Module 9

Question 1

The retina - anatomy

Answer 1

10 layers from outer (choroid) to inner (vitreous), developed from neuroectoderm,

• RPE - layer next to choroid, non-pigmented over tapetum, important for phagocytosis of spent photoreceptor pigment, important for metabolite movement and vit A metabolism, melanin absorbs free radicals, microvilli project to surround photoceptor outer segments ^SA. Area where most retinal detachments happen.
• photoreceptor layer - outer segments of rods and cones. Rods - low light. Cones - vision during daylight. Rods>cones. Cones concentrated in area centralis. Phototransduction - process of visual stimulus conversion into neuronal signal. Inner segments separated from nuclei by the external limiting membrane.
• external limiting membrane - thin membrane, cell junctions attaching inner segments of rods and cones to Muller cells.
• outer nuclear layer - photoreceptor nuclei, axons and muller cell processes
• outer plexiform layer - terminal branches of photoreceptor axons, synapses with horizontal and bipolar cells.
• inner nuclear layer - horizontal, bipolar, muller and amacrine cells bodies. Muller cells extend from external to inner limiting membrane - support the retina. The others maintain connection between photoreceptors and ganglion cells.
• inner plexiform layer - 2nd synaptic layer. Vertical synapses between bipolar and retinal ganglion cells, lateral synapses between amacrine, bipolar and RGCs (enhances motion detection).
• ganglion cell layer - cells bodies of RGCs. one cell thick apart from central retina/visual streak.
• nerve fibre layer - axons from RGCs, running centripetally without branching to optic nerve exiting globe through the lamina cribosa. Majority synapse in lateral geniculate nucleus. Blood vessels in NFL, GCL and IPL
• inner limiting membrane - basement membrane, terminations of muller cells

Question 2

Retinal vasculature

Answer 2

Outer retina (RPE and photoreceptor layer) - supplied by choroid
Inner and mid retina are supplied by retinal vessels - short posterior ciliary arteries. 

Holangiotic - cats and dogs, 3-5 major veins visible converging on ONH, dogs anastomose in a circle on ONH, arterioles radiates from the periphery 10-20 in dogs, 3-4 in cats. Arc around a clear area 3-4 lateral to disc = area centralis.
Rats and mice also holangiotic

Merangiotic - rabbits; blood supply nasal and temporal parts of the inner retina

Paurangiotic - guinea pig, vessels are minute and only extend a short distance from the ONH.

Question 3

Assessment of the retina

Answer 3

1) visual behaviour and light reflexes
2) ophthalmoscopic examination
3) diagnostic tests

Question 4

Ophthalmoscopic examination

Answer 4

Direct and indirection ophthalmoscopy - dilated with tropicamide.
Fundal exam: vitreous, retina, retinal vasculature, tapetum, non-tapetal fundus, ONH, choroid

Close/distant direct ophthalmoscopy.
Indirect ophthalmoscopy - binocular with head mounted stereoscopic view or monocular with light source and 20D lens.

Question 5

Normal fundus

Answer 5

Tapetal fundus roughly triangular and located dorsally, base of triangle located just above or below ONH.
Polyhedral cells containing reflective crystals of zinc cysteine. Orange, yellow, green or blue or absent in colour dilute animals.
End on blood vessels in the choroid - dark spots - “stars of winslow” Cats> dogs.
Tapetum development commences at 7 weeks and is complete by 4 months.

Non-tapetal fundus: heavily pigmented, dark brown or grey, homogenous. RPE. In colour dilute this may be lightly or non-pigmented and the choroidal vasculature seen through it.

ONH - beginning of ON, composed of retinal ganglion cell axons. Elevated portion = papilla, central depression = physiological cup. White in dogs due to myelination. Pseudopapilloedema when myelination continues into NFL, not pathological, seen in golden retrievers. Cat - unmyelinated.

