What Is Your Neurologic Diagnosis?

Yael Merbl Department of Clinical Sciences, Washington State University, Pullman, WA

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Annie Chen Allen Department of Clinical Sciences, Washington State University, Pullman, WA

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 DVM, MS

A 1.5-year-old 16-kg spayed female Australian Cattle Dog was evaluated at a veterinary teaching hospital because of sudden-onset paraparesis that had progressed to paraplegia over the past 3 days. The dog had difficulty urinating on the day of presentation. The dog’s history was otherwise unremarkable, and its vaccination status was current. The dog had outdoor access, and trauma could not be ruled out. A physical examination, CBC, serum biochemical analyses, and abdominal radiography were performed by the referring veterinarian; there were no abnormal findings. The dog was referred to the veterinary neurology service. On admission, the dog was assessed by a board-certified veterinary neurologist.

Neurologic examination

Assessment

Anatomic diagnosis

In this dog, the paraplegia with normal spinal reflexes was consistent with a T3-L3 spinal cord myelopathy. The intermittent thoracic limb hyperextension was suggestive of a lesion between the border cells region (L1-L4) and T3.

Likely location of a single lesion

A T3-L3 spinal cord myelopathy was considered the most likely location of the lesion.

Etiologic diagnosis

Differential diagnoses for acute deteriorating paraparesis-paraplegia in a 1.5-year-old dog included trauma with associated instability, inflammatory (immune-mediated myelitis) and infectious (opportunistic bacterial, distemper virus, fungal, and parasitic [Toxoplasma gondii or Neospora caninum] infection) diseases, bleeding disorders, abnormal vasculature, and neoplasia (nephroblastoma and lymphosarcoma considered most likely). Fibrocartilaginous embolic myelopathy and diskospondylitis with either pathological fracture or empyema causing spinal cord compression were considered less likely because of the progressive nature of the dog’s disease and lack of abnormal historical or physical examination findings. Congenital CNS anomalies or degenerative diseases could not be ruled out but were considered less likely owing to the rapid deterioration of the dog’s condition and spinal hyperesthesia.

Diagnostic Test Findings

Clinicopathologic analyses had been performed by the primary veterinarian. Results of a CBC were unremarkable. No kidney-, liver-, or electrolyte-related biochemical abnormalities were detected. Cerebrospinal fluid analysis revealed a total nucleated cell count of 155 cells/µL and RBC count of 96,867 cells/µL. A differential cell count revealed 79% neutrophils, 8% small lymphocytes, and 13% large mononuclear cells. The neutrophils were segmented and nondegenerated. The CSF sample was considered hemodiluted. The ratio of the total nucleated cell count to the RBC count suggested there was no primary inflammation. No pathogens were evident. Owing to the small sample size, microprotein concentration was not assessed.

Magnetic resonance imaging was performed, and transverse and sagittal T2-weighted, T2*-gradient echo, and STIR images; transverse and sagittal T1-weighted images with and without IV gadolinium administration; and a dorsal T1-weighted image with gadolinium were acquired with a 1.5-T magnet (Figures 1 and 2). Magnetic resonance imaging revealed focal contrast enhancement of the spinal cord extending from the cranial aspect of L2 to L3, with patchy intramedullary contrast enhancement extending caudally and overlying the L2 vertebral body and cranial aspect of L3. In addition, the spinal cord became markedly enlarged at the L2-L3 level. Marked intramedullary T2 hyperintensity was present extending from the caudal aspect of L1 to L3, and there was patchy T2 hyperintensity surrounding the central canal extending cranially to the approximate level of T11. The radiologist concluded the mass was either intradural-extramedullary or intramedullary in origin, extending from L1 to L3 with moderate associated spinal cord edema and gliosis. Given the young age of the animal and the lumbar location of the mass, nephroblastoma was considered most likely.

Figure 1
Figure 1

Sagittal T2-weighted (A) and T1-weighted postcontrast (B) MRI images of the caudal thoracic and lumbar portions of the vertebral column of a 1.5-year-old Australian Cattle Dog that had a sudden onset of paraparesis that had progressed over 3 days. A—Notice the focal elongated hyperintensity at the level of the caudal aspect of L1 to L3 with widening of the spinal cord and loss of the dorsal and ventral CSF columns. B—The T11-L7 vertebral bodies and spinal cord are shown. A focal well-demarcated, heterogeneously contrast-enhancing oval mass involving the spinal cord dorsal to L2 and L2-3 intervertebral disk space is noted. Additionally, caudal to the lesion, patchy intramedullary contrast enhancement is evident.

