Clinical Exposures: Intervertebral disk disease: An unusual cause of a cat's lameness and tail weakness

A 10-year-old 8.6-lb (3.9-kg) spayed female domestic medium-haired cat had been evaluated by the referring veterinarian because of lethargy, right pelvic limb lameness, lumbar discomfort, reluctance to jump, and tail weakness. The owner had reported that the signs had appeared acutely and had progressively worsened over two weeks.

The cat had been adopted as a stray about five years earlier and was currently allowed indoors and outdoors. The results of a feline leukemia virus (FeLV) antigen test performed eight months earlier had been negative, and routine vaccinations, including FeLV, were current.

A radiographic examination of the pelvis, stifles, and lumbosacral spine performed by the referring veterinarian had revealed a narrowed L6-L7 intervertebral disk space. A compressive myelopathy had been suspected, and the cat had been hospitalized and treated empirically with dexamethasone (1.29 mg/kg orally once daily for five days) and butorphanol tartrate (0.4 mg/kg subcutaneously as needed). The cat had been referred to the Veterinary Neurological Center in Las Vegas for further evaluation and diagnostic testing after it had shown no improvement.

Physical and neurologic examinations

On presentation at the Veterinary Neurological Center, a physical examination revealed a bright, alert animal with a temperature of 102 F (38.9 C), heart rate of 210 beats/min, and respiratory rate of 50 breaths/min. The oral mucous membranes were pink and moist, and the capillary refill time was 1 second. Other than mild gingivitis, a flaccid tail, and perianal soiling with urine and feces, the cat appeared to be in good physical condition.

A neurologic examination revealed delayed hopping in the right pelvic limb, reduced hock flexion bilaterally, an absent cutaneous trunci reflex at all levels, hyperesthesia on palpation over the lumbosacral spine and tailhead, and an absence of voluntary tail movement. The cat's tail was flaccid, but its gait appeared normal. Anal tone was present, and the bladder was small on palpation. The remainder of the physical and neurologic examinations was unremarkable. The absence of the cutaneous trunci reflex was not necessarily clinically relevant because it can be absent in normal cats. These findings localized the lesion to the caudal lumbar intumescence (L6-S1), or cauda equina.

Figure 1A. A lateral radiograph showing a large mineralized opacity between L6 and L7.

Differential diagnoses and diagnostic testing

Our differential diagnoses for this cat's progressive myelopathy included neoplasia (primary or metastatic), infectious or inflammatory spinal cord disease (toxoplasmosis, feline infectious peritonitis [FIP], coccidioidomycosis, discospondylitis), or intervertebral disk protrusion or herniation.

The complete blood count results were normal. The serum chemistry profile revealed elevated albumin (4.2 g/dl, normal = 2.5 to 3.9 g/dl) and triglyceride (216 mg/dl, normal = 25 to 160 mg/dl) concentrations. The serum thyroxine concentration was normal (1.1 µg/dl, normal = 0.8 to 4 µg/dl). A urinalysis revealed alkalinuria (pH 7.5, normal = 5.5 to 7), proteinuria (+2, normal = negative), and struvite crystalluria (+4, normal = negative). The results of FeLV antigen and feline immunodeficiency virus (FIV) antibody tests, feline toxoplasmosis serologic tests (i.e. IgG, IgM), and a feline coronavirus immunofluorescent antibody test were negative.

A ventrodorsal radiograph of the cat's spine showing a large mineralized opacity between L6 and L7.

Figure 1B

For the spinal diagnostic procedures, anesthesia was induced with thiopental and maintained with isoflurane, and the cat received mechanical ventilation. Survey radiography of the thoracolumbar spine revealed narrowing of the L6-L7 intervertebral disk space and foramen. A large (5 mm diameter), spherical mineralized opacity was identified within the vertebral canal at the level of and just caudal to the L6-L7 intervertebral disk space (Figures 1A & 1B).

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 decompressive surgery.

Figure 2. A transverse CT image showing a large amount of mineralized material within the ventral vertebral canal..

Surgical treatment

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 routinely.

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.

Discussion

Intervertebral disk disease is relatively rare in cats, and few articles on feline intervertebral disk disease have been published in the veterinary literature. The incidence of intervertebral disk disease in cats in one university study was 0.12% (vs. an overall intervertebral disk disease incidence in dogs of 2%).1 The apparent rarity of feline intervertebral disk disease may prevent practitioners from including it on their differential diagnoses lists for cats with signs of spinal cord disease.

Signs of intervertebral disk disease typically manifest in middle-aged to older cats. Like dogs, cats have two recognized manifestations of intervertebral disk disease: intervertebral disk extrusion (Hansen's type I) and intervertebral disk protrusion (Hansen's type II).2 Disk protrusions in cats appear to be an age-related (in middle-aged and older cats) phenomenon associated with fibroid disk degeneration.1,3 In cats, chronic disk protrusions have been identified most commonly in the cervical spine but also appear frequently in the midlumbar spine.2,3 Disk protrusions frequently occur at more than one disk space, and the number of disks affected tends to increase with age.1,4 The presence of disk protrusions in cats does not always correlate with clinical neurologic disease.5

However, acute disk extrusion, or herniation, is frequently associated with chondroid disk degeneration, and chondroid disk degeneration appears to be a factor in most cats with clinically apparent intervertebral disk disease.3 Disk herniations appear to occur most commonly in the thoracolumbar region and the midlumbar to caudal lumbar spine.1-3 Most cats with clinical disease have radiographic changes consistent with chondroid disk degeneration (i.e. mineralization of the nucleus pulposus).4

