Muscle wasting

Last Edited By Krjb Donovan
Last Updated: Mar 11, 2014 07:42 PM GMT


I have a three year old great dane and last month was dx w/ idiopathic neuropathy when she could drink or eat. It was not long term and was able to eat and drink like normal after two weeks. Now I just had her seen because her appearance around her skull has been changing. Our dr said it was muscle wasting but could not tell me how bad it would get and if it would effect other muscles in her body. She eats good and her body weight is good but she is sleeping more often. I am deeply concerned about her. If you have any information on this PLEASE let me know. Thank you for your time.


Well there are many diseases that cause muscle wasting but the one we saw infrequently in practice was myasthenia gravis. While it's causes are not rooted in the muscles per se, its major symptom is a wasting of the muscles and it is usually noticeable around the temples first. It can be treated with steroids on a short term basis but the prognosis is guarded.

I am going to paste here all the diseases that the Merck Veterinary Manual mentions about dystrophies and other muscles diseases, but you really need to ask your vet more questions about her diagnosis and prognosis. Ask him to name the disease he thinks she has and ask if there is a positive way of testing for it.

This information may be a bit daunting, but read through it . You can ignore the breed predilections as these can affect any dog, it's just that certain breeds are more prone to some of them. I cannot find any particular one for Danes only.

Idiopathic Neuropathy is just a name for a neuropathy from which we cannot tell how or why she got it. I would bet the farm that it was the beginning of what she has now.

Here is the Merck list:

Hypertrophic neuropathy of Tibetan Mastiff dogs is an autosomal recessive disease that has been recognized in the USA, Switzerland, and Australia. It causes paraparesis by 8 wk and may progress to tetraparesis. Hyporeflexia is marked, but sensory function is preserved. Demyelination and remyelination are seen on nerve biopsy. Prognosis is guarded. Some puppies regain the ability to walk but remain weak. There is no treatment.

Alaskan Malamute polyneuropathy affects Alaskan Malamutes 10-18 mo old. There is exercise intolerance, paraparesis progressing to tetraparesis, muscle atrophy, hyporeflexia, and, in some cases, laryngeal paralysis. Electromyography shows diffuse fibrillation potentials and positive sharp waves. On nerve biopsy, there is axonal necrosis with demyelination. There is no effective treatment, although clinical signs stabilize in some patients. In most affected dogs, however, progressive disability leads to euthanasia. Congenital laryngeal paralysis is seen in Bouvier des Flandres (autosomal dominant) and Siberian Huskies, Rottweilers, and Bull Terriers <1 yr old. It results in exercise intolerance and inspiratory dyspnea. Diagnosis is confirmed by visualization on laryngoscopy. Congenital laryngeal paralysis with diffuse peripheral neuropathy is seen in several breeds, including Dalmatians, Rottweilers, and Pyrenean Mountain Dogs. Prognosis is guarded to poor. Primary hyperoxaluria (L-glyceric aciduria) is a rare inherited (autosomal recessive) neurofilament disorder of domestic shorthaired cats that results in renal disease and also produces weakness due to a peripheral neuropathy. Signs develop at 5-9 mo of age. A plantigrade stance is the most prominent sign, and spinal reflexes are sometimes reduced. Urine contains increased oxalate and L-glycerate levels. There is no treatment.

Sensory neuropathy of longhaired Dachshunds (probably autosomal recessive) causes pelvic limb ataxia at 8-12 wk of age. Urinary and GI function may also be disturbed. Paw position sense, spinal reflexes, and pain sensation are depressed, and self-mutilation can occur. There is a loss of myelinated fibers in sensory nerves and in selected areas of the spinal cord. There is no treatment, but affected dogs may have a relatively normal quality of life provided self-mutilation does not develop.

Sensory neuropathy in Pointers is seen in English Pointers (autosomal recessive) in the USA and Shorthaired Pointers in Europe. Self-mutilation of the digits is the main clinical sign, and the disease onset is before 6 mo of age. Pain perception is absent in the pelvic limbs and depressed in the thoracic limbs. There is neuronal loss in dorsal root ganglia. Prognosis is poor. There is no treatment.

Congenital myasthenia gravis (autosomal recessive) has been described in Jack Russell Terrier, Smooth-haired Fox Terrier, and Springer Spaniel puppies. It is due to either a deficiency or dysfunction of the acetylcholine receptor, and there is none of the circulating antireceptor antibody seen in the more common acquired form of the disease. Clinical signs usually start at 5-10 wk of age. The characteristic finding is an exercise-induced weakness, often associated with megaesophagus. The prognosis is more guarded than in acquired myasthenia gravis. The congenital disease has also been described in cats. A presynaptic form is seen in 12- to 16-wk-old Gammel Dansk H?nsehund dogs (autosomal recessive). Treatment consists of anticholinesterase drugs. Scotty cramp (autosomal recessive) causes episodes of muscular hypertonicity in Scottish Terrier puppies. These episodes are exacerbated by excitement, exercise, stress, and poor health and are characterized by a hypermetric gait and arching of the spine, which can cause the dog to somersault when it runs. The disorder seems to be related to faulty serotonin metabolism. Diazepam and promazines help to relieve signs.

