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THE NERVOUS

SYSTEM

The brain comprises the cerebrum, cerebellum, midbrain, and brain stem.

The cerebrum is the largest part of the brain, and is the center of learning, memory, sensory input, behavior, and voluntary movement. Diseases affecting the cerebrum are characterized by depression, alterations in personality and behavior, and seizures.

The cerebellum has two lobes. Its primary functions are to integrate motor pathways, coordinate movements, and maintain balance. Diseases of the cerebellum result in lack of coordination, unstable gait, and muscle tremors. In the midbrain and brain stem are the centers that control the respiratory rate, heartbeat, blood pressure, and other vital functions. At the base of the brain and closely connected to the midbrain and brain stem are the hypothalamus and pituitary glands. These structures are important in regulating the dog’s body temperature and hormone systems. They are also the centers for primitive responses such as hunger, thirst, anger, and fright.

The spinal cord passes down a bony canal formed by the arches of the vertebrae. The cord sends out nerve roots that combine with one another to form the peripheral nerves. Diseases of the spinal cord produce varying degrees of weakness and paralysis.

The cauda equina is the termination of the spinal cord. Diseases of the

cauda equina can produce paralysis of the tail, loss of bladder and bowel control, and paralysis of the anal sphincter. The paired cranial nerves, 12 total, arise from the midbrain and brain stem and pass directly out into the head and neck through openings in the skull. The optic nerves to the eyes, the otic nerves to the ears, and the olfactory nerves to the nasal cavity are examples of paired cranial nerves.

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Neurological Evaluation

A complete health history is of paramount importance in diagnosing unexplained neurological symptoms. Your veterinarian will want to know if the dog has been in an accident. Did she receive a blow to the head? Is she taking any medications? Has she been exposed to other dogs who exhibit similar

signs? Could she have gotten into any toxic substances? When did you first notice the symptoms? Did they come on suddenly or gradually? Have they

progressed? If so, has the progression been rapid or gradual? The age, sex, and breed of the dog are important, because some neurological diseases are genetically determined and appear in certain breeds or at certain ages. Special tests are used in addition to a standard physical examination for a dog with a possible neurological problem. Your veterinarian will manipulate your dog to check her balance, motor control, and sensory perceptions.

Diagnostic tests used in evaluating neurological function include X-rays of the skull and vertebral column, electroencephalography ( EEG) , and muscle and nerve conduction studies. A spinal tap is a procedure in which a needle is inserted into the spinal canal to remove cerebrospinal fluid for laboratory analysis. A myelogram is a spinal tap in which dye is introduced into the spinal canal so signs of spinal cord compression will be visible on X-rays. 15_067857 ch12.qxp 7/6/07 10:42 PM Page 357

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Computer-assisted tomography ( CAT scan) and magnetic resonance imaging ( MRI) enable a radiologist to see a computerized image of the structures in the brain, spinal canal, and body cavities. These examinations are now available at veterinary schools and many large veterinary hospitals.

Head Injuries

A dog’s head can be injured in many ways, including a car accident, a fall, a blow to the head, or a gunshot wound. Since the brain is encased in bone and surrounded by a layer of fluid, it takes a major blow to the head to fracture the skull and injure the brain.

SKULL FRACTURES

A skull fracture can be linear, star shaped, compound (a compound fracture opens to outside the body), or depressed (forming a depression). Skull fractures often extend into the middle ear, nasal cavity, or sinuses, creating pathways for bacteria to gain access to the brain and cause infection. In general, the larger the skull fracture, the greater the likelihood of brain injury. However, the brain can be injured even if the skull is not broken.

OPEN FONTANEL

The skull is formed by three bone plates, and the area at the top of the skull where they come together is called the fontanel. Usually these plates fuse when a puppy is about 4 weeks old, but sometimes they never completely fuse, leaving a hole at the top of the skull called an open fontanel, or molera. The open area can range in size from a 50-cent piece to a penny.

Most of the time an open fontanel will close over by the time the dog is 1

year of age, but sometimes it will remain open throughout the dog’s lifetime. These areas can be susceptible to trauma but are generally not a problem. In some dogs this condition may be associated with hydrocephalus (see page 367). Congenital open fontanel is seen primarily in Chihuahuas, but the condition can be found in all the toy breeds. Since it’s likely a hereditary problem, dogs with an open fontanel should not be bred.

BRAIN INJURIES

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Contusion (Bruising)

With a contusion, there is no loss of consciousness. After a blow to the head the dog remains dazed, wobbly, and disoriented. The condition clears gradually.

Concussion

By definition, a concussion means the dog was knocked unconscious. With a mild concussion there is only a brief loss of consciousness, while with a severe concussion the dog may be unconscious for hours or even days. When she

returns to consciousness, the dog exhibits the same signs as for a contusion. A severe concussion causes the death of millions of neurons. Recent information indicates that brain cell death does not cease within a few hours of the injury, but can continue for weeks or months.

Seizures

Seizures can occur at the time of injury or at any time thereafter. Seizures at the time of injury are particularly detrimental because they increase pressure in the skull and compromise blood flow. This worsens the effects of the injury. Seizures that occur weeks after the injury are caused by scars that form in areas where brain tissue has died.

Brain Swelling and Bleeding

Severe head injuries result in brain swelling and bleeding into and around the brain. Brain swelling, technically called cerebral edema, is always accompanied by a depressed level of consciousness and often coma. Since the brain is encased in a rigid skull, as the brain swells the cerebellum is slowly forced down through the large opening at the base of the skull. This squeezes and compresses the vital centers in the midbrain. Death occurs from cardiac and respiratory arrest.

Blood clots can form between the skull and the brain or within the brain itself. A blood clot produces localized pressure that does not, at least initially, compress the vital centers. Like cerebral edema, the first indication is a depressed level of consciousness. One pupil may be dilated and unresponsive to a light shined in the eye. Another sign is weakness or paralysis involving one or more limbs.

TREATING HEAD INJURIES

Treating shock takes precedence over managing the head injury (see Shock, page 7). If the dog is unconscious, establish an open airway by extending the head and pulling the tongue forward as far as you can beyond the level of the canine teeth.

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Signs of death are no pulse, no effort to breathe, dilated pupils, and soft eyes. Usually it is impossible to tell at the time of an accident whether such signs are reversible. Accordingly, begin administering CPR immediately if you suspect the dog is dead (see CPR, page 9).

At the scene of the head injury, before transporting the dog to the nearest veterinary hospital, be sure to:

• Handle the dog with extreme care and gentleness. Pain and fright

deepen the level of shock. Cover the dog with a warm blanket.

• Control bleeding as described in Wounds, page 42.

• Place the dog on a flat stretcher as described in Spinal Cord Injuries, page 375.

• Stabilize all fractures, if possible (see Broken Bones, page 15).

• Record a baseline neurological exam (level of consciousness, limb

movements, pupil size).

• Transport the dog with her head higher than her hindquarters; this

helps lower intracranial pressure.

Signs of cerebral edema can appear at any time during the first 24 hours after a blow to the head. The most important thing to observe is the dog’s level of consciousness. An alert dog is easily aroused (no apparent brain swelling). A semi-comatose dog is sleepy but arousable (mild to moderate brain swelling). A comatose dog cannot be aroused (severe brain swelling). Cerebral edema is treated with intravenous corticosteroids, oxygen, and

diuretics such as mannitol or furosemide. Seizures are controlled with an intravenous or oral anticonvulsant such as diazepam (Valium).

Open skull fractures require surgical cleansing and removal of devitalized bone. Depressed bone fragments may need to be elevated to relieve pressure on the brain. Antibiotics are often necessary with open fractures to prevent infection.

Only dogs who are fully alert, are not having seizures, and exhibit no neurological signs should be permitted to return home. Awaken the dog every two hours for the first 24 hours at home to check her level of responsiveness. Any change from an alert status is an indication to return at once for veterinary evaluation. In addition, be sure to check the dog’s pupils. They should be of equal size. An enlarged pupil that does not constrict when light is shined in the eyes indicates pressure on the brain. Also notify your veterinarian if the dog’s breathing becomes rapid or irregular, if she exhibits any form of muscle weakness, or if she has a seizure.

The prognosis for recovery depends upon the severity of the brain injury. When the dog remains in a coma for more than 48 hours, the outlook is poor. However, if the dog steadily improves throughout the first week, the outlook is good.

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Dogs who recover may exhibit a posttraumatic syndrome that can include

seizures, behavior changes, head tilt, and blindness.

Brain Diseases

ENCEPHALITIS (BRAIN INFECTION)

Encephalitis is an inflammation of the brain. Symptoms include fever, depression, behavior and personality changes (especially aggression), uncoordinated gait, seizures, stupor, and coma.

Canine distemper is the most common cause of encephalitis in dogs. Signs develop two to three weeks after the onset of the disease. Other causes of viral encephalitis include rabies, pseudorabies, and herpesvirus. Rabies is a very serious disease, but with present-day vaccination programs the disease is not common among domesticated animals. Canine herpesvirus produces an

encephalitis in puppies younger than 2 weeks of age.

Bacterial encephalitis is caused by organisms that enter the brain via the circulatory system, such as bacterial endocarditis, or by direct extension from an infected sinus, nasal passage, or an abscess in the head or neck. Migrating foreign bodies such as porcupine quills or grass awns may get into the central nervous system. Fungal brain infections (caused by cryptococcosis, blastomycosis, or histoplasmosis) are rare causes of encephalitis, as are protozoan infections. Tick-borne rickettsial diseases, notably Rocky Mountain spotted fever and canine ehrlichiosis, are infrequent causes. These diseases may also

involve the spinal cord.

Postvaccination encephalitis is rare with modern vaccines. It was most likely to occur when modified live virus distemper vaccine was administered at the same time as modified live parvovirus vaccine in puppies less than 6 to 8 weeks old. This is not usually seen with current vaccines and vaccination schedules.

Lead encephalitis is seen primarily in young dogs who chew on materials that contain lead, such as paint and drywall, especially in older buildings. Lead alters brain metabolism and causes inflammation and swelling. Central nervous system signs are often preceded by vomiting, diarrhea, or constipation. The diagnosis is confirmed by an elevated blood lead level. Meningitis is an infection of the surface of the brain and spinal canal. It is caused by infected bite wounds about the head and neck and bacterial infections that travel to the brain from the sinuses, nasal passages, or middle ears. Aseptic meningitis is a nonbacterial disease of unknown cause. It affects large-breed dogs 4 to 24 months of age.

The diagnosis of encephalitis or meningitis is based on analysis of cerebrospinal fluid obtained by spinal tap. Serologic tests may identify the cause of the inflammation.

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Treatment: Corticosteroids are used to reduce inflammation and swelling of the brain. Seizures are controlled with anticonvulsants. Antibiotics are used to treat bacterial infections. Rickettsia are extremely sensitive to tetracycline and doxycycline. Dogs who recover from encephalitis may develop seizure disorders and other neurological symptoms. Rabies is almost always fatal. GRANULOMATOUS MENINGOENCEPHALITIS

This common inflammatory brain disease in dogs is abbreviated GME. The

cause is unknown. Female dogs of small breeds, especially terriers, Dachshunds, Poodles, and Poodle crosses, are predisposed. Although GME can occur at any age, most affected dogs are 2 to 6 years of age.

A chronic form of GME called Pug encephalitis occurs as an inherited disease in Pugs between the ages of 9 months and 4 years. It often begins with seizures, confusion, and loss of memory. This form of the disease has also been seen in Yorkshire Terriers and Maltese.

GME can affect all parts of the brain (the disseminated form), or only specific areas (the focal form). There is a rare ocular form that targets the optic nerves of the eyes.

The disseminated disease appears suddenly and progresses over a matter of weeks. It is characterized by incoordination, stumbling, falling, circling, head tilt, seizures and, dementia.

The focal disease begins with symptoms such as those of a brain tumor.

Behavior and personality changes may predominate. The focal disease progresses to the disseminated disease over a period of 3 to 6 months. The ocular disease is characterized by sudden blindness with a dilated

pupil. It progresses to the disseminated disease more slowly than does the focal disease.

GME can be suspected when a toy dog such as a Poodle inexplicably develops confusion, disorientation, seizures, or other neurological signs that progress rapidly over a matter of weeks. A spinal tap with analysis of cerebrospinal fluid helps confirm the diagnosis. A CAT scan or MRI is useful in determining the form and location of the disease.

Treatment: Corticosteroids and immunosuppressive drugs may slow the progression of GME and provide temporary relief for several months.

However, GME is almost invariably a progressive and fatal disease.

BRAIN TUMORS AND ABSCESSES

Brain tumors are not common. They tend to occur in middle-aged and older dogs. The highest incidence is found in the short-nosed breeds that have large-domed heads, including the Boxer, Bulldog, and Boston Terrier. Tumors 15_067857 ch12.qxp 7/6/07 10:42 PM Page 362

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that can metastasize to the brain include cancers of the mammary glands, prostate, and lungs, as well as hemangiosarcoma.

