|
NEUROMUSCULAR CASE OF THE MONTH - JANUARY 2001
Stiff-stilted gait in a 4 year old FS Boxer
Contributed by Dr. Kim Knowles
Veterinary Neurological Center
Phoenix, AZ 85040
Clinical History
The dog presented with a 4-5 week history of weight loss (10 lbs.), lethargy, anorexia, and a stiff-stilted gait. There had been some vomiting (bile) which
was intermittent and may have been associated with a diet change. Complete blood counts and serum chemistry profiles performed on 3 occasions showed moderate
elevations in alkaline phosphatase (alk phos) and creatine kinase (CK). Serum antibody titers for C. immitis and E. canis were negative.
The dog was treated with metronidazole and amoxicillin for suspected liver disease. The dog recently received Etogesic. |
Figure 1. |
Physical Examination
A stiff, stilted gait which worsened with exercise was present. The dog would nose dive in the front after walking 40 feet.
Cranial nerves and mentation were normal. Spinal reflexes were normal to slightly decreased. A disorder of neuromuscular transmission,
myopathy or neuropathy were suspected.
Diagnostic Testing
Serum CK - 6087 IU/L (10-200 IU/L)
Acetylcholine receptor antibody - 0.11 nmol/l (<0.6 nmol/l)
Antinuclear antibody titer - Negative
Thoracic radiographs - No abnormalities observed
Electrodiagnostics - Electromyography showed myopathic discharges (bizarre high frequency discharges), increased insertional activity,
and fibrillations in distal appendicular muscles primarily.
|
Muscle biopsy: A fresh frozen biopsy from the cranial tibial muscle showed multifocal areas of mononuclear and eosinophilic cellular infiltration consistent
with a diagnosis of inflammatory myopathy/polymyositis. (H&E). Since infectious agents including T. gondii and N. caninum were not
identified, immune mediated or paraneoplastic etiologies were likely. |
Figure 2. |
|
Treatments and Clinical Outcome
Prednisone therapy was initiated at 20 mg twice daily for 3 days with gradual tapering over an approximately 2 month period.
Sucrafate was also included as a stomach protectant. Clinical evaluations over the following 2 months showed the dog was doing
well with the CK concentration returning to the normal range. The dog could not be tapered off of the prednisone without return
of clinical weakness. Approximately 6 months after the original diagnosis the dog presented with weakness(Fig.A) and a moderate
size mass in the muscle of the left rear leg (Fig. B). Repeat thoracic radiographs showed a diffuse nodular pulmonary pattern
suspected to be infectious or neoplastic (Fig. C). Cytology of a tracheal wash and lung aspirate supported a probable pyogranulomatous
pneumonitis. Aerobic, anaerobic, and fungal cultures of blood, the tracheal wash, and the muscle mass were negative. A biopsy
of the muscle mass showed marked cellular infiltration composed predominantly of histiocytes with accumulations of degenerating
neutrophils in necrotic areas (Fig. D). Most of the histiocytes contained mitotic figures. A diagnosis of diffuse, aggressive
histiocytic lymphoma was made with a poor prognosis. The dog was euthanitized. Additional tissues evaluated at necropsy including
lymph node (not shown) and lung (Fig. E) showed marked histiocytic infiltration with almost complete obliteration of the normal
architecture.
Conclusion
In humans, the incidence of associated malignancy and polymyositis may be up to 28% and increases with age (1). The
associated neoplasia in humans is most frequently a carcinoma (2). The detection of a neoplasm may precede or follow the onset
of polymyositis. In most cases, the muscle disease and the malignancy develop within a year of each other (3). In the dog
of this report, neoplasia was identified 6 months following the diagnosis of polymyositis. When possible, the removal of the
tumor sometimes results in improvement of the muscle weakness; on occasion, the reappearance of muscle weakness coincides
with tumor regrowth. The incidence of malignancy associated polymyositis in dogs is not known. We suspect that the original
diagnosis of polymyositis in this dog was a paraneoplastic syndrome. This association of polymyositis and malignancy should
alert clinicians to the possibility of an underlying neoplasm in dogs with polymyositis and warrant the initial search for
and continued monitoring for neoplasia in these dogs. |

Figure A.

Figure B.

Figure C

Figure D.

Figure E. |
References
1. Callen JP (1988). Malignancy in polymyositis/dermatomyositis. Clin Dermatol 6:55.
2. Manchu LA, Pritchard KI, Tenenbaum J et al (1985). The frequency of malignant neoplasms in patients with polymyositis-dermatomyositis:
A controlled study. Arch Intern Med 145:1835.
3. Engel AG, Hohlfeld R, Banker BQ. The polymyosits and dermatomyositis syndromes. In: Engel AG, Franzini-Armstrong C (eds). Myology.
McGraw-Hill, New York, 1994;1335.
Back to Top
|