NOSS

Both botulism and tetanus are caused by clostridial toxins. So why does botulism cause a flaccid paralysis whereas tetanus causes a spastic paralysis?

- Tetanus acts within the spinal cord, after being tracked retrogradely back up motor nerves from the muscle (whereas botulinum toxin works at the neuromuscular junction). - Tetanus prevents the release of neurotransmitters in so called "Renshaw cells" , which normally act to INHIBIT motor neurones which leads to EXCITATION - and the spastic paralysis that is seen with tetanus.

what are C6-T2 spinal cord myelopathy clinical signs?

- Tetraparesis and ataxia all limbs - Proprioceptive deficits all limbs - intact/DECREASED spinal reflexes THORACIC limbs, , (INCREASED pelvic) - Intact or decreased muscle tone thoracic limbs (increased pelvic) - prayer position (image) TWO-ENGINE/DISCONNECTED GAIT possible because of increased muscle tone in pelvic limbs. wide based ataxia in pelvic limbs with short stilted pelvic limbs. two different speeds. - Horner's syndrome possible - Urinary dysfunction possible, but uncommon - Tetraplegia uncommon

what is the schiff-sherrington posture? what is the mechanism? what are other clinical signs?

- acute T3-L3 spinal cord injuries - BORDER CELLS (L1-L7 spinal cord segments) which provide inhibition to extensor muscles thoracic limbs: "disinhibition" - PARAPLEGIA with INCREASED extensor tone. in thoracic limbs. - differentiation from cervical lesion: thoracic limbs neurologically NORMAL. (cervical, not normal) - indication of LOCALISATION, not prognosis. - common to have urinary problems.

what is polysaccharide storage myopathy (type 1)? signalment, CS, Mechanism, Testing, Tx?

- affects QH, Warmbloods, draught horses, cobs, many others - Heritable (autosomal dominant) - high prevalence in some breeds (>50%) CLINICAL SIGNS: - causes exertional rhabdomyolysis - occasionally muscle atrophy/weakness in draught breeds MECHANISM - abnormality of glucose metabolism - mutation of glycogen synthase 1 gene in skeletal muscle TESTING: - DNA test now available - hair pluck. some horses don't have the mutation tho (PSSM2). all inherited from same ancestor - Muscle biopsy: internalised nuclei (nonspecific) - sign of muscle regeneration - polysaccharide inclusions on PAS stain. resistant to amylase digestion. Tx: - same as RER (high fat, low carb diet) - regular, daily EXERCISE. start with just hand walking and increase every day

what are common subjective abnormalities on a radiograph associated with CVM/S of LA?

- caudal extension of dorsal vertebral lamina (roof of the spinal canal): if it extends too far caudally, the animal can have compression. - caudal epiphyseal flare ("ski ramp"): floor of the spinal canal comes up towards the caudal aspect of the vertebrae. can get pinched at that location. - step formation between the vertebrae (they are not perfectly aligned).

what is EPM (equine protozoal myeloencephalitis)? transmission, pathology?

- caused by a parasite (sarcocystis neurona) in the USA. - cycles b/w opossums and birds, but horses can pick up from cont. pasture, act as dead-end host. - often MULTICENTRIC, can sit for long periods of time before causing CS. CS: many diff. presentations - combination of cranial nerve problems, muscle atrophy, ataxia, etc.

what are clinical signs of cerebellar dysfunction? what about vestibulocerebellear?

- cerebellar ataxia - wide based stance - hypertonous (spacticity) - decerebellate rigidity - intention tremor - abnormal menace response VESTIBULOCEREBELLUM (FLOCCULONOULAR LOBE): vestibular dysfunction - vestibular ataxia - head tilt - positional strabismus - pathological nystagmus unilateral = IPSILATERAL

what are ddx for equine spinal ataxia?

- cervical vertebral malformation/stenosis (CVM/S) - EHV1 myeloencephalitis - equine degenerative myeloencephalopathy (EDM) - trauma - migrating parasites - equine protozoal myeloencephalitis (EPM) - ryegrass staggers

how is PRA diagnosed? (3)

- clinical history (night blindness) - breed, testing 1) HYPEREFLECTIVE tapetum (thinning of retina as photoreceptorsdie - shiny eyes) 2) VASCULAR attenuation (thinning) and optic nerve looks pale. 3) late stage - CATARACTS

how is CVM/S diagnosed? how effective is myelography?

