Infections of the nervous system


Distemper

Distemper is caused by a virus which is similar in structure to human measles virus. It is a serious disease of dogs which kills almost every dog that contracts it. It causes high fever, pneumonia, runny eyes, runny nose and diarrhea. Distemper usually strikes young puppies up to four months of age. “Chewing gum fits” are common in puppies with distemper. Distemper also causes seizures in older dogs. Vaccination usually prevents the disease but it is not 100% effective. Distemper is seen in dogs, foxes, wolves, ferret, mink, skunk, raccoon and coatimundi.

Nervous signs include:

  • localized muscle twitch, such as in the leg or facial muscles
  • paresis or paralysis, often most noticeable in the hind limbs as ataxia, followed by tetraparesis and tetraparalysis
  • “chewing-gum fits” – convulsions characterized by salivation and often chewing movements of the jaw

The seizures become more frequent and severe, and the dog may fall on its side and paddle its legs; involuntary urination and defecation often occur. An infected animal may exhibit any or all of these neurologic signs during the course of the disease. Infection may be mild and inapparent or lead to severe disease manifest by most of the above signs. The course of the disease may be as short as 10 days, but the onset of neurologic signs may be delayed for several weeks or months.

Rabies

This disease is infects all mammals but it is more prevalent in carnivores and bats. Rabies can affect the animal in many ways causing a variety of signs that range from normal behavior to rage and furious behavior to complete paralysis. The first classical phase begins with an animal that shows apprehension, nervousness, anxiety, and a variable fever. Friendly animals become shy or irritable and may snap, whereas fractious animals become more docile and affectionate. The pupils usually dilate. The animals will usually bite at or chew the site where he was bitten until it bleeds. This period will last for only 2 to 3 days.

The furious stage of the disease lasts from 1 to 7 days. The animals become irritable and fearful of light. They over-respond to sounds or quick movements. As they become more restless they begin to roam, usually becoming more irritable and vicious. Dogs may eat wood or other objects. They usually will avoid contact with people but when caged they become disoriented and will bite the bars or walls. Muscular incoordination develops and seizures may happen as this phase progresses. If they do not die during a seizure they usually progress to paralysis then die. Cats more consistently develop the furious form of the disease and may make vicious attempts to attack anyone moving. Some cats will run continuously until they die of exhaustion.

The dumb or paralytic phase usually develops within 2 to 4 days after the first signs develop. Paralysis of the larynx develops as well as loss of control of the face and jaw muscles. The dog begins to salivate excessively and rapid breathing whips the saliva into frothy foam. Dogs may be thought to be “choking on a bone” causing the veterinarian to become exposed during an examination. The paralytic stage lasts for 2 to 4 days. The animals usually go into a coma and dies. The paralytic disease in cats follows the furious stage at around the fifth day of illness. This stage in cats may be the only stage seen.

More information on Rabies can be found in the vaccination pillar™

Cerebellar Hypoplasia

Cerebellar hypoplasia is seen in kittens after in utero infection with feline panleukopenia virus. The virus attacks the cells that are dividing most rapidly – in adults this is gut tissue, in the fetus the brain cells are affected. Affected animals are ataxic and poorly coordinated; they wobble when they try to move. The condition is non-progressive, and affected animals may make suitable pets.

Porto-Caval Shunt or Portosystemic Shunt

The most common circulatory anomaly of the liver in both dogs and cats is the portosystemic shunt (PSS). A PSS is a connection between the portal vessels and systemic circulation that diverts blood flow, in varying degrees, from the liver. Decreased blood flow causes atrophy of the liver and subsequent dysfunction, decreasing liver metabolism of neurotoxins. Clinical signs of hepatic encephalopathy are frequently noted and can be most severe after feeding, especially after a high-protein meal.

