Introduction
A 1-year-old 24.8-kg neutered male Collie cross was referred for neurologic evaluation because of a 3-week history of right pelvic limb lameness that had progressed to ambulatory paraparesis. Radiography performed by the referring veterinarian revealed the presence of 8 lumbar vertebrae and mildly reduced muscle mass of the right pelvic limb. The other structures were radiographically unre-markable. Results of clinicopathologic analyses indicated that the dog had mildly high hemoglobin concentration, mildly low globulin concentration, and mildly high glucose concentration. Administration of meloxicama (0.1 mg/kg, PO, q 24 h for 1 week) and strict rest was recommended for the dog; with treatment, the owner perceived an improvement in the dog's comfort but fecal incontinence and weakness in both pelvic limbs had developed.
On physical examination, the dog was very bright, alert, and responsive. No abnormalities were detected. Findings of thoracic auscultation were unremarkable. A neurologic examination was performed.
Assessment
Anatomic diagnosis
| Problem | Rule out location |
|---|---|
| Moderate lumbosacral hyperesthesia | Focal or diffuse lesion of the meninges, articular facets, nerve roots, intervertebral disks, vertebrae, ligaments, muscles, or subcutaneous tissues of the lumbosacral region. |
| Paraparesis, decreased bilateral pelvic limb proprioception, and decreased left pelvic limb segmental spinal reflexes | Bilateral pelvic limb peripheral neuropathy (worse on left side) or lumbosacral spinal cord (L4-S3) lesion. |
| Urinary incontinence | Urethral sphincter; ectopic ureters; urinary bladder; detrusor muscle; hypogastric, pelvic, or pudendal nerves; or sacral spinal cord (S1-S3) lesion. |
| Fecal incontinence | Intestinal disease, anal sphincter disease, or sacral spinal cord (S1-S3) lesion. |
Likely location of 1 lesion
L4-S3 spinal cord segments
Etiologic diagnosis—Differential diagnoses considered for the dog included inflammatory or infectious meningomyelitides (autoimmune, viral, protozoal, bacterial, or fungal cause) or degenerative conditions, such as intervertebral disk extrusion or protrusion or degenerative lumbosacral stenosis. Neoplastic conditions were considered but thought less likely given the young age of the dog. Because of the progression of clinical signs, vascular diseases were considered unlikely. Signs of pain were present, which made anomalous conditions, such as subarachnoid diverticulum, unlikely.
Further diagnostic testing included a full CBC and serum biochemical analysis to assess for any changes associated with the progression of clinical signs, reevaluate the dog's general health status, and provide evidence of systemic disease. Given the lack of notable abnormalities identified by the previously performed radiographic examination, MRI of the lumbosacral portion of the spinal cord and vertebral column was performed.
Diagnostic test findings—The results of the serum biochemical analysis and CBC were largely unremarkable with cholesterol concentration of 8.0 mmol/L (reference range, 3.8 to 7.0 mmol/L) and triglyceride concentration of 0.3 mmol/L (reference range, 0.56 to 1.14 mmol/L), which were not considered clinically important.
The dog was sedated and anesthetized for MRI. Images were obtained with a 0.4T magnetb from L2 to Cd2 before and after administration of gadolinium-based contrast agentc (0.1 mmol/kg, IV, once). Multiplanar images were acquired as follows: sagittal and transverse T2-weighted fast-spin echo, sagittal short tau inversion recovery, transverse T1-weight pre- and postcontrast (from the caudal aspect of L4 to mid L6), and sagittal and dorsal T1-weighted post-contrast images.
On T1- and T2-weighted images, there was a hyperintense (compared with the spinal cord), ovoid, broad-based lesion along the left side of the spinal cord and extending the length of the vertebral body of L5 (Figure 1). This lesion appeared to arise from an intradural extramedullary location, which was supported by the presence of a so-called golf tee sign caudal to the lesion on sagittal images. The lesion had moderate homogeneous contrast enhancement and was 2.1 cm in length, 1 cm in height, and 1.1 cm in width. The lesion occupied almost the entire cross section of the spinal canal and caused displacement of the spinal cord toward the right side with severe spinal cord compression. At the level of maximum compression, the spinal cord was severely flattened and decreased in cross-sectional area by approximately 95%. On sagittal T2-weighted and STIR images, there was mild intramedullary hyperintensity extending from the caudal aspect of L4 to the cranial aspect of L6. There was no evidence of associated peripheral nerve root enlargement within the intervertebral foramen or paraspinally, and no visible extension of the lesion into the surrounding vertebral column. Additional findings included the presence of 8 lumbar vertebrae and mild muscle atrophy in the left pelvic limb.