- clinical, neurological exam - subjective + objective interpretation of standing cervical radiographys (steps, ski ramps, inter/intra-vertebral ratios) - referral techniques (myelography, not always that useful. often done at C6-7, or atlanto-occipital space). lots of false positives + negatives. inherent risks with procedure. useful if contemplating surgery to see where compression is occurring. - CT: not easy to scan entire neck. - CSF analysis usually normal. - scintigraphy: used in orthopaedics for chronic lameness. not useful for wobbler's syndrome. image: mild scoliosis (subluxation of lower vertebrae) usually SIGNALMENT (young, male, fast-growing) and lateral x-rays of standing horse.

what is a mature cataract?

- complete opacity of the lens (marble-white appearance) - no tapetal reflex - blind surgery indicated.

how is cataract surgery conducted?

- corneal incision with blade - hole in anterior lens capsule - create opening with forceps - fill eye so it doesn't collapse - photoemulsification probe: ultrasound power that acts like a jackhammer and emulsifies lens protein while filling it with fluid so it doesn't collapse. emulsified particles from the lens are aspirated from the probe. what is remaining is softer cortex material. - irrigation/aspiration probe: vacuum created that removes fluid and fills it with other fluid. - once all lense material remove, an artificial lens is implanted - close corneal wound with simple interrupted sutures. nylon/vicryl. WITHOUT lens: patient can see but is very farsighted (-14)

after emergency tx of status epilepticus, how should you maintain homeostasis of the animal?

- correct hypovolaemia (IVFT) and hypoxia (O2) - aggressive cooling to correct hyperthermia - correct underlying/developing electrolyte abnormalities, hypoglycaemia - if intoxicated: decontaminate, supportive care (wash, gastric lavage, vomit, etc) - monitor HR, RR effort, Sp02, blood pressure, ECG, rectal temp. - if suspect intracranial pathology: consider referral MRI +/- CSF analysis.

what is the posture involved in a spinal disease?

- crouched (kyphosis) - low head carriage - schiff-sherrington (T3-L3)

describe the mechanism, ddx, and CS of proprioceptive ataxia.

- disruption of proprioceptive information reaching the brain for processing and perception. - animal less effectively aware of feet/limbs, inconsistent stride length, inconsistent foot placement DDX: most common, because spinal cord diseases - therefore also often paretic b/c it disrupts both ascending and descending motor information.

what is articular process joint osteochondrosis? (OCD)

- failure of normal endochondral ossification, resulting in thickening and retention of the hypertrophic zone of the growth cartilage - important cause of lameness in horses. It is usually seen in young rapidly growing animals, and it affects males more commonly than females. can be severe. fragments of bone, fissure lines across processes. sequelae: degenerative joint disease. CVM-2

what are behavioral signs of seizures? contrastingly, what events can MIMIC seizures?

- fly catching (limbic), lip smackin, hypersalivation, moving backwards, limb movements. certain rhythmicity. MIMIC: - syncope (partial/complete loss of consciousness, lack of motor activity). shorter duration, no post-ictal signs - Narcolepsy: stimulated often by excitement, food, pharmacologically - Pain - Vestibular Syndrom - Movement disorder. usually have a spastic phase, often triggered by exercise.

what are the peracute spinal conditions of dogs?

- fracture/ luxation - acute non-compressive nucleus pulposus extrusion (often lateralised) - ischaemic myelopathy (+/- fibrocartilagenous embolism) peracute, lateralised, non-painful, stable)

what are the characteristics of a breed related/genetic cataract?

- genetic defect but not congenital. - genetically determined morphology/progression (you can look it up) - juvenile or adult onset - MOST COMMON, always NUCLEAR (not inherited). morphology/progression genetically determined. often just doesn't progress and just sits there.

what are the causes of mydriasis?

- glaucoma (primary/secondary) - dysautonomia: deregulation of autonomic system - fear - central blindness

describe diabetic cataractogenesis. how is it treated/prevented?

