TREATMENT AND OUTCOME
The following day, a modified hemi laminectomy was performed at L3-L4, and all compressive material was removed. Small fragments
of the lesion were submitted for aerobic and anaerobic bacterial culture. The remainder of the collected fragments were submitted
for histologic examination. Intravenous cefazolin (22 mg/kg) was administered every 90 minutes during surgery. For the initial
24 hours after surgery, intravenous fentanyl (3 μg/kg/hr) was administered by constant-rate infusion for analgesia.
The patient recovered well, and at the time of discharge 72 hours after surgery, the dog was ambulatory in the pelvic limbs
with mild general proprioceptive ataxia and upper motor neuron paresis. We prescribed an approximately two-week tapering schedule
of oral prednisone (0.5 mg/kg once a day for five days, then 0.25 mg/kg once a day for five days, then 0.25 mg/kg once a day
every 48 hours for five days). The patient also received oral cephalexin (22 mg/kg orally t.i.d.) for 14 days postoperatively.
We recommended slow leash walks for two weeks, with a gradual return to normal activity over the ensuing two to three months.
The aerobic and anaerobic bacterial cultures yielded no growth. Histologic findings included highly reactive periosteal proliferation,
irregular and degenerative articular cartilage, reactive synovial cells, and regenerating chondrocytes. The morphologic diagnosis
was severe locally extensive periosteal proliferation with moderate cartilaginous hyperplasia, consistent with degenerative
On reexamination four weeks after surgery, the dog exhibited minimal pelvic limb ataxia. The owner also reported that the
dog had displayed only two episodes of fecal incontinence since surgery.
Myelopathy due to vertebral articular process, or facet, hypertrophy and subsequent spinal cord compression is infrequently
described in the veterinary literature.1,2 It is generally thought that malarticulation between the cranial and caudal vertebral articular processes leads to joint
instability and progressive hypertrophy. Two possible reasons for such malarticulation are prior trauma or a congenital malformation,
the latter of which is more likely.1-3
Some researchers have theorized that caudal vertebral articular process dysplasia, based on imaging findings in four dogs,
offers a reasonable explanation for vertebral articular process hypertrophy.2 This theory proposes that congenital hypoplasia or aplasia of the caudal vertebral articular process leads to chronic instability
of the affected intervertebral space. Over time, progressive hypertrophy of the cranial vertebral articular process, as well
as adjacent soft tissue structures (e.g. synovium, ligamentum flavum), leads to vertebral canal impingement and spinal cord compression.2 This explanation likely applies to the dog in this case and is consistent with the histologic findings. Considering the
chronicity of the dog's problem and the massive hypertrophy of the vertebral articular process, it is not surprising that
a primary defect (i.e. dysplastic caudal vertebral articular process) was not identified on either imaging or histologic examination.
Other possible explanations for articular process hypertrophy include joint infection and abnormal mechanical loading of the
joint; the latter phenomenon is suspected to be due to altered intervertebral joint movement secondary to degenerative intervertebral
disk disease.3 Breed-associated vertebral articular process hypertrophy has been described in Shiloh shepherds and Scottish deerhounds.1,3 In a family of Shiloh shepherds, hypertrophied vertebral articular processes in the thoracolumbar region, causing spinal
cord compression, were described.1 In Scottish deerhounds, arthrosis of the synovial articulations at C2-C3 was associated with cervical hyperesthesia, in
the absence of myelographic evidence of spinal cord compression.3 To the our knowledge, there are no other reports of vertebral articular process hypertrophy-associated myelopathy in Great