Question 6

General pathological changes of the fundus

Answer 6

Changes in reflectivity: neurosensory retina is transparent.
Hyporeflectivity: retinal detachment, choroidal effusion, inflammatory exudates, neoplasia
Hyperreflectivity: atrophy or degeneration - inherited, toxic, infectious or inflammatory
Pigment: pigmentation or colour changes of tapetum, loss of pigmentation, hyperpigmentation or pigment clumping in the non-tapetal area
Vascular changes: attenuation, dilation, sausaging, colour changes, perivascular cuffing
Haemorrhage: above, below, or in retina
*subretinal - large and dark
*intra-retinal - smaller and lighter, dots and blots
*superficial retinal - flame shaped following nerve fibres
*Vitreal haemorrhages - keel boat

Haemorrhage can be distinguished from pigment using green light: haemorrhage appears black and pigment is brown

Detachments: focal to total (infundibular). Focal greyish and dull, well-demarcated border. Larger appear like a membrane or curtain hanging from ora serrata or ONH.

ONH: changes in size, profile or colour

Question 7

Diagnostic tests

Answer 7

US: conscious with LA sterile US gel. If fundic view is blocked by opacity e.g. mature cataract. Retinal dz, vitreal dz, neoplasia, subretinal infiltrates. Other eye for comparison. Advanced US techniques: colour doppler to detect blood flow e.g. hyaloid arteries, contrast enhanced US (‘microbubble’ study).

Electroretingram (ERG): indications - to establish retinal activity prior to cataracts sx, and to diagnosis SARDS (flat line). yes-no ERGs; short ERG protocol after brief period of dark adaptation (20 minutes). Pupils dilated with tropicamide.
a waveform = photoreceptor activity, b = bipolar cell activity, c = RPE
Conscious, sedated or UGA depending on unit
*Positive electrode - contact lens on cornea
*reference electrode - subdermal needle 3-4cm behind the lateral canthus
*ground electrode - subdermal needle at occiput
Many variables and best carried out according to a standardised protocol.

Question 8

Diagnostic tests

Answer 8

Fluorescein angiography: serial fundic photographs are taken in rapid sequence following IV bolus of fluorescein. To investigate retinal vascular disease. Can induce emesis and anaphylaxis (the latter mainly cats)

Optical coherence tomography: humans for retinal and ON dz. Similar to US, light rather than sound waves. Images in a colour scale.

Question 9

Conditions of the retina - Developmental - CEA

Answer 9

Collie eye anomaly (CEA): congenital bilateral condition, abnormal mesenchymal differentiation.

Ophthalmoscopically: choroidal hypoplasia/dysplasia - pale patch lateral of ONH.
+/-Colobomas of ONH pink or grey, retinal vessels dip into them.
+/- secondary retinal detachments, haemorrhage

Choroidal hypoplasia is inherited - autosomal recessive, coloboma inherited unknown - polygenic.

Border, smooth and rough collies, Shetland sheepdog, Lancashire heeler.
Best seen at 5-7 weeks, mild cases may be masked after this by RPE - “go-normal”, rate 53-63%

Question 10

Conditions of the retina - Developmental - retinal dysplasia

Answer 10

Retinal dysplasia
Anomalous differentiation of the retina, folding of neurosensory retina
Non-progressive. Causes: viral, vitamin A deficiency, X-irradiation, certain drugs and intrauterine trauma. MOST ARE INHERITED.
Affect on vision depends on severity

• Focal/multifocal: central fundus, around dorsal retinal vessels and dorsal to optic disc. Rosettes or folds. grey-green dot or streaks in tapetal fundus, grey-white in non-tapetal fundus. No effect on vision. ACS, CKCS, ESS, golden retriever, Hungarian puli, Labrador retriever and Rottweiler
• Geographic: larger irregular or horseshoe shaped, tapetal>non-tapetal. Partial retinal detachments in centre. Hyperreflectivity with time in dysplastic areas and look like post-inflammatory chorioretinal scar. Impact on vision can be severe. CKCS, ESS, golden retriever, labrador retriever
• Total: completely detached, floating in the vitreous, attached only at ONH, blind with searching nystagmus. Bedlington terrier, labrador retriever and Sealyham terrier.