- glucose pathways of the eye are oversaturated with hyperglycaemia - QED glucose becomes sorbitol, which cannot leave the lens. - leads to SWELLING and RUPTURES of the lens capsule around the equator/posterior pole, leading to SEVERE inflammation aldosereductase: can inhibit in dogs with diabetes to prevent the cataracts if early enough.

what is the anatomy of the vestibular system? what are the two labyrinths and how do they differ?

- hair cell receptors -- CN VII (vestibular portion of vestibulocochlear nerve) -- 4 vestibular nuclei in the medulla oblongata inner ear: housed in petrous portion of temporal bone outer bony OSSEUS LABYRINTH of inner ear: contain PERILYMPH - 3 semicircular canals - vestibule inner MEMBRANOUS LABYRINTH: contain ENDOLYMPH - 3 semicircular ducts - utricle and saccule

what are the clinical signs of a vestibular system dysfunction?

- head tilt (towards lesion) - vestibular ataxia (towards side) - tight circling (towards side) - pathological nystagmus (fast phase away. spontaneous or induced. can be horizontal, vertical, or rotatory depending on dust) - abnormal vestibulo-ocular reflex - positional strabismus (abnormal eye position. VENTROLATERAL DEVIATION of eye on affected side) - IPSILATERAL LOSS of extensor muscle tone - nausea/vomiting due to unequal input to vomiting sencre.

what factors are most important for crossing the BBB?

- high lipid solubility - small mol. size - low plasma protein binding - ionisation: only NEUTRAL drugs can enter. increased hydrogen bonds = more polar = bad. GLUCOSE: good uptake (lots of transporters)

when might different substances accumulated in the anterior chamber?

- hyphaemia: blood (a) - Hypopion: WBC (b) - Keratic Precipitates: specks of inflammatory material that sit on the corneal endothelium. sign of CHRONIC inflammation (c) - Fibrin: inflammation inside the eye, blood-aqueous barrier leaks - Lens Luxation: whole lens in anterior chamber (D) - tyndall effect: cells/fibrin floating in AC with - aqueous flare (E)

When should you refer an eye case to a specialist?

- if you are not confident in your diagnosis or tx plan - unable to perform a complete examination - risk of losing the eye/sight - complex cases or requiring further investigation

What can cause redness in the anterior chamber/vitreal cavity? what can accumulate in there?

- intraocular bleeding (HYPHEMA). blood in the anterior chamber - hyphema. can also get hypopion (WB), aqeous flare (PROTEINS), or fibrin. DDX: - inflammation (uveitis) - trauma - intraocular neoplasia - retinal detachment - glaucoma - congenital defects - systemic conditions: hypertension, thrombopathy, coagulopathy, etc.

what are signs of an immature cataract?

- involvement of nuclear and cortical regions - tapetal reflex is still visible on retroillumination - decreased vision potential surgery candidate

what is the cause of corneal transparency?

- lack of BV/cells - no pigment - ACTIVE control mechanisms of water content (state of relative dehydration) - smooth surface - highly ORGANISED lattice arrangement of collagen fibrils. most POWERFUL refractive surface of the eye.

how should you manage the bladder in animals with spinal disease?

- manual bladder expression - repeated aseptic catheterisation - indwelling foley catheter with closed collection system

what is the pathology of EDM (equine degenerative myeloencephalopathy)? prognosis?

- neuronal fibre degeneration/demyelination in WHITE MATER of ascending and descending tracts of spinal cord - mild thoracic region often worst afected - degen. lesions in spinal, brainstem nuclei causes: - vit E deficiency? - free radical induced neuronal damage? - familial predisposition/genetic cause likely (morgan horses) image: WHITE part is most affected: ventral (motor) and lateral (propriopceptive) - paresis + ataxia. PROGNOSIS: poor. may stabilise with high dose Vit. E therapy.

what are signs of a BILATERAL vestibular dysfunction? ddx?

- no asymmetry: balance lost to both sides - low stance, crouched - wide head excursions from side to side - walk slowly to avoid falling - absent nystagmus ddx: bilateral otitis media/interna, bilateral idiopathic vestibular syndrome

what is the 5 finger rule for degenerative lumbosacral stenosis (DLSS)?