Symptoms depend on the tumor’s location and rate of growth. Tumors in

the cerebrum produce seizures and/or behavioral changes. The dog may

exhibit a staggering gait, head tilt, nystagmus (rhythmic movement of the eyeballs), and limb weakness or paralysis. These signs are progressive and continue to worsen. Late signs are stupor and coma. A brain abscess is a collection of pus in or around the brain. The signs are similar to those of a brain tumor. These dogs will often have a fever. There may be a prior infection in the oral cavity, inner ear, or respiratory tract.

Treatment: The diagnosis of tumor or abscess is made by neurological examination and special tests, including EEG, cerebrospinal fluid analysis, and CAT scan or MRI. Surgical removal of benign brain tumors may be possible in some cases. Chemotherapy and radiation therapy have not proven to be effective against most brain tumors in dogs. There may be temporary improvement with corticosteroids and anticonvulsants. Abscesses are treated with high doses of antibiotics. Corticosteroids are usually contraindicated. The outlook for recovery is guarded.

STROKE

Strokes are not common in dogs. A stroke can be caused by bleeding into the brain, obstruction of an artery caused by an embolus, or clotting of a cerebral artery. An embolus is a clot that develops at another site and travels through the vascular system to a smaller vessel, where it becomes lodged and interrupts blood flow to the area served by that artery. This results in death of tissue in the affected area, a condition called infarction. Most strokes in dogs are caused by emboli.

Bleeding in the brain is seen with ruptured cerebral blood vessels and brain tumors. Spontaneous bleeding may occur with coagulation disorders.

Disseminated intravascular coagulation is a cause of both bleeding and infarction. Some hemorrhagic strokes occur for unknown reasons. Infarctions can occur with Rocky Mountain spotted fever, hardening of the arteries associated with hypothyroidism, and for unknown reasons.

The onset of stroke is sudden. The signs depend on the location and extent of the bleeding or brain infarction. They include behavioral changes, disorientation, seizures, weakness or paralysis on one side of the body, stupor, and coma. Large strokes are often accompanied by cardiac arrhythmias and collapse. The diagnostic workup is similar to that for a brain tumor.

Treatment: Treatment involves the use of corticosteroids to prevent brain swelling and anticonvulsants to control seizures. Dogs who survive the first few days have a good prognosis for recovery. The long-term outlook depends on controlling or eliminating the underlying disease.

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Hereditary Diseases

Hereditary nervous system diseases are not common. Most run in families. Affected individuals should not be bred.

HEREDITARY MYOPATHIES (MUSCULAR DYSTROPHY)

Muscular dystrophy is actually a group of genetically determined diseases in which there is a progressive degeneration of skeletal muscle (the muscles that are attached to the skeleton). Nerves and muscles work hand in hand, so

damaged nerves will lead to damaged muscles. Weakness is the predominant sign. The diagnosis can be suspected by finding high serum CPK levels.

Many of these problems will require a muscle biopsy for an accurate diagnosis. One of the best places to send samples is the Comparative Neuromuscular Laboratory of the University of California at San Diego.

Some of the more common disorders are listed here.

Hereditary Myopathy of Labrador Retrievers

This disease is inherited as an autosomal recessive trait. Signs of weakness begin at between 6 weeks and 7 months of age. There is a marked decrease in exercise tolerance. An affected pup may have difficulty holding up her head, bunny hop when running, and collapse after brief exertion. The disease may affect the muscles involved in chewing and swallowing, resulting in drooling and the development of megaesophagus. Exposure to cold greatly exacerbates the symptoms.

Treatment: Diazepam (Valium) given twice a day benefits some puppies. It is important to prevent stress and chilling, and to warm a pup quickly if she is exposed to cold. The disease often stabilizes or improves by 6 to 12 months of age. Many dogs are able to live a normal life. If drooling and megaesophagus develop, however, the outlook is guarded.

Breeding dogs can be tested by the Alfort School of Veterinary Medicine

in Maisons-Alfort, France, to see if they carry this defect.

Sex-Linked Muscular Dystrophy

This disease affects Golden Retrievers, Irish Terriers, Samoyeds, Rottweilers, Belgian Tervurens, and Miniature Schnauzers. It is transmitted on the X chromosome from the dam. Affected pups are weak at birth and often die. Those who survive develop a stilted gait, drooling, muscle wasting, and stunted growth. The condition may stabilize temporarily by 6 months of age, but later progresses.

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Bouvier des Flandres Myopathy

This disease affects only the muscles of swallowing, resulting in regurgitation and megaesophagus. Signs appear at about 2 years of age. With severe megaesophagus the outlook is guarded.

Treatment: The only treatment is to tend to the symptoms of Megaesophagus (see page 258).

Distal Myopathy of Rottweilers

This disease affects the legs and feet, producing an abnormal stance with splayed toes and weak hocks.

Treatment: There is no treatment.

Myotonia

This disease affects Chow Chows, Staffordshire Terriers, Rhodesian

Ridgebacks, Cavalier King Charles Spaniels, Great Danes, Golden Retrievers, and Irish Setters. Signs appear when the pups begin to walk. They include stiffness upon rising and walking. This is followed by a progressive stiffening of the gait as the dog exercises.

Treatment: Off-label use of the drug procainimide may help with signs in some dogs.

DEGENERATIVE MYELOPATHY

This is a degenerative disease of the spinal cord that appears to run in families. It occurs primarily in middle-aged German Shepherd Dogs but has been diagnosed in many breeds. It is the most common cause of hindquarter weakness in German Shepherds and their crosses. The Siberian Husky, Old English Sheepdog, Rhodesian Ridgeback, Weimaraner, and other large breeds are also affected. Among smaller dogs, older Pembroke Welsh Corgis are seen with

this problem.

The disease manifests itself as a slowly progressive weakness or paralysis of the hind limbs, along with an unsteady gait suggestive of hip dysplasia. The toenails on the hind feet may show abnormal wear from dragging on the

ground. This disease appears to be autoimmune in nature and similar to multiple sclerosis in people.

Treatment: Treatment with corticosteroids and/or vitamin supplements has not proven to be effective in curing or reversing the problem. Still, about 50

percent of dogs will show some improvement when given the medications

aminocaproic acid and n-acetylcysteine. Dietary supplements are also helpful—

tofu, vitamins C and E, coenzyme Q (Q 10), and green tea for their antioxidant properties. A regular exercise program, customized for each dog’s capabilities, is also helpful.

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INHERITED NEUROPATHIES

There are a number of rare diseases in which sensory and motor nerves degenerate. With loss of sensation and motor function, an affected dog does not feel the position of her limbs, is unable to position them correctly to prevent stumbling, and fails to withdraw a leg from a painful stimulus.

The diagnosis is made by sensory and motor nerve conduction studies.

There is no cure, but because of the slow progression of the disease some dogs live comfortably for many years. Most of these neuropathies are inherited as autosomal recessive traits. Some of the most common ones are noted here. Neuropathy of German Shorthaired and English Pointers is first noted at 3 to 4 months of age. The pup with this sensory neuropathy begins to lick and bite at her paws, which become swollen, reddened, ulcerated, and eventually mutilated. Loss of sensation can extend up the limb and involve the trunk. The mode of inheritance is autosomal recessive.

Dachshund sensory neuropathy begins in longhaired Dachshunds at 2 to 3 months of age. It is characterized by uncoordinated gait, urinary incontinence, and loss of sensation over the entire body. Self-mutilation of the penis may be the first sign in males.

Global cell leukodystrophy is caused by an enzyme deficiency that results in degeneration of nerve cells. It occurs in West Highland White Terriers, Cairn Terriers, Beagles, Pomeranians, and Poodles. Signs are unsteady gait, head tremors, nystagmus (a rhythmic movement of the eyeballs), and blindness. Scotty cramp is an autosomal recessive disease in Scottish Terriers where puppies show increased muscle tone when excited, stressed, or exercising vigorously. They show a stiff, hyper gait. Diazepam (Valium) helps, and most of these dogs can be comfortable pets.

Hypertrophic neuropathy in Tibetan Mastiffs begins at 7 to 12 weeks of age and is characterized by hind-limb weakness that progresses to generalized weakness and, ultimately, an inability to stand. Some dogs maintain a degree of strength. This is an autosomal recessive disease.

Polyneuropathy in Alaskan Malamutes shows up at about 12 to 18

months of age. Initially, dogs show exercise intolerance but this can progress to paralysis. Some dogs may stabilize, but most dogs continue on a downward trend. Treatments have not been effective.

Hypomyelination diseases manifest when myelin, which forms a sheath around nerve fibers, is not completely developed at birth. The result is that nerve impulses are conducted very slowly. Hypomyelination occurs in Chow Chows, Weimaraners, Samoyeds, and Bernese Mountain Dogs. One form,

called the shaking puppy syndrome, is a sex-linked recessive trait that affects only males.

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activity and disappear with sleep. Severely affected puppies show uncoordinated body movements and are unable to stand. There is no cure for the disease. Tremors in Chow Chows and Weimaraners may improve gradually and disappear by 1 year of age.

WHITE DOG SHAKER SYNDROME

This syndrome occurs primarily in adult dogs with white coats, although dogs with other coat colors are occasionally affected. The disease occurs most often in small breeds, including West Highland White Terriers, Maltese, Bichons Frises, and Toy and Miniature Poodles.

It is characterized by the sudden appearance of tremors, sometimes accompanied by wild and random movements of the eyes. The disease affects the cerebellum, which coordinates muscle movement. Sudden trembling that

involves the entire body and head is the main sign. The dog does not shake while sleeping, but the more she moves, the worse the tremor gets. These tremors can be disabling.

The cause is unknown, but an autoimmune basis has been suggested.

Treatment: See your veterinarian if your small dog suddenly develops a tremor that seems to get worse. Corticosteroids reverse the shaking within a few days. Some dogs require extended treatment. About 25 percent of dogs retain some degree of tremor for life. With refractory cases, diazepam

(Valium) may be added to control tremors.

CEREBELLAR DISEASES

Cerebellar degeneration is a slowly progressive disease in which the nerve cells in the cerebellum die. The disease has been described in numerous

breeds, including the Kerry Blue Terrier, Gordon Setter, rough-coated Collie, Great Dane, Labrador Retriever, Golden Retriever, Cocker Spaniel, Airedale Terrier, Samoyed, Cairn Terrier, and Bullmastiff.

Affected puppies appear normal for the first two months of life, but then begin to show uncoordinated body movements such as jerking, stumbling,

falling, and overreaching with the paws. Although there is no cure, cerebellar degeneration stabilizes in some puppies, allowing them to remain active. Cerebellar hypoplasia is a condition in which the cerebellum is abnormally small at birth. A hereditary form has been reported in Airedales, Gordon Setters, and Chow Chows. A nonhereditary form has been described

in Bull Terriers, Weimaraners, Dachshunds, and Labrador Retrievers. Signs are similar to those of cerebellar degeneration, but are observed shortly after birth when puppies first begin to crawl. Some puppies compensate and make good pets.

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Lissencephaly is a condition seen rarely in Lhasa Apsos, Irish Setters, Wire Fox Terriers, and Samoyeds. The brain is smooth without the gyri or folds normally seen. Affected dogs may show behavioral abnormalities, including difficulty housetraining and sometimes seizures. HYDROCEPHALUS

Hydrocephalus is caused by the excessive accumulation of cerebrospinal fluid in the ventricles of the brain. The enlarged ventricles damage the cerebral cortex by compressing it against the skull. Most cases are congenital. Some are acquired through trauma, brain infections, or tumors.

Breeds with an increased risk of congenital hydrocephalus include the

Maltese, Yorkshire Terrier, Chihuahua, Lhasa Apso, Pomeranian, Toy Poodle, Cairn Terrier, Boston Terrier, Pug, Pekingese, and Bulldog.

Hydrocephalus causes seizures, partial or complete blindness, and dementia. The diagnosis is made by skull X-rays, ultrasound of the ventricles and, in difficult cases, by CT scan or MRI. A characteristic enlargement of the dome of the skull occurs in congenital hydrocephalus, but this may not be seen until the puppy is several months old.

An increase in ventricular size without clinical signs has also been noted. This is called subclinical hydrocephalus. In certain lines of toy breeds with a high incidence of clinical and subclinical hydrocephalus, EEG screening and breeding only dogs with normal EEGs has reduced the incidence of hydrocephalus.

Treatment: This is directed toward decreasing the production of cerebrospinal fluid with corticosteroids and diuretics. Surgery has been beneficial is some cases. The long-term prognosis is favorable if diagnosis and treatment is begun before the brain is damaged. Nonetheless, affected dogs often appear dull and have a limited ability to learn.

Seizure Disorders

A seizure is caused by an abnormal burst of electrical activity within the brain, commonly in one of the cerebral hemispheres. The electrical activity sometimes spreads out and involves other areas, including the midbrain.

A typical grand mal seizure is preceded by a period of altered behavior, called the aura. During the aura dogs may be restless and anxious, cry out, demand affection, or seek seclusion. The actual seizure normally lasts less than two minutes, and is characterized by collapse with rigid extension of the legs. The dog becomes unconscious and may stop breathing for 10 to 30 seconds. This is followed by rhythmic jerking of the legs (which resembles running or paddling). Some dogs also chomp, chew, drool, or urinate and 15_067857 ch12.qxp 7/6/07 10:42 PM Page 368

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defecate. As the dog regains consciousness there is a postseizure state characterized by disorientation and confusion. The dog may stumble into walls and appear blind. The postseizure state can persist for minutes or hours. Grand mal seizures are typical of epilepsy.

