ISSN 2398-2969      

Optic neuropathies

icanis
Contributor(s):

Kyle Braund


Introduction

  • Congenital or acquired (more common).
  • Include optic neuritis, optic nerve head atrophy and optic nerve hypoplasia.
  • Cause: inflammation, eg granulomatous meningoencephalitis, canine distemper, neoplasia, trauma, acute toxicity, eg lead, organochlorine poisoning.
  • Signs: unilateral or bilateral blindness.
  • Diagnosis: signs.
  • Treatment: steroids for inflammatory lesions, no treatment for hypoplasia or atrophy.
  • Prognosis: guarded.

Pathogenesis

Etiology

Predisposing factors

General
  • Presently unknown.

Specific

  • Presently unknown.

Pathophysiology

  • Degeneration, inflammation, space occupying lesion, trauma, toxicity, or hypoplasia of optic nerve → loss of optic nerve function → loss of visual pathways and pathways for direct pupillary light reflex → blindness and dilated pupils which are unresponsive to light → repeated episodes of optic neuritis → optic nerve head atrophy.

Timecourse

  • Typically acute onset in dog with optic neuritis.
  • Some dogs have a return of vision within days of treatment, others may show only gradual improvement over months.
  • Recurrences are not uncommon.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • McEntee K et al (1995) Closantel intoxication in a dog. Vet Human Toxicol 37 (3), 234-236 PubMed.
  • Brooks D E et al (1991) The treatment of canine ocular blastomycosis with systemically administered itraconazole. Prog Vet Comp Ophtha(4), 263-268 VetMedResource.
  • Turnquist S E et al (1991) Unilateral optic nerve hypoplasia and hydrocephalus in a Pekingese. Cornell Vet 81 (3), 305-311 PubMed.
  • Boldy K L et al (1989) Uveodermatologic syndrome in the dog - clinical characteristics and treatment of a disorder similar to human Vogt-Koyanagi-Harada syndrome. Vet Focus (3), 112-114 VetMedResource.

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