Ischemic Optic Neuropathy in a Dog with Acute Bilateral Blindness and Primary Systemic Hypertension.

A 6-year-old neutered female Jack Russell terrier was investigated for sudden onset prechiasmatic bilateral blindness, left circling, reduced proprioception in the right pelvic limb and right facial allodynia. Electroretinography was normal. Magnetic resonance imaging (MRI) examination revealed that the right optic nerve and the optic chiasm were hyperintense on diffusion weighted imaging and hypointense on apparent diffusion coefficient map consistent with ischemic optic neuropathy. A concurrent lacunar infarct was detected in the left rostral colliculus. Primary systemic hypertension was diagnosed based on blood pressure measurement and no detectable abnormalities on hematology, comprehensive serum biochemistry, urinalysis including protein/creatinine and cortisol/creatinine ratios and thoracic/abdominal imaging. Prednisolone for 10 days and amlodipine long-term were administered. Vision was not recovered after 7 months. Repeat MRI supported the diagnosis of ischemic lesions and revealed a recent striatocapsular infarct. Ischemic optic neuropathy is a well-recognized cause of blindness in humans and should be included as a differential diagnosis for acute prechiasmatic blindness in dogs.

The effect of prophylactic topical carbonic anhydrase inhibitors in canine primary closed-angle glaucoma.

OBJECTIVES: To determine the effect of 1% brinzolamide, 2% dorzolamide hydrochloride or combination 2% dorzolamide hydrochloride/0 · 5% timolol to delay the elevation of the intraocular pressure in second eyes of dogs with primary closed-angle glaucoma. METHODS: Analysis of retrospectively collated data from 40 dogs with primary closed-angle glaucoma, where the non-affected eye was treated prophylactically with brinzolamide (n = 10), dorzolamide (n = 18) or combination dorzolamide/timolol therapy (n = 12). RESULTS: The 40 treated dogs (median age of 76 · 2 months) comprised 25 females/15 males, 19 entire/21 neutered. Twenty dogs developed glaucoma in the contralateral eye (median time of 9 · 2 months). No statistically significant difference was identified during treatment failure between the treatment groups (P = 0 · 66). The second eye remained normotensive in 20 dogs; four dogs until the conclusion of the study (median: 27 · 0 months), three dogs until death (median: 15 · 4 months), seven dogs until lost to follow-up (median: 11 · 6 months). Out of these 20 dogs, treatment was discontinued because of lack of owner compliance in two dogs and following a local drug reaction in four dogs (median: 8 · 9 months). CLINICAL SIGNIFICANCE: There was no evidence that the tested drugs delayed elevation of intraocular pressure in contralateral eyes of dogs with primary closed-angle glaucoma.