A focal motor or partial seizure is one in which the jerking or twitching is limited (at least initially) to a particular part of the body. A focal seizure usually indicates a specific brain lesion, such as a scar, tumor, or abscess. Seizures are commonly associated with brain injury, encephalitis, heat

stroke, brain abscess, brain tumor, stroke, poisoning, kidney failure, or liver failure. Seizures associated with a concussion frequently occur weeks or months after the head injury and are caused by a focus of scar tissue in the brain. Postencephalitic seizures occur three to four weeks after the onset of

encephalitis. Distemper, in particular, is characterized by attacks that begin with chomping, tongue chewing, foaming at the mouth, head shaking, and

blinking, all followed by a dazed look.

Postvaccination seizures have been described in puppies under 6 weeks of age following inoculation with a combined distemper-parvovirus vaccine.

This is extremely rare with current vaccines.

A bitch may develop low blood calcium levels after whelping and have

seizures. A sudden drop in blood sugar (hypoglycemia) can also trigger a seizure. This occurs in newborn pups with cardiopulmonary syndrome (discussed in Why Puppies Die, page 494). It can also occur in small-breed puppies who have not been fed adequately. A common cause of hypoglycemia is giving too much insulin to a diabetic dog. Common poisons that cause seizures are animal baits such as strychnine,

antifreeze (ethylene glycol), lead, insecticides (organophosphates), and chocolate. Seizures caused by organophosphates are preceded by drooling and muscle twitching. Exposure to a spray, dip, or premise treatment suggests the diagnosis. There are a number of conditions that, while not true seizures, are often mistaken for them. Bee stings, for example, can cause frenzied barking followed by fainting or collapse. Cardiac arrhythmias can be mistaken for seizures because they cause loss of consciousness and collapse.

Treatment: If the dog is in a dangerous location at the time of the seizure, move her to a safe site. Otherwise, do not disturb the dog during or after the seizure, as this may trigger further seizures. Despite the old wives’ tale, do not pull out the dog’s tongue or wedge something between her teeth. Dogs can’t swallow their tongue.

Note the length of the seizure. As soon as the seizure is over, notify your veterinarian, because he or she will want to examine the dog to diagnose and treat the underlying cause.

Seizures lasting more than five minutes (status epilepticus seizures) or cluster seizures (several seizures one after the other without a return to consciousness) are emergencies. They must be stopped with intravenous Valium or other anticonvulsants to prevent permanent brain damage or death. Seek

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immediate veterinary attention. Status epilepticus has a poor prognosis, because it is usually caused by poisoning or a serious brain disease.

EPILEPSY

Epilepsy is a recurrent seizure disorder that may be idiopathic or acquired. Acquired epilepsy has an identifiable cause, such as a mass of scar tissue in the brain following a head injury. Idiopathic epilepsy occurs in up to 3 percent of dogs and accounts for 80 percent of recurrent seizures. The cause is unknown, although an imbalance in chemicals that transmit electrical impulses in the brain has been suggested. Seizures, usually of the grand mal type, begin between 6 months and 5 years of age.

Breeds in which the condition is inherited include Beagles, Dachshunds,

Keeshonden German Shepherd Dogs, Belgian Tervurens, and others. Breeds

with a high incidence, but in which inheritance has not yet been established, include Cocker Spaniels, Collies, Golden Retrievers, Labrador Retrievers, Irish Setters, Poodles, Miniature Schnauzers, St. Bernards, Siberian Huskies, and Wire Fox Terriers. Even mixed breeds can be afflicted with epilepsy. If the diagnosis is truly epilepsy, the attacks must be recurrent and similar. Epileptic seizures usually become more frequent with time. Your veterinarian will ask you to keep a log of the frequency of seizures and to provide a description of the dog’s behavior before, during, and after each seizure. A typical epileptic seizure has three phases: an aura, a generalized grand mal seizure, and a postseizure state—as described in the previous section. All three phases may not be seen, because many seizures occur while the dog is resting or asleep. Furthermore, in some cases the seizure is atypical. Instead of a classic grand mal convulsion, the dog exhibits strange behavior such as frenzied barking, licking or chewing at herself, staring into space, or snapping at invisible objects. This is called a psychomotor seizure and is believed to arise from a center lower in the brain (not the cerebrum).

Focal motor seizures, as already discussed, indicate a lesion in the brain. An abnormal neurological exam or EEG during a period when there have been no recent seizures also indicates a lesion in the brain. These findings eliminate the diagnosis of epilepsy. Further diagnostic tests include a spinal tap with cerebrospinal fluid analysis, skull X-rays, and a CT scan or MRI.

Treatment: A number of newer drugs are available for treating epilepsy. However, anti-epileptic drugs, either singly or in combination, are not 100

percent effective. The best one can hope for is that treatment will significantly decrease the number and severity of the seizures while increasing the seizure-free interval between them. In general, treatment is indicated if there are two or more seizures a month, or more than 10 to 12 seizures a year. Cluster seizures and status epilepticus are other indications to start treatment. Phenobarbital continues to be the single most effective drug for treating epilepsy in dogs. Its principal initial side effect is sedation. Most dogs, 15_067857 ch12.qxp 7/6/07 10:42 PM Page 370

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however, develop a tolerance to the sedative effects within a few weeks. In some dogs, it can cause liver damage. Potassium bromide can also be used to treat epilepsy. More dogs respond to phenobarbital than to potassium bromide alone, but potassium bromide has no potential to cause liver damage. Rarely, it will cause hind leg stiffness, but this is reversible if the drug is stopped. Many dogs are best controlled by a combination of phenobarbital and potassium bromide. A few dogs are well controlled on potassium bromide alone. If seizures cannot be controlled with phenobarbital and potassium bromide, other drugs, such as Clonazepam, Valproic acid, Clorazepate, and many others can be added. The dosages and rates of action of all anticonvulsants are variable. Regular monitoring of serum drug levels is essential—both to control seizures and to avoid toxicity. Liver enzymes are monitored as well. The two common causes of treatment failure are not maintaining adequate drug levels and not giving the drugs as often as directed. A missed dose of an anticonvulsant can precipitate a seizure. It is important to work closely with your veterinarian. Acupuncture and dietary changes may also help to reduce the number and

extent of seizures.

Research is under way to identify the defective gene or genes responsible for epilepsy so that dogs can be identified as carriers before being bred. Affected dogs may not have their first seizure until 3 to 5 years of age, by which time they may have already been bred. No dog known to seizure from suspected epilepsy should be bred.

NARCOLEPSY AND CATAPLEXY

Narcolepsy and cataplexy are uncommon disorders of the sleep mechanism in which a dog is excessively sleepy all day (narcolepsy) or experiences sudden muscle paralysis and collapse (cataplexy). Between attacks the dog is completely normal. Narcolepsy can occur without cataplexy, and vice versa, although narcolepsy alone is difficult to recognize in dogs.

A dog may have one or many episodes of collapse in a day, each lasting a few seconds or up to 30 minutes. The attacks can usually be reversed by petting the dog or making a loud noise.

Treatment: There are several effective drugs available to prevent narcolepsy and cataplexy. Dogs afflicted with the inherited form (mainly Doberman Pinschers, Dachshunds, and Labrador Retrievers) often improve as they grow older. This is an autosomal recessive problem in these three breeds. OptiGen has a DNA test to identify carriers before dogs are bred.

COMPULSIVE BEHAVIORS

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the dog may be sitting quietly and suddenly starts to bite at imaginary flies. These dogs can usually be distracted and never lose consciousness. Cavalier King Charles Spaniels are one breed in which this behavior is seen.

In the tail biting/spinning sequence, the dog is intent on trying to catch her tail and spins rapidly. These dogs may become so intent that it is difficult to break their concentration. Bull Terriers and German Shepherd Dogs may have an inherited component to this behavior.

Treatment: For dogs with these disorders, veterinary behaviorists work with a variety of behavior-modulating drugs, along with behavior modification. These are off-label uses of these drugs, so you need to work closely with your veterinarian and do not give your dog any of these medications without veterinary guidance. Clomipramine and fluoxetine are two drugs that are

sometimes prescribed; clomipramine is approved for use in dogs.

AGGRESSIVE BEHAVIORS

Some syndromes in dogs, such as rage syndrome and sudden-onset aggression, may have a physiological basis such as seizures or a metabolic disturbance in serotonin levels. These dogs may suddenly switch from acting normally to viciously attacking whomever or whatever is nearest. Minutes later, the dogs often act as if nothing happened.

English Springer Spaniels and Cocker Spaniels may have an inherited predisposition to these problems. Aggressive behavior has also been associated with hypothyroidism in Golden Retrievers, German Shepherd Dogs, and

Shetland Sheepdogs. Thyroid levels should be checked in any dog with newly appearing aggressive behavior.

Treatment: Whether this is truly a physical problem or a behavioral one has not been fully determined. Any dog showing these signs should be worked up for a physical problem and also seen by a veterinary behaviorist. Using behavior modification and behavior modifying medications, some of these

dogs can become relatively safe pets. If there is an underlying physical problem that can be treated, it should be. Coma

Coma is a depressed level of consciousness. It begins with confusion, progresses through stupor, and ends up with complete loss of consciousness. A dog in a coma is insensitive to pain and cannot be awakened. Coma occurs with oxygen deprivation, brain swelling, brain tumor, encephalitis, and poisoning. Many diseases that cause seizures progress to coma. Following a head injury with cerebral concussion, coma can occur without progressing through the earlier stages.

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Low blood sugar (hypoglycemia) is a common cause of coma. It tends to

occur in toy-breed puppies and adult hunting dogs after a long day in the field. A common iatrogenic cause is giving too much insulin to a diabetic dog (see Diabetes Mellitis, page 300). Another cause of coma is prolonged hypothermia (see Cold Exposure, page 17).

Coma related to high fever and heat stroke is a serious complication that leads to permanent brain damage and is usually preceded by seizures. Vigorous efforts must be made to bring down the fever (see Heat Stroke page 22). Coma is also especially ominous when it is associated with brain trauma or when it occurs in the late stages of kidney or liver disease.

Common poisons that may cause coma are ethylene glycol (antifreeze),

barbiturates, kerosene, turpentine, arsenic, cyanide, organophosphates,

plants, chocolate, and lead. A dog found in a coma in a closed car or in an airtight space may have smothered or developed carbon monoxide poisoning (see Drowning and Suffocation, page 20).

Treatment: First determine the level of consciousness and whether the dog is alive. If the dog shows no signs of life, begin CPR (as described on page 9). An unconscious dog can choke on her vomitus, so pull out the tongue and

clear the airway with your fingers. If the dog has a foreign body, such as a piece of meat, obstructing the airway, treat as described for Choking, page 316. Wrap the dog in a blanket and proceed at once to your veterinarian.

Weakness or Paralysis

There are several diseases—none of them very common—that attack the

motor nerves, causing weakness and paralysis but leaving the sensory nerves intact. These diseases resemble one another and are difficult to tell apart. TICK PARALYSIS

The saliva of a variety of ticks contains a toxin that affects the motor nerves, producing weakness and paralysis. Signs appear about one week after a dog has been bitten by the tick. Over the next 48 to 72 hours, the dog grows progressively weaker. Sensation to a pin prick is normal. In time, the paralysis reaches a level where the dog collapses and is unable to lift her head. Death can occur from respiratory arrest.

Treatment: Presence in a wooded area suggests the diagnosis. Seek veterinary attention whenever a dog exhibits unexplained weakness. Tick paralysis can be prevented by removing ticks promptly from the dog and using the

methods of tick control described in Ticks, page 123. Most dogs show dramatic improvement with tick removal, but may need supportive care for a while.

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BOTULISM

Botulism is a paralytic disease caused by neurotoxins produced by the bacteria Clostridium botulinum. The disease is acquired by eating infected carcasses or improperly canned vegetables and meats.

Treatment: The outlook for recovery is good if the disease does not progress rapidly. Antitoxins are available. Mildly affected dogs recover without treatment. COONHOUND PARALYSIS

The cause of this disease is unknown. It is believed to be an immune-mediated disease with antibodies directed at the dog’s own peripheral nerves. The agent triggering the immune reaction may be a virus or a bacteria. It occurs most often in hunting dogs one to two weeks after having had contact with a raccoon. The illness is not limited to Coonhounds. Paralysis begins as weakness in the hindquarters and progresses forward

until the dog is unable to stand. During this time the dog remains anxious but alert. The paralysis can affect the muscles involved in respiration and swallowing. It reaches its peak at about 10 days. Muscle atrophy may be dramatic.

Treatment: Good nursing care is the main treatment. Full recovery may take weeks or months.

MYASTHENIA GRAVIS

This is a rare disease caused by a deficiency of acetylcholine receptors, normally present at the junction of nerve endings and muscle cells. When an animal decides to move a muscle, the nerve endings release acetylcholine, which is a neurotransmitter. The acetylcholine carries the nerve impulse across the junction, where acetylcholine receptors respond and send the nerve impulse on its way. A reduction in the number or function of these receptors produces generalized muscle weakness, made worse by exercise. Weakness is most

apparent in the hindquarters. Dogs with myasthenia gravis have difficulty getting up and exhibit a swaying or staggering gait. There is a focal form of myasthenia gravis that affects only the muscles involved in swallowing. The dog is unable to swallow solid food and develops enlarged, dilated megaesophagus. Aspiration pneumonia often follows.

