Neurology Case Study
By: Joseph Eagleson, DVM, DACVIM(Neurology)
Board-Certified Neurologist & Neurosurgeon
“Linus,” a 7-year-old, 3.5 kg, male neutered, terrier mix, was presented to the VSEC Neurology service for a chronic progressive upper motor neuron (UMN) tetraparesis and general proprioceptive ataxia. Since adoption 6 years ago, the owner always noted an abnormal gait.
Three months prior to presentation to VSEC, Linus had an acute decline in his function and developed neck pain. Linus was seen at another specialty hospital and was diagnosed with an atlantoaxial (AA) subluxation via sedated radiographs (see Figure 1).
Figure 1
This is a pre-operative lateral cervical spine radiograph. The arrow is pointing to increased distance between the spinous process of the axis and the dorsal arch of the atlas. The asterisk is over the cranial body of C2. Note the dorsal displacement of the body of the axis into the vertebral canal as well as the absence of the dens.
Linus was treated with corticosteroids, tramadol, and rest. Linus improved from this acute decline; however, he was gradually getting worse over the last two months prior to presentation to VSEC.
On neurological examination, the mentation was normal. Linus was ambulatory with a UMN tetraparesis and general proprioceptive ataxia. Postural reactions were delayed in all four limbs, with the right side being worse. Myotatic and withdrawal reflexes were normal in all four limbs. The cutaneous trunci reflex was normal. Muscular tone was normal to increased in all four limbs. There was no evidence of discomfort. Neuroanatomical diagnosis was consistent with a first through fifth cervical vertebrae (C1 through C5) spinal cord lesion. Given the findings of the previous radiographs, AA subluxation was still thought to be the cause of Linus’ clinical signs. However, due to the chronicity of the problem it was decided that MRI should be pursued to determine the integrity of the spinal cord as well as rule out any other comorbidities (e.g. Chiari-like malformation) that could be contributing to the clinical signs.
Magnetic resonance imaging was performed which confirmed an AA luxation. The dens was absent and there was a T2 weighted intramedullary hyperintensity within the spinal cord at the level of the AA articulation consistent with edema or gliosis (scarring). Linus recovered from anesthesia uneventfully. Surgical stabilization was recommended which was performed ten days later without complication (see Figure 2).
Figure 2
This is a post-operative lateral cervical spine radiograph. A ventral fixation was performed using trans-articular pins as well as screws and methyl methacrylate. The dorsal displacement of C2 is no longer present and C1 and C2 are in proper alignment.
Atlantoaxial subluxation is encountered most often in young small-breed dogs, particularly Yorkshire terriers, Chihuahuas, and miniature poodles; however, any breed can be affected. A systematic review of 336 published cases found the mean age of onset to be 21.3 months. The majority of cases present before a year of age. The clinical presentation may be acute or chronic, with clinical signs ranging from mild cervical pain or tetraparesis to tetraplegia, respiratory compromise, and death. Atlantoaxial subluxation results in caudal and dorsal displacement of the axis in relation to the atlas and flexion of the AA joint, which may cause compression and concussion of the spinal cord. The typical cause of AA subluxation is loss of the ligamentous intervertebral support, which often coincides with a congenital malformation of the dens. Trauma to the cranial cervical vertebral column may also result in AA subluxation secondary to fracture of the dens or ligamentous rupture. Atlantoaxial subluxation is often diagnosed radiographically. The typical radiographic features include: increased distance between the spinous process of the axis and the dorsal arch of the atlas; dorsal displacement of the body of the axis into the vertebral canal; and absence, agenesis, or dorsal deviation of the dens. When not obvious, flexion of the neck will often make the subluxation more apparent; however, flexion can lead to further spinal cord injury. Computed tomography (CT) or CT combined with myelography can be used to identify spinal cord compression and provide accurate evaluation of the dens. Magnetic resonance imaging (MRI) can be used to evaluate the vertebrae and to identify spinal cord compression. Magnetic resonance imaging is particularly sensitive for the identification of intraaxial spinal cord abnormalities.
Treatment of AA subluxation consists of either conservative management or surgical stabilization. Although numerous risk factors affecting the prognosis of AA subluxation have been assessed, only age at onset and duration of clinical signs have been associated with prognosis. Specifically, affected dogs <2 years of age and with a duration of clinical signs <10 months were associated with a positive outcome following surgical stabilization. Similarly, when treated conservatively, affected dogs with a duration of clinical signs <30 days were significantly more likely to have a positive outcome.
Linus’ situation was unique in that he was older than average at the time of presentation and he had been displaying clinical signs consistent with a C1-C5 myelopathy for years. Both of these factors are not associated with a positive outcome whether the treatment is surgical or conservative. However, Linus was continuing to decline in the face of conservative management. Therefore, it was recommended that surgery be pursued with the goal of preventing further decline in function. Anytime there is evidence of a chronic spinal cord injury, as in the case of Linus, the prognosis for improving function is guarded. Typically, there has already been irreversible damage to spinal cord at the time of treatment. So the primary goal of surgery is to stop progression. It’s still possible that function can improve, but an owner should not make the decision to pursue surgery with that expectation. Linus is currently 3 weeks post-surgery and he is slightly improved from his pre-operative status. Although he’s a bit wobbly on his feet, he is pain free, walking, and off of all medications.
Dr. Joseph Eagleson, is a Board-Certified Neurologist & Neurosurgeon at the Veterinary Specialty & Emergency Center. The Veterinary Specialty & Emergency Center operates state-of-the-art emergency and specialty veterinary hospitals that are open 24/7/365 in both Levittown PA and Philadelphia PA. For more information about our world-class emergency and specialty care, please visit VSEC on the web at www.VSECVET.com.
References:
- N. Plessas, H.A. Volk. Signalment, clinical signs and treatment of altantoaxial subluxation in dogs: a systematic review of 336 published cases from 1967 to 2013. J Vet Intern Med, 28 (2014), pp. 944–975
2. Kent, J.S. Eagleson, D. Neravanda, et al .Intraaxial spinal cord hemorrhage secondary to atlantoaxial subluxation in a dog. J Am Anim Hosp Assoc, 46 (2010), pp. 132–137