Question 11

Inherited retinopathies - Canine progressive retinal atrophy (PRA)

Answer 11

Multiple breed-related, bilateral symmetrical conditions involving photoreceptor degeneration, age depends on breed variation
Labrador retriever, ECS, toy and miniature poodles: PRCD
Autosomal recessive in prcd mutation but in some breeds do see dominant or x-linked forms.
Poor night vision manifests as reluctance to go outside in the dark, clinginess, bumping into things.
Eventually total blindness.
Retinal thinning - hyperreflectivity. Vascular attenuation progressing to absence of retinal vasculature. Pigment clumping in non-tapetal fundus. Pale atrophic ONH.
2ndary cataracts due to waste products from degenerate retina, hence pre-operative ERG in cases of cataracts to establish function prior to sx

Question 12

Feline progressive retinal atrophy

Answer 12

Pedigree cats.

• Abyssinian cat: autosomal dominant (CrxRdy), changes at 8 weeks, complete degeneration by 3-4 months. rod-cone dysplasia.
• Abyssinian and somali cats, also siamese and ocicat: autosomal recessive (rdAc), ophthalmoscopic changes 18 months to 2 years, end-stage by 3-5 years. CEP20.
• Persians: AIPL1. autosomal recessive. Also affects Chinchilla, himalayan and exotic shorthair breeds.
• Bengal: autosomal recessive, PRA-b, blindness in the first year of life

Question 13

Retinal Pigment Epithelial Dystrophy (RPED)

Answer 13

RPE primarily, retina secondary.
Border Collie, ECS, Golden retriever, Labrador retriever, smooth and rough collies, Briard and Polish Lowland Sheepdog.
Similar lesions seen in Vitamin E deficiency
ECS with RPED have low levels of a-tocopherol, may be inherited vitamin E deficiency.
Accumulation of autofluorescent lipopigment in the RPE cells.
Spots of brown pigment which become larger and distributed throughout the tapetum. Retinal atrophy –> hyperreflectivity around pigment. Progresses to end-stage atrophy, more generalised hyperreflectivity.
Vision affected at late stage, do not progress to total blindness and better at low light levels.
Dx: fasting plasma a-tocopherol and if low then supplemented with 600-900 IU of natural source a-tocopherol BID. Halts dz but does not reverse.

Question 14

Neuronal ceroid lipofucinosis (NCL)

Answer 14

Looks similar to PRA but breeds are different
Inherited progressive dz - brain and retinal atrophy
Border collie, Polish Owczarek Nizinny and tibetan terrier
Blindness and neurological abnormalities caused by accumulation of autofluorescent lipopigments in neurons
PON and tibetan terrier see retinal signs before CNS signs.
Ophthalmoscopic signs - hyperreflectivity and vascular attenuation

Question 15

Canine multifocal retinopathy (CMR)

Answer 15

Inherited multifocal retinopathy
First in Pyrenean Mountain Dog (recessive), subsequently Coton deTulear, English mastiff, Bull mastiff, Dogue de Boredeaux, Cane Corso, Autstralian Shepherd, Lapponian Herder.
Lesions at 11 weeks, grey/tan patches, raise/bullous at times.
Peripheral tapetal fundus but progressively spread throughout the fundus around ONH.
Do not progress past 1 year old and rarely cause visual problems
Mutations: bestrophin gene (cBEST1), designated cmr1 (PMD, AS, mastiffs), cmr2 (Coton deTulear) and cmr3 (lapponian herder)
Tests available

Question 16

Retinal dystrophy in the Briard

Answer 16

Congenital, night blindness.
ERG abnormalities at 5 weeks, ophthalmoscopic signs not seen until 2-3 years.
Sheen or alteration in tapetal colour, yellow-white spots throughout fundus
Autosomal recessive, mutation RPE65.