Normally, the blood from the placenta bypasses the liver and goes into circulation via the ductus venosus, a blood vessel found in the fetus. A failure of the ductus venosus to close causes an intrahepatic shunt, while extrahepatic shunts are usually a developmental abnormality of the vitelline veins, which connect the portal vein to the caudal vena cava. Thus in the juvenile and adult animal with PSS, blood from the intestines only partly goes through the liver, and the rest mixes into general circulation. Toxins such as ammonia are not cleared by the liver. Most commonly, extrahepatic shunts are found connecting the portal vein or left gastric vein to the caudal vena cava.

Congenital PSS is a hereditary condition in dogs and cats, its frequency varying depending on the breed. The shunts found mainly in small dog breeds such as Shih Tzus, Miniature Schnauzers and Yorkshire Terriers, and in cats such as Persians, Himalayans, and mix breeds are usually extrahepatic (outside the liver), while the shunts found in large dog breeds such as Irish Wolfhounds and Labrador Retrievers tend to be intrahepatic (inside the liver).
Acquired PSS is uncommon and is found in dogs and cats with liver disease such as cirrhosis causing portal hypertension, which is high blood pressure in the portal vein.

Symptoms of congenital PSS usually appear by six months of age and include failure to gain weight, vomiting, and signs of hepatic encephalopathy (a condition where toxins normally removed by the liver accumulate in the blood and impair the function of brain cells) such as seizures, depression, tremors, drooling, and head pressing. Urate bladder stones may form because of increased amounts of uric acid in circulation and excreted by the kidneys.
Surgery is the treatment of choice for a shunt. Where this is not an option it is treated as liver failure. Dietary protein restriction is helpful to lessen signs of hepatic encephalopathy, and antibiotics such as neomycin or metronidazole and other medicines such as lactulose can reduce ammonia production and absorption in the intestines. The long term outlook is poor for any form of portosystemic shunt.

Hepatic Encephalopathy

When the liver is damaged toxic substances normally removed by the liver accumulate in the blood and impair the function of brain cells. Liver disease can be acute or chronic. The clinical signs of hepatic encephalopathy include seizures, depression, tremors, drooling and head pressing. Urate bladder stones may form because of increased amounts of uric acid in circulation and excreted by the kidneys.

Treatment of acute symptoms involves fluid therapy and enemas to reduce toxin production by gut bacteria. Once the animal has been stabilized, treatment is aimed at preventing recurrence. Protein-restricted diets should be fed. If needed, oral lactulose (0.1-0.5 mL/kg, PO, bid-tid) along with antibiotic therapy, either neomycin (22 mg/kg, PO, bid) or metronidazole (7.5 mg/kg, PO, bid) are recommended. Antibiotic therapy works synergistically with lactulose

Congenital Deafness

Congenital deafness is primarily associated with Dalmatians but has also been recorded in a number of breeds including Australian Blue Heelers and Shepherds, English Setters, Boston Terriers and Old English Sheepdogs. It is linked to blue eye color in white cats.

White Shaker Dog Syndrome

This disease, as the name suggests, is characterized by generalized tremors occurring in young, predominantly small dogs; Maltese and West Highland White Terriers are commonly affected. It has also been reported in Bichon Frise, Poodles, Beagles and Yorkshire Terriers. The disease is seen in dogs from 9 months to 3 years. The tremors are usually mild affecting all four limbs and the head. The tremors worsen with excitement or handling. The disease responds to corticosteroids.

Laryngeal Paralysis

Laryngeal paralysis occurs in middle-aged and older dogs. Large breeds, such as Labrador Retrievers, Golden Retrievers, and Saint Bernards, are predisposed. Most cases are idiopathic (no known cause) but a few cases are due to trauma or neoplasia affecting the neck or mediastinum. Hypothyroidism is also a potential cause. The clinical signs are changes in the voice, laryngeal stridor (harsh noise during breathing), and a dry cough. In severe cases, exercise intolerance and episodes of respiratory—especially inspiratory—distress and cyanosis occur. . Diagnosis is based on examining the vocal folds while the animal is lightly anesthetized. The vocal folds and arytenoid cartilages do not open properly during inspiration. Treatment of idiopathic laryngeal paralysis consists of surgery, such as laryngeal tie back. Surgery does not restore normal laryngeal function but is usually successful in reducing the severity of the dyspnea. A potential complication of surgery is aspiration of food or liquid.

