Assessment Anatomic diagnosis

Etiologic diagnosis—Differential diagnosis categories considered included degenerative, anomalous, infectious or inflammatory, and traumatic causes. Given the young age of the dog, neoplasia was considered unlikely, but lymphoma, vertebral osteoma, and vertebral osteosarcoma were considered as possible differential diagnoses. There was no history of trauma, although the dog did play off leash with other dogs. Nutritional factors were deemed unlikely contributors to the problem because of the owner's adherence to feeding the dog a recommended veterinary diet without supplementation. Further diagnostic testing was delayed because a CT examination had already been performed and images were available for evaluation. Additional diagnostic tests (eg, MRI of the dog's head and neck and genetic analyses) were discussed with the owner, but eventually declined.

Diagnostic test findings—The previously obtained CT images of the C1-T7 region of the dog's vertebral column were available for evaluation (Figure 1). The images had been acquired with a 16-slice CT scanner^a in the transverse plane with the following settings: 120 kVp, 180 mA, and a 1-mm slice thickness. Assessment of the transverse images revealed variable spinal canal stenosis and right-sided displacement of the spinal cord in the cervicothoracic region of the vertebral column from the level of the C1 through T7 vertebrae. The spinal canal stenosis was most notable at the levels of C3, C4, and T1–3. The spinal cord was markedly compressed laterally. Osseous proliferation of the left vertebral pedicles; transverse, dorsal, and articular processes; and lamina was noted with heterogeneous hypo- and hyperattenuation. Maximal transverse mid-vertebral spinal canal diameters were measured. Maximal transverse midvertebral spinal canal diameters were as follows: C1, 21.6 mm; C2, 10.7 mm; C3, 6.2 mm; C4, 9.8 mm; C5, 11.9 mm; C6, 13.2 mm; C7, 15.4 mm; T1, 11.9 mm; T2, 7.2 mm; T3, 7.6 mm; T4, 10.1 mm; T5, 9.4 mm; T6, 9.5 mm; and T7, 9.2 mm.

Transverse CT images of the C2 (A), C3 (B), T1 (C), and T2 (D) vertebrae of a 16-week-old Rhodesian Ridgeback that developed progressive tetraparesis and ataxia after a sudden onset of signs of neck pain. Notice the displacement of the spinal canal to the right, the displacement of the left transverse foramen in C3, and marked spinal canal stenosis in C3, T1, and T2. Images provided courtesy of AniCura Diergeneeskundig Verwijscentrum Dordrecht.

Citation: Journal of the American Veterinary Medical Association 255, 9; 10.2460/javma.255.9.1009

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Transverse CT images of the C2 (A), C3 (B), T1 (C), and T2 (D) vertebrae of a 16-week-old Rhodesian Ridgeback that developed progressive tetraparesis and ataxia after a sudden onset of signs of neck pain. Notice the displacement of the spinal canal to the right, the displacement of the left transverse foramen in C3, and marked spinal canal stenosis in C3, T1, and T2. Images provided courtesy of AniCura Diergeneeskundig Verwijscentrum Dordrecht.

Citation: Journal of the American Veterinary Medical Association 255, 9; 10.2460/javma.255.9.1009

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Transverse CT images of the C2 (A), C3 (B), T1 (C), and T2 (D) vertebrae of a 16-week-old Rhodesian Ridgeback that developed progressive tetraparesis and ataxia after a sudden onset of signs of neck pain. Notice the displacement of the spinal canal to the right, the displacement of the left transverse foramen in C3, and marked spinal canal stenosis in C3, T1, and T2. Images provided courtesy of AniCura Diergeneeskundig Verwijscentrum Dordrecht.

Citation: Journal of the American Veterinary Medical Association 255, 9; 10.2460/javma.255.9.1009

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At this point, differential diagnoses were multiple vertebral osteosarcomas or osteochondromas, atypical tumoral calcinosis, hamartomas, or otherwise abnormally developed vertebrae (vertebral dysplasia). Owing to the painful and diffuse or multifocal nature of this condition, severe spinal cord compression and resultant neurologic dysfunction, and noticeable progression of signs in a short period, the prognosis for the dog without treatment was deemed very poor. Medical management was not considered an option given the young age of the dog and severity of signs. Surgical treatment was considered, but the dog's prognosis was still deemed to be poor and considerable surgery-associated risks were involved given the extensive lesions. The owner elected euthanasia (by IV administration of pentobarbital solution), which was considered an acceptable option. Given that a sibling of the dog was purported to have died as a result of an unconfirmed cervical vertebral fracture, postmortem examination and histologic examination of affected tissues were strongly recommended. Pedigree analysis was not performed because of missing data.

Postmortem examination revealed macroscopic deformities of the C2-T2 vertebrae. All deformities were mostly lateralized to the left. Microscopically, no signs or cellular characteristics of inflammation or neoplasia were found. In the left pedicles of C3 and T1, several individual or paired well-differentiated thin-walled vascular structures separated by histologically normal bone marrow or bone tissue were identified. Endothelial cells covered the inner walls of the structures. The vertebral vasculature, bone tissue, and bone marrow were otherwise unremarkable. These vascular structures were postulated to be a result of venous congestion or primary malformation (hamartoma). The spinal cord had signs of absolute compression and bilateral asymmetric, mostly ventrolateral axonal degeneration. The cause of the bony deformities remained elusive. Vertebral dysplasia was considered the most appropriate term for the combined findings.