A congenital form of myasthenia gravis is inherited as an autosomal recessive trait. It occurs in Jack Russell Terriers, Springer Spaniels, and Smooth Fox Terriers.

An acquired form of myasthenia gravis occurs in all breeds, but is seen most often in Golden Retrievers, German Shepherd Dogs, Labrador Retrievers,

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Dachshunds, and Scottish Terriers, often occurring at 1 to 4 years of age or 9 to 13 years of age. Acquired myasthenia gravis is an immune-mediated disease in which auto-antibodies are directed at and destroy the acetylcholine receptors. Hypothyroidism can occur at the same time as autoimmune myasthenia

gravis. Occasionally, myasthenia gravis is related to a tumor of the thymus gland, but this is rare.

The diagnosis of myasthenia gravis is based on neurological examination. One test involves injecting a drug called edrophonium chloride. This drug blocks the enzyme that breaks down acetylcholine, resulting in higher concentrations of this neurotransmitter at the receptor sites. The test is positive if muscle strength improves after the injection. A serologic test for diagnosing autoimmune myasthenia gravis is available.

Treatment: Drugs are available that increase the concentration of acetylcholine at receptor sites, thereby reversing muscle weakness. These drugs can be given as a syrup or by injection. The dose varies according to the dog’s activity and stress levels. Close veterinary monitoring is required. Drugs to counter immune responses may also be helpful.

Megaesophagus is treated as described on page 258. Thymus gland tumors

are removed surgically. Hypothyroidism responds to thyroid replacement

therapy (see page 142). With appropriate treatment, the outlook for complete recovery and the return of normal swallowing is good.

HYPOKALEMIA (LOW SERUM POTASSIUM)

Hypokalemia, a condition in which the dog has low serum potassium, is a

metabolic cause of generalized muscle weakness. Loss of potassium occurs with severe vomiting. It also occurs with the long-term use of diuretics that cause the kidneys to excrete potassium, such as Lasix (furosemide). Other causes of hypokalemia include bloat, diabetic ketoacidosis, and Cushing’s syndrome.

Treatment: The diagnosis is made by measuring serum potassium levels. Weakness disappears as potassium is replaced and the underlying cause is corrected. Close veterinary supervision is required until normal levels are restored. Spinal Cord Diseases

Injuries and diseases of the spinal cord generally produce weakness and paralysis in one or more limbs and/or the tail. Spinal cord diseases do not cause seizures, nor do they produce changes in personality or behavior. This sets them apart from brain diseases. However, injuries to peripheral nerves may be difficult to distinguish from spinal cord injuries.

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SPINAL CORD INJURIES

Spinal cord injuries are associated with ruptured discs and vertebral fractures and dislocations caused by accidents such as automobile accidents, gunshot wounds, and falls.

Immediately after a spine injury, there may be neck or back pain, weakness or paralysis of the legs, a stumbling gait, loss of feeling in the limbs, and urinary or fecal incontinence. Signs that get worse after an injury are often caused by tissue swelling, which interferes with the blood supply to the spinal cord and may cause permanent paralysis.

A pelvic fracture can be mistaken for a spinal fracture. In both cases the dog is unable to bear weight on her hindquarters and shows pain when handled in the injured area. Thus it might appear as if the outlook is poor, even though a dog with a broken pelvis often makes a complete recovery.

Treatment: Dogs with spinal cord trauma usually have life-threatening injuries that take precedence and require immediate attention (see Treating Head Injuries, page 358). All dogs who are unconscious or unable to stand should be considered to have spinal cord injuries until proven otherwise. Handle these animals with extreme care to protect the spine. Vertebral fractures are unstable. Flexing the neck or back may compress the spinal cord and worsen the injury.

Transport a dog with a back injury on a flat surface. Duct tape over the shoulders and hips prevents this dog from moving his back.

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At the scene of the accident, move the dog as gently as possible onto a flat surface, such as a piece of plywood, and transport to the nearest veterinary clinic. Sliding the dog onto a blanket and lifting the corners is an acceptable way to transport her if a makeshift stretcher is not available.

Spinal cord injuries are treated with corticosteroids and diuretics such as mannitol to prevent further swelling at the site of the injury. Good nursing care and physiotherapy are extremely important in preventing complications and hastening recovery. Surgery may be necessary to relieve pressure on the spinal cord or to stabilize a fractured vertebra.

A dog with mild bruising of the spinal cord begins to recover in a few days. However, if the cord has been lacerated or severely damaged, paralysis or death may be the result.

INFECTIONS AND TUMORS

Infections of the vertebrae, discs, and spinal cord are uncommon. Most bacterial infections occur after trauma or from infected wounds close to the spine. Viral, fungal, rickettsial, and protozoan diseases that cause encephalitis can also cause spinal cord infections (known as myelitis). The diagnosis of

myelitis is made by spinal tap and cerebrospinal fluid analysis.

Tumors can involve the spinal cord, nerve roots, or structures around the cord. Symptoms are caused by the compression of the cord or the nerves coming out from the cord. Benign neoplasms such as meningiomas, and bony growths called osteophytes (see Spondylosis, page 380), may also cause compression. Malignant tumors include osteosarcomas and lymphosarcomas.

Treatment: Treatment of myelitis involves the long-term use of antibiotics, selected after culture and sensitivity tests. Surgery may be necessary to remove a foreign body, drain an abscess, obtain material for testing, or relieve pressure on the spinal cord.

Some benign tumors can be removed surgically. Malignant tumors

usually are not removable but may respond temporarily to radiation and/or chemotherapy.

RUPTURED DISCS

A disc is a cushion of cartilage that sits between the vertebrae and acts as a shock absorber. It is composed of a rim of tough, fibrous connective tissue that surrounds a gel-like center called the nucleus. When a disc ruptures, one of two things may happen. The first is that the fibrous capsule breaks, allowing the inner nucleus to push out through the opening and impinge on the spinal cord or a nerve root. This type of rupture is called a Hansen Type 1. The second is 15_067857 ch12.qxp 7/6/07 10:42 PM Page 377

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In this drawing, (A) is a normal disc; (B) is an acute Hansen Type 1 disc rupture; (C) is a Hansen Type 2 disc rupture.

that the entire disc, surrounded by an unbroken capsule, can bulge outward. This is called a Hansen Type 2.

The diagnosis of ruptured disc is made by neurological examination and imaging studies including spine X-rays, a myelogram, and possibly a CT scan or MRI. Ruptured discs in the back of the Hansen Type 1 occur in small breeds such as the Dachshund, Beagle, Cocker Spaniel, Pekingese, and small mixed breeds. In fact, ruptured discs are more frequent in Dachshunds than in all other breeds combined.

The capsule begins to degenerate at about 2 to 9 months of age, and signs of impingement on the spinal cord appear at 3 to 6 years of age. About 80 percent of Type 1 ruptured discs occur in the lower back between the last thoracic and the first two lumbar vertebrae. Most of the remainder occur in the neck. There is often a history of mild trauma, such as jumping off a sofa, but normal movements are sufficient to cause a Type 1 rupture. Occasionally, more than one disc becomes ruptured.

The symptoms of a Type 1 rupture usually come on gradually but can

appear with sudden explosiveness. The main sign is pain. The dog holds her back stiffly and may cry or whine when patted or handled in the injured area. She usually refuses to walk up stairs or jump into a car. Neurological signs include weakness, lameness, and a wobbly gait. A dog experiencing the severe back pain of an acute rupture will have a hunched-up position and a tight abdomen. The dog may pant and tremble. Sudden disc ruptures can produce

complete hindquarter paralysis.

Hansen Type 2 discs ruptures occur in the larger breeds, including German Shepherd Dogs and Labrador Retrievers. The entire disc, surrounded by its capsule, gradually impinges on the spinal canal. Symptoms appear in dogs 5 to 12 years of age. Because the process is gradual, symptoms progress slowly.

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Both these dogs suffer from hindquarter paralysis caused by a Type 1 back disc rupture.

Ruptured discs in the neck of the Hansen Type 1 cause a dog to carry her head low and rigidly, making the neck look shorter. This type of injury is extremely painful. A dog will often cry out when patted on the head and

refuse to lower her head to eat and drink. Weakness and lameness involve the front legs. Complete paralysis of all four legs does occur but is rare.

Hansen Type 2 neck discs occur with the wobbler syndrome discussed on

page 379.

Treatment: A dog with a sudden onset of symptoms of paralysis requires immediate veterinary evaluation. If surgery is indicated, the best outcome is when it is performed within 24 hours.

Most disc problems involving pain or mild paresis improve with rest and

medication. The dog should be closely confined for two to four weeks to allow the disc to return to its former position. Corticosteroids reduce swelling and inflammation. Analgesics relieve pain.

Dogs with neck disc problems should be walked with a chest harness rather than a collar.

Disc injuries that cause paralysis require special handling and transporting, as described for Spinal Cord Injuries, page 375. The most common surgery is called a laminectomy. It involves opening the spinal column and removing the extruded disc material. Dogs undergoing surgery will still need a period of careful rehabilitation afterward.

A newer method is to use of proteolytic enzymes to dissolve the disc material. This is called chemonucleolysis. This may only be appropriate for dogs who are in pain without neurologic deficits. If there are neuological signs, surgery is often the better option because it relieves pressure on the spinal cord more quickly.

Acupuncture and physical therapy may be incorporated into treatment

protocols.

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FIBROCATILAGINOUS EMBOLIC MYELOPATHY

This problem occurs when small emboli of disc material break off and block spinal cord blood vessels. Dogs often show a short period of pain followed by weakness ranging from mild ataxia to paralysis. Signs may be on only one side. This problem is seen more often in large to giant breed dogs, but also

Shetland Sheepdogs and Miniature Schnauzers.

Treatment: Most dogs show at least a partial recovery after treatment with corticosteroids.

WOBBLER SYNDROME

Wobbler syndrome is a disease that results from compression of the spinal cord in the neck. The compression is caused by vertebral instability related to either a malformed cervical vertebrae or a ruptured Hansen Type 2 neck disc. Both may be accompanied by hypertrophy (enlargement) of the ligament that runs down the vertebral canal beneath the vertebrae. Ligament enlargement is believed to be a reaction to instability of the spine.

Most cases of wobbler syndrome occur in Doberman Pinschers over 5 years

of age, and to a lesser extent in Great Danes under 2 years of age, but other breeds can also be affected. Ruptured discs are more common in Doberman

Pinschers, while vertebral malformations predominate in Great Danes. The malformed vertebrae may be related to the long neck and rapid rate of growth in Great Danes.

The principal sign of both conditions is a progressive loss of coordination in the rear legs, accompanied by a peculiar, wobbly gait. Weakness or partial paralysis affects the front legs as the disease progresses. Manipulating the neck up and down is painful and may exacerbate the paralysis. The diagnosis is made by X-rays of the cervical spine and by a myelogram.

Treatment: Medical treatment is similar to that described for ruptured discs. Dogs with mild symptoms may respond to medical management. More

severely affected dogs respond best to a surgical procedure that decompresses the spinal cord and stabilizes the vertebral column. Dogs will require extensive rehabilitation after the surgery. Acupuncture and cervical collars may help. Breed factors and genetic influences appear to contribute to the wobbler syndrome. Until more is known about the exact cause, affected individuals should not be bred.

CAUDA EQUINA SYNDROME

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spina bifida (a developmental defect in the bones of the lower back), infections of the spinal cord and disc spaces, spinal cord tumors, and lumbosacral vertebral canal stenosis.

Lumbosacral vertebral canal stenosis is an acquired disorder in which there is instability of the spine in the lower back. There may be a congenital component that produces narrowing of the bony canal. German Shepherd Dogs are most often affected.

The early signs of the cauda equina syndrome include pain in the lower

back (lumbosacral area), difficulty getting up, and recurring lameness in one or both hind legs. Testing for sensation in the lumbosacral area reveals an increased sensitivity to touch and pinprick. This is the key to early diagnosis. In more advanced cases there is weakness or partial paralysis in the hind limbs and urinary and/or fecal incontinence. The anal sphincter may be completely relaxed.

Treatment: Medical management is similar to that described for ruptured discs. It is most successful when symptoms are mild. Surgical decompression and bone fusion can be considered for dogs who do not respond to medical management and for those with progressive hind limb weakness. Dogs with a paralyzed bladder or rectum are unlikely to benefit from treatment.

SPONDYLOSIS (BONE SPURS)

Spondylosis is characterized by the presence of osteophytes—bone spurs that form around intervertebral discs as a dog ages. They usually do not produce symptoms. On rare occasions, spurs project into the spinal canal and cause symptoms similar to those of a ruptured disc. A fusion of the osteophytes, called spondylosis deformans, restricts movement of the vertebral column and causes pain and stiffness. Large-breed dogs are most often affected.