Facial nerve paralysis

The facial nerve wraps around the ear and runs over the jaw. This makes it susceptible to damage. Facial nerve damage can be caused by trauma, middle ear disease, damage during surgery to the ear and hypothyroidism. Symptoms of facial nerve paralysis are dropping of the eyelids, lips, ear and face on the affected side, there may also be drooling.

Coonhound Paralysis

This disorder is also referred to as “coonhound paralysis” since a great number of hounds developed an ascending flaccid paralysis following contact with raccoons. Coonhound paralysis can affect any age, breed or sex of dog or cat, although the condition is rare before the age of 6 months. The onset of signs begins as rear leg weakness which rapidly ascends over 24-48 hours until the animal is quadriplegic. Occasionally, the condition can start in the fore legs and then progress to quadriplegia. Physical examination is usually within normal limits (an old raccoon bite might be apparent in hounds). Usually, there are no cranial nerve signs; however, in severe cases, the bark may be altered, swallowing impaired and facial nerve signs be evident. In some cases, respiration is impaired necessitating respiratory support. There is no specific treatment and recovery takes several weeks.

Traumatic injuries

Radial Nerve Paralysis
The radial nerve extends the elbow, carpus and toes. It is the largest nerve in the front leg. Radial nerve paralysis is the most common nerve injury in dogs: it can be easily damaged by trauma as it passes laterally along the humerus. The symptoms of radial nerve paralysis are paralysis of the front leg, in a flexed or bent position. There is loss of sensation on the upper and outside portion on the leg.

It is very important to protect the affected limb during the recovery period. With the dog or cat unable to control his front leg, the paw drags on the ground causing abrasions. When muscles lose their nerve connections they begin to atrophy or shrink, usually within five days of the injury. Physical therapy may be helpful to maintain blood flow in the atrophying muscles. If the injured nerves begin to re-grow, the animal may experience abnormal sensations from the affected limb. This condition is called paraesthesia. The abnormal sensations may lead to self-mutilation of the limb. In this case amputation of the limb may have to be considered if the behavior cannot be controlled.

Brachial Plexus Avulsion
The brachial plexus is a bundle of nerves that conducts signals from the spine to the shoulder, foreleg and paw. The brachial plexus can be damaged if the foreleg is pulled away from the body – brachial plexus avulsion, for example during a car accident. The signs are paralysis of a foreleg, muscle wasting, Horner’s Syndrome and loss of the Panniculus Reflex. The nerves are stretched or torn and treatment relies on physiotherapy, time and prevention of damage to the paw. If after 6 months no function has returned amputation is necessary.

  • Horner’s Syndrome— drooping upper eyelid, constricted pupil and a sunken appearance to the eye – is seen on the same side as damage to nerve roots at T1 and T2. In children Horner’s syndrome causes difference in eye color.
  • Panniculus Reflex— This is the reflex in which a skin pinch over the flank region results in a skin twitch bilaterally over the whole flank. It is used to localize spinal lesions.

Toxins

The following drugs are toxic to the nervous system in certain animals or at high doses:

  • Amitraz
  • Ivermectin (collies)
  • Metronidazole
  • Pyrethrum (cats)
  • Streptomycin (causes deafness in cats)

Other common toxins that affect the nervous system:

  • Alcohol
  • Antifreeze (ethylene glycol)
  • Lead
  • Metaldehyde (slug killer)
  • Organophosphate insecticides
  • Botulism

The successful treatment of toxicity is dependent on how quickly the animal is brought in for treatment and knowing what has been ingested. Always ask the owner to bring the package if they still have it. Even in animals that do not have many signs of illness a total body function should be carried out to make sure there is no long term damage.

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