History
A 1-year-old 24.3-kg (53.5-lb) neutered female Golden Retriever was referred for evaluation of generalized proprioceptive ataxia. The neurologic signs were first observed a month earlier, when the owners obtained the dog from a rescue center. The previous history was unknown. No exercise intolerance or signs of pain at rest or after exercise were observed. The owners observed no progression of the clinical signs, and the dog was reported to be otherwise healthy.
At the referral examination, the dog was alert and responsive. Findings on physical examination were unremarkable. No abnormalities were detected on CBC or serum biochemical analysis.
Neurologic examination revealed generalized proprioceptive ataxia, accompanied by mild intermittent scuffing of the left pelvic limb. Intermittent hypermetric steps of the left thoracic limb were observed as well as intermittent knuckling at rest. The postural responses were severely decreased in the left pelvic and thoracic limbs and mildly decreased in the right pelvic and thoracic limbs (ie, no paw positioning deficits, but subjectively mildly delayed hopping reaction). A mildly reduced withdrawal reflex of the left thoracic limb was observed, whereas the rest of the segmental spinal reflexes were within reference limits. The cutaneous trunci reflex was intact. The menace response was also intact, and no abnormalities were detected during cranial nerve examination. Hyperesthesia could not be elicited on gentle palpation of the vertebral column or manipulation of the neck.
The neurologic examination findings were suggestive of myelopathy in the C6-T2 portion of the spinal cord, most likely lateralized to the left. Magnetic resonance imaging of the cervical vertebral column was performed (Figure 1).
Sagittal T2-weighted (A) and T1-weighted (B) MRI images of the cervical vertebrae and transverse T2-weighted images at the level of C4-C5 (C) and C5–C6 (D) of a 1-year-old 24.3-kg (53.5-lb) neutered female Golden Retriever that was referred for evaluation of chronic nonprogressive generalized proprioceptive ataxia.
Citation: Journal of the American Veterinary Medical Association 252, 3; 10.2460/javma.252.3.281
Determine whether additional imaging studies are required, or make your diagnosis from Figure 1—then turn the page →
Diagnostic Imaging Findings and Interpretation
Stenosis of the vertebral canal is seen at C4 through C6, as evidenced by smooth, thick hypointense new bone formation and sclerosis of the dorsal lamina and ligamentous flavum hypertrophy. Severe dorsolateral spinal cord compression is present at C4 through C6, which is most severe at C4 through C5 on the left side. On the T2-weighted images, there is a focal area of intramedullary hyperintensity (compared with that of unaffected gray matter of the spinal cord) at the site of the compression, most likely compatible with gliosis and spinal cord atrophy. On the basis of signalment, clinical signs, and MRI findings, a presumptive diagnosis of vertebral malformations resulting in cervical vertebral canal stenosis and spinal cord compression was made.
Treatment and Outcome
Surgical decompression was performed. Surgery consisted of a continuous dorsal laminectomy at C4 through C6. The dorsal laminae and the amorphous ligamentous flavum were confirmed as the source of the spinal cord compression. No intraoperative complications were recorded, and no postoperative neurologic deterioration was noted. Postoperative care consisted of analgesia (combination of opioids and NSAIDs), exercise restriction for 4 weeks, and physical therapy. Marked improvement was observed at reevaluation 4 weeks after surgery when only mild postural responses deficits were observed on the left thoracic limb. Two months after surgery, the owners reported almost complete resolution of the clinical signs with mild intermittent scuffing of the left pelvic limb. Six months after surgery, the dog was stable and the previously reported scuffing of the left pelvic was observed only after long walks.
Comments
The young female Golden Retriever of the present report had cervical vertebral canal stenosis associated with malformed vertebral lamina and ligamentum flavum hypertrophy. To the authors' knowledge, a similar vertebral arch anomaly has only been described for Basset Hounds.1 The combination of malformed vertebral laminae and ligamentum flavum hypertrophy has also been associated with cervical osseous-associated spondylomyelopathy. However, in the latter case, these anomalies are commonly combined with deformed articular processes.2,3 In the dog of the present report, the articular processes were not malformed and were not involved in the disease process. Cervical spinal cord compression caused by an enlarged ligamentum flavum has been reported in a Rottweiler4; however, vertebral abnormalities were not present in that dog. The underlying cause of this congenital malformation is unknown. Genetic predisposition or mutation has been postulated,1 but it remains unclear. Although clinical signs commonly appear before 2 years of age, they also have been observed in older dogs.1
Same images as in Figure 1. In the T2-weighted and T1-weighted sagittal views (A and B), there is C4–C6 dorsolateral stenosis of the vertebral canal (arrows), most severe at C4 through C5 on the left side. A focal area of spinal cord intramedullary hyperintensity (compared with that of unaffected gray matter of the spinal cord) compatible with gliosis is present at the site of compression. In the transverse T2-weighted views (C and D), there is enlargement and malformation of the dorsal lamina (dl) and ligamentum flavum hypertrophy (arrows), causing dorsolateral spinal cord compression. Notice that the articular processes (ap) have a normal appearance and are not involved in the disease process.
Citation: Journal of the American Veterinary Medical Association 252, 3; 10.2460/javma.252.3.281
Dorsal lamina and spinous process deformity can be recognized on survey radiographs.1 However, MRI, CT myelography, or myelography is necessary to demonstrate spinal cord compression. Computed tomography may be useful in combination with MRI to differentiate whether the compression is the result of malformation of osseous (ie, dorsal lamina) or ligamentous (ie, ligamentum flavum) structures.
Serial MRI in 1 dog1 revealed progressive hypertrophy of the ligamentum flavum that occurred subsequently to the primary bone abnormalities. This suggests that the spinal cord compression is most likely caused by ligamentum flavum hypertrophy rather than vertebral malformation and that related clinical signs are slowly progressive in accordance to the increasing degree of ligamentous fibrosis.
The outcome is considered favorable after decompressive laminectomy. Cervical dorsal laminectomy has been associated with transient postoperative neurologic deterioration.5 In the case described in the present report, uneventful clinical recovery was observed after surgery. This could be possibly related to the mild degree of the neurologic signs prior to surgery. It also has been suggested that the ligamentum flavum may not cause sustained spinal cord compression in the same way as bony malformation because of its relatively soft structure.1
Findings in the dog of the present report indicated that malformed dorsal laminae and ligamentum flavum hypertrophy can occur in young Golden Retrievers; this should be considered as a possible differential diagnosis when signs of cervical myelopathy occur in this breed.
References
1. De Decker S, De Risio L, Lowrie M, et al. Cervical vertebral stenosis associated with vertebral arch anomaly in the Basset Hound. J Vet Intern Med 2012;26:1374–1382.
2. Cooper C, Gutierrez Quintana J, Penderis R, et al. Osseous associated cervical spondylomyelopathy at the C2–C3 articular facet joints in 11 dogs. Vet Rec 2015;177:522–526.
3. da Costa RC. Cervical spondylomyelopathy (Wobbler syndrome) in dogs. Vet Clin North Am Small Anim Pract 2010;40:881–913.
4. Baum F III, de Lahunta A, Trotter EJ. Cervical fibrotic stenosis in a young Rottweiler. J Am Vet Med Assoc 1992;201:1222–1224.
5. De Risio L, Muñana K, Murray M, et al. Dorsal laminectomy for caudal cervical spondylomyelopathy: postoperative recovery and long-term follow-up in 20 dogs. Vet Surg 2002;31:418–427.
