by Dr. Jonathan Huska
A 6 month old, intact female Yorkshire Terrier was referred to the Toronto Veterinary Referral Hospital (TVRH) Neurology Service with an approximately 10 day history of cervical spinal pain. Clinical signs were initially reported as yelping in pain while holding the head low with a guarded neck carriage. There was no history of previous pain or neurological deficits. No obvious trauma had been observed, however the patient resided with 6 other dogs, one of which was a large breed dog.
Their referring veterinarian had seen the dog approximately 5 days after the onset of clinical signs. Examination at that time was reported as unremarkable. A complete blood cell count, serum biochemistry, and serum bile acids were also unremarkable. Orthogonal view radiographs of the cervical spine had been performed (see Figure 1).
Figure 1. Lateral cervical radiographs obtained approximately 5 days after onset of cervical spinal pain.
The patient was treated with gabapentin and meloxicam. Episodes of pain continued to occur, prompting referral to TVRH.
On presentation to the TVRH Neurology Service, low guarded head carriage was noted and pain was easily elicited with gentle palpation of the cervical spine. The patient was ambulatory with mild tetraparesis, worse on the left side. Postural reactions were mildly delayed in the left thoracic limb and left pelvic limb, and normal in the right thoracic and right pelvic limb. Physical and neurological examinations were otherwise unremarkable.
What is the lesion localization?
What is your diagnosis?
Based on the findings of tetraparesis and cervical spinal pain, a cervical myelopathy was suspected. Lesion localization was the C1-T2 spinal cord segments, with the C1-C5 segments more likely than the C6-T2 segments due to normal spinal reflexes (i.e. withdrawal reflex). The lesion was likely worse on the left side compared to the right side due to the postural deficits being unilateral. Referral radiographs demonstrated an increased space between the dorsal lamina of the atlas and the dorsal spinous process of the axis (see Figure 2), indicative of atlantoaxial (AA) instability and subluxation.
Figure 2. Lateral cervical radiographs demonstrating the increased space between the axis and atlas (line).
Subluxation of the axis relative to the atlas can occur due to trauma, but is most commonly due to congenital instability, which is often precipitated by a traumatic event. Congenital malformations leading to instability are most frequent in toy breed dogs, often leading to clinical signs at a young age, though dogs can become affected at any age. The atlas and axis are bound together by multiple ligaments, which allow unique pivoting motion in a longitudinal plane. The apical ligament of the dens and the transverse ligament of the atlas bind the dens to the atlas. The dorsal atlantoaxial ligament attaches the dorsal spinous process of the axis to the dorsal lamina of the atlas. Severe trauma can lead to rupture of the ligaments causing AA subluxation. Congenital malformations such as aplasia of the dens, hypoplasia of the dens, dorsal angulation of the dens, and absence of the transverse ligament can lead to AA instability and resulting AA subluxation.
Clinical signs that occur with AA subluxation are due to over flexion of the AA joint leading to concussive and compressive spinal cord trauma. Particularly, dorsal movement of the dens into the spinal canal can cause significant compression of the cervical spinal cord. Clinical signs can range from neck pain, to a mild cervical myelopathy (ambulatory with ataxia and paresis), severe myelopathy (non-ambulatory tetraparesis or tetraplegia), to death from acute respiratory paralysis.
Diagnosis can often be made with cervical radiographs performed in a neutral position, which reveal an increased space between the dorsal lamina of the atlas and dorsal spinous process of the axis (see Figure 2), dorsal displacement of the axis into the vertebral canal, and/or congenital malformations of the dens. Flexed radiographs of the cervical spine are not recommended and are absolutely contraindicated. While flexed radiographs may further emphasize instability, this can lead to acute and dramatic worsening of clinical signs. Advanced imaging (CT, MRI), has largely replaced the need for flexed view studies and is often utilized to provide further information about the congenital anomalies present and to facilitate surgical planning. Myelography has also largely been replaced by MRI and CT, due to the potential adverse effects associated with contrast administration in these patients.
In this patient the radiographs were indicative of AA subluxation; CT was performed to further evaluate the AA, and confirmed subluxation of the AA, with dorsal angulation of the dens into the spinal canal and fracture of the dens (see Figure 3). Fracture of the dens in this patient was considered consistent with congenital malformation, as the dens forms from separate cranial and caudal ossification centres, and incomplete ossification has been observed in dogs.