Question 17

Canine Stargardt Disease

Answer 17

Labrador.
Dilated pupils, retained menace response.
Greyish hyporeflective areas in the visual streak and peripheral tapetal fundus on exam
Younger dog - streak of altered reflectivity dorsal to ONH, no obvious visual deficits.
ABCA4 ‘loss-of-function’ mutation

Question 18

Genetic testing for inherited retinopathies

Answer 18

Genetic testing invaluable for adult onset diseases which is often after breeding age
Blood or cheek swabs but are only available for certain conditions hence eye panellist exams still advised
Genetic tests are specific and only test for the one mutation
Golden retriever has 4 forms of PRA identified, there are tests for 3 of them!

Question 19

Acquired Retinopathies - uveodermatological disease

“vogt-koyanagi-Harada-like syndrome”

Answer 19

UVD - uveodermatological disease
Rare multisystemic autoimmune disease. T-cell mediated process directed at one or more antigenic components of melanocytes in the eye and skin.
Granulomatous anterior uveitis +/- chorioretinitis, vitiligo and poliosis of periocular skin, lips, muzzle and nasal planum.
Lymphocyte, plasma cells, epithelioid cells, macrophages
Lichenoid interface dermatitis with pigmentary incontinence in the dermis
Do not see neuro signs like in people
Spitz breeds: akita, samoyed, siberian husky
Skin lesions - T cells and macrophages (Th1 immunity)
ocular lesions - B cell and macrophages (Th2 immunity)
Sequalae to uveitis - retinal detachment, intractable secondary glaucoma –> enucleation
Tx: CCS, systemically and topically, atropine, non-PGF2a anti-glaucoma meds e.g. CAI. +/- ciclosporin

Question 20

Sudden Acquired Retinal Degeneration Syndrome (SARDS)

Answer 20

Acute bilateral blinding condition - no tx.
Vision is lost suddenly over a period of days
Middle-aged, overwt, small breed, FN
Cushingoid symptoms (PUPD, wt gain, ^ALP, ALT, cholesterol and bilirub)
Most neg on ACTH stim
Likely immune mediate attack on photoreceptors, anti-retinal antibodies in affected dogs
Fundus may be normal but a few months later will see retinal degeneration and end-stage retina
Dx: ERG, chromatic PLR testing - unresponsive to red light, slow response to bright white, response to blue light.

Question 21

Taurine deficiency

Answer 21

Taurine - sulphur containing amino acid, essential in cats.
Deficiency causes characteristic retinopathy.
Begin with granular appearance in tapetal fundus –> hyperreflective area in area centralis –> lesion on nasal side –> coalesce –> eventually entire retina
Taurine: highest concentrations in the inner and outer segments of photoreceptors of photo receptors, protects them from light and chemical damage.
Lesions remain lifelong so may not indicate current taurine deficiency.
plasma taurine <40nmol/l is indicative of a problem.
Stages:
1- granular appearance
2- hyperreflective area in area centralis
3- lesion on nasal side
4- two foci coalesce
5- entire fundus

Question 22

Enrofloxacin toxicity

Answer 22

Acute irreversible degeneration in cats. 0.008% of cats treated with enrofloxacin
Marbofloxacin and orbifloxacin at high doses
Degeneration of outer retinal layer on histo, ERGs extinguished
Differences in ABCG2 binding protein (transports molecules across cell membranes)
Blindness and mydriasis
Granular tapetum early on, ^reflectivity, retinal vasculature attenuation, progresses to diffuse hyperreflectivity, vessel loss, pigment loss, clumping in non-tapetal fundus.
Only use if no other choice, consider split dosing. Avoid rapid IV.