Treatment: Dogs with the pain and stiffness of spondylosis deformans respond well to analgesics. Surgery to remove osteophytes and decompress the spinal cord may be benefit dogs who are not helped by analgesics.

Acupuncture and physical therapy will help some dogs, as well.

Peripheral Nerve Injuries

An injury to a nerve results in loss of sensation and/or muscle movement in the structures affected by that nerve. With complete paralysis the leg hangs limply. With partial paralysis, the dog stumbles when attempting to put

weight on the leg. Common injuries are stretches, tears, and lacerations. Stretches involving the brachial and radial nerves are usually caused by auto accidents or falls in which the front leg is jerked away from the trunk. A similar stretching of the femoral or sciatic nerves can cause a paralyzed back 15_067857 ch12.qxp 7/6/07 10:42 PM Page 381

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leg. Nerves can be crushed when a vehicle rolls over the leg. Bone fractures and muscle injuries often occur at the same time.

Another cause of nerve paralysis (usually temporary) is the injection of an irritating medication into the tissue surrounding a nerve. This problem does not occur frequently, but can be a cause of concern when it does. The correct procedure for giving injections is described on page 567. (Also see Horner’s Syndrome, page 176.)

Treatment: Lacerated nerves do not regenerate. The paralysis is permanent. Stretched nerves may (but do not always) return to normal. Those that do recover begin to improve in three weeks and may continue to improve for 12 months. If recovery does not occur, the dog may benefit from amputation of the paralyzed leg. Electroacupuncture to stimulate nerves may encourage healing.

DEAD TAIL OR LIMBER TAIL

This condition has been seen in Labrador Retrievers, Pointers, Setters,

Foxhounds, and Beagles. The dogs will hold their tails totally limp or out away from their body three to four inches, then hanging limply. Most often this occurs after a strenuous day of hunting or swimming—especially if the water is cold.

Dogs may act as if the tail is painful. It appears to be a sprain or strain of the tail muscles and nerves after working much harder than usual.

Treatment: Rest and anti-inflammatory medications usually result in a normal tail in just a few days.

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13

C h a p t e r

THE

   

MUSCULOSKELETAL

SYSTEM

The dog’s skeleton is made up of 319 bones—about 100 more than humans

have. Although the number of bones is roughly the same in all breeds, there is considerable variation in the size and shape of individual bones, as the result of selective breeding.

The place where two bones meet is called a joint, or articulation. In some joints there is a cushioning pad of cartilage interposed between the bones. This pad is called a meniscus. A damaged meniscus can deteriorate and

inflame the joint. Abnormal wear and tear on joint surfaces and joint cartilages leads to arthritis. In many cases the abnormal wear and tear is the result of poor joint conformation associated with inherited orthopedic abnormalities such as hip dysplasia. Joint position is maintained by the ligaments, the tendons, and a tough

fibrous capsule surrounding the joint. Together, these structures provide stability and hold the joint together. Joint looseness (called laxity) is caused by stretching of these support structures. Laxity enables the ends of the bones to slip partly out of position. When the joint capsule ruptures, the bones slip completely out of position. This is called dislocation.

The skeletal anatomy of humans and dogs has much in common, including

similar terminology. However, there are significant differences in the angles, lengths, and position of the bones. The dog’s hock, for example, is actually the heel bone in humans. While people walk on the soles of their feet, dogs walk on their toes. Humans carry all their weight on their hips. Dogs carry 75 percent of their weight on their shoulders and front legs. 383

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Veterinarians, dog breeders, and dog show judges use specific terms to

describe a dog’s overall composition and structure. Conformation is how the various angles, shapes, and parts of the dog’s body conform to the breed standard. Standards for purebred dogs describe the ideal conformation for each breed. These standards are based, to a certain extent, upon aesthetic considerations, but they also take into account the breed’s original purpose as a working dog. Most breed standards provide some information on the desired angle or

slope of the bones of the shoulders, pelvis, and limbs. These angles are determined using imaginary lines drawn horizontally and vertically through the plane of the standing dog.

Another term used to judge the physical attributes of a dog is soundness. When applied to the musculoskeletal system, it means that all the bones and joints are in correct alignment and are functioning as intended. In particular, in a dog with good skeletal conformation the alignment of the legs allows equal distribution of weight, equal bone pressure, and equal strain on the supporting ligaments when the dog is standing naturally or moving at a trot. Limping or Lameness

Limping indicates a structural problem, pain, or weakness in the involved leg. It is a common sign of bone and joint disease, but it also occurs with muscle and nerve injuries.

DETERMINING THE CAUSE

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leg is involved? A dog often holds up the paw or places less weight on a painful leg, especially one that has been recently injured. A dog usually takes shorter steps on a painful or weak leg. You may notice that his head bobs or drops as his weight comes down on the painful leg. With chronic lameness, the dog may simply take very short strides with no obvious limp. This is also true if more than one leg is injured or hurts. The dog’s head bobs up on the painful side and down on the side with the sound leg.

Having identified which leg is involved, try to identify the specific site and possible cause. First examine the foot and look between the toes. Many cases of lameness are due to foot injuries such as sprains, pad lacerations, broken nails, and penetrating puncture wounds caused by thorns and splinters. Carefully feel the leg from the toes up. Locate areas of tenderness by applying gentle pressure. You may also feel areas of swelling. Next, flex and extend all joints from the toes to the shoulder looking for resistance (lack of easy movement). Resistance is a sign of joint pain, which will be evident when the dog attempts to pull the leg free. If you aren’t sure if something you feel is normal, check the dog’s other leg. You have one for a comparison for both front and rear leg problems.

Having located the site of pain, the next step is to try to determine the cause of the pain. Consider the following:

Infected areas are red, warm, and tender, and are often associated with skin lacerations or bite wounds. There may be purulent drainage from the wound. The limp grows steadily worse. An abscess may be developing.

The dog may have a fever. Dogs often lick at abscessed or wounded areas.

Sprains and strains occur suddenly and are often accompanied by swelling and bruising. Usually the dog is able to bear some weight on the leg. The lameness may persist for days or weeks.

Fractures and dislocations cause severe pain and the dog is unable to bear weight on the leg. There is some degree of deformity. The tissues

are swollen and discolored from bleeding.

Inherited orthopedic diseases generally come on gradually. Young to middle-aged dogs are commonly affected. There may be few local findings to explain the lameness. Swelling, if present, is often slight. The lameness persists and grows worse with time.

Degenerative joint disease, also called arthritis or osteoarthritis, is the most common cause of lameness in older dogs. The lameness is worse

when the dog wakes up and improves as he moves about.

Spinal cord injuries and peripheral nerve injuries (discussed in chapter 12) produce weakness or paralysis without pain in one or more limbs.

Bone tumors are evidenced by a firm mass or swelling with or without signs of inflammation (see page 538). Pressure over a bone tumor causes

varying degrees of pain. Consider this diagnosis in a mature dog with an unexplained limp. Bone tumors are more common in large-breed dogs.

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DIAGNOSTIC TESTS

X-rays of the bones and joints are used to diagnose fractures and dislocations. They are also helpful in distinguishing bone growths from soft tissue swellings. Note that many cases of lameness occur without positive findings on conventional X-rays. A bone scan (also called nuclear scintigraphy) is an imaging technique that uses radioactive isotopes injected into the body and X-ray equipment to form a picture of the bone and surrounding tissue. These scans are especially useful in diagnosing bone cancers and determining the extent of their spread. Because of the cost and the restrictions on using radioactive isotopes, bone scans are performed only at medical centers and schools of veterinary medicine.

A CT scan or MRI may be of benefit in special circumstances, particularly with tendon, ligament, and muscle damage, but their availability and cost of these studies limit their usefulness.

Synovial fluid is a viscous joint lubricant that contains hyaluronic acid. The fluid can be removed using a sterile needle and syringe. Analyzing this fluid helps determine the cause of joint swelling. Normal synovial fluid is clear and pale yellow. Blood in the fluid indicates recent joint injury. Pus indicates joint infection (septic arthritis) . Bone and Joint Injuries

Emergency treatment for fractures is discussed in Broken Bones, page 15. A fracture (or even a suspected fracture) is always an emergency and requires immediate veterinary attention.

OSTEOMYELITIS (BONE INFECTION)

Bacterial contamination and subsequent infection is a hazard whenever bone is exposed. It occurs most often with open fractures. Other causes are gunshot wounds and animal bites that become infected and progress to adjacent bone. In rare cases osteomyelitis is caused by blood-borne bacteria or fungi. This occurs in dogs receiving chemotherapy and those suffering from illnesses that impair immunity.

Signs of acute osteomyelitis are excessive pain, lameness, fever, and swelling. In dogs with chronic osteomyelitis there is an intermittent purulent discharge through the sinus tracts connecting the bone to the skin. The diagnosis is confirmed by X-rays and a culture of the bone.

Treatment: Bone infection is a most difficult problem to treat. It is essential to remove all devitalized bone and leave the wound open for daily dressing changes and wound irrigation. Bacterial cultures of the infected bone aid in selecting appropriate antibiotics.

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Osteomyelitis associated with nonhealing fractures is treated by stabilizing the fracture with plates and screws and implanting a sterile bone graft. SPRAINS

A sprain is an injury caused by sudden stretching or tearing of the ligaments in and around the joint, or the joint capsule itself. Signs are pain over the joint, swelling of the tissues, and temporary lameness.

Treatment: If the dog is unable to put weight on the leg, seek veterinary consultation to rule out a fracture or dislocation. This is true for any injury that fails to improve in 24 hours. X-rays should be taken.

It is most important to prevent further injury by resting the affected part. Restrict activity by confining the dog in a small area. Apply cold packs to the injured joint for 15 to 30 minutes, three or four times a day for the first 24 hours. Use a chemical cold pack or put crushed ice in a plastic bag. Wrap the pack in a towel and secure it in place over the injured joint with a loose gauze wrap. An alternative method is to run cold water over the affected leg for 5 to 10 minutes, three or four times a day. After the first 24 hours, switch to warm, moist compresses for 15 to 30 minutes, three times a day for the next two to three days. Apply as described for cold packs. Avoid hot compresses, which can burn the skin.

Analgesics may be prescribed by your veterinarian to relieve pain (see

Over-the-Counter Drugs for Home Veterinary Use, page 571). One disadvantage of pain relievers is that they may allow the dog to begin using the leg while the injury is still fresh. This can delay healing, but if the dog’s activity is restricted this is not a problem. Anti-inflammatories may hasten healing by reducing swelling and inflammation around the area. Keep the dog off the leg by confining him in a small, closed area. Take him out on a leash only to eliminate. Allow at least three weeks for successful healing. Incomplete healing is associated with prolonged lameness and the later development of degenerative arthritis in the joint. TENDON INJURIES

Tendons can be stretched, partly torn, or ruptured. Strained tendons follow sudden wrenching or twisting injuries. The tendons of the forepaws (front and back) are strained most often. The signs of tendon injury are lameness, pain on bearing weight, and painful swelling over the course of the tendon.

Rupture of the Achilles tendon at the hock joint can be caused by sudden and extreme flexion of the hock. This injury tends to occur in Greyhounds and sporting and performance breeds. The Achilles tendon is the one most often severed in dog fights and car accidents. Rupture of the Achilles tendon causes a dropped hock.

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The Achilles tendon in the

heel is the one most often

ruptured in dogs.

Inflammation of a tendon is called tendonitis. This injury follows strenuous field or road work and overuse of the limb.

Treatment: This is the same as described for sprains (see page 387). A ruptured Achilles tendon should be surgically repaired. Surgery will be followed by a long course of rest and rehabilitation.

MUSCLE STRAINS

Muscle strains are caused by stretching or tearing the muscle fibers or by overuse of a muscle following strenuous field or road work. Signs are lameness, swelling of the muscle, tenderness over the injured part, and bruising.

Bruising may be difficult to see beneath the fur.

Treatment: Initial treatment is similar to that described for sprains (see page 387). The dog should be rested for at least three weeks.

LUXATION (DISLOCATED JOINT)

A strong force is necessary to rupture a joint and displace the bones. Such injuries are usually caused by auto accidents and falls from a height. Signs of a

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dislocated joint are sudden pain and inability to use the limb. The elbow or knee may be bent, with the leg pointing either toward or away from the body. The affected leg may be either shorter or longer than the opposite leg.

When the bone is removed from

the joint it belongs in, it is important

to realize that the soft tissues, such as

ligaments, tendons, and muscles, are

often torn or damaged as well. Simply

replacing the bone may not be

enough, because the support tissues

that hold the joint together also need

to heal.

Subluxations (also called luxations)

are dislocations in which the bones

are only partly out of joint. Some

subluxations are congenital, but most

are caused by trauma. The limb does

not shorten and joint deformity is

minimal.

Dislocations and subluxations affect

the hips, stifles, shoulders, elbows, and

the small joints that make up the hocks

and wrists. Subluxations of these

smaller joints can be caused by a sudden force, such as jumping from a This dog shows subluxation of the left height.

hip, with outward rotation of the knee

Treatment: Veterinary examina-and inward rotation of the heel. tion is necessary to rule out fractures

and to replace the dislocated bones—a procedure that requires anesthesia. The treatment of other life-threatening injuries may take precedence. After reduction (replacement of the dislocated joint), the limb is immobilized in a sling or splint.

