A 4 yr old, intact female cocker spaniel was presented for investigation of acute, progressive lethargy/hypersomnia; vestibular signs; and cataplexy. A narcolepsy-cataplexy episode with associated hypertension and bradycardia was triggered… Click to show full abstract
A 4 yr old, intact female cocker spaniel was presented for investigation of acute, progressive lethargy/hypersomnia; vestibular signs; and cataplexy. A narcolepsy-cataplexy episode with associated hypertension and bradycardia was triggered during examination. There was no evidence of arrhythmia on electrocardiography during the episode. Hematology, serum biochemistry, and thoracic and abdominal imaging were unremarkable. MRI of the brain and cerebrospinal fluid analysis were compatible with meningoencephalitis of unknown origin affecting the mesencephalon, pons and rostral medulla oblongata. The dog was started on immunosuppressive treatment with prednisolone and cytosine arabinoside, which was subsequently switched to cyclosporine. Narcolepsy-cataplexy episodes could initially still be triggered by offering food; however, they gradually became shorter and less frequent until they completely subsided along with all other clinical signs after 3 wk. No relapse occurred over a 32 mo follow-up period from the diagnosis. Repeated MRI revealed marked reduction in the lesion size; cerebrospinal fluid analysis revealed no abnormalities. Although very rare, symptomatic narcolepsy/cataplexy can occur in dogs and can be secondary to brainstem encephalitis. Cardiovascular changes can occur in association with narcolepsy/cataplexy and should be considered when dealing with patients presenting with these specific clinical signs.
               
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