- older large breed dogs (GSD overrepresented) - progressive clinical signs - transitional vertebrae often present in dogs with DLSS (between L and S vertebrae). associated with increased risk if you see it but poor correlation w/clinical signs (like spondylosis) - DIAGNOSIS: CT or MRI. however - can have obvious radiological abnormalities presents in clinical normal dogs

how are horses with idiopathic seizures usually managed?

- oral phenolbarbitone (but 2-3k/year) - no ridden exercise for at least a year MRI not usually very useful. often euthanise.

how does ocular proptosis have different prognostics in cats?

- orbital rim is nearly ALL limited by bone, which means globe is well protected to trauma - QED a LOT of force is req'd to cause globe proptosis. often associated to RTA (road traffic accidents), orbital fractures, globe rupture, and blinding of OTHER EYE secondary to PULLINg at the level of optic chiasma

what are the parasitic diseases affecting the CNS of LA?

- ovine encephalomyelitis (louping ill) - ixodes - coenurosis (gid) - taenia multiceps also nervous coccidiosis, sarcosystis

what tests should be done before cataract surgery?

- owner compliance - DEFINITELY electroretinogram (see back of retina) and ocular US - also CBC/chemistry, urinalysis, dental exam image: lens placed into dog's eyes. able to see immediately but cannot move to focus. without lens, dog will be very far-sighted.

what should be involved in the hands-on opthalmic exam?

- palpation/gentle repulsion of globes: they SHOULD move back because there is a fat pad. if not - space-occupying lesion. - closer exam of adnexa: conjunctiva, episclera, cornea - palpebral reflex: medial AND lateral canthus. - menace response (don't waft) - vestibulo-ocular reflex (train nystagmus)

what are reasons for seizure tx failure?

- poor compliance - incorrect choice of AED or dose - systemic disease (renal, hepatic compromoise) - ∆ in body weight - incorrect Dx (structural pathology) - tolerance developed - refractory seizures can also use gabapentin, pregabalin, levetiracetam, zonisamide, felbamate.

what is the hands-on neuro exam?

- postural rxn testing (knuckling, hopping, extensor trust). - spinal reflexes: withdrawal (testing C6-T2, L4-S1) - patellar: L4-L6. must be relaxed. - perianal: S1-S3 - cutaneous trunci: sensory C8-T1 decreased: LMN (C6-T2, L4-S3) increased: UMN (C1-C5, T3-L3)

what can be concurrent clinical signs with acquired small globe (phthisis bulbi)?

- protruded nictiting membrane - chronic keratitis leading to partially pigmented cornea - absent menace response, dazzle reflex, PLR. in this case: secondary to trauma.

what are the general principles of treatment of neuromuscular disease?

- recumbent patients: supportive care (skin, fluid, bladder) - severe weakness may need ventilations - aspiration pneumonia: monitor and treat promptly physiotherapy/hydrotherapy essential to maintain muscle mass - ATROPHY is MAJOR concern

what are 7 general causes of blindness?

- symblepharon: partial or complete adhesion of palpebral and bulbar conjunctiva (eyelid issues. most common in cats>dogs, 2ary to FHV-1) - keratitis (corneal abormalities/pigmentation) - persistent pupillary membranes (not v. severe) - uveal problems/uveitis (hypopion, hyphaemia) - CATARACTS - GLAUCOMA - posterior segment (fundic: vitreous, retina, optic nerve)

what are clinical signs of a C1-C5 spinal cord segment?

- tetraparesis, ataxia all limbs - proprioceptive deficits all limbs - INTACT OR INCREASED SPINAL REFLEXES all limbs, muscle tone all limbs POSSIBLE: - horner's syndrome - urinary dysfunction (uncommon) - tetraplegia uncommon

what are indications of an L4-S3 spinal cord myelopathy?