Depending on the extent of the injury, the dog is placed on strict crate rest or allowed limited exercise on a short leash. Physical therapy with exercises that move the joint passively through a limited range of motion, and activities such as swimming, help the dog recover strength and joint flexibility. Joint surgery is necessary for dislocations that cannot be reduced by manipulating the limbs. Surgery gives the best results for recurrent dislocations and for subluxations of the wrists and hocks. Surgery may also be required to repair associated soft tissue injuries.

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A restriction bandage is used to immobilize the leg of this Poodle.

STIFLE INJURIES

The stifle joint is stabilized by a number of ligaments. The two large ligaments that cross in the middle of the joint are the cranial and caudal cruciates. The ligaments that stabilize the sides of the joints are the medial and lateral collaterals. The meniscus is a cushion of cartilage between the femur and the tibia and fibula.

Rupture of the cranial cruciate is a common and serious injury of the stifle. It occurs in all breeds at all ages, but is more likely to occur in younger, active dogs. There may be a congenital or developmental predisposition in some

dogs (see Osteochondrosis, page 400). If one tears, unless it is repaired, the ligament in the other knee also eventually tears. The sudden onset of rear leg lameness suggests a rupture. The lameness

may disappear with rest, then recur with exercise. In some cases the presenting sign is persistent lameness in one or both hind legs. The diagnosis is confirmed by palpating the stifle joint. In many cases the medial collateral ligament is also damaged.

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Rupture of the medial or lateral collateral ligament usually is caused by a severe blow to the side of the joint or a twisting motion, especially at speed. The affected ligament may be stretched, partially torn, or completely severed. Diagnosis is made by manipulating the joint and looking for a degree of looseness. Severe blows to the stifle may also cause joint fractures. Dogs may need to be anesthetized for a thorough evaluation of the stifle.

Injuries to the meniscus are associated with injuries to the cruciates. If a cruciate injury goes untreated, secondary damage to the meniscus occurs in the weeks and months that follow. The end result is degenerative arthritis and permanent lameness. Isolated meniscus injuries are rare in dogs.

Treatment: The treatment of choice for ruptured cruciate ligaments is surgical repair. If this is not done, the joint becomes unstable and is subject to further damage. Following surgical repair, physical therapy and restricted exercise (as described for Luxation, page 388) are important for successful recovery. The complete rehabilitation program may take months for dogs to return to near full athletic performance levels.

Collateral ligaments that have been stretched but not torn usually heal satisfactorily with rest and restricted activity. Meniscal injuries respond well to surgical removal of the damaged part of the cartilage.

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Inherited Orthopedic Diseases

Inherited bone and joint diseases have a genetic basis, despite the fact that only a certain number of offspring will be affected. If, after a careful veterinary examination, one of these conditions is diagnosed in your dog, do not breed the animal.

HIP DYSPLASIA

Hip dysplasia is the most common cause of rear leg lameness in dogs. The highest incidence occurs in large-breed dogs, including St. Bernards,

Newfoundlands, Rottweilers, Chesapeake Bay Retrievers, Golden Retrievers, German Shepherd Dogs, Labrador Retrievers, and many others. Smaller

breeds are also affected, but are less likely to show symptoms.

Hip dysplasia is a polygenic trait. That is, more than one gene controls the inheritance. Environmental factors such as diet are also involved. The hip is a ball-and-socket joint; the ball is the head of the femur and the socket is the acetabulum of the pelvis. In a dysplastic hip, the head of the femur fits loosely into a poorly developed, shallow acetabulum. Joint instability occurs as muscle development lags behind the rate of skeletal growth. As the stress of weightbearing exceeds the strength limits of the supporting connective tissue and muscle, the joint becomes loose and unstable. This allows for free play of the femoral head in the acetabulum, which promotes abnormal wear and tear.

Feeding a very high-calorie diet to growing dogs can exacerbate a predisposition to hip dysplasia, because the rapid weight gain places increased stress on Hip dysplasia, showing progressive increase in the joint space and increasing joint wear.

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Upward displacement is the most common type of subluxation in canine

hip dysplasia.

the hips. Being overweight supports the genetic potential for hip dysplasia, as well as other skeletal diseases. A diet with an imbalance of calcium and phosphorous is bad for bone development. Another factor that can bring on the symptoms of hip dysplasia is inappropriate exercise during the period of rapid bone growth. Young dogs should be discouraged from jumping up and down from heights in situations where they land on their back legs (such as jumping up to catch a ball), and from standing up on their back legs (which dogs do when they stand up against a fence or window to get a better view). They should also avoid running on pavement. Dogs with hip dysplasia are born with hips that appear normal but progressively undergo structural changes. The age of onset is 4 to 12 months. Affected puppies may show pain in the hip, walk with a limp or a swaying gait, bunny hop when running, and experience difficulty in the hindquarters when getting up. Pressing on the rump can cause the pelvis to drop. With the puppy on his back, the rear legs may not extend into the frog-leg position without causing pain. An X-ray of the hips and pelvis is the only reliable way of determining

whether a dog has hip dysplasia. Good X-rays require heavy sedation or anesthesia. The standard view is taken with the dog lying on his back with his rear legs parallel and extended. The knees (stifles) are rotated internally. Care is taken to be sure the pelvis is not tilted.

Hip dysplasia is graded according to the severity of X-ray findings. In ideal hips, the femoral head fits tightly into a well-formed hip socket with a minimum of space between the head of the femur and the acetabulum. The hip ball is almost completely covered by the socket.

Normal hips are rated Excellent, Good, or Fair, depending on how closely they match the ideal. Dysplastic hips are rated Mild, Moderate, or Severe. If the findings are not clear, the hips are rated Borderline.

In a dog with mild hip dysplasia, the X-rays will show mild subluxation

(increased space in the joint) with the hip ball partway out of the socket. There are no changes associated with degenerative arthritis.

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An X-ray of normal hips. The femoral

Moderate dysplasia. These loose hips

heads fit tightly into well-formed

are partly out of their sockets and the

sockets.

femoral heads are beginning to flatten.

In a dog with moderate hip dysplasia,

the hip ball is barely seated into a shallow acetabulum. Arthritic changes begin to appear. These include wear and flattening of the femoral head, a rough appearance to the joint surfaces, and the

beginning of bone spurs.

In a dog with severe hip dysplasia, the

head of the femur is completely out of

the joint and arthritic changes are

marked. Once arthritis is noted, the condition is irreversible. But even with arthritis, some dogs are not lame. The

onset of lameness is unpredictable, and

some dogs may go most of their lives with

Severe dysplasia with degenerative

dysplastic hips but no lameness. Others

arthritis. Note bilateral subluxations

and bone spurs on the femoral

develop lameness as puppies.

heads and rims of the sockets.

The OFA maintains a hip dysplasia

registry for purebred dogs (see appendix

D). An OFA-certified radiologist will review hip X-rays taken by your veterinarian and, if the conformation of the hips is normal for the breed, certify the dog as Excellent, Good, or Fair and assign him an OFA number. As an

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Dogs must be 24 months of age or older to be tested. Some female dogs will show subluxation when X-rayed around an estrus cycle, so OFA recommends

not X-raying females around a heat period or within three to four weeks of weaning a litter.

The OFA registry is closed. That means if the dog is found to have hip dysplasia, the information remains confidential unless the owner marks off on the application that all results may be made public.

Dog breeders often request preliminary evaluations on hip status before

selecting puppies for show and breeding stock. The OFA accepts preliminary X-rays for puppies as young as 4 months of age. Their own analysis reveals that these evaluations are about 90 percent accurate when compared with followups at 24 months of age. Another method of evaluating hips was developed at the University of

Pennsylvania Veterinary School and is now administered by PennHip via the University of Pennsylvania (see appendix D). PennHip X-rays are taken using the traditional OFA views, but additional views are also required. Distraction pressure is applied with special techniques to look for joint laxity by seeing how much the joint can be distracted (pulled apart). This is done very carefully and to a set standard. These views are used to gauge joint laxity, which can be measured in puppies, starting at 16 weeks of age. The joint laxity does not change as the dog ages.

Dogs X-rayed for PennHip measurements are compared only to other dogs

of the same breed. Your dog then receives a joint laxity distraction index (DI) number, ranging from 0.0 (perfect) to 1.1 (severely dysplastic). PennHip suggests that only dogs in the top half for their breed with respect to joint laxity (that is, those with the tightest joints) be used for breeding. Those dogs who fall into the lower half, which are the ones with the loosest hips, have a greater chance of developing hip dysplasia in the future. In general, dogs with a DI of .3 or less are unlikely to develop degenerative joint disease.

Finally, the Institute for Genetic Disease Control (GDC) in Animals

maintained a separate hip dysplasia registry for some time, although its database has now been merged with OFA’s (with the exception of some eye and tumor problems). The GDC certifies dogs starting at 12 months of age. The GDC’s registry is open. That is, the GDC provides information on affected as well as normal dogs to anyone making an inquiry.

The GDC requests that veterinarians palpate the stifle joints for patella luxation at the time the hip X-rays are taken. They also request that copies of pedigrees be submitted with X-rays.

A genetic test for hip dysplasia that is applicable for a number of breeds is under development through VetGen. However, the mode of inheritance is

still not clearly understood, making it difficult to develop a test.

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Rimadyl, and a joint chondroprotectant such as Cosequin or Adequan to

relieve pain and inflammation and to repair damaged cartilage. Weight loss and moderate exercise are also important. These agents are discussed in more detail in Degenerative Joint Disease, page 401.

It is important to exercise lame dogs on a leash and not allow them to run, jump, or play as long as they exhibit pain. Swimming is an excellent exercise that improves muscle mass and joint flexibility without overstressing the hips. After reviewing the X-rays, your veterinarian may recommend hip surgery. Early surgery in selected puppies can prevent some cases of degenerative joint disease. Surgery is also indicated for dogs who continue to experience pain and lameness despite medical treatment.

There are five surgical options; technical factors govern the choice. Triple pelvic osteotomy and femoral osteotomy are two operations performed on

puppies who do not have degenerative joint changes. The goal of both is to position the femoral head more deeply in the acetabulum. Normal joint function is thus maintained and arthritis may not develop, although this is not always the case.

Pectineus myectomy is a relatively simple operation in which all of the

pectineus muscle is removed on both affected sides. This operation does not slow the progress of joint disease but does relieve the pain for some time. Femoral head and neck excision arthroplasty is an effective operation that provides relief for intractable hip pain. The head of the femur is removed, allowing a fibrous union to replace the ball-and-socket joint. The operation is usually reserved for dogs who weigh less than 36 pounds. Total hip replacement is the most effective procedure for dogs 9 months and older who have disabling degenerative joint disease in one or both hips. The operation

removes the old joint and replaces it with a new, artificial joint. The procedure requires special equipment and is usually performed by an orthopedic specialist. Good results are obtained in more than 95 percent of cases.

Dorsal acetabular rim arthroplasty—building up the acetabular rim with

bone from other sites in the body to create a deeper socket—is another surgical option that is currently the subject of investigational studies.

Prevention: Preventing excessive weight gain in puppyhood and keeping the puppy from placing undue stress on the hips will delay the onset of hip dysplasia in many dogs with a genetic predisposition. It may also lead to a less severe form of the disease. Feed puppies a quality food in amounts appropriate for normal (but not accelerated) growth. Puppies at risk for hip dysplasia should be fed a calorie-controlled diet, as described in Feeding Weaned Puppies, page 510. Overweight puppies should be given a calorie-restricted diet. Discuss this with your veterinarian. Vitamin and mineral supplements have no proven benefit in preventing or treating hip dysplasia, and may even be detrimental if given in excess.

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among littermates who have one dysplastic parent. Experience shows that

repeatedly using only dogs with normal hips for breeding stock significantly reduces the incidence of hip dysplasia in susceptible bloodlines.

Information on breed risk is available through the OFA and PennHip. In

breeds in which hip dysplasia is a particular problem, prospective puppy buyers are advised to check pedigrees for OFA, PennHip, or GDC certifications, particularly for sires and dams. Ideally, you will also be able to find evaluations of littermates of the sires and dams, as well as the grandparents.

LEGG-PERTHES DISEASE

Legg-Perthes disease is caused by a vascular necrosis of the femoral head. Avascular necrosis means death of bone in the head of the femur resulting from an interruption in the blood supply. It is not clear what causes this, but genetic factors may be involved.

The disease occurs most often in toy-breed puppies between 4 and 11 months of age. Large breeds are occasionally affected. Avascular necrosis occurs in both hips in about 15 percent of cases. Occasionally, it is the result of a traumatically dislocated hip caused by trauma such as an auto accident or a fall from a height. Weight bearing causes the dead bone beneath the cartilage of the femoral head to collapse. This fractures the cartilage and causes a gradual destruction of the hip joint.

Signs are severe lameness and sometimes the inability to bear weight on

the leg. Muscle wasting is pronounced and the joint loses some range of

motion. The affected leg may be shorter than the opposite normal leg. A standard X-ray of the hips and pelvis establishes the diagnosis.

