Module 8 Flashcards
Glaucoma
How is aqueous produced? Where? What causes glaucoma?
Physiological control of IOP
Constant production and drainage.
Aqueous, from non-pigmented epithelium of ciliary body. 80% active, 20% by diffusion and ultrafiltration.
Active: CO2 + H2O –> (catalyse by carbonic anhydrase) H2CO3 –> HCO3- + H+
Movement of bicarbonate ions into the posterior chamber creates osmotic gradient, water from ciliary stroma moves into posterior chamber as well.
Hence, how carbonic anhydrase inhibitors drop IOP
Junction of base of iris and corneoscleral tissue = iridocorneal angle which includes drainage apparatus; the pectinate ligaments and ciliary cleft (full of trabecular meshwork tissue) = conventional drainage
Unconventional drainage = uveoscleral outflow
IOP only increases in glaucoma as a results of increased outflow resistant, not from hypersecretion of aqueous.
Normal variations in IOP
RR 15-25mmHg Variations: -instrumentation used -age of dog; may decrease with age -Head position; head up or dorsal recumbency ^IOP -Restraint; vigorous may ^ IOP -Forced lid opening; ^IOP -Breed; terriers, fluctuant IOP -Obesity and A-BP
Gonioscopy required to asses drainage angle in dogs, not required for cats. Not dilated and LA applied.
Glaucoma; “The Glaucomas”
Glaucoma = increased IOP –> damage to retina and ON that results in total irreversible blindness.
A complex of several separate entities. Prolonged elevated IOP in our species. Humans have a form of normotensive glaucoma. Most profound damage is on ONH with ganglion cells –> visual field loss.
Clinical signs. Acute. Dogs only.
Pain - nociceptors in cornea and globe. Behavioural changes. Ocular signs; blepharospasm, photophobia, increased lacrimation.
Corneal oedema - endothelial pumps actively transports solutes out of the stroma into the aqueous. ^IOP interferes with this and the excess water disrupts the stromal lamellae. Less marked in lower IOP, chronic cases and cats. Deep corneal vessels - brush border may be seen, especially secondary to uveitis.
Mydriasis - pressure induced paresis or paralysis of iris sphincter muscle, moderate to dilate pupil. In some cases pupil may be constricted.
Episcleral congestion - common feature, engorged vessels run at right angles to the limbus, do not move when conj moved. Not all cases of episcleral congestion = glaucoma as can also occur in uveitis/panopthalmitis, episcleritis, retrobulbar-space occupying lesions.
Vision loss - ONH damage results in loss of vision. Second eye is usually starting to be affected by time of presentation. Os rarely notice unilateral blindness but signs include:
-Loss of menace in affected eye
-loss of dazzle response to bright light
-loss of consensual and direct PLRs
-absence of tracking response to cotton-wool ball (patch eye not being tested)
-inability to negotiate a maze (patch other eye)
In early stages vision loss could be reversible, but once >few days or very high IOP then prospects poor.
Chronic glaucoma. Dogs and cats.
Uncontrolled acute glaucoma or insidious onset presenting at point of irreversible damage. Pain and corneal oedema tend to be less obvious. In addition to acute glaucoma signs you can see:
- Neovascularisation from limbus, superficial arborising pattern, pigment deposition secondary to this.
- Globe enlargement from stretching of the ocular tunics, marked in young animals. Differentiate from exophthalmos - which is normal globe pushed forward. Exophthalmos see TEL prominence. Hydrophthalmos see TEL pushed in medial canthal region.
- Descemet’s fracture or Haab’s striae seen as greys streaks
- Lens luxation due to zonular fibre rupture. Must establish if lens luxation is cause or effect of glaucoma
- Cupping of optic disc - ONH bowed backwards through cribriform plate (a perforated region of sclera which allow ON to leave the globe). Best seen with bionocular indirect ophthalmoscopy.
