Peracute Tetraparesis in a Boston Terrier

History

A 5.5-year-old castrated Boston terrier was presented with a peracute history of tetraparesis. About 2 hours before presentation, the dog had jumped off a bed and fallen to one side. According to the owners, their dog had difficulty getting up, especially when using his left limbs, but had not cried out or appeared to be in pain.

The dog had a medical history of osteoarthritis, and dental extractions had been performed within the past year. The only medications on record were a daily glucosamine–chondroitin supplement and monthly heartworm and flea preventatives. The dog’s vaccinations were up-to-date.

Physical Examination

Mild dental calculus and gingivitis and a few missing teeth were noted. The rest of the examination was unremarkable.

Neurologic Examination

• Mentation: Alert and appropriate

• Posture: Knuckled in the left thoracic limb (with the dorsal aspect of the paw on the ground), with the left thoracic limb being held more laterally when standing; slow to rise to a standing position

• Gait: Barely ambulatory tetraparesis, much more severe on the left (especially the left thoracic limb) and mild proprioceptive ataxia with a tendency to fall toward the left

• Postural reactions: Absent placing and hopping in the left thoracic limb; decreased placing responses in the pelvic limbs; normal in the right thoracic limb

• Cranial nerves: All intact and unremarkable

• Spinal reflexes: Absent withdrawal and myotatic reflexes in the left thoracic limb; increased withdrawal (with crossed extensor) and increased myotatic reflexes (clonic patellar reflex) and Babinski reflex present in the left pelvic limb; normal withdrawal and myotatic reflexes in the right thoracic and pelvic limbs

• Spinal pain: No pain apparent on palpation of the calvarium, neck, or remainder of the spinal column

Where would you localize the lesion?

Lesion localization: C6-T2 left lateralized spinal cord segments

Differential Diagnoses (acute nonpainful C6-T2 spinal cord lesion)

• Fibrocartilaginous embolism (FCE), also known as ischemic myelopathy

• Acute noncompressive annulus pulposus extrusion (ANNPE), also known as low-volume high-velocity disk rupture

• Type I intervertebral disk disease (with extrusion)

• Trauma (causing fracture, luxation, or hemorrhage)

• Inflammatory disease

• Neoplasia

Inflammatory disease would fit with the patient’s signalment but is somewhat less likely because of the peracute history. Neoplasia is less likely, given the patient’s age.

Figure 1

Magnetic resonance imaging (MRI) of the cervical spine: T2-weighted transverse image at the level of C6 (A) and T2-weighted midsagittal image (B). Evidence of hyperintensity within the spinal cord parenchyma (arrows) is consistent with a diagnosis of fibrocartilaginous embolism (FCE).

Diagnostics

• Complete blood count (CBC), serum chemistry panel, and urinalysis results were within normal limits.

• Cervical spinal radiography showed no evidence of abnormalities.

• Magnetic resonance imaging (MRI) of the cervical spine (Figure 1) showed a T2-weighted hyperintense slightly wedge-shaped left-sided lesion within the spinal cord, extending from the cranial aspect of C6 to the cranial aspect of C7. The intervertebral disks at C2-3 and C6-7 showed reduced signal intensity on T2-weighted imaging, consistent with dehydration. The most likely cause of the lesions seen was FCE and less likely ANNPE or primary inflammatory disease. 

• Cerebrospinal fluid (CSF) was collected from the cerebellomedullary cistern after the MRI. The cell count was 9 nucleated cells/mm3 and 1 erythrocyte/mm3 (normal, <5 cells/mm3), with protein of 40.5 mg/dL (normal, <25 mg/dL). The sample showed increased cellularity with 48% large mononuclear cells, 41% neutrophils, and 11% small mononuclear cells. This mild mixed pleocytosis was consistent with FCE.

Diagnosis

Fibrocartilaginous embolism (FCE) at C6-7

Outcome

Based on diagnostic findings, the patient remained hospitalized for 2 days of in-hospital physical rehabilitation, including underwater treadmill therapy. The owners were shown how to perform physical therapy exercises at home, including passive range of motion, massage, and standing exercises. Video 2 shows the dog’s progress 2 weeks after the injury occurred. The dog re-presented for outpatient physical therapy twice a week for 7 weeks. At the final evaluation, the neurologic examination was almost normal, with only subtle weakness noted in the left thoracic limb.

Discussion

FCE, also referred to as ischemic myelopathy, is an occlusion of the spinal vasculature by fibrocartilaginous material likely originating from the nucleus pulposus. There are many hypotheses speculating how the disk material enters the spinal vasculature, although the exact cause is unknown. One hypothesis is that a Valsalva-like maneuver predisposes the patient to this condition, such as straining to defecate, one of the most common associations found with FCE in humans.¹

FCE causes a peracute onset of neurologic signs that typically do not progress beyond 24 hours. The clinical signs reflect location of the lesion within the spinal cord and are typically asymmetric. Although reports^2,3 have described this disease as nonpainful, patients may yelp in pain prior to onset of neurologic signs; in some cases, the pain can persist for the first 24 hours following injury. FCE is reported more often in large-breed dogs but has also been described in small-breed dogs, with increased risk for miniature schnauzers.⁴

Definitive diagnosis is achieved with histopathology at necropsy, but antemortem diagnosis is based on a combination of clinical features, diagnostic imaging, and CSF analysis.⁵ Treatment consists of supportive nursing care and physical therapy. Corticosteroid therapy has not proven beneficial and is not recommended, as associated side effects may increase risk for infection, especially in recumbent patients.

Prognosis ultimately depends on the severity and extent of spinal cord injury.  Recovery rates range from 58% to 84%.³ Negative prognostic indicators include severe neurologic deficits (eg, loss of nociception), symmetric neurologic signs, lower motor neuron signs, lack of improvement within the first 14 days after injury, and owner unwillingness to pursue treatment.³

Devon Wallis Hague, DVM, DACVIM (Neurology), is clinical assistant professor at University of Illinois Urbana–Champaign. Dr. Hague completed a rotating medicine and surgery internship at VCA Veterinary Referral and Emergency Center in Norwalk and Shelton, Connecticut, after which she completed a neurology specialty internship at the Center for Veterinary Specialty in Carrollton, Texas. Dr. Hague joined the faculty at Illinois after completing a private practice neurology residency in northern Virginia.