![]() ![]() The diagnosis was idiopathic efferent parasympathetic pupillary defect, laryngeal paralysis, and tracheal and bronchial collapse. No other abnormalities were present on gross or light microscopic examination of the other organ systems. Small foci of chronic pneumonia, likely related to the laryngeal paralysis and the tracheal and bronchial collapse were the only detectable abnormalities. Abnormalities were not detected on routine gross and light microscopic examination of the central nervous system, recurrent laryngeal nerves, and eyes. Anesthetic recovery was difficult and the owners requested euthanasia and a postmortem examination. Magnetic resonance imaging was recommended, but declined by the owners. Laryngoscopy confirmed bilateral laryngeal paralysis and bronchoscopy revealed a severe (grade 3) tracheal collapse, as well as collapse of the mainstem bronchi. Images from thoracic radiographs and fluoroscopy were unremarkable. Its respiratory signs were considered most likely due to chronic tracheal collapse and laryngeal paralysis. The dog had failed to respond to prior symptomatic oral antibiotic and corticosteroid therapy. The neurologic examination failed to identify any additional neurologic defects and results from a complete blood (cell) count (CBC), serum biochemical panel, and urinalysis were within normal reference ranges. The hyper-response of the previously dilated pupil was suggestive of a postganglionic efferent parasympathetic defect (Adies pupil) ( 1, 2) or, less likely, dysautonomia ( 3, 4). The resultant pupillary constriction established that iris sphincter atrophy was not present. Both pupils constricted within 1 h however, the left pupil constricted within 20 min. We performed topical parasympathetic stimulation 1 drop 1% pilocarpine was placed on both corneas and the responses of the pupils were timed. The presence of an intact oculocephalic reflex confirmed a functional trochlear nerve, but it did not exclude a defect in the Edinger Westphal nucleus, the parasympathetic portion of the oculomotor nerve, or left iris sphincter muscle atrophy. Afferent pupillary defects and glaucoma were excluded in this dog based on the menace responses and lack of abnormalities on ophthalmoscopic examination. Anisocoria due to dilatation of 1 pupil develops most commonly in dogs secondary to asymmetrical ipsilateral iris atrophy, topical application of atropine or atropine-like medications, glaucoma, afferent pupillary defects (retinal detachment, optic neuritis, optic nerve neoplasia), and rarely dysautonomia or efferent pupillary motor defects. Our clinical diagnosis was left internal ophthalmoplegia. No abnormalities were noted on biomicroscopic and indirect ophthalmoscopic examination. Biomicroscopic (Osram 64222 Carl Zeiss Canada, Don Mills, Ontario) and indirect ophthalmoscopic (Heine Omega 200 Heine Instruments Canada, Kitchener, Ontario) examinations were completed. The right pupil was dilated with tropicamide (Mydriacyl Alcon Canada, Mississauga, Ontario). The intraocular pressures were estimated with an applanation tonometer (Tonopen XL Biorad Ophthalmic Division, Santa Clara, California, USA) to be 16 mm Hg bilaterally. Schirmer tear test (Schirmer Tear Test Strips Alcon Canada, Mississauga, Ontario) values were 20 mm/min bilaterally. The right direct and left to right consensual pupillary light reflexes were also present. The menace responses, and the palpebral and oculocephalic reflexes were present in both eyes. The anisocoria was most pronounced in photopic conditions and the right pupil was fully mobile. The anisocoria had been present for a few weeks, while the cough and dyspnea had been noted for several months. The dog had been referred to the WCVM for laryngeal paralysis and anisocoria ( Figure 1). Vaccinations for Canine distemper virus, Canine parvovirus, and Rabies virus were current. A 4-year-old, toy poodle dog was examined by the ophthalmology service at the Western College of Veterinary Medicine (WCVM) as an internal consult for the internal medicine service. ![]()
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