Figure 3. Sagittal CT 3D reconstruction demonstrating AA subluxation and fracture of the dens (arrow).
Dogs with AA instability and subluxation can be treated either medically or surgically. Medical management is recommended for dogs with mild signs, and involves placement of a cervical splint for at least 6 weeks. The splint must completely immobilize the AA junction, with the goal to provide a fibrous union at the AA junction. The success rate of medical management varies, with one study citing 10 dogs with a good outcome 1 year following removal of the splint (62.5%); the other 6 dogs failed to improve and were euthanized.
Surgical stabilization is advocated for dogs with severe clinical signs, the goal of treatment being reduction of the subluxation as well as stabilization of the AA junction. Numerous surgical procedures have been described, making direct comparisons of surgical techniques difficult. Success rates range from 85.3% for surgical procedures with a ventral approach to 88.9% for those with a dorsal approach. Postoperative neurological deficits tend to be higher with dorsal approaches (55.5%) than ventral approaches (29.1%). Surgical stabilization can be complicated in many patients by greater anaesthetic risks, immature bone, small physical size, and the small corridor for implant placement. Other factors found to negatively affect prognosis in dogs with AA luxation regardless of treatment technique were chronicity of clinical signs, older age at onset of clinical signs, and potentially more severe clinical signs at time of treatment.
Our patient was treated surgically using a dorsal technique with non-absorbable sutures described by Sanchez-Main et al. The technique places a double strand of non-absorbable suture between the muscles of the atlantooccipital and atlantoaxial joints to provide reduction and stabilization. By not requiring osseous implants, the surgical risks are greatly reduced. The dog was pain-free immediately post-operative and was discharged with improvement in neurological signs. At follow-up examination (6 weeks post-surgery) she remains pain-free with a normal neurological examination.
Beaver, et al. Risk factors affecting the outcome of surgery for atlantoaxial subluxation in dogs: 46 cases (1978-1998). J Am Vet Med Assoc. 200;216(7):1104-9.
Parry, et al. Computed tomography variation in morphology of the canine atlas in dogs with and without atlantoaxial subluxation. Vet Radiol Ultrasound. 2010;51(6):596-600.
Sanchez-Masian, et al. Dorsal stabilization of atlantoaxial subluxation using non-absorbable sutures in toy breed dogs. Vet Comp Orthop Traumatol. 2014;27(1):62-7.
Slanina. Atlantoaxial instability. Vet Clin North Am Small Anim Pract. 2016;46(2):265-75.
Stigen, et al. Acute non-ambulatory tetraparesis with absence of the dens in two large breed dogs: case reports with a radiographic study of relatives. Acta Vet Scand. 2013;17(55):31.
Watson, de Lahunta. Atlantoaxial subluxation and absence of transverse ligament of the atlas in a dog. J Am Vet Assoc. 1989;195(2):235-7.
Dr. Huska graduated from the Ontario Veterinary College (OVC) with his Doctor of Veterinary Medicine (DVM) in 2008. He completed a rotating internship in small animal medicine and surgery the following year at the Atlantic Veterinary College (AVC) before returning to the OVC to complete a residency in Neurology. Obtaining both a Doctor of Veterinary Science (DVSc) and board-certification in neurology (Diplomate of the American Veterinary College of Internal Medicine-Neurology), he then went on to start the Neurology Service at the Toronto Veterinary Emergency Hospital (TVEH) in 2012. After establishing the service at TVEH, Dr. Huska worked as the head of the Neurology Service at the Alta Vista Animal Hospital (AVAH) in Ottawa, before returning in 2017 to continue the growth of the TVEH Neurology Service. While he enjoys all aspects of small animal clinical neurology, Dr. Huska has a special interest in diseases of the muscle (myopathies), epilepsy, and cerebellar disorders. Personally, he enjoys being active outdoors with hiking, snow shoeing, camping, fishing, and ultimate frisbee (‘ultimate’ makes it sound more cool). He is an avid rugby fan, but most of all enjoys quality time spent with family. Currently he is the adoptive parent to two handsome cats, and a dog who has undergone multiple successful spinal surgeries.