Congenital myoclonus of Labrador Retrievers (familial reflex myoclonus) causes muscle spasms/hypertonicity from an early age. Puppies may be unable to walk or even maintain a sternal position due to extensor rigidity. The prognosis is very poor.

Hypokalemic myopathy of Burmese cats (autosomal recessive) causes periodic paralysis or weakness with ventral flexion of the neck. Cats are affected at 3-4 mo of age. Serum CK is markedly increased. Dietary supplementation of oral potassium usually produces a favorable response (eg, potassium gluconate solution at 2-4 mEq or mmol/cat, PO, sid, until serum potassium levels are stable).

X-linked muscular dystrophies have been described in Irish Terriers, Golden Retrievers, Miniature Schnauzers, Rottweilers, Samoyeds, German Shorthaired Pointers, Groenendaeler Belgian Shepherds, Brittany Spaniels, Rat Terriers, Labrador Retrievers, Japanese Spitz dogs, and also in cats. All are due to mutations in the dystrophin gene. Males show muscle stiffness, dysphagia, and weakness at an early age, along with a plantigrade stance and muscle atrophy as the animal gets older. Initial muscle hypertrophy may be marked, particularly in cats. Diagnosis is facilitated by the initial massive increases in serum levels of CK and by demonstration of hyalinized and mineralized muscle fibers on biopsy. Prognosis is guarded to poor. At present, there is no treatment. A novel congenital muscular dystrophy has recently been reported in cats associated with deficiency of merosin (laminin α2), in which degenerative changes occur in both muscles and peripheral nerves. Labrador Retriever myopathy (autosomal recessive) causes a stiff gait and marked muscle atrophy in puppies of both sexes. Signs worsen with cold, stress, or exercise, and affected dogs may be unable to keep their heads elevated in a normal position from as early as 3 mo of age. Tendon reflexes are usually absent. Signs stabilize by 6-8 mo of age, and the prognosis is favorable so that affected dogs can make good pets. There is preferential atrophy of type II muscle fibers.

Dermatomyositis of Collies and Shetland Sheepdogs (inherited as a dominant trait with variable expressivity) causes atrophy and weakness of the masticatory and distal limb muscles from a few months of age, sometimes associated with trismus and megaesophagus. These signs are combined with a dermatitis over the face and extremities. The clinical signs may wax and wane and, in general, do not become severely debilitating. Polymyositis and dermatitis are evident on histopathologic examination. This disorder has also been seen in Beauceron Shepherds, Pembroke Welsh Corgis, Australian Cattle Dogs, Lakeland Terriers, Chow Chows, German Shepherds, and Kuvasz dogs.

Glycogen storage diseases can cause muscle weakness and exercise intolerance in young dogs and cats. Examples include glycogenosis types II (Lapland dogs), III (German Shepherds and Akitas), IV (autosomal recessive in Norwegian Forest cats), and VII (English Springer Spaniels). Mitochondrial myopathy has been described in Clumber and Sussex Spaniels and in Old English Sheepdogs. Mitochondrial myopathies result in exercise intolerance and collapse, and blood lactate and pyruvate levels are often increased after exercise. Ragged red fibers, indicating increased numbers of mitochondria, may be seen on muscle biopsy. Inherited disorders of carnitine metabolism are another cause of mitochondrial myopathy; they may cause accumulation of lipid vacuoles within muscle fibers.

Nemaline rod myopathy (probable autosomal recessive) in cats causes weakness and later a hypermetric gait at 6-18 mo of age. Patellar reflexes are depressed, and muscle atrophy develops progressively. Large numbers of nemaline rods are found in skeletal muscle fibers. The prognosis is poor. A similar disorder is seen sporadically in young dogs. Central core myopathy has been described as a cause of weakness, muscle atrophy, and exercise intolerance/collapse in young Great Danes in the UK. Signs begin around 6 mo of age. Prognosis is poor.

Congenital megaesophagus is inherited in Wirehaired Fox Terriers and Miniature Schnauzers, and possibly also in German Shepherds, Great Danes, Irish Setters, Newfoundlands, Shar-Peis, Greyhounds, and Siamese cats. Clinical signs include regurgitation and aspiration pneumonia. Prognosis is guarded.

I hope you can get to the root of this and my best wishes to you and your girl. You have a right to be worried.Please let me know what you discover.


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