Treatment: Medical therapy involves restricting activity and administering analgesics. Some dogs may improve, but surgery generally produces the best results. Surgery involves either a femoral head and neck excision arthroplasty or a total hip replacement, as described in Hip Dysplasia, page 392 . It is difficult to do hip replacement surgery on very small dogs.

The GDC maintains a Legg-Perthes registry, which is now merged with OFA, for breeds in the Terrier Group. OFA also has a Legg-Perthes registry for a variety of breeds. The determination can be made from standard hip X-rays. LUXATING PATELLA (SLIPPING KNEECAP)

The patella, or kneecap, is a small bone that protects the front of the stifle joint on the rear leg. The patella is anchored in place by ligaments and slides in a groove in the femur called the trochlea. If the groove is too shallow, the patella will slip out when the knee bends. When the patella slips out to the inside of the knee joint, it’s called medial luxation. When it slips out to the outside, it’s called lateral luxation.

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Luxating patella is usually an inherited developmental defect. Rarely, it is acquired through trauma.

Medial luxation is more common. It occurs in toy, miniature, and large

breeds, and is apparent in some puppies when they begin to walk. In others it appears later. The patella may slip in and out of place, resulting in a gait that is sometimes normal and sometimes not. When the patella is out of place, the affected leg is usually carried with the stifle joint bent and the foot turned inward. The condition is bilateral in about 25 percent of cases.

Lateral luxation occurs in large and giant breeds at 5 to 6 months of age. A knock-kneed stance is the most noticeable sign. The foot often twists outward as weight is placed on the limb. Both knees are almost always involved.

In the early stages, luxating patella may not be painful. But pain can

increase as the grooves are polished smoother by the slipping action of the kneecap and as arthritis develops in the joint.

The diagnosis of luxation is made by attempting to push the patella out of the trochlear groove. The degree of luxation is graded 1 to 4, depending on how easy it is to dislocate the patella and whether the patella returns spontaneously to the trochlear groove. This manipulation should only be done by breeders or veterinarians experienced in this technique. Preliminary veterinary screening for medial patella luxation should be done on dogs of toy and small breeds at 6 to 8 weeks of age, before these pups are sent to their new homes.

Treatment: A Grade 1 luxation may never worsen, and these dogs may need only medical treatment to deal with any pain that develops. For other dogs, though, surgery to deepen the trochlear groove and repair any loose or torn ligaments is usually recommended. The specific operation depends on the age of the dog and the type of luxation.

The OFA maintains a patellar luxation registry and issues certificates to all dogs who palpate normal at 12 months of age or older. The GDC maintains a medial patella luxation registry for breeds in the Terrier Group and also issues certificates to dogs who palpate normal at 12 months of age or older. The GDC is attempting to accumulate information on patella luxation based on palpating patellas when dogs are X-rayed for hip dysplasia. This GDC registry is now merged with OFA.

Dogs with genetically determined patella luxation should not be bred.

ELBOW DYSPLASIA

Elbow dysplasia is a common cause of front-leg lameness in large-breed

dogs. Breeds predisposed to elbow dysplasia include the Golden Retriever, Labrador Retriever, English Setter, English Springer Spaniel, Rottweiler, German Shepherd, Bernese Mountain Dog, Chow Chow, Chinese Shar-Pei,

Newfoundland, and others.

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The elbow joint is composed of the humerus, which articulates with the

radius and ulna, and those two bones. The anconeal process unites with the ulna at about 6 months of age. It forms a curved depression in the ulna. The coronoid process forms part of the lower curved bone of the ulna.

Dogs with elbow dysplasia have one or more of the following inherited

developmental defects, which may occur singly or in combination: ununited anconeal process, fragmented medial coronoid process, osteochondritis dissecans of the medial condyle of the head of the humerus, and incongruity of growth rate between the radius and ulna resulting in curvature of the radius. The first three defects are related to osteochondrosis (discussed on page 400). The fourth is related to an enlargement of the epiphyseal growth plate at the head of the radius.

Signs of elbow dysplasia usually appear in puppies at 4 to 10 months of age, but some dogs may not show signs until adulthood, when degenerative joint disease starts. The signs consist of varying degrees of front-leg lameness that worsens with exercise. Characteristically,

the elbow is held outward from the chest

and may appear swollen.

The diagnosis is made using detailed

X-rays of the elbow joint, taken in extreme

flexion. Radiologists are particularly interested in the appearance of the anconeal process of the ulna. In a dog with elbow

dysplasia, the anconeal process has a

rough, irregular appearance due to arthritic

changes. Another sign of dysplasia is

widening of the joint space associated with

a loose, unstable joint. X-rays may be difficult to interpret before a pup is 7 months of age. A CT scan may be required to demonstrate a fragmented coronoid process. The OFA evaluates X-rays and maintains registries for dogs with elbow dyspla-The wide stance and swollen elbow sia. Dogs must be 24 months of age or joints of a dog with bilateral elbow older to be certified by OFA, although it dysplasia.

accepts preliminary X-rays on growing

pups for interpretation only.

Treatment: Medical treatment is similar to that described for Hip Dysplasia, page 392. Surgery is the treatment of choice for most dogs. Several factors, including the age of the dog and the number and severity of the defects, govern the choice of surgical procedure. The more defects in the elbow, the greater the likelihood that the dog will develop degenerative arthritis—with or without surgery.

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OSTEOCHONDROSIS

Bone lengthening is a continuous process in which rapidly growing cartilage at the ends of bones becomes calcified and is gradually incorporated into the bone. Osteochondrosis is a disease caused by a defect in the calcification process of this growing cartilage. In a dog with osteochondrosis, the cartilage is calcified in an irregular instead of a uniform fashion. This creates areas of uncalcified, defective cartilage over the ends of the bones. With stress on the joint, the defective cartilage breaks into loose fragments called joint mice. This process, which is accompanied by joint pain and swelling, is called osteochondritis dissecans. Osteochondrosis most often involves the head of the humerus in the shoulder joint. It also occurs in the elbow, where it is responsible for many of the defects of elbow dysplasia. Osteochondrosis occurs less commonly in the stifle and hock joints. In the stifle, osteochondrosis involves the femur at its articulation with the tibia. Symptoms of intermittent lameness may look like luxating patella. In the hock, osteochondrosis involves the articulation between the tibia and the talus (the first bone of the hock).

Osteochondrosis is a common disease of rapidly growing large-breed puppies. The first signs show up at between 4 and 8 months of age. The symptoms may resemble those of panosteitis (see this page), another disease that causes lameness in growing puppies. The typical presentation is gradual lameness that seems to stem from the shoulder, elbow, stifle, or hock in a young dog of one of the large breeds. Lameness often gets worse with exercise. Symptoms may appear following a traumatic episode such as jumping down stairs. Pain is present on flexing and extending the joint. X-rays may show fragmentation of joint cartilage or a loose piece of cartilage in the joint. The diagnosis may not be made definitively until the dog is 18 months of age.

Treatment: Medical treatment involves restricting activity and prescribing analgesics and chondroprotectants, as described for the treatment of degenerative joint disease, page 401. Preparations that contain polysulfated glycosaminoglycan (such as Adequan) may be of benefit in limiting further cartilage degeneration and relieving pain and inflammation.

In most cases surgery will be required to scrape away defective cartilage and remove any joint mice. The best results are obtained in the shoulder and elbow joints. The results are less favorable for the hock, which is a small joint, and for the stifle, which is a more complex joint. In the hock and stifle, degenerative joint disease is likely to occur over time.

PANOSTEITIS (WANDERING LAMENESS)

Panosteitis is a disease of large, rapidly growing puppies between 5 and 12

months of age. The disease has been described in German Shepherd Dogs,

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Doberman Pinschers, Great Danes, Irish Setters, St. Bernards, Airedale

Terriers, Basset Hounds, Miniature Schnauzers, and other breeds. The cause is unknown, but an inherited polygenic trait is suspected. Males are affected four times more often than females. Suspect this disease if your puppy exhibits intermittent lameness in one or more legs that is unrelated to trauma.

A characteristic sign is the tendency for pain and lameness to shift from one limb to another over the course of several weeks or months. That’s why this disease is sometimes called wandering leg lameness. Pressure over the shaft of an affected bone elicits pain. X-rays show a characteristic picture of increased density in the affected long bone. Panosteitis must be distinguished from other causes of lameness in growing puppies, including osteochondrosis, elbow dysplasia, and hip dysplasia.

Treatment: The disease is self-limiting, but lameness may persist for several months. Symptoms usually disappear by the time the dog is 20 months old. Analgesics prescribed by your veterinarian can be given to relieve pain. If the dog is severely affected, restrict exercise.

Arthritis

Arthritis is a degenerative condition that affects one or more joints. Most cases occur in dogs with an inherited orthopedic disease such as osteochondrosis or hip dysplasia, or those with a joint injury. Some cases of arthritis are related to an immune-mediated joint disease or a joint infection.

OSTEOARTHRITIS (DEGENERATIVE JOINT DISEASE)

Osteoarthritis is a common disease that affects one out of five dogs during their lifetime. The problem isn’t confined to older dogs. Hip dysplasia, ruptured cruciate ligaments, patella luxation, joint trauma, and other joint conditions can cause degenerative arthritis, even in young dogs. Large-breed dogs are affected more often than small dogs. Heavy dogs are more likely to experience symptoms because of the extra strain placed on ligaments and joints. Dogs with degenerative arthritis experience varying degrees of lameness, stiffness, and joint pain, which is more apparent in the morning and after getting up from a nap. They often exhibit irritability and behavioral changes associated with increasing disability. Cold and damp surroundings increase pain and stiffness. Degenerative arthritis is progressive, and in time makes the dog’s life miserable.

The diagnosis is made by joint X-rays that show bone spurs at points where the ligaments and the joint capsule attach to the bone. There may be varying degrees of joint space narrowing and increased density of bone around the joint. 16_067857 ch13.qxp 7/17/07 11:02 PM Page 402

402 • DOG OWNER’S HOME VETERINARY HANDBOOK

Treating Osteoarthritis

Degenerative joint disease is incurable, but treatment can substantially improve the dog’s life. Treatment involves physical therapy and weight control, the use of analgesics and corticosteroids to relieve pain and improve function, and the use of chondroprotective agents to repair joint cartilage and prevent further damage. Acupuncture is another therapy that has shown good results for arthritic dogs. All of these should be used at the same time. (See the chart on pages 404–405 for an overview of medications used to treat osteoarthritis.)

Acupuncture and physical therapy are alternative or additional ways to

make arthritic dogs comfortable.

In severe cases, surgical fusion of painful joints, such as the hock or elbow, relieves pain and restores limb movement in some dogs.

Physical Therapy

Moderate exercise is beneficial because it maintains muscle mass and preserves joint flexibility. Excessive exercise, however, is counterproductive. Arthritic dogs should not be allowed to jump up and down and should never be encouraged to stand up on their back legs. Dogs with pain and lameness should be exercised on a leash or a harness. There are veterinary physical therapists who can help design an exercise (and weight loss) program.

Swimming is an excellent exercise that improves muscle mass without

overstressing the joints. Exercise can be increased as the dog improves with the use of medications.

Overweight dogs should be encouraged to lose weight, as described in

Weight Reduction, page 308. Being overweight seriously complicates the treatment of osteoarthritis.

Nonsteroidal Anti-Inflammatory Drugs

These are anti-inflammatory medications, but they do not repair or heal cartilage. Ideally, they would be used along with supplements and given with food. These do provide rapid relief from pain.

A few NSAIDs have chondroprotective characteristics, which means they

protect against the breakdown of cartilage. Others, such as aspirin, actually destroy cartilage in the dosage required for pain relief. This is one reason why aspirin is used less frequently for treating osteoarthritis.

The NSAIDs most often recommended are prescription medications.

Newer medications have been developed that offer significant advantages

over aspirin and the older NSAIDs. Rimadyl (carprofen) is an excellent drug with a low incidence of gastrointestinal side effects that has proven itself over time. It must be given daily. Rimadyl provides good pain relief and seems to slow the arthritic process. There are no detrimental effects on cartilage. Labrador Retrievers, and possibly a few other breeds, may show a higher predisposition for liver toxicity with Rimadyl. Etogesic (etodolac) is another 16_067857 ch13.qxp 7/17/07 11:02 PM Page 403

THE MUSCULOSKELETAL SYSTEM • 403

newer NSAID. It requires only one dose a day. This drug may prove as effective as Rimadyl. These drugs are available through your veterinarian by prescription. See the chart Osteoarthritis Medications (pages 404–405) for other drugs that may be used. Note that many over-the-counter NSAIDs used for pain

control in people are dangerous when given to dogs. Do not use any drugs with- out veterinary approval, and never use more than one NSAID at the same time. Due to potential serious side effects, dogs on these drugs should have blood work first to assess liver and kidneys. The drugs may prolong bleeding times and interfere with clotting, and have the potential to cause life-threatening liver and kidney problems and gastrointestinal ulcerations. Nausea and vomiting may be the first indication of trouble. Blood work should be rechecked every six months, or sooner if there are problems. These drugs should not be combined or given with steroids.