Question 23

Chorioretinitis

Answer 23

• Choroid and retina usually become inflamed simultaneously
• (retinochoroiditis far less common, except neospora)
• Traumatic, neoplastic, immune-mediated, or infectious
• Dogs: viral - canine distemper. Bacterial - leptospirosis, borreliosis. Protozoal - toxoplasmosis, neosporosis. Parasitic - toxocariasis, angiostrongylosis.
• Cats: viral - FIP, feline panleucopaenia, FeLV, FIV. Bacteria - mycobacteriosis. Protozoal - toxoplasmosis.
• Inflammatory lesions can be uni or bi and are usually irregular in shape, rarely bilaterally symmetrical unlike inherited retinopathies

Question 24

Acute Chorioretinitis

Answer 24

In the tapetal fundus - retinal oedema/cellular infiltration are seen. Grey hyporeflective areas, indistinct border +/- haemorrhages.
Haemorrhage characteristic of rickettsial infections.
Pigmentation of RPE over tapetum
Non-tapetal fundus - active inflammatory lesions are grey/white, perivascular cuffing may be seen; grey or white accumulations of inflammatory cells around the retinal blood vessels
Retinal detachments - grey areas with distinct borders, exudate has accumulated between photoreceptors and RPE and lifted off the neurosensory retina.
Granulomatous lesions - fungal
Secondary = vitreous syneresis (haze or liquefaction), ONH swelling/haemorrhage

Question 25

Chronic Chorioretinitis

Answer 25

Inflammation progressing for some time, or has abated, appearance is different
Irregular well-demarcated areas of hyperreflectivity +/- pigmented centres due to hypertrophy/hyperplasia of RPE
Colour changes or destruction of tapetum can occur
Exposure of choroid vessels or sclera
Non-tapetal fundus: well-demarcated area of depigmentation, exposure of choroidal vessels, pigment clumping.
Retinal vessels crossing inflammatory lesions may be attenuated, tortuous or delineated by pigment. Choroidal vessels may be atrophied.
+/- ONH atrophy

Question 26

Retinal detachments

Answer 26

neuroretina is separated from RPE –> retinal degeneration in the area

• Congenital - CEA or TRD
• Rhegmatogenous - tear allows fluid from vitreous in primary (shih tzu) or seconday (trauma, sx, laser etc)
• Non-rhegmatogenous - 1) exudative - fluid or cell accumulation from hypertension, chorioretinitis, neoplasia, or 2) traction - fibrous tissue develops in vitreous from IO haemorrhage or inflammation (sx or trauma)
• steroid responsive - exudative detachment, dx of exclusion, GSD types, can reattach following systemic steroids.

Question 27

Treatment of retinal detachments

Answer 27

Find primary cause if possible
Work up:
1) ophthalmic exam
2) general CE
3) haematology and biochemistry (+ T4 in cats, clotting profile in dogs)
4) BP
5) serology/PCR for location and travel history for infectious dzs
6) Chest rads and abdo US - r/o neoplasia or infection - pyo!

If all neg then CCS for 10 days and then taper. Prognosis deteriorates once retina detached for more than a few days. Retinal degeneration will follow. Sx repair for rhegmatogenous types, only offered at two sites in UK. Diode retinopexy more common, prevents enlargement of existing tears - transsclerally or transpupillary.

Question 28

Retinal vascular disease - hypertension

Answer 28

Systemic hypertension: BP >160mmHg. Primary/essential or secondary (more likely).
Dogs: renal dz, HAC, phaeochromocytoma, primary aldosteronism, DM, hypoT4
Cats: renal, hyperT4, primary aldosteronism, DM
Renal dz most common, especially in cats, 1 in 5 cats with CRD are hypertensive.

Hypertension damage to eye:

1) retinal arterioles constrict in response to ^BP
2) sustained constriction –> ischaemic necrosis of vessel walls
3) ^vascular permeability –> serous retinal exudates, haemorrhage and oedema
4) choroidal vascular changes, subretinal fluid accumulation and retinal detachment
5) RPE ischaemic damage –> retinal detachment

Fundic exam: arterial tortuosity, retinal oedema, pre, intra and sub-retinal haemorrhage. Partial or total retinal detachments. Papilloedema, haemorrhage in vitreous or anterior chamber.