- thoracic limbs normal - paraparesis and ataxia pelvic limbs, paraplegia possible - intact or DECREASED spinal reflexes, muscle tone pelvic limbs - urinary dysfunction common (LMN bladder) - possible flaccid tail - possible decreased perianal reflex

what can cause redness in the anterior uvea/iris hyperaemia/iris rubeosis? what about posterior uvea (retina)? (4)

- uveal bleeding - uveal tumours - engorgement of normal vascularisation (2ary to uveitis) - formation of new vasculature over the iris surface: pre-iridial fibrovscular mebranes PIFM (2ary to uveitis, intraocular tumours, retinal detachment, glaucoma.) posterior uvea: intraocular bleeding, similar mechanisms to anterior.

what is EDM (equine degenerative myeloencephalopathy)? signalment? clinical signs?

- variety of breedss, but often neuroaxonal dystrophy in Morgan horses - clusters on certain farms - 6 months - 2 years old (young) - rare but underdiagnosed because not recognised. CS: symmetric ataxia, weakness. - hindlimbs >> forelimbs (moreso than wobbler's syndrome) - hyporeflexia over trunk (panniculus reflex can be reduced/absent)

what is a dynamic stenosis (CVM type 1)? what is the signalment, location?

- when the neck is flexed or hyperextended, the vertebrae move excessively causing cord compression. (partial subluxation squeezing spinal cord like a tube of toothpaste) - commonly affects middle fo the neck C3-C5, seen most frequently in young animals, fast growing young male thoroughbreds - often worse with flexion (C3-C5) and extensions (C5-C7) - often acute, but can be chronic.

what presenting signs can accompany congenital microphthalmia?

- young - small palpebral fissure - periocular wetness - 2ary nictiting membrane protrusion

What is TEL follicular proliferation? causes, signalment?

- young animals, allergies, and certain infections (cats) - mainly present in the inner side - usually accompanied by hyperaemia

what diseases can make the eye appear large? how can you differentiate between large and protruded eye?

1) BUPHTHALMNIA: - primary glaucoma - secondary glaucoma (to intraocular tumour, chronic uveitis, systemic hypertension) 2) RED HERRINGS: - globe pushed forward due to orbital mass (exopthalmia) or ocular proptosis - corneal disease, anisocoria (corneal abscesses, anterior lens luxation), different coloured eyes - check line PERPENDICULAR to SKULL axis to see if right globe appears protruded forward

what are clinical signs of cerebellar dysfunction? what is NOT a clinical sign?

1) DYSMETRIA, often HYPERMETRIA. - increased rate = often slow to initiate movement, then sudden, jerky movements. - increased range (excessive flexion, large exaggerated movements). - increased force. burst-like.- wide based stance 2) truncal ataxia (swaying, titiubation - nodding) 3) hypertonia: increased muscle tone due to loss of inhibition of UMN, muscle spindles. excessive extensor tone. 4) INTENTION TREMOR: fine head/neck, often when goal-oriented 5) abnormal menace response (it goes through the cerebellum) 6) DECEREBELLATE posture (extension of thoracic limbs, flexion of pelvic under body) 7) NOT paresis: cerebellum doesn't activate LMN. only UMN.

what are clinical signs of a forebrain dysfunction? (mental status, gait, posture, etc)

1) MENTAL STATUS: obtunded. behavioral changes (thalamic) 2) SEIZURES, hemi-neglect syndrome 3)GAIT: compulsive circling, headpressing, pacing, proprioceptive ataxia (contralateral to lesion), tetraparesis 4) POSTURE: head turn, body turn (pleurothonous) towards side of lesion

how can the eye appear small? (3)

1) MICROPHTALMIA: maldevelopment of the globe + structures during foetal stage - young, small palpebral fissure, periocular wetness, 2ary TEL protrusion 2) PHTHYSIS BULBI: globe trauma causing atrophy of the globe 3) RED HERRINGS: - enopthalmia (retracted globe) due to ocular pain (like ulcers), reduced BW, or fat loss (old cats) - anisocoria (diferent pupil sizes)

what are 3 channelopathies?

