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Archive for February, 2012

The intervertebral discs are structures located between the bodies of the vertebrae and act as shock absorbers. They are composed of a rim of tough, fibrous connective tissue covering surrounding a gel-like center. A Hansen Type I rupture occurs when the fibrous capsule breaks, allowing the inner nucleus to push out through the opening and impinge on the spinal cord or a nerve root. A Hansen Type II occurs when the entire disc, surrounded by an unbroken capsule, impinges on nerve tissue.

Hansen Type I ruptures usually occur in small breeds such as Dachshunds, Beagles, Cocker Spaniels, Pekingese, and small mixed breeds. Ruptured discs are more common in Dachshunds than in all other breeds combined. The capsule can start to degenerate when the dog is only 2 to 9 months of age. Nearly eighty percent of Type 1 ruptured discs occur in the lower back between the last thoracic and the first two lumbar vertebrae. The history often includes jumping off a sofa or stairs, but any abrupt movement can be sufficient to cause a Type 1 rupture. It is also possible for more than one disc to rupture.

The symptoms of a Type I rupture usually progress gradually but can appear suddenly. The dog holds her/his back stiffly and may vocalize with pain or snap at the hand palpating in or around the injured area. The dog will usually refuse to walk up stairs or jump into a car. Neurological signs include weakness, lameness, and a wobbly gait. A dog experiencing severe back pain resulting from an acute rupture usually assumes a hunched-up position with a tight abdomen and may pant and tremble. Sudden ruptures can result in complete hindlimb paralysis.

Dogs with a Hansen Type I rupture in the neck usually carry their head low and stiff and are in extreme pain. The dog will often cry out when patted on the head and refuse to lower her head to eat or drink. There may be weakness and/or lameness of the front legs. Complete paralysis of all four limbs can occur but is rare.

Hansen Type II disc ruptures occur most in German Shepherds, Labrador Retrievers and other larger breeds. With this condition the entire disc, surrounded by its capsule, gradually impinges on the spinal canal. Symptoms usually appear gradually and progress slowly in dogs 5 to 12 years of age.

Your veterinarian can presumptively diagnose a ruptured disc by doing a neurological examination and prove it with imaging studies including spine X-rays, a myelogram, and possibly a CT scan or MRI.

Dogs still able to walk but with pain and mild weakness can be treated by confining them to a cage for a minimum of two weeks with appropriate anti-inflammatory drugs and drugs for pain control. If there is no improvement, or the dog’s condition worsens during this time, surgery is necessary. Surgery for disc disease involves surgical decompression of the spine by removal of bone over the spinal cord a laminectomy or partial bone removal (hemilaminectomy) and removal of the extruded disk material impinging on the spinal cord thus relieving the compression of the cord. Obviously, a very well trained and experienced veterinary surgeon is necessary for these procedures.

The prognosis for these cases depends upon the degree of injury and the location. Most patients that retain motor function have a good chance for recovery. If motor function is compromised the prognosis is more guarded and if deep pain perception is absent, a return to normal is less likely. We have all seen those photos of paralyzed dogs suspended in a two-wheeled cart who suffered this condition and still function as loved pets.

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Cardio” obviously pertains to the heart, “myo” pertains to muscle and “pathy” signifies pathology or abnormality. Therefore, cardiomyopathy is pathology or abnormality of the heart muscle. We describe two kinds of cardiomyopathy; hypertrophic and dilated. Both types occur because of genetic mutations in one or more of the various proteins that comprise the heart muscle.

A study published in 1993 in the American Journal of Cardiology compared lesions found in 38 humans, 51 cats and 10 dogs that died of spontaneous hypertrophic cardiomyopathy. The authors of the paper discovered almost identical changes in all of the subjects.

Hypertrophic cardiomyopathy results in an increase in the volume of the heart muscle. As the muscle, usually that of the left ventricle, the chamber of the heart responsible for pumping blood out into the body, is forced to work harder it becomes thicker. As this happens the muscle also becomes stiffer, less compliant, and the result is that the ventricle is less able to relax and fill with blood during the resting phase between beats, called diastole. Eventually the left ventricle cannot fill enough to pump enough blood to meet the metabolic demands of the body and the resulting condition is “heart failure”. These same changes can also occur in the right ventricle, the heart chamber responsible for pumping blood to the lungs. Sometimes both chambers are afflicted. The results are left heart failure, right heart failure or total heart failure. Hypertrophic cardiomyopathy seems to be particularly prevalent in Maine Coon, Maine Coon crossbreds and Ragdoll cats.