Dx: BP, fundic exam, thoracic ausc, bloods to assess renal and thyroid function.
Cats - Doppler best. Dogs - oscillometric best. Systolic BP should be measured.

Tx: lowering BP ASAP, txing underlying condition as soon as possible and maintain around 140mmHg. Ca channel blocker - amlodopine. ACE inhibitor benazepril added in if hypertension remains uncontrolled or if proteinuria. Monitor BP every 4-6 months once stable. Telmisartan (semintra) now licensed for tx.

Question 29

Retinal vascular disease - hyperviscosity syndrome

Answer 29

Elevated serum protein levels –> hyperviscosity. Monoclonal gammopathy or polycythaemia
Underlying dz: neoplastic or infectious (erhlichiosis or FIP)
Tortuous and dilated retinal vessels - sausaging and box-car appearance.
Retinal or vitreal haemorrhage, retinal detachments
Dx: blood tests

Question 30

Hyperlipidaemia

Answer 30

Elevated plasma cholesterol/triglycerides.
Primary - miniature schnauzer, Burmese cat.
Secondary - DM, pancreatitis, hypoT4, liver dz, high fat diet, transient episode
Blood milky appearance - lipaemia retinalis - pale pink engorged vessels
BAB has to be compromised for lipoproteins to access anterior chamber.
Chicken or egg… uveitis pre-existing or hyperlipidaemia causes uveitis?
Work up: diet hx, bloods - haem and biochem, fasting triglycerides and cholesterol, T4, urinalysis.
Lipoprotein analysis may be required.

Question 31

Diabetic retinopathy

Answer 31

Retinal vasculature changes and cataract. Retinal lesions in 1 in 5 dogs - haemorrhages and microaneurysms.

Question 32

Neoplastic and proliferative conditions

Answer 32

Primary: rare in retina, may see:

• Choroidal melanoma - darkly pigmented mass underlying retina and tapetum adjacent to ONH, benign. Retinal detachment and haemorrhages can occur
• astrocytoma, teratoid medulloepithelioma, retinoblastoma

Secondary:

• lymphoma most common. Ophtho exam - chorioretinitis, retinal haemorrhages, tapetal changes, pipilloedema.
• extension of anterior ocular tumours, ON, EO tissue or mets.
• feline carcinoma mets characteristic sectoral infarctions within the choroid. Wedge shaped areas of tan/grey discolouration of the tapetum fanning out from the ONH

Question 33

Neoplastic and proliferative conditions

Answer 33

Primary: rare in retina, may see:

• Choroidal melanoma - darkly pigmented mass underlying retina and tapetum adjacent to ONH, benign. Retinal detachment and haemorrhages can occur
• astrocytoma, teratoid medulloepithelioma, retinoblastoma

Secondary:

• lymphoma most common. Ophtho exam - chorioretinitis, retinal haemorrhages, tapetal changes, pipilloedema.
• extension of anterior ocular tumours, ON, EO tissue or mets.
• feline carcinoma mets characteristic sectoral infarctions within the choroid. Wedge shaped areas of tan/grey discolouration of the tapetum fanning out from the ONH

Question 34

Granulomatous Meningoencephalitis (GME)

Answer 34

Immune mediated
idiopathic non-suppurative meningoencephalitis
Retinal detachments especially in the papillary area due to effects on ONH

Question 35

Vitreous - embryology

Answer 35

Embryology:

• Primary - hyaloid and its branches which nourish the lens, mesenchymal cells, collagenous fibrils, macrophages.
• secondary - fetal fissure closes, fill the space of the posterior segment. Expansion of secondary vitreous leads to atrophy of primary vitreous. Central zone - cloquet’s canal, mittendorf’s dot on posterior lens capsule. Regression complete a few weeks post birth
• tertiary - condensation of collagen fibres between lens equator and optic cup. Non-pigmented ciliary epithelium may be involved in their formation

