An 8-year-old female, spayed Labrador retriever presented for severe paraparesis. The dog was diagnosed 2 weeks prior as a healthy ketotic diabetic and was started on 18 units (0.5 U/kg) Humulin-N insulin injected subcutaneously twice daily. Paraparesis developed 1 week later and seemed to worsen with exercise. The owner reported no regurgitation or vomiting. Other than polyuria and polydipsia, the owner did not note any signs of systemic disease. Blood work performed by the referring veterinarian included a chemistry analysis (including creatine kinase), TT4, CBC, and urinalysis. Significant abnormalities noted were hyperglycemia (550 mg/dL), 3+ glucosuria, trace ketonuria, and TT4 of 0.7 µg/dL. A free T4 was not performed.
Physical and Neurological Exam
Abnormalities were limited to the neuromuscular system. A mild paraparesis was noted with a short-strided, choppy gait that progressed to a nonambulatory state in the pelvic limbs (Go to video clip). The dog also had a slightly diminished palpebral reflex bilaterally, intact general proprioception, absent patellar reflexes bilaterally, absent cranial tibial reflex on the left side, and decreased withdrawal strength in all four limbs.
On admission electrolytes were normal and the blood glucose was 605 mg/dL. Urinalysis revealed 3+ glucosuria but no ketonuria. Following exercise that resulted in a nonambulatory paraparesis, edrophonium chloride (4 mg; 0.13 mg/kg) was administered intravenously. There was no improvement in strength following injection. Serum was submitted for identification of acetylcholine receptor antibodies. Thoracic radiographs did not reveal any abnormalities.
Following the initial evaluation, myasthenia gravis was highly suspected based primarily on the gait abnormalities and decreased palpebral reflexes. Pending results of the acetylcholine receptor antibody test, the dog was placed on pyridostigmine bromide (15 mg; 0.5 mg/kg) orally every 12 hours. Two days later the dog was still very weak in the morning but seemed stronger 2 hours after receiving the pyridostigmine bromide. However, a glucose curve demonstrated that the blood glucose never dropped below 480 mg/dL. The insulin dosage was increased to 23 units twice daily and the pyridostigmine bromide dosage increased to 30 mg orally every 6 hours.
Diagnosis and Outcome:
The acetylcholine receptor antibody titer was within the reference range at 0.01 nmol/l (canine reference <0.6 nmol/l). The following day the owner reported muscle strength was improving and, that morning, the dog was able to walk 1/8 mile. Due to the negative response to edrophonium and the negative serology, pyridostigmine bromide was discontinued. Several days later the owner reported that the dog was running and improving daily as the diabetes was under better control (Go to video clip). The resolution of muscle weakness with glycemic control in this dog is very similar to the quick resolution of clinical weakness in cats with diabetic neuropathy. Uncontrolled diabetes mellitus should be considered in dogs with a “myasthenic” presentation.