Presumed neuroprotective therapies prescribed by veterinary ophthalmologists for canine degenerative retinal and optic nerve diseases.

OBJECTIVE: To investigate veterinary ophthalmologists' use of presumed neuroprotective therapies for degenerative retinal and optic nerve diseases in dogs. PROCEDURES: An online survey was sent to 663 board-certified veterinary ophthalmologists who were Diplomates of the American College of Veterinary Ophthalmologists (ACVO), Asian College of Veterinary Ophthalmologists (AiCVO), Latin American College of Veterinary Ophthalmologists (Colegio Latinoamericano de Oftalmólogos Veterinarios, CLOVE), or European College of Veterinary Ophthalmologists (ECVO). The survey was created using Qualtrics® software and focused on the prescription of presumed neuroprotective treatments for canine glaucoma, sudden acquired retinal degeneration syndrome (SARDS), progressive retinal atrophy (PRA), and retinal detachment (RD). RESULTS: A total of 165 completed surveys were received, representing an overall response rate of 25%, which was comparable across the four specialty colleges. Of all respondents, 140/165 (85%) prescribed some form of presumed neuroprotective therapies at least once in the last five years: 114/165 (69%) for glaucoma, 51/165 (31%) for SARDS, 116/165 (70%) for PRA, and 50/165 (30%) for RD. The three most recommended neuroprotective reagents were the commercial Ocu-GLO™ Vision Supplement for animals, amlodipine, and human eye supplements. CONCLUSIONS: Despite lack of published clinical efficacy data, the majority of surveyed board-certified veterinary ophthalmologists previously prescribed a presumed neuroprotective therapy at least once in the last five years in dogs with degenerative retinal and optic nerve diseases.

Magnetic resonance imaging characteristics of equine head disorders: 84 cases (2000-2013).

The equine head is an anatomically complex area, therefore advanced tomographic imaging techniques, such as computed tomography or magnetic resonance imaging (MRI), are often required for diagnosis and treatment planning. The purpose of this multicenter retrospective study was to describe MRI characteristics for a large sample of horses with head disorders. Horses imaged over a period of 13 years were recruited. Eighty-four horses met the inclusion criteria, having neurological (n = 65), sinonasal (n = 14), and soft tissue (n = 5) disorders. Magnetic resonance imaging accurately depicted the anatomy and allowed identification of the primary lesion and associated changes. There were good correlations between MRI findings and intraoperative or postmortem results. Magnetic resonance imaging showed the exact localization of the lesions, their size, and relation to surrounding structures. However, in the neurological group, there were 45 horses with no MRI abnormalities, 29 of which had a history of recurrent seizures, related to cryptogenic epilepsy. Magnetic resonance imaging was otherwise a valuable diagnostic tool, and can be used for studying a broad range of head disorders using either low-field or high-field magnets.

Optic neuropathy in a herd of beef cattle in Alberta associated with consumption of moldy corn.

A group of beef cattle in eastern Alberta was investigated due to sudden onset of blindness after grazing on standing corn in mid-winter. Fumonisin-producing Fusarium spp. were isolated from the corn. Blindness was due to an optic nerve degeneration suspected to be secondary to fumonisin mycotoxin.

Neuropathie optique dans un cheptel de bovins de boucherie en Alberta associée à la consommation de maïs moisi. Un groupe de bovins de boucherie de l'est de l'Alberta a fait l'objet d'une enquête en raison de l'apparition soudaine de cécité après avoir brouté du maïs sur pied vers le milieu de l'hiver. Fusarium spp., qui produit la fumonisine, a été isolé dans le maïs. La cécité a été attribuable à la dégénération du nerf optique ayant pour cause suspectée la mycotoxine fumonisine.(Traduit par Isabelle Vallières).

Contralateral optic neuropathy and retinopathy associated with visual and afferent pupillomotor dysfunction following enucleation in six cats.

PURPOSE: To investigate contralateral optic neuropathy and retinopathy following enucleation in 6 cats. METHODS: Retrospective study. The medical records of cats with contralateral visual and afferent pupillomotor dysfunction following enucleation presented to the Animal Health Trust (AHT), Newmarket, UK, between January 1994 and January 2010 were reviewed. Information recorded included history, signalment, ophthalmic findings, electroretinography (ERG) (2/6) and MRI (3/6) findings and long-term outcome. Pearson's chi-square tests were used to compare breed proportions (P < 0.05). RESULTS: Six cats aged 1.5 to 11 (median 5.5) years presented with mydriasis and/or visual deficits noted immediately following enucleation. Enucleation involved optic nerve (ON) ligation in all of the four cases for which this information was available. Ophthalmic findings included mydriasis with absent pupillary light reflex (PLR) (4/6), incomplete PLRs (2/6), absence of dazzle reflex (4/6) and absence of menace response (4/6). Funduscopy initially revealed multifocal peripapillary retinal lesions, with subsequent progressive optic nerve head (ONH) and retinal atrophy. ERG recordings revealed normal outer retinal function at 6 and 22 weeks (2/2). On MRI, the optic chiasm (OC) ipsilateral to the enucleation could not be identified and the contralateral OC was atrophied (3/3). CONCLUSIONS: The acute afferent ON deficits following enucleation, progressive ONH atrophy, normal outer retinal function and MRI demonstrating OC pathology are consistent with chiasmal injury due to traction on the ON during enucleation. Rostral traction on the globe to facilitate ON ligation is contraindicated in cats.

