Introduction

Spinal malformations previously reported in the literature in dogs and cats include neural tube defects, vertebral column malformations, vascular malformations, and arachnoid diverticula; however, most reports of spinal malformations are in dogs with only a few reports in cats.^1–8

Previous reports of cervical vertebral malformations in cats are even less numerous and have been limited to transitional C7 vertebra and severe hypoplasia of the occipital condyles, hypoplasia of the dens, and atlantoaxial instability and subluxation^.2,4 Incomplete ossification of cervical vertebrae has only previously been reported in dogs.^9–12

This case report describes the presentation, imaging findings, treatment, and outcome of a case of nonambulatory tetraparesis in a cat suspected to be caused by dynamic spinal cord compression secondary to multiple cervical vertebral malformations including incomplete ossification of cervical vertebrae. To the authors’ knowledge, this is the first report of a case of incomplete ossification of cervical vertebrae in a feline patient in the English-language, peer-reviewed literature.

Case Report

A 21 wk old, 2 kg neutered male domestic shorthair was referred with a 24 hr history of acute-onset severe nonambulatory tetraparesis with no known inciting cause. The patient had regular outdoor access during daylight hours and had remained confined indoors since normal ambulation was last observed by the owner 3 hr previously. The owner found the patient in lateral recumbency in his bed reportedly unable to move any limbs. The owner and primary veterinarian reported no previous abnormalities in ambulatory, respiratory, or urinary function.

Investigations by the primary veterinarian prior to referral included blood sampling for hematology, biochemistry, and electrolytes as well as conscious lateral, dorsoventral thoracic, and abdominal radiography. Creatine kinase (CK) was not included in the biochemistry panel. Significant findings included increased alanine aminotransferase (ALT; reference 12–115, >1000 U/L on day 1, 902 U/L on day 2) on biochemistry and transitional L7 vertebra on radiography. Treatment by the regular veterinarian included IV fluid therapy with 0.9% sodium chloride^a (2–4 mL/kg/hr), buprenorphine^b (0.02 mg/kg IV q 8 hr), ranitidine^c (1 mg/kg IV q 12 hr), and clavulanate-potentiated amoxicillin^d (8.75 mg/kg subcutaneously once).

On presentation, the patient was laterally recumbent but demonstrated appropriate mentation and responsiveness. The patient was tachypneic (44–52 breaths per min) without dyspnea and thoracic auscultation was within normal limits. Neurologic examination revealed nonambulatory tetraparesis with intermittent extensor rigidity of all four limbs. Assessment of postural reactions revealed absent paw placement and hopping in the right thoracic and pelvic limbs and markedly reduced paw placement and hopping in the left thoracic and pelvic limbs. Spinal reflexes were normal in all four limbs. There was no evidence of spinal pain. Nociception was normal in all four limbs. Cranial nerve examination revealed no abnormalities. Neurolocalization was to the C1–C5 spinal cord segments. Abdominal palpation revealed a soft, medium-sized bladder from which grossly normal urine could be expressed with firm digital pressure. There was no external evidence of traumatic injury. Remaining clinical examination was unremarkable.

In view of the C1–C5 myelopathy, cervical manipulation and jugular venepuncture were avoided and only peripheral venepuncture was performed. Measurement of packed cell volume, total solids, analysis of venous blood gas, and electrolytes during triage was unremarkable.

