Clinical History
The dog presented for a three week history of progressive tetraparesis and difficulty in eating, urinating and defecating. A left sided thoracic limb lameness was the initial abnormality. There was rapid progression to involve all four limbs resulting in inability to ambulate.  The owner also reported the dog gradually lost facial expression.

Physical and Neurological Examination
No specific abnormalities were identified on general physical examination.　On neurological examination, the dog had a non-ambulatory tetraparesis with slight right-sided head tilt. Muscles of mastication were moderately atrophied. Postural reactions were absent in all four limbs. Spinal reflexes were reduced (reduced withdrawal in all four) to absent (absence of both patellar reflexes). Other cranial nerve abnormalities include trigeminal (in all three branches) and facial nerve weakness. Sensory evaluations were normal. The urinary bladder was distended and easily expressed. The neurological localization was consistent with generalized lower motor neuron disease. One week after the initial presentation, the head tilt and masticatory muscle atrophy became more prominent. Voluntary movement of all limbs was still present but decreased from the initial evaluation, particularly in the left forelimb which had minimum voluntary motor activity.

Diagnostic Testing

CBC and serum chemistry profile including creatine kinase– No abnormalities

Blood Lead– <1ug/dl

Canine distemper virus–
            Serum IgG: 1:320
            CSF IgG: negative
            Serum IgM: negative
            CSF IgM: negative
Toxoplasma gondii: negative in serum and CSF
Neospora caninum: negative in serum and CSF

Urinalysis– suspect urinary tract infection (UTI)

Urine culture and sensitivity– an aerobe was cultured which was sensitive to all tested antibiotic including ampicillin

Thoracic and abdominal radiographs– No abnormalities

CSF Analysis– No abnormalities

Muscle and Nerve Biopsies
With the exception of scattered atrophic fibers, the muscle biopsy was generally unremarkable (not shown). Predominant pathological changes consistent with demyelination were present in the peroneal nerve biopsy specimen. The density of myelinated fibers was subjectively appropriate (A). Fully (arrow) and partially demyelinated nerve fibers were present with closely placed foamy macrophages around some fibers (B). Small numbers of thinly myelinated nerve fibers were present suggesting remyelination.

Conclusion and Clinical Outcome
The most likely cause of this acquired demyelinating neuropathy is immune mediated disease. Other differential diagnoses including infectious diseases, paraneoplastic syndrome or lead toxicity were considered less likely in this case based on the clinical evaluation and diagnostic testing. Prednisolone therapy was initiated at an anti-inflammatory dosage, and was increased to an immunosuppressive dosage after receipt of the histopathology report.  Gradual improvement was noted after one month of treatment with prednisolone and methylcobalamin. There was no further progression of the neuropathy and the dog regained  facial expression soon after initiation of treatment. The head tilt, difficulty in eating, and difficulties in urination and defecation gradually resolved over the month. Spinal reflexes were still reduced to absent in all four limbs. The dog, however, regained good voluntary movement in all limbs and began to attempt to raise up. However, the dog still crawled around when moving. The UTI was treated with ampicillin and resolved. Addition of cyclosporine resulted in a little further improvement.