Magnetic resonance images obtained from a 1-year-old dog with a 3-week history of right pelvic limb lameness that progressed to ambulatory paraparesis and subsequently fecal and urinary incontinence. A—Transverse T2-weighted image obtained at the level of the midbody of the L5 vertebra. The lesion is hyperintense (compared to the spinal cord) and occupies almost the entire cross section of the spinal canal. The spinal cord is displaced toward the right side with severe spinal cord compression. The dorsal CSF-epidural fat signal is attenuated. B—Sagittal T2-weighted image obtained from L2 to S1. The lesion at the level of the L5 vertebral body has an ovoid and broad-based appearance; notice a so-called golf-tee sign (arrow), which is characteristic of an intradural extramedullary location. Notably, the dog has 8 lumbar vertebrae. C—Dorsal T1-weighted postcontrast image from L2 to S1 demonstrating moderate homogeneous contrast enhancement of the lesion at the level of the L5 vertebral body with no visible extension into the surrounding vertebral column. The lesion is lateralized to the left, consistent with the dog's neurologic examination findings, and appears to be extramedullary. D—Sagittal T1-weighted postcontrast image from L2 to Cd3 in which the lesion is homogeneously contrast enhanced. Some degree of cranial intramedullary extension is difficult to fully exclude.
Citation: Journal of the American Veterinary Medical Association 259, 6; 10.2460/javma.259.6.601
On the basis of the imaging findings, differential diagnoses for the intradural extramedullary contrast-enhancing lesion included neoplastic disease, such as meningioma, peripheral nerve sheath tumor, lymphoma, plasma cell tumor, or paraganglioma. A nephroblastoma was considered less likely given the caudal location of the lesion. Congenital anomalies, such as cavernous angioma and hamartoma, were considered much less likely because of the lesion's solid and homogeneous MRI appearance. A fungal granuloma was considered unlikely given the dog's geographic location.
Surgical excision of the lesion with adjunct radio-therapy was discussed with the dog's owner; however, given the concern for ongoing morbidity, the owner opted for the dog to be euthanized while anesthetized and gave consent for postmortem examination. On gross postmortem examination, the spinal cord at the level of the L5 vertebral body was thickened, firm, and pale, which confirmed the intradural location of the lesion. The affected portion of spinal cord was removed en bloc and submitted for histologic examination. Histologic examination of that section of the spinal cord confirmed the presence of an intradural mass that had compressed and multifocally infiltrated the nerve roots and spinal cord. The mass was encapsulated and composed of a disorganized mixture of epithelial, blastemal, and mesenchymal cells. The epithelial population was composed of cuboidal to columnar cells arranged in tubules and occasionally forming densely cellular tufts (primitive glomeruli). These neoplastic cells each had variably distinct cell borders and scant to moderate amount of eosinophilic cytoplasm and an irregularly oval nucleus with densely clumped chromatin and 1 or 2 generally distinct nucleoli. Among these cells, there were 2 mitotic figures/hpf (40X). The blastemal cell population was composed of roundish to occasionally polygonal cells arranged in sheets; these cells had indistinct cell borders, very scant cytoplasm, and a high nuclear-to-cytoplasmic ratio. The nuclei of these cells were irregularly round to oval with densely clumped chromatin and 1 to 3 variably distinct nucleoli. Among the blastemal cells, there was 1 mitotic figure/hpf. The mesenchymal component was minimal and consisted of few spindle-shaped cells loosely arranged in vague streams, with < 1 mitotic figure/hpf. Edema and spheroids were evident in the adjacent compressed spinal cord and nerve roots. Despite the atypical anatomic location, this neoplasm was considered to have unequivocal histologic features of an ectopic spinal nephroblastoma.