Bilateral vision loss in a captive cheetah (Acinonyx jubatus).

The following case report describes a 1-year-old female cheetah (Acinonyx jubatus) with bilateral blindness and unresponsive pupils. For comparison, a second healthy 2.5-year-old male cheetah without visual deficits was also examined. Clinical examination of both animals included biomicroscopy, indirect ophthalmoscopy, tonometry, and electroretinography. The young female cheetah showed no menace response, no direct or indirect pupillary light reflex, and no dazzle reflex in either eye. Fundus lesions, as detected by indirect ophthalmoscopy, are described for the female animal. In both eyes, the fundus color was green/turquoise/yellow with multiple hyperpigmented linear lesions in the tapetal area around the optic nerve. The optic nerve head was dark gray and about half the normal size suggesting bilateral optic nerve hypoplasia and retinal dysplasia or differentially optic nerve atrophy and chorioretinal scarring. The ERG had low amplitudes in the right eye but appeared normal in the left eye compared with the male cheetah. Blood levels did not suggest current taurine deficiency. This is addressed to some degree in the discussion. Bilateral optic nerve hypoplasia or optic nerve atrophy is a rare anomaly in cats and has not yet been described in a cheetah.

Unilateral optical nerve hypoplasia in a Beagle dog.

Unilateral (left eye) optic nerve hypoplasia was detected in a six-month-old male Beagle dog. Vision testing indicated that the left eye had poor vision and testing the pupillary light reflex showed the left eye to have an absence of the afferent pathway of the reflex but it had a normal efferent pathway. Ophthalmoscopy revealed a small-sized optic disc, winding retinal artery and dilated retinal vasculature in the left globe. Electroretinography showed no abnormal findings even in the left globe. Histopathologically, the left optic nerve was markedly hypoplastic and was composed of sparse neural elements and a moderate amount of connective and glial tissues. In the retina of the left globe, the nerve fibre layer and the ganglion cell layer were reduced in thickness, although a small number of ganglion cells were still present. There were no abnormal findings detected in the right globe and the right optic nerve. The brain appeared normal macroscopically.

Myelin vacuolation, optic neuropathy and retinal degeneration after closantel overdosage in sheep and in a goat.

Toxicity of closantel, a halogenated salicylanilide anthelmintic, is described in 11 sheep and a goat, humanely killed 4-70 days after accidental overdosage. Status spongiosis of the cerebrum and cerebellum was present, its severity decreasing with time after treatment. Ultrastructurally, vacuoles in the cerebral white matter were seen to be intramyelinic due to splitting of myelin lamellae at the intraperiod lines, indicating myelin oedema. In the optic nerves, Wallerian degeneration and eventual fibrosis and atrophy of the nerves followed myelin vacuolation. Lesions in the optic nerves were particularly advanced in the intracanalicular portion, indicating a compressive neuropathy within the optic canal. Acute retinal lesions consisted of papilloedema, necrosis of the outer retinal layers (especially the photoreceptor layer), and retinal separation in tapetal and non-tapetal areas. In more chronic cases, the outer nuclear layer was diffusely attenuated and generally reduced to a single row of cells.

Acute Blindness.

Sudden loss of vision is an ophthalmic emergency with numerous possible causes. Abnormalities may occur at any point within the complex vision pathway, from retina to optic nerve to the visual center in the occipital lobe. This article reviews specific prechiasm (retina and optic nerve) and cerebral cortical diseases that lead to acute blindness. Information regarding specific etiologies, pathophysiology, diagnosis, treatment, and prognosis for vision is discussed.

Congenital pits of the optic nerve head. I. Experimental studies in collie dogs.

In three collie dogs with a congenital pit of the optic nerve and associated serous macular detachment, no connection between the subarachnoid space and the pit or subretinal fluid could be demonstrated with subarachnoid injection of India ink or with serial sections of the eyes. A direct communication between the vitreous, the pit, and the subretinal space could be demonstrated, however, in all three dogs. Flow of India ink particles from the vitreous to the pit and into the subretinal space was demonstrated. Indirect evidence to support the above mechanism in humans includes the biomicroscopic observation of channels coursing from the pit toward the subretinal space and the presence of posterior vitreous detachment or liquefaction of the vitreous in patients with optic pits and macular detachment.

Cataracts and optic nerve hypoplasia in turkey poults.

Newly hatched commercial turkey poults culled because of grossly visible cataracts were studied. A total of 43 affected and 23 unaffected control poults at various ages were necropsied, and the ocular changes in affected poults were compared with those of aged-matched controls. Affected poults had consistent cataracts coupled with a marked depletion in retinal inner plexiform, ganglion cell, and optic nerve fiber layers, with a resultant reduction in the size of the optic nerves. Lesions were seen in 1-day-old poults. Lens changes included microphakia and lens fiber degeneration throughout the lens, with nuclear liquefaction. The depletion in the numbers of retinal ganglion cells did not appear to progress over several weeks time. The ganglion cell depletion was not uniform within the retina. The cause for these ocular changes is unknown.

