Surgical management of vertebral malformation in a Manx cat

Abstract

A 15-week-old Manx kitten was presented for evaluation of progressive hind limb paresis and ataxia. Spinal radiographs and computed tomography revealed a malformation of T3 causing thoracic spinal cord compression. Decompressive surgery consisting of dorsal laminectomy, without vertebral stabilisation, resulted in improvement of clinical signs.

Vertebral congenital malformations of the spinal column are not uncommon in dogs and are seen less frequently in cats. ¹ Wedge-shaped vertebral deformities or hemivertebrae are often identified as incidental radiographic findings. Hemivertebrae are encountered most frequently in the brachycephalic, screw-tailed breeds of dogs. Uncommonly, this condition can present with other concurrent neural anomalies. ^2,3 Clinical signs, if present, are due to spinal cord attenuation or stretching, most commonly resulting in chronic progressive myelopathy. In dogs spinal cord compression causing neurological deficits may be treated by surgical decompression and stabilisation. ^4–8 Information about congenital vertebral malformation affecting cats and their treatment is sparse. ^9–13

A 15-week-old male Manx kitten was referred for evaluation of progressive hind limb paresis of a few days duration. Another kitten, born to the same Manx parents in a previous litter, was identified with spinal deformities in the mid-thoracic and caudal lumbar spine. That animal developed ataxia, which progressed very rapidly to complete hind limb paralysis.

The kitten presented to our referral centre had a short stumpy tail. It was bright and alert, weakly ambulatory in the pelvic limbs and fell often when walking. Neurological examination revealed normal mentation and normal thoracic limb function. Myotatic reflexes were not elicited, although withdrawal reflex and conscious proprioceptive testing was normal in both thoracic limbs. The kitten was able to right itself from lateral recumbency, but conscious proprioception with stepping reflex were delayed in both pelvic limbs. Patellar and flexor reflexes were elicited normal in both pelvic limbs. Cutaneous trunci reflex and perineal sensation were present. Deep pain sensation response was elicited in all four limbs. No evidence of pain was elicited on palpation of the thoracic or lumbar spine. The kitten had a normal appetite and was eating and drinking normally. Urination and defecation were considered normal. Based on normal function of the front limbs and the presence of normal myotatic reflexes in both hind limbs, abnormality was expected to involve T3–L3 spinal cord segments.

Lateral and ventro-dorsal survey spinal radiographs and computed tomographic images of the thoracic and lumbar vertebrae were obtained under general anaesthesia. Marked kyphosis of the vertebral column was present, centered at the level of T2–T3 vertebral segments (Fig 1). The bodies of T2 and T4 were malaligned (Fig 2).

Fig 1.

The body of the third thoracic vertebra is displaced craniodorsally (arrow) in a manner that narrows the neural canal within the second thoracic vertebra.

Fig 2.

The vertebral elements of T2–T4 are clustered together because of malformation of T3. T2 and T4 appear abnormally shaped.

The neural canal within the second thoracic vertebra was obstructed by the body of T3, which was misplaced (Figs 3, 4).

Fig 3.

Reconstructed sagittal CT image of the vertebral column demonstrating craniodorsal displacement of the body of T3 (arrow) within the neural canal.

Fig 4.

The transaxial reconstructed CT image at the level of T2 illustrates the body of T3 (labeled T3) within the neural canal of T2. The dorsal spinous process of T2 (T2a) and the body of T2 (T2b) are also labeled.

Due to the progressive nature of the neurological abnormalities, surgical decompression was indicated. ^5,7 In sternal recumbency, a dorsal midline skin incision was made from the midcervical to the mid-thoracic region. The cranial thoracic vertebral column was exposed with bilateral reflection of the epaxial musculature. Dorsal spinous processes of the T1, T2 and T3 were removed and dorsal laminectomy, centered over the T1–T3, was executed using a micro drill (Stryker). The laminae with mammillary and caudal articular processes were removed to enable full spinal cord width exposure. The spinal cord appeared sharply ventroflexed, bending over the body of T3. No gross parenchymal abnormalities were seen. Absorbable gelatine sponge (Gelfoam; Pharmacia & Upjohn) was placed over the spinal cord. No attempt was made to stabilise or re-align the spinal column. Intermuscular and subcutaneous space closure was achieved using polydioxanone (PDSII; Johnson & Johnson) and skin was approximated with polypropylene (Prolene; Johnson & Johnson) suture material. Peri-operative cephalotine sodium (Cephalotine sodium; MaynePharma) was administered at the dose 22 mg/kg intravenously at induction of anaesthesia. Peri-operative and early postoperative analgesia was carried out by constant rate infusion of fentanyl citrate (Sublimaze; Janssen-Cilag).

Twenty-four hours after surgical decompression, the kitten was non-ambulatory with severe pelvic limb paresis, but good voluntary movements were present in both pelvic limbs. Urination was achieved by manual expression. By the eighth postoperative day, the kitten was able to support itself in a standing position. Severe ataxia was persistent. Urination and defecation was voluntary when the animal was supported in a litter tray. The kitten was discharged to home care 12 days after the surgery, severely ataxic and weakly ambulatory, with normal urinary and faecal continence.