1) Sarcolemmal sodium pump: hyperkalaemic periodic paralysis in quarter horses. potassium is not uptaken into muscle fibre, leading to increased K, paralysis/weakness/fasciculations. 2) ryanodine receptor (RYR1): malignant hyperthermia in mixed breed dogs, landrace pigs, quarter horses. calcium keeps leaking out of SR. muscles go rigid and ATP breaks down causing heat. - can cause anaesthetic deaths in humans from halothane, iso - exacerbated by stress. can cause PALE PORK. stress of transport causes a bout of malignant hyperthermia. 3) Calcium ATPase: congenital psudomyotonia of Chianina cattle. calcium can't return to SR. excessive contraction of muscles.

what are two major mechanisms of eye wetness and relevant ddx?

1) Trigeminal nerve irritation (increased tear production): corneal ulcer... hairs: - distichiasis (hairs in meibomian gland opening, irritate eye) - trichiasis (normal hairs growing towards cornea and touching) - ectopic cilia - Foreign bodies (conjunctival, grass seeds) look behind third eyelid (+ dacryocystits) - entropion (eyelid margin rolled inwards). can be congenital, acquired (age) or blepharospasm/spastic entropion - prolapse of gland of third eyelid/nictitians. "cherry eye" - prevents drainage of lacrimal punctan, can irritate cornea - lymphoplasmacitic infiltrate of the cornea (Chronic superficial keratitis/german shepherd keratitis) - eyelid masses 2) DRAINAGE problems: jones test to confirm - congenital abnormalities: lacrimal puncta atresia (common in dogs), micropuncta - eyelid abnormalities: eurybelaphron, entropion, eyelid coloboma/agenisis, ectropion, or diamond eye (entropion + ectropion + macroblepharon) - NSL block: unilateral, chronic. dacryocystitis (FB, idiopathic), or bonny disease (neoplaia)

what are the efferent outputs of the vestibular system? (5)

1) UMN SPINAL CORD - stimulate IPSILATERAL EXTENSOR in limbs, trunk, neck, inhibit contralateral extensor (head tilt) 2) BRAINSTEM NUCLEI of CN III, IV, VI to innervate EXTRA-OCULAR muscles and coordinate eye mvmts with head/neck (nystagmus) 3) CEREBELLUM to inform of head position, ensure approtiate posture, coordinate movements 4) SENSORY CORTEX OF BRAIN for conscious proprioception of head/mvmt 5) VOMITING CENTRE in RETICULAR FORMATION: motion sickness

what are the most common seizure disorders in horses?

1) arab foals: congenital, grows out of it 2) foals with perinatal asphyxia (neonatal maladjustment syndrome) 3) adults: due to structural or metabolic brain disease (migrating parasites, trauma, accidental intra-carotid injections)

how can you surgically treat deep ulcers?

1) conjunctival graft 2) corneo-conjunctival transposition 3) corneal grafting: - frozen/fresh cornea from donor -biologic collagenous grafting material: A-cell (Porcine urinary bladder, lamina propria, BioSiSt from porcine SI) - Amnionic membrane

what are causes of corneal ulcers? what are the main 4 ddx for SUPERFICIAL ulcers?

1) foreign bodies (sharp, thorny things) 2) ulcerative diseases - KCS (keratoconjunctivitis sicca) - lid conformation esp if they can't blink - mechanical irritation (trichiasis, districhiasis - meibomian, ectopic cilia - not visible) - entropion/ectropion (rolling eyelids/malformed). treatable. - degnerative processes: lipid spots/calcium mineralisations SUPERFICIAL ulcers: - scratches - KCS - Mineralisation (calcium) - Feline herpesvirus - SCCED (spontaneous chronic corneal epithelial defect)

describe the mechanism of signs of a vestibular disease if a lesion is affecting the right side. (which direction would things be? why)

1) lesion affecting RIGHT vestibular apparatus 2) decreased input from RIGHT horizontal SEMICIRCULAR duct 3) perceived as moving head to the LEFT 4) INCREASED EXTENSOR in LEFT limbs, trunk, muscles, decreased tone on right 5) HEAD TILT to the RIGHT, with leaning, falling, or rolling to the RIGHT 6) JERK OF EYES to the LEFT (direction head perceived to be moving) TL;DR: HEAD TILT/FALLING TO SIDE WITH NO ACTIVITY NYSTAGMUS IN OPPOSITE DIRECTION

what are two optic nerve diseases?

