Diagnostic Ophthalmology

History and clinical signs

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. Vaccinations for Canine distemper virus, Canine parvovirus, and Rabies virus were current. The dog had been referred to the WCVM for laryngeal paralysis and anisocoria (Figure 1). The anisocoria had been present for a few weeks, while the cough and dyspnea had been noted for several months. The left pupil was fixed and dilated. The anisocoria was most pronounced in photopic conditions and the right pupil was fully mobile. The menace responses, and the palpebral and oculocephalic reflexes were present in both eyes. The right direct and left to right consensual pupillary light reflexes were also present. Schirmer tear test (Schirmer Tear Test Strips; Alcon Canada, Mississauga, Ontario) values were 20 mm/min bilaterally. The intraocular pressures were estimated with an applanation tonometer (Tonopen XL; Biorad Ophthalmic Division, Santa Clara, California, USA) to be 16 mm Hg bilaterally. The right pupil was dilated with tropicamide (Mydriacyl; Alcon Canada, Mississauga, Ontario). Biomicroscopic (Osram 64222; Carl Zeiss Canada, Don Mills, Ontario) and indirect ophthalmoscopic (Heine Omega 200; Heine Instruments Canada, Kitchener, Ontario) examinations were completed. No abnormalities were noted on biomicroscopic and indirect ophthalmoscopic examination.

Figure 1.

Marked anisocoria in a 4-year-old toy poodle.

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Discussion

Our clinical diagnosis was left internal ophthalmoplegia. 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. Afferent pupillary defects and glaucoma were excluded in this dog based on the menace responses and lack of abnormalities on ophthalmoscopic examination. 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. We performed topical parasympathetic stimulation; 1 drop 1% pilocarpine was placed on both corneas and the responses of the pupils were timed. Both pupils constricted within 1 h; however, the left pupil constricted within 20 min. The resultant pupillary constriction established that iris sphincter atrophy was not present. 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 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 dog had failed to respond to prior symptomatic oral antibiotic and corticosteroid therapy. Its respiratory signs were considered most likely due to chronic tracheal collapse and laryngeal paralysis. Images from thoracic radiographs and fluoroscopy were unremarkable. Laryngoscopy confirmed bilateral laryngeal paralysis and bronchoscopy revealed a severe (grade 3) tracheal collapse, as well as collapse of the mainstem bronchi. Magnetic resonance imaging was recommended, but declined by the owners. Anesthetic recovery was difficult and the owners requested euthanasia and a postmortem examination. Abnormalities were not detected on routine gross and light microscopic examination of the central nervous system, recurrent laryngeal nerves, and eyes. Small foci of chronic pneumonia, likely related to the laryngeal paralysis and the tracheal and bronchial collapse were the only detectable abnormalities. No other abnormalities were present on gross or light microscopic examination of the other organ systems. The diagnosis was idiopathic efferent parasympathetic pupillary defect, laryngeal paralysis, and tracheal and bronchial collapse.

The etiology and pathogenesis of the neurologic abnormalities in this dog remain unknown. Pupillotonia, Adies pupil, and a tonic pupil are synonymous terms for internal ophthalmoplegia (5). Adies pupil is actually a misnomer in the dog. Humans with Adies pupils also experience a loss of deep tendon reflexes, which has not been identified in dogs (5). Pupillotonia is an appropriate term for this uncommon, rarely reported condition of dogs (1,2). The clinical diagnosis of pupillotonia or dysautonomia is based upon response to topical parasympathomimetic stimulation, after a thorough ophthalmic examination has excluded all afferent pupillary defects (6). The dilated pupils of dogs with dysautonoamia will respond to topical parasympathomimetic stimulation, similar to pupillotonia (3–5). However, we felt that dysautonomia was less likely, as this rare condition usually causes bilateral mydriasis, elevated nictitans, and multiple gastrointestinal signs (3,4). Laryngeal paralysis has been reported to occur in approximately 30% of dogs with tracheal collapse; however, pupillotonia has not been associated with it (7). Postmortem examination failed to identify a cause for the largyngeal paralysis or the pupillotonia. Light microscopy excluded dysautonomia, as apoptotic and degenerate autonomic ganglia were not observed (4).

Uneven pupils are common clinical manifestations of multiple intraocular, extraocular, neurological, and central nervous syndrome disorders. They can be challenging to diagnose for even the experienced veterinarian.