The other type of cardiomyopathy, dilated, is the yang of hypertrophic’s yin. The myocardium dilates and becomes thinner rather than thicker. This condition is also most often a genetic defect and thought to be an autoimmune disease as are Lou Gehrig’s disease, Cohn’s disease, lupus, and many others. The myocardium stretches and becomes weaker over time. Eventually the affected heart chamber(s) stretch to the point where the beating muscle looses strength. When it contracts it can no longer expel enough blood and heart failure occurs. Again, either the left, right or both ventricles can be affected. Large breeds of dogs, especially Irish Wolfhounds and Doberman Pinschers, seem to be the most afflicted by this condition but it has been found in German Shepherds, Boxers, and English Cocker Spaniels, mixed breeds and occasionally other breeds. For unknown reasons dilated cardiomyopathy kills males 2-3 times more commonly than it does females.

Genetic lesions resulting in myocardial changes closely resembling cardiomyopathy have been reported in Polled Hereford cattle, mustached tamarinds (monkeys) and pygmy sperm whales. Cardiomyopathies can also develop as the result of persistent rapid heart rate, high blood pressure, either systemic or pulmonary, diseases of the outflow valves of either the right or left ventricles (aortic or pulmonary valves), following treatment with certain chemotherapeutic agents, following obstruction of the coronary arteries, and after exposure to a host of toxic substances.

If your pet shows signs of lethargy, labored breathing, decreased levels of activity and tiring easily take it to your veterinarian for a checkup. The earlier a heart condition is caught the more successful the treatment and/or management is.

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This behavior is known as “cribbing”. There is evidence that cribbing releases chemicals in the brain known as endorphins. Some horses learn to arch their neck and swallow air without needing to grasp an object with their teeth, but this is rare. Some horses will also get into a habit of chewing wood.

Cribbing can result in several unhealthy outcomes. Grasping and pulling on hard objects can wear down the teeth or damage them. The pulling motion, if frequent and intense, can result in abnormal neck muscle development. Some claim that pain (from colic or ulcers) causes cribbing. Horses that crib do seem to have a higher frequency of colic and ulcers than the normal horse population. However, research suggests that horses fed grain rather than pasture and/or those fed 1 or 2 times per day rather than multiple times, are more likely to get ulcers or colic. I believe colic does not cause cribbing and cribbing does not cause colic, but both can be the result of unnatural feeding.

Cribbing is a compulsive habit, probably the result of boredom and/or anxiety. Not all bored or anxious horses will develop this habit but is most common in horses kept in their stalls, or small enclosures, for long periods without adequate mental stimulation. If a horse cribs, other horses may copy the behavior. Once the habit becomes ingrained, it can be difficult to correct. Because cribbing releases endorphins in the brain, it is, effectively, a drug addiction. As with any drug addiction, kicking the habit is hard. Here are some recommended treatments:

1) Provide mental stimulation, additional exercise, training, etc. Occupy more of the horse’s time.

2) Remove the horse to a more enjoyable environment such as a pasture with other horses. Providing pasture time will usually reduce the frequency and intensity of cribbing, but may not stop it.

3) Paint the objects that the horse grabs with something that tastes unpleasant. This is most effective when combined with providing lots of pasture time. There are a number of products designed for this purpose as well as many home made recipes. Make sure that what you use is not poisonous.

4) If your horse cribs on fences, putting an electric wire along the top of the rails might work.

5) Fit the horse with a cribbing strap. This collar will prevent, or make it uncomfortable for the horse to swell its neck to suck in air.

6) Calming medication, usually anti-depressants, but I don’t support behavior modification with drugs.

7) Fit the horse with a special muzzle that allows it to eat but not to grasp with his front teeth. I have seen something like this but have no idea where to find one.

8) A last resort is surgery to cut the muscles used to arch the neck.

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