1) optic neuritis - meningoencephalitis of unknown origin - from infectious diseases (distemper, erlichia, crypto) - CS: looks blurry/swollen, hyperemia of papilla, vascular congestion, or peripapillary haemorrhages 2) optic nerve neoplasia. (optic nerve meningioma)

what are the phases of an epileptic seizure?

1) prodrome: behaviour changes that occur hours or days before a seizure. 2) aura: animal feels something is about to happen, might be clingy/needy, etc 3) ICTAL phase: seizure 4) POST ICTAL phase: can be bilateral blindness, obtundation, lethargy, etc. can be days after the seizure. can also be hyperactivity, etc. normally a pattern for each patient as to behavior if you do a neuro exam after a seizure 24 hr after a seizure, you might repeat the exam to make sure they aren't just post-ical

what are the 3 forms of ataxia? when are they most seen and how do they display?

1) proprioceptive: unaware of limbs, inconsistent movements. spinal cord diseases. often paretic. most common. 2) vestibular: loss of equilibrium: head tilt, leaning/falling, circles. lateralised. drunken. 3) cerebellar: dysmetria, hypermetria, truncal ataxia, hypertonia, intention tremours, decerebellate posture, absent menace response

what types of fundic diseases can lead to blindness?

1) retinal dysplasia (inherited, bilateral, spaniels) 2) Progressive Retinal Atrophy (night to day blindness) 3) Acute: SARDs/IMR 4) Retinal Detachment (

what is the emergency tx for status epilepticus?

1) systemic stabilisation. ensure patent airway, adequate ventilation, CV status. place IV catheter (very difficult in seizuring dog). if rectal temp > 40 C, start passive cooling. 2a) emergency diagnostic eval. blood glucose, electrolyte, blood gas eval (where available). ECG: arrhythmias <72 hrs following. 2b) drug therapy. - GLUCOSE - DIAZEPAM (.5 mg/kg) or MIDAZOLAM (.2 mg/kg IV) up to 3x. cross BBB in seconds, first-line emergency tx. only for around 15-20 minutes, so you need something that lasts longer. - Phenobarbitol (2-4 mg/kg) up to 20 mg/kg in 24 hrs - Leviticeram (60 mg/Kg IV) but it's EXPENSIVE if persists: consider CRI of medetomidine, benzo, or propofol. can also use potassium bromide (600 mg/kg 1-5 days) , ketabmine, +/- inhalational anaesthetics. continuous EEG MONITORING to TAPER anticonvulsants.

what are ways to tease out proprioceptive difficulties in the horse?

1) walk them with their head up 2) walk them blindfolded 3) walk them down a hill 4) backing up 5) circling often it's very subtle. you can try to do a hopping response: lift up leg, push to the side. only do with experienced handlers.

what is the origin of all the cranial nerves?

1: olfactory bulb 2: diencephalon (it's not really a nerve) 3/4: midbrain 5: pons 6-12 : medulla

which 4 cranial nerves are parasympathetic (autonomic)?

3, 6, 9, 10.

how can articular process DJD cause bilateral lameness?

5 + 6: osteosclerotic new bone it causes BILATERAL FORELIMB LAMENESS the nerves that make up the brachial plexus leave the spinal cord at the intervertebral foraminae between the two arrows. as the new bone is formed, it puts pressure on the nerve roots. in the same way that disc disease can cause sciatica via the nerve roots. the horse was euthanased.

what is the way to approach a spinal disorder in the small animal?

6-finger rule: 1. localisation 2. onset (acute, peracute, chronic) 3. progression (not many disorders improve spontaneously, but a few will improve by themselves in a few hours.) 4. symmetry (not often TRULY asymmetrical) 5. pain (not painful if spinal cord) 6. signalment (species -- cats vs. dogs), breed (daschsund has IVDD), age questions to ask: - is it NEUROLOGICAL (is there proprioception?) - how many limbs are affected? all four (C1-C5, C6-T2) or only pelvic (T3-L3, L4-S3) - are there spinal reflexes?

what sort of mutations do DMD (duchenne MD)/Becker MD patients have? how does that affect prognosis? how can we use this for therapy?