Computed tomography (CT) of the spine was performed^e under sedation without contrast and revealed multiple abnormalities of the C2 and C3 vertebrae (Figures 1, 2). The C2 vertebra appeared transitional with elongated, flattened transverse processes, and a more circular vertebral body reminiscent of C1. A hypoattenuating gap was present in C2 between the body and left neural arch with a position that would normally be consistent with the suture line normally seen between the left neural arch and the centrum/intercentrum complex and was therefore considered to be incompletely ossified. The dorsal arches of C2 were also not fused together, remaining separated by a sagittal plane cleft. The dens was present on the cranial aspect of the C2 vertebral body and articulated with C1 but appeared thickened and elongated compared with normal. The spinous process of C3 was bifid with the two sides of the spinous process not fused dorsally and remained separated from the pedicles of the neural arch by two further asymmetric hypoattenuating gaps. The pedicles and neural arch of C3 were hypertrophied compared with normal. Secondary to these malformations, there was vertebral canal stenosis from C2 to C3. Thoracic CT was also acquired which demonstrated a 20 mm diameter bulla in the dorsal right caudal lung lobe, an 11 mm diameter bulla in the ventral right cranial lung lobe, a 2 mm bulla in the dorsal left cranial lobe, and a 4 mm soft tissue nodule in the ventral left cranial lung lobe. The cervical epaxial and hypaxial muscles and liver parenchyma visible in the cranial abdomen were unremarkable.

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MRI was recommended to further assess the spinal cord but was declined by the client in favor of conservative management. Contrast CT was considered to further assess the epaxial musculature for evidence of external trauma but was not performed as the vertebral abnormalities identified could explain clinical signs.

Medical therapy initiated by the primary veterinarian was discontinued as the patient was not considered to be in pain and there was no indication of an infectious process or gastrointestinal pathology. Intravenous fluid therapy was discontinued shortly after presentation as the patient was eating and drinking readily when offered. The patient remained hospitalized for 3 days under close observation, particularly for neurological deterioration, dyspnea, and urinary dysfunction. Food and water were offered and recumbency was alternated every 3 hr during the first 24 hr of hospitalization while the patient was unable to autonomously adjust body position. Bladder size and tone were assessed through digital palpation, and the bladder was expressed when it was palpably firm. On day 2 of hospitalization (4 days following the onset of clinical signs), the patient was able to shuffle around the kennel and voluntarily urinate in a low-profile litter tray. The bladder was palpably soft and small following these episodes of urination.

Five days following the onset of clinical signs, the patient was weakly ambulatory, exhibiting moderate tetraparesis and ataxia in all four limbs, with only intermittent support required to stand and walk. At this time, postural reactions were mild-to-moderately delayed (similarly on the left and right), spinal reflexes were normal in all four limbs, and muscle tone was normal in all four limbs. Gentle palpation of the neck revealed no evidence of spinal pain, although a full assessment was not performed given the findings on CT. Neck range of motion was considered normal based on visualization of patient physical activity; however, digital manipulation of the neck was not performed given the findings on CT. Voluntary urination had been observed multiple times during hospitalization without evidence of urinary incontinence. Repeat hematology and biochemistry at this time revealed reduced ALT 319 U/L (reference 15–45) and was otherwise unremarkable. CK and electrolytes were not included in the biochemistry panel. Mild tachypnea persisted throughout hospitalization.

The patient was discharged 5 days following the onset of clinical signs with instructions to restrict exercise through crate confinement for 4 wk with short periods of closely supervised, controlled walking outside the crate permitted three times daily as physiotherapy and to ensure that voluntary urination occurred at least once daily.

The owner reported gradual improvement in neurologic function over the 4 wk following discharge. At this time, the owner reported that the cat was strongly ambulatory without assistance with no evidence of ataxia or tetraparesis, other than reluctance to jump, and that daily voluntary urination had been observed.