Question 36

Vitreous - anatomy and physiology

Answer 36

2/3 eye volume. Lens sits in Hyaloid fossa.
Central portion - funnel-shaped tracts, cloquet’s canal in centre
99% water, 1% collagen, hyalocytes, soluble protein and hyaluronic acid.
Intermingle with fibres of inner limiting membrane forming weak attachments
stronger attachments at the : Hyalocapsular ligament and ora ciliaris retinae and pars plana (vitreous base), ONH
Hyalocytes - derived from macrophages, contain high number of lysosomes suggesting phagocytic role and produce hyaluronic acid in vitro

Functions: Transmit light, mechanical support, maintain position of retina, metabolic properties

Question 37

Vitreous - Pathology

Answer 37

Degeneration: ageing process or as a result of ocular disease

• Syneresis - vitreal collagen framework breaks down - liquefaction. Collagen clumps - floaters. Strand or clumps swirling around in the liquefied vitreous. Can lead to detachments. Primary in bichon frise, whippet, italian greyhound
• Asteroid hyalosis - does not liquefy, fixed sparkling particles in the gel, calcium/phospholipid complexes, does not affect vision.
• Synchysis scintillans - liquefaction, swirling particles when head is moved, settle ventrally when still. “snowstorm”. Cholesterol particles, doesn’t impact vision but is a result of other ocular dz which may do so.

Haemorrhage: avascular so bleeding from persistent embryological vessels or adjacent structures. PHTVL/PHPV, CEA, hypertension, trauma, coagulopathies, uveitis, chorioretinitis, retinal detachment, IO sx. Vitreous haemorrhages - breakdown of blood products is toxic to retina, formation of fibrous vitreal membranes –> traction bands

Inflammation: hyalitis/vitritis - inflammatory response from adjacent structures, inflammatory cells, proteins and blood enter vitreous. Haze which may make fundic examination impossible.

Traction bands: following inflammation or haemorrhage - retinal detachment.

Question 38

Conditions of vitreous - congenital/developmental

Answer 38

Persistent hyaloid artery: most species atrophies within the first few weeks of life, small worm arising from the posterior lens capsule, +/- cataract, +/- blood, rare the whole artery persists, Doppler US may demonstrate if patent. Glial remnant on optic disc are termed Bergmeister’s papilla.

Persistent tunica vasculosa lentis: not common, web like strands or punctate pigmented opacities, not usually associated with cataracts or effect on vision

Persistent hyperplastic tunica vasculosa lentis/persistent hyperplastic primary vitreous: parts of hyaloid and tunica become hyperplastic during early development and combined with incomplete regression. may see a few pigmented dots on posterior lens capsule to dense fibrous plaques containing vascular elements. Cataracts and other lens anomalies may be seen. Vision depends on level of abnormalities. Can occur in any breed by inherited in staffies and dobies.
Grading for dobies:
1) retrolental pigment dots, minor posterior capsular cataracts
2) more intense central posterior capsular cataract, yellow-brown capsular/retrolental fibrous tissue. +/- PPM
3) PTVL + grade 2
4) posterior lenticonus + grade 2
5) grade 3+4
6) as above but lens coloboma, microphakia, accumulations of pigment and blood

Question 39

Acquired vitreal abnormalities

Answer 39

Degenerative changes as before

Vitreal cysts: uveal origin - incidental

Neoplasia: arise from other adjacent structures or cause hyalitis

Parasites: migrating parasites - T. canis, D. immitis, A. vasorum, death may elicit significant inflammation, sx removal may be indicated.

Question 40

Optic nerve

Answer 40

Anatomy: intraocular - ONH can be visualised. depression centrally - physiological cup. Ganglion cells axons - converge on ONH, joined in bundles or fascicles which are separated by glial cells and lamina cribrosa at level of choroid and sclera.