Citation: Journal of the American Veterinary Medical Association 260, 4; 10.2460/javma.20.08.0470

Figure 2
Figure 2

Transverse (A, B, and C) and dorsal (on the right) T1-weighted postcontrast MRI images of the lesion. Panels A, B, and C are images acquired at the levels indicated in the image on the right. Notice the possible meningeal involvement (B).

Citation: Journal of the American Veterinary Medical Association 260, 4; 10.2460/javma.20.08.0470

Treatment options for the dog included excisional biopsy with or without radiation therapy and palliative treatment with glucocorticoids. Given the potential poor long-term prognosis and financial constraints, the owners chose to euthanize the dog by injection of pentobarbital sodium and phenytoin sodium. A necropsy was performed at the owners’ request.

Grossly, the lumbar spinal mass was a 1.5×1.2×0.6 cm, firm, pale red, well-circumscribed, intramedullary soft tissue nodule. Histologically, the L2 spinal cord segment was infiltrated by a densely cellular to paucicellular, nodular, unencapsulated neoplasm that extended into the caudal L1 and cranial L3 spinal cord segments and multifocally invaded the overlying meninges. Immunohistochemical staining of representative sections of the neoplasm revealed cytoplasmic immunoreactivity for vimentin and laminin, with no immunoreactivity for cytokeratin, glial fibrillary acidic protein, or S100. Given the overlap of the histologic appearance and immunoreactivity with that of several tumors, it was concluded that the exact histogenesis of this neoplasm could not be definitively determined. Primary differential diagnoses included neurofibroma and meningioma and possibly schwannoma (although considered less likely).

Comments

The mass in the dog of the present report was interesting in that the rapid deterioration of clinical signs along with the age and breed of the dog were more suggestive of a traumatic insult or inflammatory or infectious disease. Neoplasia can never be ruled out on the basis of history alone; however, tumors are generally much rarer at a younger age. Spinal cord neoplasms are often categorized initially on the basis of the anatomic area in relation to the dura and spinal cord (ie, extradural, intradural-extramedullary, and intramedullary).1 Depending on growth characteristics and biological aggressiveness of tumors, they can expand and extend from one localized anatomic area to another.1 Results of diagnostic imaging that appear supportive of one location versus another can affect the patient’s prognosis and influence the owners’ decision regarding the preferred treatment option. Tumors of the spinal cord are less common in dogs of a young age; however, ectopic nephroblastoma should be considered for a young dog with the neuroanatomical localization described for the dog of the present report.2,3 A case series3 of 10 dogs with spinal nephroblastoma revealed that tumors confined to an intradural-extramedullary space were associated with superior survival times (range, 176 to 560 days), compared with tumors that had intramedullary involvement (range, 38 to 269 days). Given the intramedullary involvement of the tumor in the dog of the present report, the dog was speculated to have had a poor long-term prognosis.

Surprisingly, results of necropsy suggested the tumor in this dog was most likely a meningioma or neurofibroma. Among primary spinal cord tumors in dogs, meningioma is the most common; however, reports of meningioma in dogs at such an early age are scarce.4,5 In dogs, meningiomas in the lumbar portion of the spinal cord are more likely to be high grade, compared with meningiomas in the cervical portion of the spinal cord; moreover, these tumors in younger dogs tend to be more biologically aggressive, as evident in the case described in the present report.4 Some MRI characteristics suggest a mass is more likely to be a meningioma,6 including meningeal involvement (ie, broad-based attachment and dural tail sign), T1-weighted hyperintensity, and T1-weighted postcontrast homogeneity and well-defined contrast enhancement. These characteristics were subtle in the dog of the present report, perhaps supporting the undetermined origin of this tumor. This case was atypical in its clinical presentation, imaging characteristics, and postmortem diagnosis. The authors’ recommendations to owners are based on the diseases that are considered to be more common on the basis of signalment and onset of clinical signs. In the case described in the present report, the owners were given a guarded to poor long-term prognosis for the dog. It is important to remember that the diagnosis in many cases represents the most probable diagnosis in the absence of histopathologic evidence.

Acknowledgments

The authors declare that there were no conflicts of interest.

References

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