What Is Your Neurologic Diagnosis?

Brandi N. Petrukovich Veterinary Emergency Clinic and Referral Centre, Toronto, ON M4W 3C7, Canada.

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Greg A. Kilburn Veterinary Emergency Clinic and Referral Centre, Toronto, ON M4W 3C7, Canada.

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A17-month-old 35.4-kg (77.9-lb) sexually intact male Doberman Pinscher was evaluated because of a 3-week history of progressive neurologic deficits. Two weeks prior, the dog developed dysphagia and vomiting; at that time, physical examination and diagnostic test findings had been unremarkable, although facial asymmetry was evident when the dog was panting. A few days later, the dog was noted to have a left head tilt, ataxia, and dysphagia. The dog's free thyroxine (assessed by dialysis), thyrotropin, and thyroglobulin autoantibody concentrations were all considered normal. The result of Lyme disease testing was consistent with previous vaccination or natural exposure to Borrelia burgdorferi. There were no radiographic abnormalities of the vertebral column. Despite treatment with meloxicam (initiated 2 weeks prior to referral), the neurologic signs progressed. At the referral evaluation, mild petechiation along the labial mucosa was the only physically detectable abnormality.

Etiologic diagnosis—Differential diagnoses for this dog included inflammatory disease (meningoencephalitis), progressive compressive lesions, and developmental disorders. Many infectious causes of CNS inflammation are associated with infections in tissues outside of the CNS. In those cases, the most direct route to diagnosis may be evaluation and assessment of samples obtained from extracranial sites. Noninfectious inflammatory disease (meningoencephalitis of unknown etiology) was also considered. Space-occupying lesions resulting from neoplasia, and epidermoid or dermoid cysts were considered. Cerebrovascular accident was not considered likely because of progression of the clinical signs. Because results of comprehensive blood analyses were unremarkable, the diagnostic plan included MRI of the brain and collection of a CSF sample from the cerebellomedullary cistern.

Diagnostic test results, supportive care, and outcome—The dog was admitted to the hospital for supportive care and further diagnostic testing. Magnetic resonance imaging was performed with a 0.2-T MRI unit. Multiplanar T2-weighted, T1-weighted, and fluid-attenuated inversion recovery images were obtained before and after IV administration of gadodiamide (0.2 mL/kg [0.09 mL/lb]). Imaging revealed a well-defined 1.5-cm-diameter spherical intra-axial mass at the right cerebellopontomedullary angle (Figure 1). The mass was hyperintense on T2-weighted images and isointense on fluid-attenuated inversion recovery and T1-weighted images; contrast enhancement of the mass was not evident. There was moderate mass effect and compression of the cerebral aqueduct but minimal ventricular enlargement.

Figure 1—
Figure 1—

Transverse T2-weighted image of the brain (at the level of the rostral medulla) of a young dog that was evaluated because of a 3-week history of progressive neurologic deficits. A hyperintense intra-axial spherical mass is visible in the right cerebellomedullary pontine angle (arrow). There is a moderate mass effect and compression of the cerebellum and brainstem. Scale on the right is in millimeters.

Citation: Journal of the American Veterinary Medical Association 247, 9; 10.2460/javma.247.9.1015

Analysis of a CSF sample obtained from the cerebellomedullary cistern revealed a WBC count of 0 WBCs/μL (reference range, < 4 WBCs/μL), RBC count of 3 RBCs/μL (reference range, 0 RBCs/μL), and protein concentration of 15 mg/dL (reference range, < 25 mg/dL). Cytologic examination findings for the CSF sample were unremarkable. On the basis of the diagnostic test results, neoplasia was considered the most likely diagnosis and options for treatment were discussed. The owners elected for palliative treatment.

During hospitalization, the dog's condition improved slightly but not sufficiently to provide a good quality of life. Progressive neurogenic atrophy of the right masticatory muscles developed as a result of trigeminal nerve involvement. The dog was unable to stand or walk without assistance and continued to have intermittent vertical nystagmus. Given the dog's poor prognosis, the owners requested euthanasia on day 7 of hospitalization. The brain was removed and submitted for histopathologic examination at the owner's request.

Grossly, the anterior to central right brainstem was expanded by a 2 × 1.5-cm gray-tan, mildly granular firm mass, which was fairly well demarcated from the surrounding brain. There was compression of the anterior lobes of the cerebellar cortex, being more severe on the right. On the basis of histopathologic findings and the fact that some tumor cells were positive for glial fibrillar acidic protein and tumor cells were negative for cyclic nucleotide phosphodiesterase, the final diagnosis was a poorly differentiated high-grade astrocytoma (glioblastoma).

