CLINICAL SIGNS of Canine DM. “Diagnosis” is by process of elimination, since regular neurological tests aren’t satisfactory, except perhaps for the presence of a brain fluid protein in the lumbar area of the cord. True diagnosis is only possible upon autopsy. Initially, the dog does not seem to realize what position his rear legs are in; soon he will begin to drag his toenails and the top part of his paws, and may tremble as if palsied. The dog sooner or later begins to atrophy in the haunches and croup. He may “dance” with the rear limbs because he does not realize how high he is stepping. Proprioception is the ability of the animal to recognize the location of his limbs, and this is increasingly lost in the afflicted dog. He will get his hocks “tangled up” (one hooked behind the other) and trip over them or drag both. Later, he will have more difficulty getting up and “steering” the rear quarters. Eventually, he will be unable to get up on all four legs, and by this time most owners will have decided upon euthanasia. There were only two cases in the U.K. study, that were maintained for two years after first signs of thoracic limb involvement, such as stumbling in front; these had both been in a “K-9 Kart” for more than 12 months, their back halves being supported by the wheeled contraption. My own cut-off date for euthanasia is when a dog can no longer get up and squat to defecate. Everyone has to decide on his own deadline, but you must have a plan and stick to it, or the event will be even harder on you. It is not possible to diagnose CDRM definitively in life. A presumptive diagnosis could be made, however, based on typical history and clinical signs. Clinical signs of CDRM had been well documented. The dogs showed a slowly progressive pelvic limb ataxia and paresis with loss of proprioception. Initially they scuffed the middle two toes of one or both hind feet. Subsequently they developed problems with circling and with stairs, especially going down; they often scuffed, misjudged distances and showed hypermetria (ataxia in which intended movements overreach the intended goal). The dogs were often affected asymmetrically [more or earlier in one limb than the other] although both pelvic limbs were usually involved. Disuse muscle atrophy developed over the trunk and hindquarters several months after disease onset. With time, prolonged scuffing resulted in excoriation and ulceration of the feet. Eventually the disease resulted in marked paraparesis; the dogs could not rise without assistance and would pull themselves along with their thoracic limbs. A degree of faecal and urinary incontinence would often develop late in the disease. Dogs maintained beyond this stage could show thoracic limb signs. It had been reported that brain stem involvement eventually occurred (Clemmons, 1992) which could result in a number of signs including asymmetrical tetraparesis, cranial nerve abnormalities and altered mental status. The clinical signs were inexorably progressive and whilst they may have stabilised for short periods of time, improvement did not occur. Typically, the signs, which developed as the disease progressed, were as follows: wearing of the nails became increasingly noticeable and more persistent; all dogs started to have problems turning, developing a tendency for the hindquarters to fall to the outside on a turn. These difficulties were more obvious on slippery surfaces and on stairs. Most cases were still keen to exercise at this stage. Crossing of the pelvic limbs then developed, where one leg would get caught behind the other, which often resulted in the dog falling over. Collapsing to one side when walking in a straight line followed. Eventually, after a period of six to 18 months, the dogs were unable to rise to a standing position, so pulled themselves along with their thoracic limbs. In the brain, the lateral vestibular nucleus (LVN) is the one most commonly affected in DM. The axons of all these cells pass to the spinal cord in the vestibulospinal tract. Cerebello-vestibular fibres from the cerebellar cortex provide a feedback mechanism between the vestibular nuclei and the cerebellum. Maintenance of equilibrium or orientation of the body in the vestibular righting reflex is largely reflex activity governed primarily by general proprioceptive impulses from muscles, tendons and joints in the trunk and limbs, and special proprioceptive nerve endings which initiate impulses conveyed via the vestibular nerve to the vestibular nuclei. The LVN, by way of that vestibulospinal tract, exerts a facilitatory effect on spinal reflexes that control muscle tone, especially to maintain appropriate posture or strength of supporting and balancing movements. This is compromised in the case of DM, and the dog is unable to sense that its rear feet are not in the right place or doing the right thing, and likewise is unable to exercise normal control over them. These tracts have an effect on the spinal cord nuclei supplying the antigravity (i.e. the postural and extensor) muscles. [Thus, the DM-affected dog will tend to gallop or bunny-hop rather than trot or walk with as much extension of the hocks as previously or normally.] A failure in the normal activity of the vestibular system due to DM or other lesions may cause disequilibrium, staggering, postural changes, falling or rolling to the same side, and other reactions.
Posted on: Sun, 24 Aug 2014 04:26:42 +0000
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