What Is Your Neurologic Diagnosis?

Michaela J. Beasley Small Animal Clinic, College of Veterinary Medicine, Auburn University, Auburn, AL 36849.

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Andrew Shores Small Animal Clinic, College of Veterinary Medicine, Auburn University, Auburn, AL 36849.

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John T. Hathcock Small Animal Clinic, College of Veterinary Medicine, Auburn University, Auburn, AL 36849.

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A 5-year-old 25-kg (55-lb) castrated male Siberian Husky was evaluated because of sudden onset of circling 7 days earlier. Muscle atrophy of the right temporalis muscle became evident 5 days prior to the scheduled appointment. Bilateral corneal dystrophy and keratoconjunctivitis sicca of the right eye were diagnosed by the referring veterinarian approximately 1 month prior to the onset of the clinical signs.

During physical examination, the dog was quiet, alert, and responsive. No abnormalities were detected during auscultation of the heart and lungs; heart and respiratory rates were within reference limits. The mucous membranes were pink and slightly dry with a capillary refill time of < 2 seconds. Marked atrophy of the right temporalis muscle and enophthalmos and ptosis, both of the right eye, were noted.

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What is the problem? Where is the lesion? What are the most probable causes of this problem? What is your plan to establish a diagnosis? Please turn the page.

Assessment

Anatomic diagnosis

Problem 
Circling to leftCerebrum or brainstem
Vestibular ataxia; head tilt to left; horizontal nystagmus with fast phase to rightCentral or peripheral vestibular system
Falling to right; extensor hypertonus of left limbsRostral portion of brainstem
Decreased proprioception in right fore- and hind limbsCervical portion of spinal cord, brainstem, or cerebral cortex
Absent palpebral reflex on right (with normal menace response); temporalis muscle atrophy on right sideRight trigeminal nerve or peripheral nerves
Ptosis and enophthalmos of right eyePeripheral nerves or sympathetic trunk

Likely location of lesion

Right flocculonodular lobe of the cerebellum or right supramedullary part of the caudal cerebellar peduncle

Etiologic diagnosis—Rule out disease processes included neoplasia, infectious or inflammatory disease, ischemic or vascular event, parasitic migration, degenerative process, trauma, or an idiopathic cause.

The diagnostic plan included clinicopathologic analyses (to establish general health status and identify any factors that would put the dog at risk during anesthesia), radiography (to rule out any gross metastatic disease and determine cardiac and respiratory stability for anesthesia), magnetic resonance imaging evaluation of the cranial vault (to identify any masses or hemorrhagic or ischemic event process in or surrounding the brain tissues), and CSF analysis (to evaluate for inflammatory, neoplastic, or infectious disease processes).

Diagnostic test findings—Results of a CBC indicated mild eosinophilia. Abnormalities detected via serum biochemical analyses included mildly low creatine kinase activity, mildly high creatinine concentration, moderate hypophosphatemia, mild hyperglycemia, and mild hypercholesterolemia. Results of urinalysis were within reference limits.

Thoracic radiography (3 views) revealed a diffuse interstitial pulmonary pattern in all lung lobes, which was considered appropriate for the age of the dog. The cardiovascular structures appeared radiographically normal; there was no evidence of pulmonary metastasis. Magnetic resonance imaging of the brain was performed in transverse, sagittal, and dorsal planes; T1-, T2-, and T2*-weighted images were obtained with and without administration of contrast medium. In T2-weighted images obtained without contrast medium administration, there was a large area of nonhomogeneous increased signal intensity (relative to the surrounding brain tissue) on the midline and right side of the midline at the level of the rostral portion of the brainstem and ventral right portion of the cerebellum. The lateral and third ventricles were large, possibly as a result of compression of the CSF outflow tract by the mass. Marked muscle atrophy of the right temporalis muscle was evident. On T1-weighted images obtained without contrast medium administration, the mass had decreased signal intensity relative to the surrounding brain tissue. In the T1-weighted image obtained after contrast medium administration, the mass was markedly contrast-enhanced and well defined (Figure 1). Analysis of a CSF sample was not performed because the magnetic resonance imaging findings were indicative of a mass and because of the risk of brain herniation.

Figure 1—
Figure 1—

Transverse T1-weighted magnetic resonance image (obtained after administration of contrast medium) of the head of a dog that was evaluated because of sudden onset of circling 7 days earlier. Notice the area of marked contrast enhancement indicative of a mass located in the right ventral cranial vault that has caused deviation of the brainstem and cerebellum to the left. Also notice the large lateral ventricles and muscle atrophy of the right temporalis muscle.