Comments

For the dog of the present report, the right hemiparesis could be explained by right-sided brainstem dysfunction; however, the left-sided head tilt, loss of balance, and falling to the left indicated left vestibular system dysfunction. The combination of signs could be indicative of either multifocal disease or paradoxical vestibular disease. The latter is caused by lesions in the caudal cerebellar peduncle or flocculonodular lobe of the cerebellum.1 Normally, peripheral and central vestibular disease can be easily localized because head tilt, loss of balance, and falling are directed toward the side with the least vestibular activity (in other words, the side bearing the lesion).2 Paradoxical disease results from a lesion causing a lack of inhibition of the vestibular cell bodies. The result is excessive discharge of their neurons effectively overriding normal vestibular function on the side without the lesion. Clinically, this gives the appearance of decreased vestibular function on the otherwise normal side.2 Right-sided proprioceptive ataxia and postural deficits are indicative of involvement of the right side of the brainstem. The tumor in the dog of this report was growing in the brainstem and secondarily causing compression of the cerebellum, which resulted in the paradoxical vestibular signs. The masticatory muscle atrophy, which developed during hospitalization, was due to compression of the motor nucleus of the trigeminal nerve located in the pons and at the level of the middle and rostral cerebellar peduncles.2

The primary lesion in the dog of this report was a poorly differentiated astrocytoma affecting the pontine region of the brainstem. Astrocytes are a type of glial cell, the supporting cells of the nervous system that are derived from spongioblasts.2 Phenotypically, astrocytic tumors are made of neoplastic cells that resemble astrocytes; however, the origin of the tumor is still considered controversial because of the lack of a recognized premalignant state.3 Although older dogs are more commonly affected, results of studies1,4 have indicated the importance of considering neoplasia in the differential diagnosis list for CNS disease in young dogs, such as the dog of the present report.

The current World Health Organization grading system for dogs differentiates tumors into low (well-differentiated), medium (anaplastic), and high (glioblastoma) grades of malignancy.5 Prognostic information is scarce in the veterinary medical literature, and survival times have been shown to vary among dogs pending treatment and with different glial cell tumors. A survival time of 3 months has been reported for a dog with an astrocytoma after surgery, chemotherapy, and radiation therapy and for a dog with glioblastoma multiforme after chemotherapy.6 In those 2 dogs, clinical signs had been present for 12 months in 1 dog and 6 weeks in the other.6 Another dog with astrocytoma survived 6 months following radiation therapy, and another dog with undifferentiated glioma survived 8 months following surgery and chemotherapy.6

For dogs with astrocytomas, treatment options include palliation with corticosteroid administration, chemotherapy, surgery, radiation therapy, or a combination thereof.7 More recently in veterinary medicine, the combination of surgery, vaccination, and gene therapy has had success.

For the dog of the present report, the key features that helped localize this lesion were right hemiparesis and left vestibular dysfunction, as explained by paradoxical vestibular disease. The normal CSF protein content and WBC count were inconsistent with an inflammatory process, yielding a tentative diagnosis of neoplasia. Radiation and chemotherapy were possible treatments; however, given the intra-axial nature of the mass, surgical removal was not possible.

References

  • 1. Wong M, Glass E, de Lahunta A, et al. Intracranial anaplastic astrocytoma in a 19-week-old Boxer dog. J Small Anim Pract 2011; 52: 325328.

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  • 2. de Lahunta A, Glass E. Vestibular system: special proprioception. In: Veterinary neuroanatomy and clinical neurology. 3rd ed. St Louis: Saunders Elsevier, 2009; 319347.

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  • 3. Stoica G, Levine J, Wolff J, et al. Canine astrocytic tumors: a comparative review. Vet Pathol 2011; 48: 266275.

  • 4. Kube SA, Bruyette DS, Hanson SM. Astrocytomas in young dogs. J Am Anim Hosp Assoc 2003; 39: 288293.

  • 5. Koestner A, Bilzer T, Fatzer R, et al. Tumors of neuroepithelial tissue. In: Koestner A, Bilzer T, Fatzer R, et al, eds. Histological classification of tumors of the nervous system of domestic animals. Washington, DC: Armed Forces Institute of Pathology, 1999; 1721.

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  • 6. Jeffery N, Brearley MJ. Brain tumours in the dog: treatment of 10 cases and review of recent literature. J Small Anim Pract 1993; 34: 367372.

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  • 7. Nakaichi M, Taura Y, Nakama S, et al. Primary brain tumors in two dogs treated by surgical resection in combination with postoperative radiation therapy. J Vet Med Sci 1996; 58: 773775.

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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 (800-248-2862, ext 6692) for case submission forms. Submissions will be sent to Dr. Karen Kline, DVM, DACVIM, for her review, except when Dr. Kline is an author.

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