A lesion at this location could have been causing the cat's neurologic signs, so we did not perform a myelogram because of
the risk of potential complications and the likelihood that no additional information would be obtained. Computed tomography
revealed a massive amount of mineralized material within the ventral vertebral canal (presumptive Hansen's type I disk herniation)
(Figure 2). Both the radiographic and CT findings were suggestive of a compressive myelopathy at L6-L7, so the cat was prepared for
Figure 2. A transverse CT image showing a large amount of mineralized material within the ventral vertebral canal..
Cefazolin (22 mg/kg intravenously every 90 minutes) was administered prophylactically during surgery. The cat was placed in
sternal recumbency, and a routine midline approach to the caudal lumbar spine was performed. After the dorsal spine of L7
was removed, a dorsal laminectomy from the caudal third of the L6 vertebral body to the L7-S1 disk space was performed. On
entry into the spinal canal, the exposed spinal nerves within the dural sac appeared to be displaced dorsally and were adhered
to surrounding structures. A durotomy was performed to enable retraction of the nerve roots and to gain access to the underlying
disk material. After the nerve roots were carefully retracted, a massive amount of gritty, friable, herniated nuclear material
causing marked compression of the surrounding nerve roots was identified and removed. Two of the most dorsally located nerve
roots appeared swollen and had small hemorrhagic foci and bruising at the compression site. After the extruded disk material
was completely removed, the laminectomy site was flushed with 0.9% sterile saline solution and re-explored, and the nerve
roots appeared adequately decompressed. A fat graft was placed over the laminectomy defect, and the surgical site was closed
Recovery and follow-up
Immediately after surgery, the cat received hydromorphone (0.025 mg/kg intravenously) for analgesia. The cat, which was ambulatory
and could urinate without assistance within five hours of surgery, was discharged within 24 hours of surgery. At that time,
the cat was normal neurologically except it could not voluntarily move its tail, and it lacked pain perception in the distal
half of its tail. The cat was discharged with oral prednisone (0.6 mg/kg orally once daily for three days) to reduce inflammation
and amoxicillin trihydrate-clavulanate potassium (16.1 mg/kg orally b.i.d. for seven days) to help prevent a postoperative
infection. We recommended four to six weeks of enforced rest (i.e. cage confinement) for the cat.
At a recheck examination 12 days after surgery, the cat appeared to be recovering well. No discomfort was elicited when the
surgical site was palpated or the pelvic limbs and tail were manipulated. The cat's gait and spinal reflexes were normal.
The cat exhibited weak voluntary movement of the proximal third of its tail, but the rest of the tail remained flaccid. Pain
perception remained absent in the distal half of the tail.
Follow-up phone conversations with the owner revealed that within one month of surgery, the cat had returned to its normal
activities, including running and jumping. Within three months of surgery, the cat had regained weak voluntary movement of
its entire tail, and at 10 months after surgery, the cat had strong voluntary movement of its tail, although it carried its
tail predominantly to the left of midline (Figure 3).
Figure 3. The cat 10 months after surgery. Note the predominantly leftward carriage of its tail.