Introduction

Minuet cats are a breed derived from the combination of Persian and munchkin parent breeds. The short limbs of Minuet cats are a characteristic inherited from munchkin cats. It has recently been reported that munchkin cats exhibit an autosomal dominant mode of inheritance for a chondrodysplastic condition, similar to osteochondrodysplasia seen in Scottish Fold cats.¹ This condition in munchkin cats is believed to predispose them to lordosis and pectus excavatum, which may be attributed to the chondrodysplastic condition; however, the detailed etiology is still unknown.² Reports have described osteochondrodysplasia in Scottish Fold cats because of an autosomal dominant gene mutation, leading to progressive skeletal deformations at the distal limbs, tail, and vertebrae.^3–5

Thoracic vertebral canal stenosis is the seventh most common spinal disease in cats, preceded by nonlymphoid neoplasia, intervertebral disk disease, fracture and luxation, ischemic myelopathy, feline infectious peritonitis virus myelitis, and lymphoma.⁶ Reports of thoracic vertebral canal stenosis in cats are limited, and most reported cases involved were middle-aged cats. In one report, all nine cats were older than 5 yr, with a median age of 9 yr.⁷ In another report, two cats were 9 and 13 yr old.⁸ Recently, a 2 yr old Scottish Fold cat was reported as the only case of onset at a young age, and the possibility of vertebral canal stenosis caused by osteochondrodysplasia was suggested.⁹ Surgical treatments for thoracic vertebral canal stenosis in cats include hemilaminectomy or dorsal laminectomy.^7–9

In dogs, reports have described thoracic vertebral canal stenosis and vertebral instability secondary to congenital vertebral anomalies.^10,11 Vertebral instability can cause acute or repetitive spinal cord injury owing to dynamic compression. In cats, vertebral instability caused by traumatic vertebral fracture or luxation has been reported.^12,13 On the other hand, a case report on cauda equina syndrome in a cat was the only one describing vertebral instability induced by a cause other than trauma.¹⁴ Vertebral stabilization using pins or screws with polymethylmethacrylate (PMMA) has been reported as a surgical treatment for trauma-induced thoracolumbar vertebral instability.¹³ To the best of our knowledge, the diagnosis and surgical treatment of thoracic vertebral canal stenosis and vertebral instability in cats have not been reported before.

The purpose of this report is to describe the successful surgical management of thoracic vertebral canal stenosis and vertebral instability in a young Minuet cat.

Case Report

An 11 mo old neutered female Minuet cat weighing 1.8 kg was presented with a 3 wk history of insidious onset of pelvic limb ambulatory paraparesis. There was no history of previous trauma. On neurological examination, the cat displayed mild paraparesis and proprioceptive ataxia affecting the pelvic limbs, with normal voluntary use of thoracic limbs. Hopping responses were delayed in the pelvic limbs. Spinal reflexes were normal, and mild discomfort was elicited on palpation of the tail. The neuroanatomical localization was a focal or diffuse spinal cord lesion between the T3 and L3 segments. Radiographs of cervical (C), thoracic (T), and lumbosacral vertebral column revealed mild spondylosis deformans of C2–T2 and subluxations of an articulation between sacral vertebrae and caudal (Cd) vertebrae as well as a Cd1–Cd2 articulation (Figure 1). The owner declined further evaluation at that time.

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Two months later, the cat was presented with a 2 day history of nonambulatory paraparesis, with no evidence of trauma. On neurological examination, hopping responses remained delayed in the pelvic limbs and spinal reflexes also remained normal. Moderate discomfort was elicited on palpation of the cranial thoracic vertebral column. The function of cranial nerves and thoracic limbs, including postural reactions and spinal reflexes, were all normal. The neuroanatomical localization was a focal or diffuse spinal cord lesion between the T3 and L3 segments. Radiographs of the vertebral column revealed marked spondylosis deformans of C1–T6 and sacral–Cd4 (Figure 1). Serum biochemistry detected a mildly elevated total protein (9.0 g/L, reference interval: 5.7–7.8) and globulin fraction of serum protein (5.9 g/L, reference interval: 3.4–4.3). Hematology was unremarkable. Serological test results for feline immunodeficiency virus and feline leukemia virus were negative. Total nucleated cell count and total protein concentration of cerebrospinal fluid analysis collected at the cerebellomedullary cistern were normal (total cell count 0/μL, reference: <3; total protein 4 mg/dL, reference: <20).