- Cataract - chronic and lens luxation and probably results from alterations in nutrition of the lens
- IO haemorrhage
- Iris atrophy - retroilluminates or holes in iris. Can also be a senile change or as a sequel to uveitis
- retinal and ONH atrophy - end stage. loss of vasculature–> ONH chalky appearance, in dog may also grey with loss of myelinated nerve fibres. Retina - hyperreflective, retinal thinning and retinal vasculature attenuation.
- equatorial staphylomas - scleral thinning and stretching, outward protrusions.
- Phthisis bulbi - previously increase IOP, pressure-induced atrophy of the ciliary processes, aqueous production drops and in extreme cases phthisis bulbi and reduction of globe size.
Classification of glaucoma
Primary (no antecedent ocular dz) or secondary (following other ocular dz). Congenital also seen rarely.
Primary: hereditary basis:
PLA: ECS, Welsh and English SS, Basset Hound, Siberian Husky, Retrievers - Lab and golden, Welsh Terrier, ACS, Great Dane, Flat-coated retriever, Hungarian Viszla, Dandie Dinmont terrier, Border collie
Open angle glaucoma: Norwegian elkhound, petit basset Griffon Vendeen, Basset Hound
Pectinate ligament abnormality/goniodysgenesis
Most common form of primary glaucoma in the UK. PLA - ligament is abnormal and made up of mesodermal sheets with perforations by intermittent flow holes. May also be narrowed. In early life sufficient drainage and normotensive. Middle ages dogs, see compromise and acute glaucoma develops.
Ciliary cleft examined with 50MHz US in studies for more info.
Not strictly congenital as now found can progress with age.
Open-angle glaucoma
Open angle in dogs prove to be a good models for the disease in humans.
Not fully understood but suggestive of glycosaminoglycans build up in the drainage system. DNA tests are available for some breeds.
Drainage angle is normal on gonio
Secondary glaucoma
Most common glaucoma seen. Cats as well as dogs. Primary dz impairs drainage of aqueous at pupil or drainage apparatus.
Blockage at pupils: lens, vitreous, total posterior synechiae/iris bombe
Blockage at drainage apparatus: inflammatory cells, fibrin/haemorrhage, tumour cells, pre-iridial fibrovascular membranes (PIFMs), peripheral anterior synechiae, iris swelling, vitreous.
Secondary glaucoma - primary lens luxation
Terrier breeds + Border collie (to lesser degree)
Anterior lens luxation with vitreous prolapse can block both sites! Rapid rise in IOP.
Can also be seen with posterior lens luxation but less common.
Lens luxation - cause of effect of glaucoma?! Careful clinical assessment and hx taking. DNA tests for many terrier breeds
Secondary glaucoma - Uveitis
Mechanisms:
- infiltration of PL and ciliary cleft with inflammatory debris
- swelling of the trabecular meshwork
- swelling of the iris reducing drainage angle
- synechiae anterior and posterior (posterior adhesions between iris and lens –> iris bombe due to aqueous build up behind the iris)
- pre-irdial fibrovascular membranes
Secondary glaucoma - neoplasia
Mechanisms:
- neoplasia directly involved in the drainage structures
- accumulation of cells blocking ciliary cleft
- development of uveitis
- angiogenic factors –> neovascular tissue growth over PL (pre-iridal fibrovascular membranes)
Uveal melanoma, primary ciliary body adenoma/adenocarcinoma, lymphoma.
Dx can be difficult if glaucoma, full dx investigation, enucleation may be only way to achieve definitive dx
Secondary glaucoma - IO haemorrhage
Causes:
- trauma, IO neoplasia, uveitis, bleeding disorders, congenital lesions
Blood and fibrin clots compromise outflow. Haemorrhage may be effect rather than cause of glaucoma
Secondary glaucoma - ocular melanosis/pigmentary glaucoma
Cairn terriers accumulate pigment in the anterior segment
insidious onset glaucoma in middle-aged and older dogs.