The most common side effect is GI bleeding. This can be difficult to diagnose and quite extensive before signs become apparent (see Stomach and Duodenal Ulcers, page 261). Misoprostol (Cytotec) is a drug that prevents ulceration and helps heal ulcers caused by NSAIDs. Sulcrafate (Carafate) is another drug that protects against mucosal damage. Your veterinarian may prescribe one of these stomach protectants if your dog is taking an NSAID for chronic arthritis.

Steroids

Oral glucocorticoids (corticosteroids) are used for their anti-inflammatory effects. Low dosages appear to protect cartilage, while high dosages (those needed to relieve pain) destroy cartilage. Future formulations may have better protective effects and a wider margin of safety.

Unfortunately, dogs are unusually sensitive to the adverse effects of both the NSAIDs and glucocorticoids. Glucocorticoids are best used for short periods in dogs with osteoarthritis who have failed to respond to NSAIDs. Longterm therapy should be reserved for dogs with immune-mediated arthritis. Steroids are regarded as highly dangerous medications with many side

effects. These can range from interfering with cartilage repair to causing increased drinking and eating (with the associated increased elimination). Long-term use can lead to liver and adrenal problems. Still, steroids can provide quick relief for many conditions, and for immune problems they may be the drug of choice. They should not be combined with any of the NSAIDs.

Most steroids, such as prednisone, are given orally, but long-lasting injections may also be used. Dosing schedules will vary greatly and usually work on a decreasing dose schedule to wean the dog off the medication, if possible, and minimize side effects.

Chondroprotectants

These compounds appear to modify the progression of osteoarthritis by preventing further breakdown of cartilage. Breakdown of cartilage is the first step 16_067857 ch13.qxp 7/17/07 11:02 PM Page 404

404 • DOG OWNER’S HOME VETERINARY HANDBOOK

in the development of degenerative joint disease. Chondroprotectants are most effective when used early in the course of osteoarthritis.

Adequan (a polysulfated glycosaminoglycan similar to glucosamine) is a

chondroprotective given by intramuscular injection twice a week for four or more weeks. It can be used as a preventive in dogs who are at high risk of developing degenerative joint disease, such as those with hip dysplasia. Other chondroprotective agents are nutraceuticals—products that lie somewhere between a nutrient and a drug. Nutraceuticals are believed to have medical value based on subjective evidence of their effectiveness, although clinical evidence based on controlled studies is lacking for many of these. Unlike drugs, nutraceuticals do not undergo an approval process and are not regulated by a federal agency. Numerous controlled studies in humans, limited studies done on dogs, and canine anecdotal reports suggest these substances do have medical value for arthritic dogs. Many of the supplements mentioned in the chart on pages 404–405 are used based on anecdotal information, not clinical studies. So far, however, these compounds appear to be both safe and effective. Osteoarthritis Medications

Nonsteroidal Anti-Inflammatory Drugs

Generic Name

Brand Name

Dosing

Special Side Effects

Aspirin

Many

Variable, best

Gastrointestinal tract

given with food

ulceration, prolonging

bleeding times

Carprofen

Rimadyl,

Once or twice

Possible idiosyncratic

Novox

daily (has a

reaction in Labrador

chewable form)

Retrievers, can cause

liver problems within

3 weeks

Deracoxib

Deramaxx

Once daily with food

Etodolac

Etogesic

Once daily

Possible association with

with food

dry eye

Firocoxib

Previcox

Once daily (has

a chewable form)

Meloxicam

Metacam

Once daily with

food (liquid)

Phenylbutazone

Butazolidine

Three times

daily with food

Piroxicam

Feldene

Daily or every

Possible cancer

other day, with food

prevention

Tepoxalin

Zubrin

Once daily with

food (rapid

disintegration tablet)

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THE MUSCULOSKELETAL SYSTEM • 405

Chondroprotectants and Other Supplements

Supplement

Use

Side Effects

Perna cannaliculus,

Cartilage protection

green lipped mussel

and repair

Minimal

Sea cucumber, sea jerky

Cartilage protection

Minimal

and repair

Chondroitin sulfate

Cartilage production and

Minimal

repair, prevents damage,

controls pain

Glucosamine

Cartilage production

Minimal

and repair

Methylsulfonylmethane, Sulfur

supplement,

Minimal

MSM

controls pain

Polysulfonated Cartilage

protection

Minimal

glycosaminoglycan (must

and repair

be given by injection)

Omega-3 fatty acids

Anti-inflammatory

Minimal

Vitamins C and E

Antioxidants

Minimal, but excessively high doses can

result in toxicity

Boswellia Anti-inflammatory

herb

Minimal

Yucca Anti-inflammatory

herb

containing steroidal saponins

Minimal

Most nutraceuticals used to treat osteoarthritis contain glucosamine, polysulfated glycosaminoglycans, and chondroitin sulfates—compounds known to be involved in the synthesis and repair of joint cartilage. Examples include Cosequin and Glycoflex. These compounds are given orally and can be considered as follow-up therapy after Adequan, or in any condition in which joint damage is anticipated or expected, such as trauma, surgery, degenerative joint disease, or immune-mediated arthritis.

Chondroprotectives may be given along with an NSAID. The combination

reduces pain and alleviates joint inflammation. The chondroprotectants can also be used to help prevent the development of osteoarthritis. There are now some prescription diets that include chondroprotectants in their formulation. Always check with your veterinarian before adding any supplements to avoid adverse interactions with medications your dog may be on. Supplements generally take a month or so to show positive effects. Dosages will vary greatly, so consult your veterinarian.

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406 • DOG OWNER’S HOME VETERINARY HANDBOOK

IMMUNE-MEDIATED ARTHRITIS

This is an unusual group of diseases in which antibodies are directed against the dog’s own connective tissue, resulting in either an erosive or nonerosive arthritis. In erosive arthritis, cartilage and joint surfaces are destroyed. In nonerosive arthritis, there is inflammation but no tissue destruction.

Rheumatoid arthritis is an erosive arthritis that occurs primarily in toy breeds and other small breeds, such as Shetland Sheepdogs, at approximately 4 years of age. It is characterized by morning stiffness, shifting lameness, and swelling of the smaller joints, particularly the wrists and hocks. Fever, loss of appetite, and lymphadenopathy are accompanying features.

Nonerosive arthritis tends to occur in midsize and large-breed dogs at about 5 to 6 years of age. The cause is unknown. Signs are intermittent fever, loss of appetite, joint swelling, and a lameness that often shifts from limb to limb. A form of nonerosive arthritis occurs with systemic lupus erythematosus. The diagnosis of immune-mediated arthritis is made by joint X-rays and specific laboratory tests. Synovial fluid analysis helps distinguish immune-mediated arthritis from infectious arthritis and osteoarthritis.

Treatment: Immune-mediated arthritis responds to anti-inflammatory and immunosuppressive drugs, including corticosteroids and chemotherapy

agents. Treatment must be continued for eight weeks or longer. Your veterinarian may use several drugs or drug combinations before determining which protocol works best for your dog. Rheumatoid arthritis is less responsive than nonerosive arthritis to drug therapy.

Light to moderate activity is beneficial, but vigorous exercise, which is most likely during periods of remission, can injure the joints and should be restricted. Overweight dogs should be placed on a calorie-restricted diet. In fact, it may be advantageous if the dog is somewhat lean. Discuss this with your veterinarian.

INFECTIOUS ARTHRITIS

Infectious diseases can produce arthritis. Rickettsial arthritis is seen with Rocky Mountain spotted fever and canine ehrlichiosis, and spirochetal arthritis with Lyme disease. (All of these are tick-borne diseases.) Fungal arthritis is a rare complication of a systemic fungal infection.

Septic arthritis is caused by bacteria that gain access to joints through open wounds, soft-tissue infections around joints, and via the bloodstream. Injecting steroids into a joint carries a small risk of introducing bacteria.

Treatment: This involves opening the joint and removing all infected and devitalized tissue. This is followed by a long-term course of antibiotics. Most of the tick-borne diseases respond to doxycycline or tetracycline. Some dogs will have permanent joint damage.

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Metabolic Bone Diseases

HYPERPARATHYROIDISM

The parathyroids are four small glands in the neck located near the thyroid gland. The parathyroid glands secrete the hormone PTH, which is essential to bone metabolism and blood calcium regulation.

Primary Hyperparathyroidism

This disease is rare in dogs. It is caused by tumors of the parathyroid glands that cause them to secrete excessive amounts of PTH. Middle-aged and older dogs are affected. The average age of onset is 10. Keeshonds seem to have a breed predisposition to this problem.

Signs are nonspecific and include loss of appetite, lethargy, excessive thirst, and frequent urination. Constipation, weakness, vomiting, muscle twitching, and a stiff gait have all been reported. The disease may not be suspected until a chemistry panel reveals a high serum calcium.

A primary parathyroid hyperplasia syndrome, in which all four parathyroid glands are enlarged, has been identified in German Shepherd Dog puppies. This is an inherited autosomal recessive trait.

Anal sac adenocarcinomas have the unique property of producing PTH, and

thus are a rare cause of pseudohyperparathyroidism (see Anal Sacs, page 289). The diagnosis of primary hyperparathyroidism can be confirmed by measuring PTH. The serum PTH is above normal in dogs with this disease.

Treatment: Surgical removal of the affected glands is the only possible treatment.

Renal Secondary Hyperparathyroidism

This is the end result of long-standing kidney disease that causes the body to retain phosphorus. The high serum phosphorus and low serum calcium stimulates the parathyroids to produce PTH. Symptoms similar to those of primary hyperparathyroidism are usually overshadowed by the kidney problem.

Treatment: Treatment is directed toward correcting the kidney disease, as described in Kidney Failure, page 423.

Nutritional Secondary Hyperparathyroidism

This disease (now rare) is caused by an excess of phosphorus or a deficiency of calcium in the diet. Vitamin D is required for calcium to be absorbed from the small intestine. Thus, a deficiency of vitamin D produces a deficiency of calcium. This can cause the parathyroid glands to produce more PTH. One cause of nutritional secondary hyperparathyroidism is feeding a diet that consists primarily of organ meats, such as hearts, livers, or kidneys. Such diets are too high in phosphorus and too low in calcium and vitamin D. Other diets low in calcium are all-vegetable diets, corn bread diets, and diets 16_067857 ch13.qxp 7/17/07 11:02 PM Page 408

408 • DOG OWNER’S HOME VETERINARY HANDBOOK

containing leftover table scraps. The disease does not occur in dogs who eat a nutritionally balanced diet.

In puppies and young dogs, signs suggest skeletal problems and include

lameness, bone pain, stunted growth, and spontaneous fractures. In adult dogs, nutritional secondary hyperthyroidism produces periodontal disease. Thinning of the jaws exposes the roots of teeth. The teeth then loosen and fall out.

Treatment: Correct the diet by feeding a high-quality balanced food—in the case of puppies, one advertised as supporting growth. Vitamin and mineral supplements should not be given unless prescribed by a veterinarian.

Affected puppies should be kept quiet and confined for the first few weeks to prevent fractures. Older dogs with advanced periodontal disease or

intractable eating habits may not eat enough of their balanced food. These dogs need restorative dentistry and may require dietary supplements.

HYPERTROPHIC OSTEODYSTROPHY

Hypertrophic osteodystrophy is a developmental disease that affects largeand giant-breed dogs 2 to 8 months of age. The cause is unknown. Hypertrophic osteodystrophy targets the long bones close to the growth

plates at the wrists and hocks. These areas become painful and give rise to lameness. The lameness ranges from mild to incapacitating. It often affects both front or both rear limbs. The bones are extremely warm, swollen, and painful to the touch. Affected dogs are reluctant to move. Some dogs develop high fever, depression, loss of appetite, and weight loss.

Bone X-rays show enlargement of the affected growth plate and increased

density of bone adjacent to the growth plate. These findings distinguish hypertrophic osteodystrophy from panosteitis and other causes of lameness in growing pups.

Treatment: There is no specific treatment for hypertrophic osteodystrophy. Symptomatic therapy involves resting the dog and giving an NSAID, available through your veterinarian. Many pups do well with on antibiotics, and some are treated with prednisone as well.

Review the pup’s diet with your veterinarian to be sure he is not being

overfed; if he is, reduce caloric intake. Discontinue all vitamin supplements. Most affected puppies have one to two episodes of hypertrophic osteodystrophy and then recover, but permanent bone changes and physical deformities may develop.

Vitamin and Mineral Supplements

Contrary to popular belief, puppies do not need vitamin or mineral supplements for their normal growth and development. Modern name-brand commercial

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THE MUSCULOSKELETAL SYSTEM • 409

puppy foods are formulated to supply all the nutrients required to sustain normal growth—provided the puppy or young dog consumes the puppy food as the sole or main source of calories. More vitamins and minerals added to the diet will not add more substance or coat to the growing dog.

When calcium, phosphorus, and vitamin D are given in excess of a dog’s

capacity to use them, growth and development can be adversely affected.

Overdosing with vitamin D causes bones to calcify in an uneven fashion. In addition, calcium may be deposited in the lungs, heart, and blood vessels. Vitamin and mineral supplements are most effective when given to elderly dogs with poor eating habits who may have developed a specific deficiency. The appropriate dose of any supplement should be determined by your veterinarian. 16_067857 ch13.qxp 7/17/07 11:02 PM Page 410

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