Citation: Journal of the American Veterinary Medical Association 234, 6; 10.2460/javma.234.6.743

A diagnosis of vestibular disease was made on the basis of clinical signs of head tilt, circling, and ataxia with falling. Because the dog had muscle atrophy of the right temporalis muscle and loss of the palpebral response in the right eye, trigeminal nerve involvement (caused by a lesion at its origin in the brainstem or elsewhere along its length) was indicated. This dog also had conscious proprioceptive deficits on the right side, which could be indicative of a brainstem lesion that can cause hemi- to tetraparesis with deficiencies in both gait and postural reactions. Conscious proprioceptive deficits could also indicate cerebellar involvement, which can cause ipsilateral decreases in conscious proprioception and postural reactions. On the basis of these additional neurologic signs, the vestibular disease was classified as central. Because dog had a head tilt to the left and was circling to the left, and the fast phase of horizontal nystagmus was to the right, a lesion was localized to the left side; however, falling to the right indicated a right-sided lesion. When the localizing signs of vestibular disease are conflicting, it is known as paradoxical vestibular disease. Lesions of the caudal cerebellar peduncle and flocculonodular lobe of the cerebellum will result in paradoxical vestibular disease. Lesions in these areas typically affect the general proprioceptive pathways afferent to the cerebellum and result in signs of conscious proprioceptive deficits ipsilateral to the lesion. Conscious proprioceptive deficits are therefore the most reliable indicators for localizing paradoxical vestibular disease to the left or right side. This dog's conscious proprioceptive deficits were on the right side, indicating a right-sided lesion. In support of this proposed localization, the trigeminal nerve deficits were also on the right side. The lesion was therefore localized to the right caudal cerebellar peduncle or flocculonodular lobe of the cerebellum, in addition to the right portion of the brainstem.1,2

Discussion

The duration of survival in dogs with primary brain neoplasia varies depending on the type and number of treatments administered. The use of surgical debulking followed by radiation therapy results in the longest median survival time. In 1 study3 of dogs with intracranial meningiomas, the median survival time associated with surgery and radiation therapy was 16.5 months (range, 3 to 58 months), compared with a median survival time of 7 months (range, 0.5 to 22 months) for dogs that did not undergo radiation therapy after surgery. In studies4,5 to evaluate the use of radiation therapy as a primary treatment of brain masses of undetermined histologic origin in dogs, median survival time was 250 to 489 days (range, 21 to 804 days). Given the size of the mass and the severe clinical signs in the dog of this report, the prognosis without treatment was grave. In dogs with primary brain masses that receive no treatment or only treatment of clinical signs, the estimated median survival time is 2 weeks to 2.5 months.4,6

Immediately following the magnetic resonance imaging procedure, the dog of this report was administered mannitol (1 g/kg [0.45 g/lb], IV, once) to decrease the edema surrounding the mass. While the owners considered surgery and radiation therapy, the dog was administered omeprazole (1 mg/kg, PO, q 24 h) to reduce CSF production because of the outflow obstruction to the ventricles, prednisone (1 mg/kg, PO, q 24 h) to decrease swelling associated with the mass, and meclizine (25 mg, PO, q 24 h) to reduce nausea associated with vestibular disease. After 2 days of medical treatment, the dog's condition improved considerably. The head tilt was still present, but ambulation was greatly improved. The owners elected surgical resection of the mass. A ventral surgical approach to the caudal brainstem7 was performed, and approximately 90% of the mass was removed. During recovery from anesthesia, the dog did not require the use of a ventilator; however, it never awoke from a semicomatose state. The dog's postsurgical small animal coma scale (modified Glasgow coma scale) score was 12 (maximum possible score, 18); serial monitoring of the coma scale score did not reveal improvement. Further complications included regurgitation during the postoperative period, which resulted in aspiration pneumonia and exposure keratitis that required treatment via grid keratotomy. The owners elected euthanasia 9 days following surgery. Results of histologic examination of the mass tissue were most consistent with a peripheral nerve sheath tumor, although it is possible that the mass was a meningioma, particularly the fibroblastic type.

References

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    De Lahunta A. Vestibular system—special proprioception. In: Veterinary neuroanatomy and clinical neurology. 2nd ed. Philadelphia: WB Saunders Co, 1983;238246.

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  • 2.

    Oliver JE, Lorenz MD, Kornegay JN. Ataxia of the head and limbs. In: Handbook of veterinary neurology. 3rd ed. Philadelphia: WB Saunders Co, 1997;216219.

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    Axlund TW, McGlasson ML, Smith AN. Surgery alone or in combination with radiation therapy for treatment of intracranial meningiomas in dogs: 31 cases (1989–2002). J Am Vet Med Assoc 2002;221:15971600.

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    Evans SM, Dayrell-Hart B, Powlis W, et al. Radiation therapy of canine brain masses. J Vet Intern Med 1993;7:216219.

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    Spugnini EP, Thrall DE, Price GS, et al. Primary irradiation of canine intracranial masses. Vet Radiol Ultrasound 2000;41:377380.

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    Heidner GL, Kornegay JN, Page RL, et al. Analysis of survival in a retrospective study of 86 dogs with brain tumors. J Vet Intern Med 1991;5:219226.

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    Klopp LS, Simpson ST, Sorjonen DC, et al. Ventral surgical approach to the caudal brain stem in dogs. Vet Surg 2000;29:533542.

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