Large amounts of pigment in anterior chamber, especially ventrally
Sporadically in other breeds - Golden retriever and WHWT.
Secondary glaucoma - Intumescent cataract
lens swelling can cause glaucoma due to effects on aqueous dynamics.
Lens induced uveitis is a more common cause of glaucoma due to leakage of lens material from hypermature cataracts
Secondary glaucoma - Vitreous prolapse
after IO surgery e.g. lendectomy or lens luxation
Obstruction to aqueous flow at pupil or at drainage apparatus. vitreal liquefaction - ageing process, can allow anterior movement of the vitreous.
Management of glaucoma
Medical or Sx, reduced IOP by decreasing production or increasing outflow
Factors to considers: duration of dz, degree of vision, underlying cause, gonioscopic findings, one-eyed case, age of patient, temperament of pt, finances
Management of glaucoma - medical
- ANALGESIA; NSAIDs +/- opiates
- Osmetic diuretics; acute cases with pressure >50mmHg. 1-2g/kg IV over 30 mins. Lasts few hours
- CAI; decrease aqueous production, 50% drop in IOP. No longer use systemic CAIs due to SE and topicals available. Dorzolamide and Brinzolamide. Dorzolamide has been shown to lower serum K+ in cats, monitoring K+ advised.
- Prostaglandin analogues; PGF2a - increase outflow via unconventional uveoscleral outflow, pronounced miosis, in an emergency used every 15 minutes for 4-6 doses but not in cases of uveitis or lens luxation. Latanoprost, travaprost, bimatoprost. Do not work in cats
- miotics; POAG, opens up trabecular meshwork, rarely used in our pts
- B-adrenergic blockers; reduce cAMP in ciliary processes. Increase outflow and combined with other drugs (e.g. dozolamide and timolol in cosopt). Timolol maleate, Betoxalol.
Management of glaucoma; Sx treatment of glaucoma
Methods to increase outflow: filtration devices. Shunted into subconjunctival tissue space. Thin piece of tubing, +/- valve and base plate. Tubing enter anterior chamber through a scleral tunnel. Aqueous is drained into tenon’s space. Scarring and fibrosis can occur after sx. Mitomycin C or 5 fluorouracil or beta-irradiation can improve this. Additional shunts also possible.
Methods to reduce aqueous production:
- cyclocryoablation; trans-scleral freezing of portions of ciliary body, visual or blind glaucomatous eyes, post-op spike in IOP, liquid nitrogen or nitrous oxide via 3mm probe, UGA, 4-8 sites 4-5mm posterior to limbus, sparing posterior ciliary arteries at 9 and 3 positions. Applied until “ice-ball” reaches corneal periphery (2 minutes). Superseded by laser.
- cyclophotocoagulation; as above but destruction with laser energy. Nd-YAG laser and diode are used. Low energy direct contact methods less complications cf. non-contact methods but less effective. Laser applied to 30-40 sites 3-4mm posterior to limbus, avoiding 9 and 3 positions. 1.2 W for 1.2 seconds. 50J per eye. Every 4th application an audible pop noise is heard due to vaporisation of fluid. Spikes post treatment common - paracentesis in eyes with potential for vision. Medical treatment 4 weeks post tx before attempt to reduce dose and frequency of CAI.
Management of glaucoma; Sx treatment of glaucoma - pharmacoablation
Pharmacoablation for blind eyes:
- gentamicin injected into the vitreous to destroy ciliary body and retina.
- UGA 0.5ml of vitreous is aspirated through sclera and 25 mg of gentamicin is injected.
- feline post-traumatic sarcoma in cats
- intractable uveitis may be seen, severe phthisis bulbi and may necessitate enucleation
Management of glaucoma; Sx treatment of glaucoma; Enucleation
Primary glaucoma - must be warned that other eye will follow
Bumper bars, echolocation used in some animals, most adjust within a few weeks and benefit from being pain free without frequent medication
Feline Glaucoma
Cats - deep chamber, allows gonio without a lens, and has a wide iridocorneal angle.
