Has anyone ever come across Central Neuro Myopathy in a lab???
I was telling my breeder that my pup was exercise intolerant and shakes when she runs after a ball or walks short distances. She then has to lay down.
It is a autosomal recessive disorder and since researching the symptoms he has found the pedigree of both the sire and dam have the gene in them.
I am so devastated. I can't find much info on this . Does anyone know of a good site to look at? My breeder is devastated as well.
He gave me one site to look at, but it won't be up until tomorrow. I don't even know if this is fatal.
oh my gosh, I'm so sorry! I don't know anything about that, but just wanted to express my sympathies! Poor pup!! Hopefully someone on here with more knowledge will be able to help you!! Have you checked veterinarypartner.com? Not sur eif they have anything helpful but they seem to have a lot of disorders listed...
The site you mentioned contains kindof the "gold standard" of CNM in labradors- diagnosis, treatments, prognosis, etc. For those who aren't aware of it, the site is: http://www.labradorcnm.com/
You can also find information at:
Usually, the prognosis for affected dogs depends on how severe they have it. To me, it doesn't sound like your baby has a very severe case if just showing "exercise intolerance," but I would probably have her tested for it just to be sure. There are many things that can cause "exercise intolerance," including muscular diseases, neurologic diseases, electrolyte abnormalities and even heart diseases.
~Julie, Rogue, Monty, and Eddy~
"The reason a dog has so many friends is that he wags his tail instead of his tongue." -Anon
Mischasmom i found this.....not sure if it helps any. sorry to hear about you puppy.
Central Core Myopathy
A myopathy has been recognized in young Great Danes beginning around 6 months of age. Clinical signs of generalized weakness exacerbated by moderate exercise [5,6]. In one report, exercise or excitement associated with feeding would induce an episode of general body tremor and collapse into sternal recumbency, with rapid recovery after a few minutes rest . Clinical weakness progressed in affected dogs, so that around 15 to 18 months of age, exercise intolerance was severe, with one dog unable to walk more than a few feet before collapsing. Elevated serum levels of CK, aspartate aminotransferase, and alanine aminotransferase have been reported. The condition is unresponsive to intravenous edrophonium chloride (Tensilon). EMG abnormalities include presence of positive sharp waves and fibrillation potentials in all muscles examined, including proximal and distal limb and trunk muscles. At necropsy, moderate atrophy of proximal limb and paraspinal muscles were noted in one dog . Approximately 50% of muscle fibers contained a central core that occupied from 20 to 80% of the fiber. The cores appeared dark staining with hematoxylin and eosin stains, lacked cross-striations, and some contained vacuoles and nuclei. The cores were found in both type 1 and type 2 fibers. In longitudinal sections, the cores sometimes extended from 50 to 150 mm along the fibers. The core structure varied from homogenous to finely granular or fibrillar. In Gomori trichome stains, scattered rod-shaped bodies were seen. Scattered necrotic and regenerating (characterized by small basophilic fibers with subsarcolemmal nuclear chains) fibers were also observed. Ultrastructurally, the cores consisted of numerous mitochondria, glycogen granules and disarrayed, irregular filament bundles attached to thickened Z-lines. No abnormalities were seen in spinal cord, peripheral nerves, or intramuscular nerve branches. The condition has some similarities to certain congenital myopathies in people, including central core disease, an autosomal dominantly inherited disorder, although in humans there is an absence of oxidative enzyme activity in the cores, which consistently affect type 1 fibers . Note that the cores resemble target fibers seen in denervating muscle , however unlike targets, cores extend along the length of the fiber . In one dog, some clinical improvement occurred following oral prednisolone therapy, although signs quickly returned upon cessation of treatment . Prognosis appears to be guarded to poor. The etiology of this myopathy is uncertain, although a possible genetic disorder involved with oxidative metabolism has been suggested .
Go to this site and order the kit. http://cnmlabrador.vet-alfort.fr/ A pedigree may be indicative but only the genetic test will be valid. How old is the puppy? CNM is usually evident by 4-6 months. Exercise Induced Collapse is something else and usually starts a little later, 18 months or so but may start at less than 1 year. Neither is necessarily fatal but you will have to alter their lifestyle. Good breeders will have had their dogs tested for CNM although the test has only been out for around a year. If a breeder doesn't know what myopathy it is, run.