Mitochondria and vesicles continually moving with axon - axonal flow. Constant protein synthesis occurs at synaptic ending (orthograde) or toward the cell body (retrograde). Axonal flow can be impeded by ^IOP.

Dogs - myelinated along entire length of nerve including ONH.
Cat - ONH unmyelinated.

Orbital portion shares meningeal sheaths of CNS: outer - dura mater which fuses with sclera, arachnoid sheath and internally pia mater which sends radial septae into the nerve.

Question 41

ON - physiology

Answer 41

Ganglion cell axon and glial cells populations:

• oligodendrocytes; myelin sheath
• astrocytes; transporting and storing metabolites
• microglia; resident macrophages, role in immune system

hyperpolarised in resting state, negative resting potential. Na channels open, inflow of Na, action potential generated along the axon. Electrical conduction more efficient by myelination and Na channels groups in gaps known as nodes of ranvier. Salutatory conduction - jumping conduction.

Retinotopic arrangement of axons - spatial arrangement in retina is maintained

Question 42

Conditions of the ON - congenital/developmental

Answer 42

ONH hypoplasia - reduction in ON axons. uni or bi. Alone or as part of MODs. Toy, mini poodles, mini LH dachshunds. Inheritance unknown. Small and grey. Retina and BV normal. Reduced vision unlike micropapilla where ONH is small but otherwise normal and has no visual defects.

ON coloboma - absence of tissue, typically at 6 o’clock position from incomplete closure of optic fissure. Collie breeds as part of CEA, or others as separate condition. Small grey/pink pits to large excavation. Vision not affected unless very large!

Question 43

Acquired condition of ON

Answer 43

Papilloedema: disc swelling associated with ^ICP, bilateral, visual deficits late in dz, brain tumours mostly, occasionally ^CSF pressure

Optic neuritis: neoplastic, immune mediated, idiopathic or infectious cause.
Infectious causes: CDV, toxo, neospora, cryptococcosis, FIP
Sudden onset blindness, fixed dilated pupils.
ONH swollen, hyperaemic, oedematous, blurred margins, loss of physiological cup. haemorrhages and peripapillary retinal oedema. If retrobulbar there may be no ophthalmoscopic signs and advanced imaging will be required to dx - potentially US but CT/MRI preferable. +/- CSF tap.
Tx: underlying cause if identified but most are idiopathic or immune mediated. CCS for 10-14 days, tapering slowly. Monitoring PLRs, and appearance of the ONH. +/- other immunosuppressives. prognosis for vision guarded.

Question 44

GME (little white fluffy dog dz)

Answer 44

young, small breed dogs. perivascular cuffing with macrophages and lymphocytes on histo.
Primary immune mediated.
CS: neurological, multi-focal brain dz.
ONs may be involved, present as a sudden onset blindness.
Papilloedema, peripheral haemorrhage, retinal detachments
Dx: CS, advanced imaging, and elevated protein and inflammation in CSF
Tx: steroids, cytosine arabinoside.
Px: weeks to years.

Question 45

ON tumours

Answer 45

Uncommon in dogs, rare in cats.

Dogs: meningioma –> exophthalmos, visual deficits, abnormalities of PLR, papilloedema, optic neuritis.
US/CT/MRI are essential part of work up.
Teratoid medulloepithelioma, gliomas, SCC, nasal and orbital tumours.

Cats: lymphoma

Question 46

ONH atrophy

Answer 46

previous inflammation; optic neuritis or trauma, or ^IOP
Dark and grey, loss of myelin, crenelated appearance. BVs absent.

Glaucoma - cupping of ONH, bowed outwards from IOP pushing on lamina cribrosa.
-Binocular indirect ophthalmoscopy or direct ophthalmoscope with negative lenses to bring into focus. each dioptre difference is 0.3mm cupping.