PLs - slender, widely separated, unbranching, gold/blue/white depending on iris colour
Glaucoma relatively uncommon in cats
RR 22.2 +/- 5.2mmHg
Hereditary predisposition Siamese and Persian, only proven in Lab strain of Siamese in the US. Few cases occur in absence of other ocular disease, older cats but uncommon
Majority are secondary..
- Uveitis - most common
- neoplasia - melanoma and lymphoma
- trauma
- lens rupture
- lens luxation - large anterior chamber so can have anterior lens luxation w/o ^IOP
- aqueous misdirection syndrome
Glaucoma is usually insidious and chronic in cats. Blepharospasm and lacrimation may be noted in the early stages, pain rarely exhibited. Mydriasis often presenting complaint. Conjunctival and episcleral congestion - red eye, to lesser extent cf. dog. Corneal oedema and bullous keratopathy in longstanding cases. Hydrophthalmos common, may lead to exposure keratopathy. Cataract and lens luxation due to stretching and breakdown of zonular fibres may occur. Retinal degeneration and ONH cupping and atrophy.
Aqueous misdirection; aqueous flows into vitreous causing it to swell and lens-iris diaphragm moves anteriorly. Closes ciliary cleft, ^IOP. Vitrectomy with lens removal is the most successful long term management.
Unilateral or bilateral. Tx difficult. Presented late with advanced and irreversible vision loss. Also primary condition needs to be managed.
Uveitis - CCS and other anti-inflammatory agents. Miotics are of little use in cats. CAI & beta blockers are useful in cats. PGF2a - will use miosis but not reduce IOP
Congenital glaucoma in cats: buphthalmos, uni or bi. Grossly enlarged globe with intense corneal oedema. Presumed catastrophic developmental abnormalities preventing drainage. Young animals - pronounced scleral stretching.
Neuro-ophthalmology
CNS, PNS, autonomic nervous system (sympathetic and parasympathetic).
Consider: hx, CS, neurological assessment, systemic exam, lifestyle of pt.
CNS = surrounded by meninges - brain, spinal cord, optic nerves CNS = collections of cell bodies are called nuclei, PNS = collections of cell bodies are called ganglia
Neuro-ophthalmology - examination
Distant examination, gait, posture, head position, tremor, ocular movements (nystagmus or strabismus)
Nystagmus: rhythmic and involuntary eye movements. Physiological (vestibulo-ocular reflex) and pathological nystagmus occur. Fast phase describes direction of nystagmus. Pendular has no direction (can be seen in congenital nystagmus - Siamese cat or pups with MODs). Spontaneous pathological - vestibular dz, CN II, IV and VI.
Strabismus: vestibular or extraocular muscle or innervating nerve dysfunction. Vestibular ventral and ipsilateral to lesion.
- CN III: medial, dorsal and ventral rectus, ventral oblique
- CN IV: dorsal oblique
- CN VI: lateral rectus, retractor bulbi
Originate in brainstem, originate rostral to caudal in numerical order, ipsilateral apart from CN IV. CN IV crosses to contralateral muscle, exits from dorsal midbrain instead of ventral also.
Direction of strabismus:
-CN III or its nucleus = ipsilateral ventrolateral with ptosis
-CN IV = ipsilateral exotropia
-CN IV nucleus = contralateral exotropia
-CN VI or its nucleus = ipsilateral esotropia (medial)
Neuro-ophthalmology - examination
Pupils - parasympathetic and sympathetic supply
Pupil size:
Anisocoria: difference in pupil size. Distant direct ophthalmoscopy in light and dark conditions. Light reflexes and vision tests.
Dilator muscle - arranged like spokes of a wheel, adrenergic sympathetic stimulation. Constrictor/sphincter muscle - like rings of a tree, cholinergic parasympathetic stimulation.