Discussion

This report describes a case of C2 and C3 vertebral malformations in a cat who had not been previously described and may have resulted in signs of a cervical myelopathy. A possible cause of the neurologic signs in this patient is traumatic spinal cord injury, which could be a result of a dynamic compression secondary to the vertebral malformation and vertebral canal stenosis. The neurologic signs could also be attributable to an acute noncompressive nucleus pulposus extrusion or vascular injury, neither of which could be excluded in this case without the use of MRI. Although CT is a useful imaging modality for assessing vertebral pathology, MRI is superior for assessing the spinal cord. Several types of spinal cord lesion are identifiable using MRI including intramedullary hemorrhage, spinal cord contusion/edema, extrinsic compression by a bone fragment, or a traumatic disc herniation or infarction, and so MRI would have helped confirm the location of the suspected spinal cord lesion and whether it corresponded with the vertebral malformations identified on CT.^13,14

Dynamic spinal cord compression is a relatively common cause of tetra- or paraparesis in dogs but is encountered rarely in cats.^9,15–20 Narrowing of the vertebral canal lowers the threshold, at which the cumulative effects of various structures encroaching on the spinal cord cause signs of myelopathy, meaning that usually innocuous activities may result in spinal cord compression and secondary neurologic clinical signs.²¹ Vertebral canal stenosis has been shown to be an important factor for the development of cervical spondylotic myelopathy in humans.²² Although not confirmed in this case, the sudden onset of clinical signs without a history of known trauma may suggest a dynamic compression of the spinal cord in the presence of vertebral canal stenosis as a likely etiology. It remains possible that the patient suffered a traumatic injury that was undetected by the owner and led to the onset of neurologic signs.

Conservative management of spinal cord injury has been described with a less predictable outcome than surgical management; however, successful outcomes have been reported in both surgically and conservatively managed canine cases of incomplete ossification of cervical vertebrae.^10,23,24 Surgical techniques described to manage cases of feline spinal malformation and trauma including decompressive (laminectomy, hemilaminectomy, and durotomy to treat compressive congenital, neoplastic, traumatic, or degenerative lesions) and stabilization (internal fixation with translaminar or spinal staples, tension bands, plates, screws and polymethyl methacrylate) techniques.^5,23,25–27 A combination of these techniques could have been considered if surgical stabilization of the spine was pursued. Further assessment of the spinal cord injury with MRI before considering treatment options was recommended but declined in favor of conservative management.

Lung bullae identified on CT may be primary (idiopathic) or secondary to inflammation, emphysema, or trauma.²⁸ Bronchopulmonary dysplasia has been previously reported as a cause of lung bullae in a 3 yr old cat and may have been the cause in this case.²⁹ Congenital pulmonary airway malformation (CPAM), also known as congenital cystic adenomatoid malformation of lung, is a rare human condition that is usually identified in utero or shortly after birth. CPAM describes congenital cystic lung lesions that arise from excessive proliferation of tubular bronchial structures, alongside which, concurrent anatomical abnormalities including cervical spinal malformations have been reported.^30–33 A condition resembling CPAM has been reported in a dog but with no reported spinal malformation.³⁴ It is possible that the present case represents a manifestation of CPAM; however, lung histopathology would be required to confirm this. Further research in this area would be useful but is limited by the low disease prevalence.

Increased ALT in this patient may have reflected an acute hepatic or muscular injury. There was no known trauma in this case, but a traumatic event possibly occurred without the owner’s knowledge. Measurement of serum CK may have helped to differentiate between a hepatic or muscular source. Repeat serum biochemistry 4 wk following discharge was recommended but not pursued for financial reasons. In addition to this, MRI would have been useful to further assess the spinal cord and confirm neurolocalization. Contrast CT would have been useful to assess the epaxial musculature for evidence of external trauma and improve sensitivity of thoracic CT.

Outcome in the present case after 4 wk of crate confinement following discharge was favorable; however, should the vertebral malformations be the cause of clinical signs, then relapse will remain possible without surgical treatment. The cervical vertebral abnormalities outlined in this report should be considered as an unusual differential for acute-onset tetraparesis in cats that localize to the cervical spine. Further research investigating CPAM-like conditions in companion animals is warranted.

Conclusion

To the authors’ knowledge, this is the first report of incomplete ossification of cervical vertebrae in a feline patient. Although not confirmed with MRI, the cervical skeletal abnormalities identified in this case may have contributed to dynamic spinal cord compression and the presenting neurological signs.