MRI^a of the brain and whole spinal cord was performed first. On another day, myelography with dynamic views, computed tomography (CT), and CT/myelography without dynamic views were performed. Precontrast T1-weighted (T1W) and T2-weighted MR pulse sequences and postcontrast T1W sequences after 0.1 mmol/kg IV gadobutrol^b administration were acquired. The spinal cord at the level of T2–4 was compressed from the ventral side on T2-weighted images (Figure 2). There were marked contrast enhancements of the ventral portion of the vertebral canal at the level of T1–3, the T2–3 intervertebral disk, and the ventral surface of the T1–5 vertebral body on T1W images with contrast. The MRI findings suggested hypertrophy and changes related with inflammation in the dorsal longitudinal ligament, intervertebral disk, and paravertebral soft tissues. The hypertrophied ligament, occupying the extradural space, was one of the lesions compressing the spinal cord. CT was performed using a 16-slice helical scanner^c (CT settings: 120kVp, 120mA, and slice thickness 0.625 mm). Myelography was performed using a subarachnoid injection of iohexol^d at L5–6 with the aid of fluoroscopy. Dynamic spinal cord compression was assessed by applying manual extension and flexion to the vertebral column in lateral recumbency.¹⁵ CT/myelography revealed the ventral and bilateral spinal cord compression at the level of T1–4. There were multiple sites of vertebral endplate osteolysis, adjacent bone sclerosis, intervertebral disk space narrowing, and spondylotic bridging (or bone formation) within the cervical and cranial thoracic vertebral bodies and pedicles, especially at the level of C6–T4. The dynamic myelogram revealed that spinal cord compression at the level of T1–4 in the neutral position worsened in the extension position and improved in the flexion position (Figure 3). This dynamic compression indicates the need for vertebral stabilization at this level. Based on the history, neurological examination, cerebrospinal fluid analysis, and imaging findings, tentative diagnoses of vertebral canal stenosis and vertebral instability at the level of T1–4 were made. This was consistent with the neuroanatomical localization of spinal cord lesion between the T3 and L3 segments.

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The anesthetic protocol consisted of premedication with atropine^e and morphine^f intramuscularly, followed by IV induction with propofol^g and maintenance on inhalation with isoflurane^h. Cefazolinⁱ was administered IV 30 min before surgery.

The cat was positioned in sternal recumbency with a towel under the sternum to induce flexion of the cranial thoracic vertebrae. The cat underwent a right-sided T1–4 hemilaminectomy and vertebral stabilization using 6 positively threaded profile pins^j and PMMA.^k The pins, 1.1 mm in diameter, were inserted, avoiding the exposed spinal cord, with two in the T1 vertebral body, one each in T2 and T3, and two in T4 (Figure 4).

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Postoperative radiography and CT revealed that the most cranial pin inserted into the vertebral body of C7 via the pedicle of T1 resulting in vertebral stabilization of C7–T4. The positioning of the other implants was satisfactory. Postoperative pain management was achieved through a continuous fentanyl^l infusion at a rate of 3 μg/kg/hr IV for 48 hr. After this period, no medication was administered. A follow-up evaluation 2 wk postoperatively confirmed that the cat was ambulatory with improved paraparesis. Three months postoperatively, the owners reported that the cat had completely returned to normal. Neurological examination failed to reveal any abnormalities. In a telephone conversation with the owner 12 mo after surgery, the cat was reported to be neurologically normal.

Informed consent was obtained from the pet owner involved in this report. Additionally, the cat described in this report was clinically treated according to contemporary standards of care.

Discussion

The cat in this case is, to our knowledge, the youngest reported instance of feline thoracic vertebral canal stenosis. All previously reported cats were middle-aged or older, with the exception of a 2 yr old Scottish Fold cat.^7–9,16 In those reports, vertebral canal stenosis was secondary to a combination of intervertebral disk protrusion and hypertrophy of the dorsal lamina and ligamentum flavum (n = 4) or articular processes (n = 2), or secondary to hypertrophy of the dorsal lamina and ligamentum flavum (n = 2), articular process (n = 2), facet joints with diffuse idiopathic skeletal hyperostosis (n = 1), vertebral body and pedicle (n = 1 [2 yr old Scottish Fold cat]), or unknown (n = 1). The most common sites in those reports of stenosis were T3–4 (38%; n = 5/13) and T11–12 (30%; n = 4/13). The affected sites in the cat reported herein were T1–4; thus, thoracic vertebral canal stenosis in cats may be more likely to develop around T3–4 or T11–12 and rarely at a young age.