Sympathetic nerve supply: thoracolumbar distribution, preganglionic sympathetic nerves travel down spinal cord, exit ventral spinal nerve roots, join sympathetic trunk which traverses through the thorax to cranial cervical ganglion (ventromedial to tympanic bulla). Postganglionic sympathetic fibre cross middle ear, pass through cavernous sinus and join ophtho branch of CN V, enter globe as long ciliary nerve. Also supplies smooth muscles and Muller’s muscle which keep lids open.
Parasympathetic nerve supply: preganglionic fibres arise in the parasympathetic nucleus of CN III. Axons run with somatic efferent fibres of CN III. Preganglionic parasympathetic fibres are superficial and susceptible to damage. Enter orbit then synapse with ciliary ganglion, post ganglionic fibres - short ciliary nerves (plus somatosensory innervation from CN V)
Arrangement of short ciliary nerves dictate pupil shape. Dogs 5-8 short ciliary nerves = round pupil. Cats 2 short ciliary nerves = elliptical pupil. Damage of one of these results in D or reverse-D pupil - allowing localisation to nasal or malar branches in cats
Neuro-ophthalmology - reflexes and responses
A reflex is an instantaneous, short-lived, predictable reaction. A response is learned and involves higher brain input, a reflex does not.
Pupillary light reflex (PLR): light stimulus, CN II afferent pathway –> optic chiasm–> crossing at pretectal nuclei. Postsynaptic axons pass to left and right parasympathetic nuclei of CN III, most cross back to opposite side. Parasympathetic stimulation of iris sphincter muscle. Doubling fibre crossing lead to stronger constriction on ipsilateral pupil.
Swinging flashlight test: move bright light source from one eye to the other. Both pupils constrict but when the light is moved to the other eye it constricts further. An abnormal reaction is if the newly illuminated pupil dilates (a positive swinging flashlight or Marcus Gunn sign) - pathognomic for unilateral or prechiasmic disease.
Neuro-ophthalmology - reflexes and responses
Dazzle: bilateral, partial blink in response to bright light shone into each eye in turn. Non-illuminated eye does not exhibit same response. CN VII damage will result in negative result. Although animal may move away from light or TEL move which would indicate intact retina and ON function.
Menace response: gentle threatening gesture, blink response. Afferent retina and CN II, efferent CN VII. Menace response is learned at approx 8 weeks. CN II –> optic chiasm–> lateral geniculate nucleus –> visual cortex –> occipital lobe of the brain. Motor cortex communicates with visual cortex –> CN VII nucleus –> eyelids. Also pathways including cerebellum
Palpebral reflex: rapid blink from touching medial and lateral canthus. Afferent CN V (ophthalmic branch at medial canthus and maxillary at lateral canthus). Efferent VII to orbicularis oculi
Neuro-ophthalmology - reflexes and responses
Corneal reflex: gentle stimulation –> eyelid closure. CN V afferent and CN VII efferent. Trigeminal long ciliary nerves provide somatic sensation of cornea. Corneal touch threshold (CCT) is measured using Cochet-Bonnet anaesthesiometer - more sensitive corneas have lower readings.
STT: qualitative tear production. Parasympathetic VII to V to lacrimal gland. Diseases involving CNs V and VII can result in decreased tear production; e.g. otitis media.
CN V provides sensory innervation to the gland (lacrimal nerve)
Vestibulo-ocular reflex: stabilises image on retina when head is moved. Evaluate by moving pts head side to side and up and down, eyes should remain central by tiny resetting movements, fast phase in direction on head movement. Driven by vestibular system - peripheral and central. Peripheral = inner ear and vestibular ganglion and vestibular potion of vestibulocochlear nerve (CN VIII). Central = vestibular nuclei and flocculonodular lobe of the cerebellum. Movement involves 3 semicircular canals, utricle and saccule and endolymph movement and perilymph causes firing of CN VIII. Synapsing in vestibular nuclei and connections made with motor neurones controlling extraocular muscles (CN III, IV and VI).
