diet (milk, cottage cheese with honey, kefir), given sweetened oatmeal (or pearl barley) porridge, and limited salt intake. As a medicine, along with other drugs (vitamin D, promedol, aminazine), calcium glucanate is prescribed, the use of which does not stop even after the dog recovers in order to avoid relapse of the disease.

Neurological diseases (disorders) in dogs

Brain diseases

Inflammatory diseases of the central nervous system in most dogs mostly manifest themselves as dangerous diseases such as meningoencephalitis. This combined disease affects the meninges (meningitis) and the brain itself (encephalitis). Sometimes it “takes over” the spinal cord. Its lesion is called "encephalomyelitis".

The disease has the following classification:

By origin - primary or secondary meningoencephalitis.
By nature - purulent and non-purulent.
According to the course - acute and chronic.

In dogs, this disease manifests itself as a complication of a number of other diseases, for example, canine distemper, rabies, viral hepatitis and even helminthiasis (toxascariasis).

Symptoms of the disease are varied and vary at different stages. At the onset of the disease, the dog’s pupils are dilated, convulsions and twitching occur, which are sometimes confused with a condition such as a nervous tic of the head in an elderly dog. Rigidity of the neck muscles, agitation, and an acute reaction to any stimuli, including light and sounds, are also noted.

With the further development of the disease, the animal becomes apathetic, indifferent, does not respond to stimuli and stops following the owner’s commands, its coordination of movements is impaired, and its limbs are paralyzed. If the inflammation is acute and purulent, the body temperature rises.

Diagnosis is confirmed by puncture with collection of cerebrospinal fluid. Treatment is associated with eliminating the underlying cause of the disease. It is carried out comprehensively, the basis is the prescription of specific antibiotics.

In addition to encephalitis and meningoencephalitis, dogs may exhibit the following diseases caused by abnormalities in brain cells:

tumors of benign and malignant nature;
hydrocephalus;
idiopathic epilepsy and other diseases.

Problems associated with brain disease can be caused by external influences, such as an animal being hit by a car, being beaten by a person or other animals, or falling.

The resulting injuries to the skull can have serious consequences, including damage to the brain.

If they do not lead to the death of the dog or make it disabled, they may manifest themselves in changes in the animal’s behavior.

Predisposing factors

Neuralgia pain is acute and paroxysmal. Any impact on the sore spot can provoke a sudden onset of an attack. Such effects (for trigeminal neuralgia) include:

Eating too hot or cold food or drink. The dog’s teeth react to a sharp change in temperature and immediately send a nerve impulse to the nerve. As a result, acute pain appears.

Abrupt switching on of bright light.

A loud, deafening sound, a sudden bang.

Touching the tip of the nose, gums, lips. If you notice that the pet you are stroking suddenly jerks its head back without any adequate reason, then this sign is a good reason to take your pet to the veterinarian.

Spinal cord diseases

Spinal cord diseases in dogs are not caused by damage to the brain, but arise due to various effects on the spine and nerve endings. They can be caused by various reasons:

Spinal injuries and fractures.
Heredity. Some breeds with a long body and short crooked limbs have a hereditary predisposition to such diseases (dachshunds, basset hounds, English and French bulldogs, pugs, etc.).
Vertebral displacements.
Inflammatory processes.
Infections.

Herniated discs are most common in dogs with hereditary defects. In this condition, the disc becomes displaced and pinched between two vertebrae. The nerve endings are damaged, and the dog suffers from serious pain and impaired mobility.

Cauda equina syndrome can occur when there is severe inflammation or injury to the lumbar and pelvic spine.

It develops a disease of the extremities, which constantly progresses and leads to persistent paralysis, dysfunction of the pelvic organs, genitourinary and excretory systems.

Unstable vertebra syndrome develops due to sudden movement of the head due to degeneration of the cervical vertebrae.

In this case, inflammation of the spinal cord membranes, a wobbling gait or the development of paralysis appears. It is believed that dogs with a long cervical spine, such as Great Danes and Dobermans, suffer from this more often than others. This condition is also often observed as a result of injury.

When injured and pinched with death of the end, there is no sensitivity in the affected area of the nerve, the animal cannot control the damaged part of the body, and paresis or paralysis develops.

Depending on the size and depth of damage to the spinal cord membranes, symptoms can affect different parts of the body. With massive lesions, the animal can be completely paralyzed.

Source: https://lorises.ru/drugoe/nevrologiya-u-sobak-simptomy.html