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-Cold, compression therapy for soft tissue injuries, preventative maintenance, and pre/post operative care.

     Wobbler disease is a condition of the cervical vertebrae (vertebrae in the neck) that causes an unsteady (wobbly) gait and weakness.  Wobbler Syndrome refers to a number of disease states in the horse. The most common is termed  (CVM) Cervical Vertebral Malformation (CVM). The malformed or compressed vertebrae press against the spinal cord and interfere with messages being sent by the brain. Therefore, the interference with normal nerve transmission from the brain to the legs leads to noticeable incoordination (ataxia). The compression, malformation or lesions of cervical vertebral malformation usually occur between the third and fifth cervical vertebrae. The Thoroughbred, Quarter Horse, and Morgan are the most commonly affected breeds.
Causes:
     The exact cause of the wobbler syndrome in horses is unknown. It is believed that the syndrome is caused by several factors: (1) genetic predisposition, (2) nutritional imbalances, (3) rapid growth, (4) physical trauma, or (5) a combination of these.

     Diagnosis of spinal cord damage requires quality radiographs of the cervical region. Radiographs will reveal signs of “lipping,” “flaring,” evidence of lesion or stenosis (narrowing) of the vertebrae to indicate whether the horse is suffering from CVM.
A myelogram is also used to show a static cord compression. The procedure involves injecting radio-opaque dye into the area surrounding the spinal cord so that it can be visualized on radiographs.

     Diagnosis of wobbler syndrome is not easy because several other causes of incoordination exist in horses, such as viruses, protozoa in the spinal cord, parasites,
tumors, or fractures. A sample of Cerebral Spinal Fluid (CSF) is sent to the lab to test for viruses, protozoa (EPM), parasites (alternate larval migration), tumors, infection and inflammation.

Veterinary surgeons in the United States have devised a surgical procedure adapted from human surgery called the cloward method for fusing vertebrae . The surgical technique involves drilling a hole between the affected vertebral bodies from underneath the neck and inserting a stainless steel prosthesis called a “Bagby Basket,” which fuses and immobilizes the vertebrae. In equine medicine, it is also referred to as "basket surgery". The surgery requires specialized instruments and takes approximately 1 1/2 hours to perform.

      Every day veterinarians across the country see hundreds of cases of laminitis, a painful disease that affects the feet of horses.  Laminitis results from the disruption of blood flow to the sensitive and insensitive laminae within the foot, which secure the coffin bone to the hoof wall.  While the exact mechanisms by which the feet are damaged remain a mystery, certain precipitating events can produce laminitis.  Although laminitis occurs in the feet, the underlying cause is often a disturbance elsewhere in the horse’s body.

     There are generally considered to be three phases of laminitis:  developmental, acute and chronic.  The developmental phase, which actually occurs before the onset of foot pain, is when the separation of the lamellae from the coffin bone is triggered.  This may be as short as 8-12 hours when the laminitis is caused by exposure to black walnut shavings or 30-40 hours in the case of grain overload.

During the developmental phase, the horse usually experiences a problem with one or more of the following organ systems: 
-GI  (colic: grain overload, pasture grass,  colitis, enteritis, devitalized intestine)
-Respiratory (bacterial pneumonia)
-Reproductive (retained placenta)
-Renal (kidney) (not eliminating toxins properly)
-Endocrine (hormonal) (Equine Metabolic Syndrome, Insulin Resistance, Cushing's Syndrome)
-Musculoskeletal (Supporting limb develops laminitis from carrying all the weight, road founder, tying up)
-Skin (cellulitis, severe burns, severe infected wounds)
-Immune (endotoxemia, exposure to toxins such as black walnut)