Pathological nystagmus - central and peripheral vestibular disease, worse in dorsal recumbency. This decompensates the vestibular system. Central - fast phase towards side of lesion, peripheral - fast phase contralateral to the side of lesion.
Central Visual Pathways
Light photons stimulate retina –> phototransduction cascade –> impulses–> retinal ganglion cells –> CN II to lateral geniculate nucleus. Arrangement of retinal ganglion cells within ON is in a retinotopic manner.
ON –> optic chiasm via optic foramen. At the base of hypothalamus decussates. Mammals with binocular vision not all fibre decussate.
Fibre from opposite visual fields in both eyes –> optic tracts.
Unilateral optic tract lesion –> bilateral visual field loss on contralateral side. Optic tract passes to the lateral geniculate nucleus, divides into two pathways, 20% fibres project to various brainstem nuclei –> ocular reflexes, 80% continue to optic radiation visual cortex of occipital lobe.
Assessment of vision: maze test, in light and dim conditions, covering each eye in turn is required to asses unilateral conditions. Visual placing in small pts
Pharmacological testing of ANS
Parasympathetic system: pilocarpine causes pupil constriction to check pupil can constrict - r/o iris atrophy
Sympathetic testing: phenylephrine is used for evaluating Horner’s syndrome. Rapid pupil dilation in postganglionic lesions cf. preganglionic lesion (20-60 minutes)
Neuro-ophthalmic dz; three categories
3 categories:
- blind with normal PLRs (distal optic tract, GME etc, other neuro signs)
- blind with abnormal PLRs (retinal degeneration, CN II etc)
- Visual with abnormal PLRs (oculomotor nerve dysfunction, internal or external ophthalmoplgia)
Horner’s syndrome
Disruption of the sympathetic innervation to the eye
CS: miosis, ptosis, enophthalmos, protrusion of nictitans membrane, hyperthermia of CN VII
First order: hypothalamus down the spinal cord to exit T1-T3
Second order: pre-ganglionic sympathetic neurons pass from spinal cord to synapse in the cranial cervical ganglion adjacent to tympanic bulla
Third order: post-ganglionic fibres pass to the eye to the iris dilator muscle, smooth muscles of the periorbita and Muller’s muscles in the upper and lower eyelids
Lesion localisation: phenylephrine - 3rd order eye will dilate in 20 minutes, 1st or 2nd will dilate in 30-40 minutes.
Middle ear dz most common, along with idiopathic form seen in golden retrievers (resolves in 8-12 weeks). Cat bites to neck should be checked for in cats with Horner’s.
Cavernous sinus syndrome
Dz process, inflammation or neoplasia, affecting cavernous sinus. Venous sinus on the floor of the middle cranial vault extending from the orbital fissure to the petro-orbital canal. CN III, IV, V, VI and postganglionic sympathetic fibres run close to this sinus. uni>bi.
CS: external and internal ophthalmoparesis (extraocular muscles, innervated by CN III, CN IV, and CN VI)
- ptosis
- reduced corneal sensation
- mydriasis
- reduced periorbital and facial sensation
Pourfour du petit syndrome
In man, recognised in cats that have had ear flushing UGA.
Mydriasis, good direct PLR, wide palpebral fissure, exophthalmos, no TEL protrusion.
Transient neuritis to post-ganglionic sympathetic fibres.
Resolves in a week or so although Horner’s syndrome can develop due to middle ear disease.
Static anisocoria (spastic pupil syndrome) and hemidilated pupil
Unilateral miosis in cats, occasionally mydriasis. With miosis pupil does not enlarge in the dark.
Hemidilated pupil where D or inverted D shape develops - one of the short ciliary nerves affected in isolation.
