I'm sorry to hear of this with your Lab. My primary differential diagnosis would be idiopathic (unknown cause) polymyositis which can initially manifest about the jaws and eyes and then generalize to the rest of the body. This is considerated to be an autoimmune disorder (her immune system would be attacking her own muscles). Here is a synopsis of this disease for you:
An autoimmune inflammatory disease of unknown pathogenesis that primarily affects appendicular musculature
Species, Age, Sex
Although any breed or age of dog can be affected, the majority of reported cases are middle-aged, large breeds. There is no apparent sex predilection.
Genetics and Breed Predisposition
Newfoundlands and boxers appear to be overrepresented. Newfoundlands tend to develop the disease at a younger age than other breeds. A substantial number of boxers with polymyositis may develop the disorder as a preneoplastic condition. A breed-specific suspected autoimmune polymyositis has recently been described in Hungarian Vizsla dogs. This latter disorder appears to primarily affect masticatory and pharyngeal muscles clinically, though other muscles are affected.
Uncommonly, dogs with autoimmune polymyositis may have concurrent masticatory myositis (which would cause her facial pain). This combination is referred to as overlap syndrome. Another uncommon associated condition in dogs with autoimmune polymyositis is thymoma.
History, Chief Complaint
Clinical signs may be acute or chronic. The animal's medical history or clinical complaints may include any combination of generalized weakness (often worsened by exercise), stiff gait, generalized muscle atrophy, dysphonia, myalgia, dysphagia, regurgitation (megaesophagus may be present), fever, and muscle swelling.
Physical Exam Findings
Physical examination findings typically concur with the animal's medical history and clinical complaints.
Etiology and Pathophysiology
This is an idiopathic autoimmune disorder.
The diagnosis is suspected in a dog with signs of regional or diffuse muscle weakness and pain. Elevation of muscle enzymes on routine serum biochemistry panels is common. A definitive clinical diagnosis is achieved with muscle biopsy results in combination with normal (negative) serologic titers for potential infectious causes.
- Infectious polymyositis (e.g., toxoplasmosis, neosporosis)
- Overlap syndrome
- Preneoplastic myositis
- Myasthenia gravis
- CBC, serum chemistry profile, urinalysis: elevated aspartate aminotransferase (AST) possible
- Serum creatine kinase: usually elevated, often markedly so
- Serologic titers for infectious diseases (e.g., toxoplasmosis, neosporosis)
Advanced or Confirmatory Testing
- Electrodiagnostics: electromyogram (EMG) is usually abnormal.
- Muscle biopsy: a nonsuppurative inflammatory infiltrate is typically evident. Immunohistochemical staining of muscle tissue can verify immunoglobulin localization to the sarcolemma.
The goal of therapy is to achieve clinical remission of myopathic signs.
Acute General Treatment
Immunosuppressive doses of prednisone (e.g., 1-2 mg/kg PO q 24h) are generally used as initial therapy.
- Once clinical remission of signs is achieved, the dosage of prednisone is slowly tapered over several months and is discontinued if possible.
- If prednisone cannot be effectively tapered or discontinued, alternative immunosuppressive drugs can be instituted (e.g., azathioprine 2 mg/kg PO q 24h for 5 days, then q 48h; or mycophenolate mofetil 5-10 mg/kg PO q 12h).
- Either inadequate or excessive immunosuppression
- Drug side effects or complications, including polyuria and polydipsia (PU/PD), polyphagia, weight gain, iatrogenic hyperadrenocorticism (glucocorticoids), bone marrow effects (azathioprine), and others
Prognosis & Outcome
The prognosis is favorable in approximately 80% of cases. Relapses may occur with tapering or discontinuation of immunosuppressive drugs.
Pearls & Considerations
When tapering prednisone in cases of autoimmune polymyositis, dose reductions should not be made more frequently than every 4 weeks.
I don't believe that a CT would be of value but referral to a specialist veterinary internist (please see here: www.acvim.org) is indicated once such extensive diagnostics have been performed which haven't clarified the diagnosis.
Please respond with further questions or concerns if you wish.