A 6-year-old castrated male Great Dane was presented to the Cornell University Hospital for Animals for evaluation of pelvic
limb ataxia and intermittent fecal incontinence. The owner reported that the ataxia had first been noticed when the dog was
about 1.5 years old and had slowly progressed. Fecal incontinence had been present for about two months. The owner noted that,
in addition to defecating normally, about every two days the dog had accidents in the house during which it appeared unaware
that it was defecating.
The patient had been evaluated at another hospital about seven months previously for the pelvic limb ataxia. At that time,
caudal cervical spondylomyelopathy had been suspected and magnetic resonance imaging had been performed, which revealed no
evidence of caudal cervical spondylomyelopathy. Cerebrospinal fluid analysis had also been performed at that time, which revealed
EXAMINATIONS AND DIAGNOSTIC TESTS
On presentation, the dog was quiet, alert, and responsive. The only abnormality identified on physical examination was hyperemia
and nail wear of the fifth digit of both pelvic limbs. No abnormalities were identified on rectal examination.
The dog exhibited moderate pelvic limb general proprioceptive ataxia when walking. A neurologic examination revealed bilateral
crossed extensor reflexes and upper motor neuron paresis in the pelvic limbs and decreased proprioceptive positioning reactions
in both pelvic limbs. The patient ambulated well with the pelvic limbs but was moderately ataxic and occasionally scuffed
the dorsum of the toes on either limb. Spinal reflexes (with the exception of the crossed extensor reflex) and muscle tone
were normal in both pelvic limbs. The thoracic limbs were normal, as was the perineal reflex.
We localized the patient's lesion to the T3-L3 spinal cord segments and decided to evaluate the thoracolumbar spine with magnetic
resonance imaging. The dog's CBC and serum chemistry profile results were within reference ranges, so the dog was anesthetized.
At the right synovial articulation of L3-L4, the articular processes (facets) were enlarged and bulbous, having substantial
new bone formation with minimal associated surrounding soft tissue. This new bone formation expanded into the vertebral canal,
causing mild right dorsolateral compression of the spinal cord (Figures 1A & 1B).
Figure: 1A & 1B. Axial T2-weighted and sagittal T1-weighted magnetic resonance images of the midlumbar region of the dog in
this report. At L3-L4, the right articular processes are hypertrophied (arrowheads) causing mild, right, dorsolateral spinal
cord compression (thin arrows).
Immediately after the magnetic resonance imaging, we evaluated the abnormal articular processes by using computed tomography.
Three-dimensional reconstruction revealed a large, smooth bridging bone formation at the right synovial articulation of L3-L4,
along with mild deformation of the right pedicle and lamina of L4 (Figures 2A & 2B).
Figure: 2A & 2B. Computed tomography three-dimensional reconstructions of the midlumbar vertebrae of the dog in this report
viewed from the right craniodorsally (2A) and dorsally (2B). At L3-L4, the hypertrophy of the right articular processes appears
as bulbous, smooth, new bone formation bridging the synovial joint. Additionally, the spinous process of L4 is mildly deviated
to the left.