FeLV, lymphosarcoma, feline dysautonomia
Hydrocephalus
Increased CSF in the cranial vault. Congenital dz, seen in toy and brachy breeds.
Enlargement of calvarium and failure of skull suture lines to fuse (open fontanelle) also common with this.
CS: behavioural changes, ataxia, seizures, ventrolateral strabismus typical ocular change (sunset)
Myasthenia gravis
abnormalities at the neuromuscular junction (acetylcholine receptors).
Congenital (rare) or acquired.
Weakened palpebral reflex and facial muscle paresis. General signs of weakness on exercise and megaoesophagus most obvious.
Lafora disease
Adult onset myoclonus inherited in mini wire hair dachshund and basset hound.
Visual stimulation such as strobe light (or slit lamp exam) can trigger twitches which can be pronounced and debilitating.
Lafora disease
Adult onset myoclonus inherited in mini wire hair dachshund and basset hound.
Visual stimulation such as strobe light (or slit lamp exam) can trigger twitches which can be pronounced and debilitating.
Fibrosing esotropia
Juvenile or giant breeds - Shar peis.
Progressive esotropia, myositis of medial rectus and dorsal oblique.
Bi > uni.
Forced duction tests dx. sx to resect fibrosed muscles will improve globe position and sight
Canine distemper
RNA Morbillivirus
Rare - vaccination
Bilateral conjunctivitis, respiratory and GI dz
KCS secondary to adenitis
Chorioretinitis
Optic neuritis - uni or bilateral blindness
Can also involve optic tracts, lateral geniculate nuclei and occipital cortex
Dysautonomia
cats "key gaskell syndrome" Autonomic nervous system dysfunction. Dehydration, decreased appetite, V+, regurgitation, bradycardia, malaise Bilateral dilated pupils Progressive and fatal Pupil will constrict rapidly with low doses of pilocarpine, normal pupil would not with doses as low as 0.1% Definitive dx usually PM
Canine: reported, less common than in cats, prognosis poor
Granulomatous meningoencephalitis (MGE)/ meningitis of unknown origin (MUO)
Idiopathic inflammatory brain disease, perivascular cuffing with mononuclear cells on histo.
Pathogenesis proposed: immune mediated, precancerous lymphoma, infectious dz
Young, small breed dogs, 3 different presentations
1-disseminated, 2- focal, 3-ocular
CS: sudden onset blindness (optic neuritis) to generalised CNS dz with seizures and postural abnormalities etc. MRI and CSF taps essential for work up.
Tx: CCS, cytosine/cytarabine, px: guarded long term may be managed for a few years
Cerebral hypoxia
Doing GA - apnoea, cardiopulmonary failure, drug overdose, hypotension
Blind ness is the most common symptom, stupor, seizures and paralysis
PLRs normal
Can make full recovery in days to months or long term affected
Idiopathic facial nerve paralysis
1/4 due to OM/OI or hypot4
Paresis of facial muscles, drooping of lip, saliva spillage
Absent or reduced menace response/palpebral
tear production normal or reduced
CKCS or CS
Topical lubricants
Immune mediated retinitis (IMR)
Differentiated from SARDS recently
Sudden onset blindness, dilated pupils
IMR sometimes night blind but not day blind, unilateral, PLR may remain.
Concurrent health issues such as neoplasia and neurological abnormalities in 20%
Retain dazzle.
Colourimic PLR testing - neg to red light but normal with blue
ERG - reduced waveform
Tx - CCS and doxycycline - some improve
Masticatory and EO muscle myositis
Young adult, typical 3-5 years
Masticatory: exophthalmos, protrusion of TEL, swelling or atrophy of MM, pain/difficulty opening mouth. pterygoid muscle swelling can compress ON = blindness in small %. Progresses to enophthalmos long term. CS, biochemistry, immunohistochemistry for antibiodies of 2M muscle fibres = dx. bxs also.
