Neurological signs in VideoVet Neurol Neurosurg J. Neurological Signs in Video;Video Supplement(1):.
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Neurological signs in Video
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Video 1: Cataplexy and presumed narcolepsy in an English Cocker spaniel.
Cataplexy and presumed narcolepsy in an English Cocker spaniel induced by feeding.
Although this dog obviously enjoyed going for a walk, that alone was not sufficient to induce cataplexy. Typically, his cataplexy was induced by feeding, but in this instance it was possible to induce it by removal of the food. Note that the hypotonia which caused the limbs to collapse also caused the spinal muscles to relax, as evident in the flaccidity of the neck. The dog also showed behavior consistent with REM sleep but this is not verifiable in the video clip.
Video 2: Cataplexy in a long-haired Dachshund.
Cataplexy induced in a long-haired Dachshund by "going for a walk".
In this dog, the simple pleasure of going for a walk was sufficient to induce cataplexy. Narcolepsy occurred during these attacks but is not verifiable in the video clip.
Video 3: Fibrotic Myopathy in a German Shepherd dog.
Fibrotic Myopathy in a German Shepherd dog.
The gait of this 9 year-old castrated male German Shepherd is typical of that seen in cases of fibrotic myopathy. In this dog there was a firm soft tissue mass judged to be in the proximal region of the left adductor muscle. The non-progressive lameness had begun when the dog collided with the door of an automobile several months earlier. The mass was not biopsied. This patient was seen by the Surgery Service and (by consultation) the Neurology/Neurosurgery Service of the Veterinary Medical Teaching Hospital of The University of California Davis. We are grateful to them for allowing the use of this video segment herein.
Video 4: Myoclonus in a dog.
Myoclonus in a dog.
As a new graduate in a busy small animal practice in the 1950's it was common to have from 2 or 3 to as many as 8 or 10 dogs in the "distemper ward" in our hospital. The mortality rate was high and, among survivors, the jerking movements which we referred to as "chorea" appeared from one or two to as many as ten weeks after the acute stages of the disease. Many of these unfortunate dogs were put to death because of the disabling effects of the myoclonus, or often simply because the owner could not cope emotionally with the problem. Sadly, a high proportion of dogs with distemper had been immunized, inadequately, with a killed virus tissue suspension or with the chick embryo origin modified live virus that was available then. The problem was so common, and so frustrating, that I remember stating passionately that I hoped that before my practice days were over we would no longer see such dogs. Soon, more effective immunization procedures became available and typical canine distemper became less and less common. Happily, distemper myoclonus has become very unusual in many urban practices of the United States. Although this is very gratifying, cases still appear from time to time, notifying us emphatically that distemper and its aftereffects have not been eradicated.
Dr. Gregg Kortz has provided this video of a case he saw a few years ago. It is typical in the character of the signs: rhythmical jerking movements, mainly of groups of flexor muscles. The myoclonus may appear in only one small group of muscles or it may be nearly body wide; sometimes it appears to affect the diaphragm, although I have not been able to verify this. This particular dog's gait is affected by the myoclonus; its gait also may reflect a degree of transverse myelopathy as well, for transverse myelopathy occurs commonly in distemper in the absence of myoclonus. It helped form the basis for McGrath's division of neurological signs of distemper into cerebral, cerebellovestibular and spinal forms; some poor dogs suffer from all forms simultaneously!
Importantly, Breazile et al, 1966 published some very interesting data indicating that the mechanism for myoclonus was located in the spinal cord. Myoclonus in a foreleg persisted after transection of the spinal cord cranial and caudal to the brachial enlargement and after cutting the dorsal roots of the relevant spinal nerves. This leaves nothing but the ventral horn cells and the interneuron pool to generate the repetitive movements! It is not clear that the disease does this through some direct action on the spinal cord gray matter. Perhaps it is an effect on the brain, which then leads to a change in the spinal cord as if the brain "taught" the spinal cord to behave in this way. (Possibly in a way similar to the development of "mirror epileptogenic foci" in the brain?).
Commentary by: T. A. Holliday, May 2000.
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