Comments
For any young dog, a history of chronic painful asymmetrical progressive L4-S3 myelopathy should alert a clinician to the possibility of neoplasia as well as more common inflammatory causes. Spinal cord nephroblastomas are embryonal tumors that are thought to arise from embryonic renal tissue that becomes trapped in the dura during fetal development and later undergoes neoplastic transformation.1 Spinal cord nephroblastomas are typically intradural-extramedullary tumors, and in dogs most commonly cause clinical signs between 0.5 and 4 years old, with neurologic deficits consistent with T3-L3 myelopathy.2
Diagnosis of spinal cord nephroblastoma is typically achieved on the basis of routine histologic findings from biopsy samples. The classic features of spinal cord nephroblastomas include the coexistence of 3 tumor cell populations in 1 neoplasm3 and the presence of multifocal glomeruloid structures resembling fetal glomeruli.2 Immunohistochemical analysis of tumor sections for Wilms tumor-1 protein can also be performed because mutation in the gene for that protein is associated with nephroblastoma in humans.4 In 1 study,2 tumor sections from 9 of 11 dogs with a histologically confirmed spinal cord nephroblastoma were positive for Wilms tumor-1 protein.
For dogs with spinal cord nephroblastomas, treatment options include cytoreductive surgery and radiotherapy. Among affected dogs, median survival time with palliative treatment only is 55 days; however, dogs treated with surgery or radiotherapy in 1 study5 had a median survival time of 374 days. In the same study,5 dogs with intradural-extramedullary tumors had a longer median survival time (380 days), compared with the finding for dogs with intramedullary tumors (140 days).
To the authors' knowledge, there is only 1 published report6 of a primary nephroblastoma located in the L4-S3 region of a dog that had L4-S3 spinal cord segment signs. For another dog with spinal cord nephroblastoma, involvement of the L4-S3 spinal cord segments was considered a result of intraspinal metastasis of a nephroblastoma from T12.7 The location of the tumor in the case described in the present report was therefore unusual because primary lesions are typically located in the T3-L3 segments. However, this dog's neurologic examination findings were consistent with L4-S3 myelopathy, and hence a second more cranially located lesion was not suspected.
This feature is published in coordination with the American College of Veterinary Internal Medicine on behalf of the specialty of neurology. Contributors to this feature should contact Dr. Helen L. Simons (hsimons@avma.org) for case submission forms. Submissions will be sent to Dr. Karen Kline, DVM, DACVIM, for her review, except when Dr. Kline is an author.
Footnotes
Loxicom, Norbrook Laboratories Ltd, Newry, Northern Ireland.
Aperto Lucente 0.4T, Hitachi, Maidenhead, England.
Dotarem, Guerbet Laboratories Ltd, Solihull, England.
References
- 1. ↑
Sale CS, Skerritt GC, Smith KC. Spinal nephroblastoma in a crossbreed dog. J Small Anim Pract 2004;45:267–271.
- 2. ↑
Brewer DM, Cerda-Gonzalez S, Dewey CW, et al. Spinal cord nephroblastoma in dogs: 11 cases (1985–2007). J Am Vet Med Assoc 2011;238:618–624.
- 3. ↑
De Lorenzi D, Baroni M, Mandara MT. A true “triphasic” pattern: thoracolumbar spinal tumor in a young dog. Vet Clin Pathol 2007;36:200–203.
- 4. ↑
Ghanem MA, Van der Kwast TH, Den Hollander JC, et al. Expression and prognostic value of Wilms' tumor 1 and early growth response 1 proteins in nephroblastoma. Clin Cancer Res 2000;6:4265–4271.
- 5. ↑
Liebel FX, Rossmeisl JH, Lanz OI, et al. Canine spinal nephroblastoma: long-term outcomes associated with treatment of 10 cases (1996–2009). Vet Surg 2011;40:244–252.
- 6. ↑
Langen N, von Puckler K, Tillmanns C, et al. Spinal nephroblastoma at an uncommon localization in a dog [in German]. Tierarztl Prax Ausg K Kleintiere Heimtiere 2017;45:115–121.
- 7. ↑
Terrell SP, Platt SR, Chrisman CL, et al. Possible intraspinal metastasis of a canine spinal cord nephroblastoma. Vet Pathol 2000;37:94–97.