Marked improvement was experienced during the first 2 months postoperatively and the cat has regained near normal function in the pelvic limbs by the 6 months of age. Myotatic reflexes were normal in both front and hind limbs at that stage. Only mild ataxia was present with conscious proprioception normal in both front and hind limbs.

At the age of 3 years, only phone call follow-up was available. The client considers the cat as near normal, fully ambulatory with urinary and faecal continence. Only occasionally unsteady in the hind legs, the cat lives outdoor and is capable of climbing trees.

Ossification of the vertebrae is usually complete by 5–9 months of age. There are three major ossification centres for each vertebrae (with the exception of C2) recognised at birth. Centres of ossification for the cranial and caudal epiphyses appear 3–4 weeks after birth. ¹⁴ Asymmetrical development of the vertebral body or failure of ossification results in malformation, such as hemivertebra.

Hemivertebrae are commonly diagnosed in dogs as an incidental radiographic finding. Clinical signs, if present, are attributed to spinal cord compression due to stenosis of the vertebral canal, spinal angulation or instability leading to a chronic progressive myelopathy. ⁵ Varying degrees of kyphosis, scoliosis or lordosis is present in the majority of cases and may be detected on physical examination.

In the canine population, hemivertebrae are most frequently seen in brachycephalic dogs with screw-tails ⁵ and German Shorthaired Pointers where the disease is present as an autosomal recessive disorder. ¹⁵ The malformation is seen sporadically in other breeds. Hemivertebrae have been reported to occur with other concurrent neural anomalies, including arachnoid cyst, meningocoele, myelocoele or spinal dysraphism. ^2,3 It has been proposed that spinal deviation causes alteration of cerebrospinal fluid flow dynamics, resulting in formation of subarachnoid diverticulae ¹⁶ and syringomelia. Use of advanced imaging techniques in combination with radiography is thus recommended to identify potential concurrent lesions.

Published data on feline vertebral column anomalies is limited. Nutritional osteodystrophy and osteoporosis was suggested as the cause of acquired thoracic vertebral malformation in an immature domestic shorthair cat, leading to lordosis and subarachnoid cyst formation. ¹⁶ Congenital vertebral anomalies, such as hemivertebrae and spina bifida are reported in domestic shorthair kittens affected by mucolipidosis II. ¹⁷ Similarly, Marioni-Henry ¹⁸ found in her study all the cats with congenital disease of the vertebral column were affected by mucopolysaccharidosis VI. Spinal cord compression has been surgically treated in two immature lions with atlantal malformations. ¹¹

No particular feline breed with predilection for hemivertebra has been identified by the authors. The absence of one to all coccygeal vertebrae is typical for Manx cats, with neural malformation, such as spina bifida and syringomyelia being reported concurrently. ^9,19 Clinical signs of this syndrome are taillessness, hypermetric or hopping pelvic limb gait, urinary and fecal incontinence with megacolon. ^10,12,20 It has been postulated that the effect of the Manx gene (M), localised in the heterozygote Manx cat, is responsible for the absence of the caudal spinal cord and overlying vertebrae. ¹⁰ Significant histopathological changes within the spinal cord have been identified in all Manx cats with gait abnormalities and faecal and urinary incontinence. The spinal cord in each case in one study showed cavitation of the dorsal spinal cord with surrounding degeneration of the dorsomedial columns. The cavitation was apparently continuous, communicating in sections with the central canal. ¹⁰ Meningocoele and meningocutaneous fistula draining cerebrospinal fluid in an immature Manx-type cats has been reported. ^9,21 This cat did not have clinical signs of a sacrocaudal abnormality, however, a related kitten also had a vertebral and spinal cord malformation suggesting a genetic cause.

In one study of dogs, the clinical signs of spinal cord compression caused by hemivertebrae are often reported to be mild and non-progressive. ²² In cases where signs of myelopathy are progressive, surgical decompression and stabilisation has been suggested with a very cautious prognosis. ⁵ Dorsal laminectomy or hemilaminectomy in combination with vertebral stabilisation has been reported in three immature dogs with hemivertebrae resulting in satisfactory outcome. ⁸ Aikawa et al ⁴ reported improved neurological function in eight (n=9) dogs after vertebral stabilisation with or without laminectomy.

Surgical stabilisation of adjacent vertebral segments after dorsal laminectomy is recommended in dogs. ^4,5,8 Various fixation techniques using external fixateur pins, Kirschner wires or screws with polymethylmethacrylate are used widely for the dorsal stabilisation of the canine spinal column. The consequence of rigid stabilisation of the immature growing spine has to be yet evaluated. Spinal column instability in our patient was of concern. But the technical difficulty of achieving spinal fixation of an immature feline vertebral column was the reason dorsal laminectomy was used as the sole treatment in this case. The reasons for the persistent ataxia are only speculative. Persisting dynamic compression, instability causing repetitive spinal cord injury or congenital spinal cord anomaly must be considered. The dynamic nature of the lesion and spinal cord pathology could have been preoperatively evaluated by myelography and MRI but these procedures were not performed for financial reasons and the overall guarded prognosis given to the client.

The outcome of both this case and of those reported elsewhere ^4,8,11 are encouraging although definitive conclusions on the best treatment for vertebral malformation cannot be drawn from the treatment of one cat.