Comments

Spinal canal stenosis is classified as a malformation originating in the fetal period of development.¹ It is defined as “a narrowing or stricture of the vertebral canal or intervertebral foramen, in any plane or level.”¹ Focal, segmental, or generalized stenosis has been described in humans.^2–4 Forms of spinal canal stenosis are classified as congenital (static from birth), developmental (active from birth), or acquired.

In veterinary medicine, spinal canal stenosis is extensively reported as a feature of caudal cervical spondylomyelopathy (osseous form).⁵ This might be considered a developmental form of spinal canal stenosis because the process may be viewed as active as an affected dog grows and clinical signs become apparent. In addition, spinal canal stenosis can be classified as absolute or relative; the distinction of these forms depends on whether the mid-sagittal spinal canal diameter is so small that neural structures are compressed.¹

With the exception of identification of spinal canal stenosis as a feature of the osseous form of caudal cervical spondylomyelopathy, relatively few veterinary reports have documented segmental congenital and developmental cases of spinal canal stenosis in dogs. Segmental impingement of the spinal cord in the cranial thoracic region of the vertebral column in Doberman Pinschers, English Bulldogs, and 2 young Dogues de Bordeaux has been reported.^6–9 To our knowledge, there are no reports of generalized spinal canal stenosis in the veterinary medical literature. Focal spinal canal stenosis is often a result of congenital (vertebral malformations), developmental (caudal cervical spondylomyelopathy), or acquired (degenerative lumbosacral stenosis) causes.^1,5,10

In veterinary medicine, it is generally accepted that, normally, the diameter of the spinal canal is greatest at the level of the first and second cervical vertebrae.¹¹ The spinal canal diameter decreases progressively caudally, but it increases again in the caudal cervical and cranial thoracic regions (cervical intumescence) before narrowing again in the caudal thoracic region of the vertebral column. In the dog of the present report, this pattern of diameter variation was not evident. Indeed, the maximal midvertebral spinal canal diameter at the level of C2 was less than the diameters at the levels of C5, C6, and C7; the maximal mid-vertebral spinal canal diameter at the level of C3 was less than the diameters for all other vertebrae. Furthermore, the maximal mid-vertebral spinal canal diameters at T2 and T3 were markedly less than the diameters for the more caudal thoracic vertebrae; the maximal mid-vertebral spinal canal diameter at the level of T1 was greatly reduced, compared with that at the level of C7.

Some reference data pertaining to ranges of spinal canal width and height and spinal cord-to-spinal canal diameter ratios in dogs are available.^12,13 However, those data were obtained from healthy adult dogs of various breeds. It has been reported and generally accepted that differences in body weight and physical build among various dog breeds and among dogs of the same breed can influence those measurements. Nonetheless, for the dog of the present report, the spinal canal measurements in several regions (most notably at the level of the C3 vertebra) were clearly drastically lower than those reported for any level of the vertebral column in healthy dogs of any body weight group in those studies.^12,13

Clinical signs of spinal canal stenosis are dependent on the localization of the stenotic region and may become apparent early in life, during the growth phase, or as the animal matures.¹ Signs can be acute or chronic and symmetric or asymmetric. Radiography can reveal regions of stenosis, but advanced imaging (CT or MRI) allows better characterization of the stenosis and nervous tissue compression and more accurate surgical planning.¹ Treatment options vary, but surgical decompression is reported to be associated with good outcomes.¹ Repeated surgery may be necessary if stenosis recurs, which may happen if surgery is performed when the stenosis is still an active process that progresses after that first surgery. In the dog of the present study, clinical signs were severe and developed early in life (ie, at 12 weeks of age). Surgery was briefly considered, but discussion of the clinical signs and CT findings led to a decision to euthanize the dog.

Postmortem findings regarding the cause of the mostly left-sided vertebral malformations in the dog of the present report were inconclusive. The presence of vascular structures in some of the bony proliferations was reason to suggest the presence of vertebral vascular hamartomas, which have been described for 2 cats previously.^14,15 In humans, multiple vertebral hamartomas have been reported, and the influence of genetic factors in their development has been proven (in cases of Cowden disease or Bannayan-Riley-Ruvalcaba syndrome).¹⁶ Also, osteochondromatosis was considered as a differential diagnosis for the dog of the present report.¹⁷ However, the histologic characteristics of osteochondromatosis did not fit the findings in this case. In embryonic development, contributions of 2 pairs of adjacent somites (sclerotomes) on each side of the notochord form the vertebrae.¹¹ Because the dog's vertebral anomalies were mostly lateralized to the left, one might conclude that this represented a form of a developmental left-sided segmentation defect.¹ However, a more general term of vertebral dysplasia was considered more appropriate. The case described in the present report involved a young dog with a severe form of spinal canal stenosis, likely attributable to anomalous development of vertebral structures; one should be mindful that clinical signs of spinal canal stenosis in dogs may become apparent at an early age.