The clinical signs of a myelopathy include spinal hyperesthesia, proprioceptive deficits, ataxia, paraparesis or paraplegia, tetraparesis or tetraplegia, urinary or fecal incontinence or retention, sensory deficits, or a flaccid tail. Broad differential diagnoses to consider in cats exhibiting signs consistent with spinal cord disease include neoplasia, trauma, infectious or inflammatory diseases, fibrocartilaginous embolism, or intervertebral disk disease.1,2,4,5

Lymphosarcoma has been reported to be the most common cause of spinal cord disease in cats, followed closely by spinal trauma.1,4 Lymphosarcoma is most common in young, FeLV-positive cats. Spinal trauma is usually the cause of spinal cord disease in cats allowed frequent outdoor access. Infectious causes to consider include toxoplasmosis, FIP, cryptococcosis, and coccidioidomycosis. Coccidioidomycosis, a regional disease, should be considered in patients living in or traveling through the southwestern United States. Fibrocartilaginous embolism and discospondylitis have been reported in cats but are relatively uncommon.2 Aortic thromboembolism and bilateral cranial cruciate ligament rupture can mimic signs of a myelopathy and should be ruled out. Pay careful attention to physical examination findings, including cardiac auscultation, palpation of peripheral pulses, and limb temperature, and orthopedic examination findings to help identify the correct cause of the clinical signs.4 Place intervertebral disk disease higher on the differential diagnoses list in middle-aged-to-older, FeLV-negative, indoor-only cats with clinical signs of a myelopathy.1

In cats presenting with a myelopathy, perform a complete blood count, a serum chemistry profile including creatine kinase activity, a urinalysis, and FeLV antigen and FIV antibody tests and measure the serum thyroxine (T4) concentration. Consider testing for FIP, toxoplasmosis, and other regional diseases based on your examination findings and your assessment of each animal's risk. Spinal survey radiography, spinal fluid analysis, myelography, CT, and magnetic resonance imaging are used to localize and identify the causes of spinal cord disease. In cats with intervertebral disk disease, spinal imaging helps identify the degree of spinal cord compression and aids in planning surgical spinal cord decompression.

In practices in which diagnostic imaging is limited to plain radiography, obtain orthogonal views of the spine in an anesthetized animal. Findings consistent with intervertebral disk herniation include narrowing of the intervertebral disk space, mineralization of the intervertebral disk, and opacification of the intervertebral foramen.1,3 Degeneration of the articular facets may also be present. Normal radiographic findings do not preclude a diagnosis of intervertebral disk herniation.

Correctly identifying intervertebral disk herniation as a cause of myelopathy is crucial because a favorable outcome can be achieved with proper treatment.2,3,5 Patients treated with conservative therapy (e.g. enforced confinement, corticosteroid administration) compared with those treated with surgical intervention appear to have a less favorable long-term outcome.3 Conservative therapy may be appropriate in cats with minimal spinal cord compression, but because cats tend to hide the early signs of discomfort, the window of opportunity for treating the disease conservatively may be missed.

The recommended treatment for most patients with clinical intervertebral disk disease is surgical spinal cord decompression and postoperative physical therapy.4-6 Physical therapy typically consists of performing passive range-of-motion exercises and massaging the muscles of the affected limbs. With surgical spinal cord decompression, the prognosis for cats with intervertebral disk disease likely mirrors the prognosis for dogs with intervertebral disk disease; that is, cats receiving spinal cord decompression surgery appear to show good neurologic recovery.6 Most cats receiving spinal cord decompression surgery show good clinical improvement; residual neurologic deficits, although common, often do not seriously affect the cat's quality of life.3 The return of pain perception and ambulation after surgery has been reported in cats that had deep pain loss before surgery.6 It is reasonable to assume that the patients with the best prognoses are those that retain deep pain perception because they are more likely to regain voluntary motor function and continence than are those without deep pain perception.

The photographs and information for this case were provided by Tracy N. Prouty, DVM, and Joli M. Jarboe, DVM, DACVIM (neurology), Veterinary Neurological Center, 4445 N. Rainbow Blvd., Las Vegas, NV 89108. Dr. Prouty’s present address is Northwest Veterinary Specialists, 16756 S.E. 82nd Drive, Clackamas, OR 97015.

REFERENCES

1. Munana KR, Olby NJ, Sharp NJ, et al. Intervertebral disk disease in 10 cats. J Am Anim Hosp Assoc 2001;37:384-389.

2. Salisbury SK, Cook JR. Recovery of neurological function following focal myelomalacia in a cat. J Am Anim Hosp Assoc 1988;24:227-230.

3. Seim HB III, Nafe LA. Spontaneous intervertebral disk extrusion with associated myelopathy in a cat. J Am Anim Hosp Assoc 1981;17:201-204.

4. Rayward RM. Feline intervertebral disc disease: a review of the literature. Vet Comp Orthop Traumatol 2002;15:137-144.

5. Knipe MF, Vernau KM, Hornof WJ, et al. Intervertebral disc extrusion in six cats. J Feline Med Surg 2001;3:161-168.

6. Kathmann I, Cizinauskas S, Rytz U, et al. Spontaneous lumbar intervertebral disc protrusion in cats: literature review and case presentations. J Feline Med Surg 2000;2:207-212.