Clinical Exposures: Intervertebral disk disease in a dog with agenesis of a cervical vertebra



Figure 1 : Lateral radiograph of the cervical spine of the dog in this case. Note the incomplete formation and separation of C3.
A 65-lb (29.5-kg) 6-year-old spayed female Doberman pinscher was presented for evaluation of a one-month history of progressive left forelimb lameness. The physical examination revealed a weightbearing lameness of the left forelimb with mild muscle atrophy in the left forelimb, especially over the spine of the scapula. No swelling, joint effusion, or pain was detected on palpation of the limb. Pain was elicited on cervical extension. A neurologic examination revealed delayed conscious proprioception of the left forelimb, with slightly delayed conscious proprioception in the left hindlimb. All segmental spinal reflexes and all other neurologic responses were normal. No other abnormalities were noted on the remainder of the physical examination. Differential diagnoses for the dog's condition included cervical intervertebral disk extrusion, cervical vertebral malformation-malarticulation, and neoplasia involving the spine, vertebrae, or brachial plexus.

Diagnostic tests


Figure 2 : Ventrodorsal radiograph of the cervical spine of the dog in this case. Note the incomplete formation and separation of the elongated body of C4.
Our diagnostic plan included a complete blood count, a serum chemistry profile, survey spinal radiography, and myelography with possible cerebrospinal fluid analysis. The results of the complete blood count and serum chemistry profile were normal.

We premedicated the dog with morphine sulfate and glycopyrrolate, both administered subcutaneously. General anesthesia was induced with thiopental sodium, given intravenously. Anesthesia was maintained with isoflurane. A survey spinal radiographic examination revealed only six distinct cervical vertebrae, with apparent incomplete separation of the second and third cervical vertebrae (Figures 1 & 2). The fourth cervical vertebral body was elongated.

Myelography was performed by injecting 0.3 ml/kg iohexol (240 mg iodine/ml) at the cisterna magna. The myelogram revealed marked extradural ventral spinal cord compression over the C5-C6 disk space (Figures 3 & 4). No change in the lesion was noted radiographically in response to traction, flexion, or extension.

Diagnosis and treatment


Figure 3 : Lateral myelogram of the cervical spine. Note the marked ventral extradural compression at C5.
The static ventral cord compression was highly indicative of a prolapsed intervertebral disk at C5-C6. The other vertebral abnormalities were consistent with cervical vertebral malformation-malarticulation. Because there was no dynamic component and the lesion was nontraction-responsive, we performed a ventral slot fenestration at C5-C6 immediately after the myelography. A large amount of degenerative disk material was removed from the spinal canal.

Postoperatively, the dog was given intravenous fluids at a maintenance rate, and 0.5 mg/kg morphine was administered subcutaneously every four to six hours or as needed for pain. We administered intravenous methylprednisolone sodium succinate intraoperatively at a dose of 30 mg/kg, followed by a 15-mg/kg dose two hours later and then every six hours for 24 hours. This was followed by administration of 0.5 mg/kg prednisone twice a day for five days and then 0.5 mg/kg every other day for five days. Famotidine was given at 0.5 mg/kg twice a day while the dog was in the hospital. Fluids were discontinued after two days, once the dog was eating and drinking normally.


Figure 4 : Ventrodorsal myelogram of the cervical spine. Note the marked ventral extradural compression at C6.
Twenty-four hours after surgery, the dog was nonambulatory and tetraparetic. While recumbent, the dog was turned over every four hours and later assisted to rise with a sling. Three days later, the dog was able to stand and walk unassisted and was discharged from the hospital with strict exercise restrictions for four weeks and harness walks only. The dog was clinically normal two weeks after surgery. Six months after surgery, the dog remained normal, with no recurrence of lameness, ataxia, or neck pain.