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Background: Hypothyroidism has been associated with a variety of neurologic signs, but the mechanism for this association is not completely understood. Hypothyroidism also is associated with hyperlipidemia that predisposes to atherosclerosis, increased blood viscosity, and thromboembolic events., Objective: The objective is to characterize neurologic signs potentially associated with hyperlipidemia and atherosclerosis in canine hypothyroidism., Animals: This study used dogs referred to North Carolina State University Veterinary Teaching Hospital for evaluation of neurologic signs., Materials and Methods: A retrospective study was conducted in which medical records of dogs with neurologic signs and a diagnosis of hypothyroidism and hyperlipidemia were reviewed. Details of the history, presenting signs, results of routine blood tests, thyroid tests, cerebrospinal fluid (CSF) analysis and diagnostic imaging, and response to therapy were compiled., Results: Three Labrador Retrievers and one Labrador Retriever cross fit the inclusion criteria. All dogs were hypothyroid and severely hyperlipidemic. Neurologic signs included tetraparesis, central and peripheral vestibular signs, facial paralysis, and paraparesis. Two dogs had an acute history and rapid resolution of signs consistent with an infarct, the presence of which was confirmed in 1 of the dogs by magnetic resonance imaging. Two dogs had chronic histories of cranial neuropathies and paraparesis. One of these dogs had evidence of iliac thrombosis and atherosclerosis on ultrasound examination. All dogs improved with thyroid hormone supplementation., Clinical Relevance: Labrador Retrievers may be predisposed to the development of severe hyperlipidemia in association with hypothyroidism. One possible consequence of severe hyperlipidemia is the development of neurologic signs due to atherosclerosis and thromboembolic events.

Background: Granulomatous meningoencephalomyelitis (GME) is an idiopathic inflammatory disease of the central nervous system. Remission often is short-lived in dogs treated with glucocorticoids. Procarbazine is T cell-specific and crosses the blood-brain barrier., Hypothesis: Dogs with presumptive antemortem diagnosis of GME given procarbazine as adjunctive therapy to prednisone will have improved long-term outcome compared with dogs given no treatment or glucocorticoids alone., Animals: Two groups were studied: (1) Dogs with presumptive antemortem diagnosis of GME treated with procarbazine and prednisone (n = 21); (2) Dogs that had a histologic diagnosis of GME at postmortem examination and received no treatment (n = 11)., Methods: Dogs with presumptive GME treated with procarbazine were identified retrospectively from medical records of 2 veterinary referral hospitals. Selection criteria required all dogs have a neurologic examination, blood work, cerebrospinal fluid analysis, and brain imaging (MRI or CT)., Results: Median survival time for all dogs studied was 5.0 months. Median survival time for dogs treated with procarbazine was 14.0 months and for untreated dogs, 0.73 months. Treatment with procarbazine was significantly correlated with survival time (P < .001). Procarbazine was the only independent predictor of survival. Prednisone was reduced in dosage or discontinued in 17 dogs. Adverse reactions to procarbazine therapy included myelosuppression in 7 dogs and hemorrhagic gastroenteritis in 3 dogs., Conclusion: These data suggest that procarbazine treatment of presumptive GME may result in greater improved long-term outcome than has been previously reported for glucocorticoid treatment alone and may complement other immunomodulatory therapies. Procarbazine-treated dogs must be monitored for adverse reactions.