Minuet cats are a breed derived from the combination of Persian and munchkin cats, the latter of which exhibit an autosomal dominant mode of inheritance for a chondrodysplastic condition similar to osteochondrodysplasia in Scottish Fold cats. This condition leads to progressive skeletal deformations at the distal limbs, tail, and vertebrae.^1,3–5 Both a 2 yr old Scottish Fold cat in the previous report and a 1 yr old Minuet cat in the present report developed hypertrophy and/or bone formation of the vertebral bodies and pedicles at a young age that could potentially be linked to these similar conditions. This might contribute to unremarkable vertebral malformation, degeneration of vertebral disks, vertebral instability, and bone formation of vertebrae resulting in thoracic vertebral canal stenosis. However, this case report did not perform genetic analysis and histopathological examination of the tissue causing stenosis.

This cat had two atypical imaging findings for thoracic vertebral canal stenosis on MRI and CT. First, MRI revealed contrast enhancements in the hypertrophied dorsal longitudinal ligament, intervertebral disk, and proliferated paravertebral soft tissues. Contrast enhancement in the paravertebral musculature on MRI has been reported in a cat with cranial thoracic vertebral canal stenosis.¹⁷ In that report, the histopathologic features of the tissue removed during the decompressive dorsal laminectomy were most consistent with a degenerative process, characterized by the proliferation of connective tissue, reflecting chronic instability. They might reflect a proliferative and inflammatory response caused by chronic instability. Additionally, this inflammatory response might indicate that the area is in an active phase, meaning that the vertebral column is in the process of regaining stability in response to instability. The second atypical finding was vertebral endplate osteolysis on CT. Generally, this CT finding suggests discospondylitis, but considering the clinical course, this seems unlikely. A previous report mentioned that munchkin cats could have impaired chondrogenesis, suggesting that the endplate osteolysis might be related to a chondrodysplastic condition.^1,5 Alternatively, it might be related to the aforementioned inflammatory response caused by chronic instability. However, the exact etiology remains unclear.

There are no clear criteria for the application of vertebral stabilization in cats, and its necessity must be assessed individually. In this case, multiple imaging findings indicated vertebral instability, leading to the decision of vertebral stabilization. The narrowing of the intervertebral disk space and sclerosis of the endplates are associated with vertebral instability caused by a slowly degenerating disk.¹⁸ Spondylosis deformans can indicate chronic vertebral instability and serve as a compensatory mechanism.¹⁹ Dynamic compression diagnosed with a dynamic myelogram indicates the need for vertebral stabilization.^10,15 Furthermore, as mentioned earlier, in this case, the proliferation and contrast enhancements of paravertebral tissues might suggest ongoing instability. However, the sites of these imaging findings on radiography, CT, and MRI did not completely align with those of dynamic compression on the dynamic myelogram. Consistent with the previous report in dogs, a dynamic myelogram in cats was effective in determining where to stabilize.¹⁰

The optimal safe implantation corridors in feline thoracolumbar vertebrae (T10–L7) have been reported, but those in C7–T4, where this cat underwent vertebral stabilization, have not.²⁰ When implants are placed in the vertebral body, the risk of iatrogenic injury to the spinal nerve root, descending aorta, caudal vena cava, pleura, lungs, intercostal arteries, sympathetic trunk, and thoracic duct must be considered.¹³ In this cat, the descending aorta and caudal vena cava were at low risk, but the trachea was at high risk. Postoperative radiography and CT were useful for confirming implant positioning, and this cat fully recovered without any complications.

Conclusion

To our knowledge, this report describes the first case of feline thoracic vertebral canal stenosis and vertebral instability. Hemilaminectomy and vertebral stabilization, using positively threaded profile pins and PMMA, allowed an excellent clinical outcome in this cat. Although the etiology remains unclear, we should be aware of the development of these disorders in young cats, especially those with a chondrodysplastic condition.

We would like to thank Dr. Daisuke Hasegawa at Nippon Veterinary and Life Science University for his support in interpreting MRI. The authors declare no conflicts of interest related to this report.