EOM: young, large breed. Exophthalmos, can become restrictive with chronicity. 2M muscle fibres are not present. Can see on CT/US but presentation is enough to dx!
TX: CS for 4-6 weeks,
Central neoplasia
Central blindness.
Globes NAD and normal PLRs depending on lesion location
Blindness may be only CS
Lesions at optic chiasm: pituitary carcinomas, optic nerve gliomas, meningiomas
If optic chiasm itself –> dilated, non-responsive pupils
Internal ophthalmoplegia and CN dysfunction may be seen
Neurogenic KCS
Acute severe KCS.
Lesion anywhere on efferent path: PS nucleus of facial nerve, CN VII itself, geniculate ganglion, or post parasympathetic fibres (CN V).
Preganglionic lesions - OM/OI. See other signs of facial nerve paralysis or horner’s.
Periorbital myositis, erosive bone lesions affecting the pterygopalatine fossa or petrous temporal bone and dental dz can cause neuro KCS
if postganglion (CN V) facial or corneal anaesthesia may accompany dry eye.
Ipsilateral dry nostril Pathognomic. TX: oral pilocarpine.
Otitis media/interna
Middle and inner ear disease –> neuro-ophthalmic dz. Horner’s, neuro KCS, CN VII paralysis, vestibular dz and ear signs.
Sudden acquired retinal degeneration syndrome (SARDS)
Idiopathic, sudden onset irreversible blindness. Dilated pupils, poss some retained dazzle.
- poss causes: toxins, autoantibodies, paraneoplastic processes, metabolic dz
- Occurs over 24hrs-2weeks. Some display PUPD. Raised cholesterol, ALKP and lymphopaenia. Raised sex hormones and cortisol following ACTH stim tests.
- Smaller breed, FN mostly but can be any
- Fundus initially appears normal but degenerates after a few weeks, hyperreflectivity, optic disc pallor, blood vessel attenuation. ERG - absent trace.
- PLR absent in red light, pos in blue due to melanopsin driving PLR despite absence of photoreceptors.
- early in dz may respond to human IV immunoglobulins but generally considered untreatable
Feline anomalies associated with albinism
- Siamese and pointed breeds - partial albinism associated with ocular abnormalities.
- Esotropia (congenital)
- Mutant allele of the albino series (at the C locus).
- Reduced ocular pigmentation - iris and fundus
- Misrouting of retinal projections to the visual cortex, too axons from temporal retina cross to opposite side projecting into the side of the brain that they shouldn’t
- Convergent strabismus/esotropia and nystagmus result.
Feline fluoroquinolone toxicity
Use with extreme caution
Irreversible retinal degeneration
low incidence
Marbofloxacin and orbifloxacin may also be implicated
Total blindness, occasionally partial or temp
Idiosyncratic reaction.
Cats with different amino acid sequence in one of the P-glycoproteins involved in transporting in fluoroquinolones across BRB and UV light stimulates fluoroquinolones to produce reactive oxygen species.
Feline leukaemia virus (FeLV)
May manifest purely neuro-ophthalmic problem initially
anisocoria or dyscoria
Spastic pupil syndrome - does not alter in the dark
Pupil abnormalities may be intermittent
Affected cats are FeLV positive and prognosis guarded
Feline nictitans membrane protrusion
Protrusion of NM with watery D+
D+ resolves before NM protrusion resolves
Tora or tora-like virus and is self-limiting
Adrenergic drops - phenylephrine, TELs will return to normal position, sympathetic involvement
No tx required
Thiamine deficiency
Cats fed raw fish and cats with severe GI dz from malabsorption
Inappetence, dilated pupils but normal vision
Ventroflexion of the head and neck follows and if untx progresses to semi-comatose state, crying opisthotonos and extensor rigidity
Dietary hx suggestive, bloods for thiamine will be low
Parenteral vitamin B administration followed by orals can cure if dx early enough