       It is a problem in one or more of these systems that results in the lamellae being exposed to trigger factors, which leads to separation from the coffin bone.  The exact nature of the laminitis trigger factors, apparently reaching the lamellae through the circulation, is not yet known.
      Sometimes no developmental phase can be recognized:  the horse is simply discovered in the acute phase with no apparent ill health or inciting problem occurring beforehand.  This appears to be the case with grass founder, although research on grass growth suggests otherwise.  That is, under certain conditions (cold nights, sunny days) grass can manufacture high enough concentrations of sugar to cause fermentation in the horse’s gut, producing trigger factors.
      The developmental phase of laminitis merges into the acute phase, which occurs from the onset of foot pain to evidence of movement of the coffin bone within the hoof.  This evidence is usually  obtained by x-rays.  After the acute phase, if the horse does not die of the disease process that caused the laminitis, it can make an apparent complete recovery or become a “sinker,”   the hallmark sign of chronic laminitis. A “sinker” is a horse whose coffin bone has lost all attachment to the inner hoof wall and dropped to the bottom of the hoof.  The chronic phase can last indefinitely with signs ranging from persistent, mild lameness to continued severe foot pain, further breakdown of the lamellae, a deformed or even sloughed hoof wall—the horse may even go down.  It is important to realize that the process which triggered the lamellae to breakdown begins to operate during the developmental phase before the first sign of foot pain.
      During the developmental phase, the specific problems of the horse often have to be attended to urgently (grain overload, tying up, retained placenta).  Unfortunately, the feet may not enter into the equation until the signs of foot pain appear.  By the time foot pain is apparent, destruction of the lamellae is under way.  In other words, foot pain is the outward sign that lamellar destruction is occurring.  To wait and see if foot pain is the sequel to another organ system’s crisis is to miss the opportunity to prevent or at least lessen lamellar damage.

-Rings in hoof wall that become wider as they are followed from toe to heel
-Bruised soles or “stone bruises”
-Widened white line, commonly called “seedy toe,” with occurrence of blood pockets and/or abscesses
-Dropped soles or flat feet
-Overweight body condition: Thick, “cresty” neck and fat pads around tail head.
-Dished hooves, which are the result of unequal rates of hoof growth 

An additional component of lamellar anatomy to be affected by overproduction of MMP is the lamellar capillaries.  As the basement membrane disappears, so do the capillaries.  The loss of these capillaries may explain why resistance to blood flow was increased 3.5 times in horses during early laminitis and also why blood bypassed the capillary bed, flowing instead through the larger arteries and veins.  These two changes in circulation are what produces the “bounding digital pulses” felt in the acute phase of laminitis and are believed to occur as a result of excess MMP. This theory of laminitis based on the triggering of MMP challenges the alternative view that laminitis develops because of circulation changes in the foot.  A current theory is that constriction of veins and high fluid pressure blocks the flow of blood through  the capillaries of the lamellae, eventually causing the lamellae to die.  However,  research has not provided any evidence that vein constriction and high fluid pressure occur.  What appears certain in several studies is that the disintegration of lamellae is caused by the uncontrolled release of excess MMP.What triggers MMP release?  A factor present in cultures obtained from the gut of the horse has been demonstrated to activate MMP and cause lamellar separation in the laboratory.  These cultures contain Streptococcus bovis, the principal bacteria responsible for fermentation of sugars during grain overload.  There is current investigation in the role of the S. bovis MMP activator in natural  cases of equine laminitis.  If it is able to cross the barrier of the gut and enter the circulation, it may be a new “cause” of laminitis.   How do the trigger factors of laminitis reach the lamellae?  There is now strong evidence that the blood vessels of the foot are dilated during the developmental phase of laminitis.  Laminitis does not occur if these blood vessels are constricted, suggesting that the trigger factors will only cause laminitis if they reach the lamellae when the blood vessels are dilated, they are at a high enough concentration, or they occur over a long enough time period. Since blood vessels constrict as the temperature decreases, keeping the feet of horses that are in danger of developing laminitis as cool as possible seems logical.  Trials to determine the effect of a slurry of iced water applied to the feet of horses are underway.  Preliminary results show that horses, unlike humans, do not regard extremely cold feet as uncomfortable.

-If insulin resistance is due to an overweight body conditoin, the goal is weight reduction; Typically when the horse obtains the desired body condition, the insulin resistance often resolves. A minimum of 10% of body weight fed in dry matter each day.
-If insulin resistance is due to Cushing's Syndrome (pituitary dysfunction), the horse should be receiving daily medication (Pergolide) to control the metabolic effects of this syndrome. Weight reduction may not be necessary if body condition is adequate.
-Low non-structural carbohydrate diet is a fundamental component to recovery.
 (No access to pasture, no treats (carrots, apples, etc), no grain other than one that is formulated as a low starch grain such as Purina's Well Solve L/S.
-Recommend soaking the hay for a minimum of 1.5hrs (longer is okay) and discarding the water (this reduces the sugar content by up to 40%)
-Feeding small, frequent meals (divide daily allowance into 3-4 meals per day) this mimics natural grazing behavior and  maintains a steady state of insulin/glucose in the blood.
-After the pain from laminitis is controlled, the feet are no longer inflamed, and there is proper trimming/shoeing/foot support, exercise for 30 minutes 3 times per week has dramatic effects on reducing insulin levels in response to glucose.