Glioma of the optic nerve with intraocular and intracranial involvement in a dog.

An anaplastic glioma of the optic nerve, involving the globe, optic chiasma and brain in a 3 1/2-year-old Labrador Retriever is described. The tumour consisted of lobules of small, dark cells intersected by a delicate fibrovascular stroma. There was a high degree of anaplasia and an average of 19 mitoses per x 200 field. The clinical signs were exophthalmos and mydriasis, followed several months later by blindness and, only terminally, by signs of brain involvement.

Internal hydrocephalus, optic nerve aplasia, and microphthalmia in CPB-WE (Wezob) and Cpb:WU (Wistar) rats.

Wistar rats of the inbred CPB-WE and the random bred Cpb:WU strains have been used in neuroanatomical studies. In both groups of rats a high incidence of hydrocephalus was observed. In the CPB-WE rats the ventricular dilatation was accompanied by optic tract lesions and microphthalmia. The present report describes the gross and microscopic findings in these rats and discusses the possible aetiology.

Treatment of serous retinal detachments associated with optic disk pits in dogs.

Serous retinal detachment, associated with optic disk pit, was diagnosed in 28 eyes of 24 dogs. Xenon arc photocoagulation was used in treatment of the detachment. Of 24 dogs, 21 were Collies. In 23 eyes, retinal detachments affected temporal and/or inferior portions of the retina. In 5 eyes, detachments were predominantly superior and/or nasal. A single photocoagulation treatment resulted in reattachments in 25 eyes. Of the 3 remaining detachments, 2 eyes improved with additional photocoagulation, and 1 eye, which was not treated further, had a complete retinal detachment.

Update on llama medicine. Ophthalmology.

Review of the limited literature on camelid eyes suggests they are anatomically similar to those of domestic livestock species, except they lack meibomian glands and have iridial folds (rather than corpora nigra). The microbial flora of the healthy camelid conjunctival sac also appears to be similar to those of domestic livestock and pets, except that no Mycoplasma have been isolated from camelids. Ocular diseases for which camelids are presented to veterinarians are numerous and varied. The most frequently presented conditions are ocular trauma and congenital abnormalities. Trauma to cornea, conjunctiva, eyelids, and sclera has been reported. Therapies for these injuries are the same as for other animals. Most congenital abnormalities are cataracts and optic nerve colobomas, but congenital eyelid defects, conjunctival cysts, and multiple ocular defects have been reported. Although these conditions are not demonstrably hereditary, breeding of animals with congenital ocular defects is strongly discouraged. Intraocular inflammatory diseases are seen commonly in camelids. Uveitis and chorioretinitis may cause permanent visual loss, usually with no indication of cause. Equine herpesvirus 1 has been isolated from camelids with severe ocular inflammation and is a known cause of chorioretinitis and neurologic abnormalities. Systemic aspergillosis causes severe chorioretinitis in alpacas. More research is needed to improve our understanding of ocular physiology and pathology in camelids. Genetic studies also are needed to establish hereditary patterns of ocular maldevelopment. Additional information from researchers and practitioners should improve our ability to recognize and treat ocular disease in camelids.

Functional and structural changes in a canine model of hereditary primary angle-closure glaucoma.

PURPOSE: To characterize functional and structural changes in a canine model of hereditary primary angle-closure glaucoma. METHODS: Intraocular pressure (IOP) was evaluated with tonometry in a colony of glaucomatous dogs at 8, 15, 18, 20, and 30 months of age. Retinal function was evaluated using electroretinography (scotopic, photopic, and pattern). Examination of anterior segment structures was performed using gonioscopy and high-frequency ultrasonography (HFU). RESULTS: A gradual rise in IOP was observed with an increase in age: 8 months, 14 mm Hg (median value); 15 months, 15.5 mm Hg; 18 months, 17.5 mm Hg; 20 months, 24 mm Hg; 30 months, 36 mm Hg. Provocative testing with mydriatic agents (tropicamide and atropine 1%) caused significant increases in IOP (35% and 50%, respectively). HFU analysis showed complete collapse of iridocorneal angles by 20 months of age. Scotopic and photopic ERG analysis did not reveal significant deficits, but pattern ERG analysis showed significantly reduced amplitudes in glaucomatous dogs (glaucoma, 3.5 +/- 0.4 muV; control, 6.2 +/- 0.3 muV; P = 0.004; Student's t-test). Histologic analysis revealed collapse of the iridocorneal angle, posterior bowing of the lamina cribrosa, swelling and loss of large retinal ganglion cells, increased glial reactivity, and increased thickening of the lamina cribrosa. CONCLUSIONS: Canine hereditary angle-closure glaucoma is characterized by a progressive increase in intraocular pressure, loss of optic nerve function, and retinal ganglion cell loss.