65%: out-of-frame deletions. exon 7 is gone, so 6 and 8 don't fit together. it's X-linked. In-frame deletions (Becker MD): missing exon 4, but 3 and 5 join together. exon 6+ 12 go together (image). they can have partially functioning muscles- reduced but functional dystrophin. longer lifespan. we can do EXON REMOVAL therapy - if we turn OUT OF FRAME exons into IN-FRAME exons, we can improve prognosis - CRISPR/Cas9 to help

how is phenobarbitol metabolised? how does that inform therapy?

67% hepatically metabolised, 33% in urine, possibly cytochrome p450 enzyme system inducer (which breaks down other drugs faster if on multimodal therapy). POOR LIVER function - higher concentration. risk of WITHDRAWAL SEIZURES: severe seizures if suddenly stop tx.

what are common causes of seizures based on age? what are the breed-specific predispositions? how might the most likely change cause if there are abnormal inter-ictal exam findings?

< 6 months: metabolic (PSS, hypoglycaemia), infectious disease, congenital 6 month - 6 years: idiopathic epilepsy, inflammatory/infectious, Metabolic >6 years: Neoplasia, idiopathic epilepsy, inflammatory/infectious. - can also get insulinomas which lead to hypoglycemic seizures breed dispositions: - retrievers, beagles, GSD, bernese, keeshonds, irish wolfhounds - jesus there is a lot of them i don't care anymore if abnormal inter-ictal: - symmetrical abnormalities: metabolic, toxic, hyrocephalus, degenerative - asymmetrical: neoplasia, inflammatory/infectious, anomalous

what are some ddx for a peripheral vestibular dysfunction?

A - congenital vestibular dysfunction M - hypothyroidism N - tumours of inner/middle ear (peripheral nerve sheath, adenocarcinoma, other) I - inflammaotry (nasopharyngeal polyp) or infectious (otitis media, interna, bacterial or fungal), idiopathic (geriatric vestibular system) T - aminoglycosides, loop diuretics (furosemide), topical cleansing agents, traumatic (head traumas

what are the focal acute/chronic ddx for a neuromuscular disease?

ACUTE: NEUROPATHY: trigeminal, facial, brachial plexus avulsion, tail-pull injury, ischaemic neuropathy JUNCTIONOPATHY: m. gravis (focal) MYOPATHY: masticatory myositis, extraocular myositis, ischaemic neuromypoathy ------------------------------------------ CHRONIC: NEUROPATHY: degenerative lumbosacral disease, peripheral nerve sheat tumour. JUNCTIONOPATHY: focal m. gravis MYOPATHY: masticatory myositis, extraocular myositis, fibrotic myopathy (gracilis/semitendinosus)

what are type I and type II acute adverse reactions for phenobarbitol? what about chronic?

ACUTE: type I: sedation/ataxia very common. resolves within 7 days. type II: - Immune mediated neutropaenia, anaemia, thrombocytopaenia: REVERSIBLE, STOP TX immediately - acute hepatotoxicity: rapid elevation of ALT. STOP - superficial necrolytic dermatitis - +/- pancreatitis, dyskenesia, anxiety. - need CBC to check enzymes, etc. CHRONIC: - PU/PD/Poyphagia - KEEP THEM ON THE SAME DIET - elevation of ALKP/ALT (mild elevations normal/to be expected) - low T4 +/- high TSH. - CHRONIC HEPATOTOXICITY: associated with high concentrations. need serum biochem every 6-12 months. test ammonia/BAST if ALT rises or albumin decreases.

what are the most common generalised acute/chronic neuromuscular ddx?

ACUTE: - NEUROPATHY: acute canine polyradiculoneuritis - JUNCTIONOPATHY: acquire m. gravis, - also: botulism, tick paralysis, hypocalcaemia, hypokalaemia, exertional rhabdo - MYOPATHY: hypokalamia, exertional rhabdo (HORSES) ---------------- CHRONIC: - NEUROPATHY: inherited or diabetic polyneuropathy - chronic inflammatory demyelination polyneuropathy - protozoal polyradiculoneuritis (NEOSPORA) JUNCTIONOPATHY: m. gravis, hypokalaemia, MYOPATHY: immune-mediated polymyosistitis, centronuclear myopathy (great dane/labs), Muscular dystrophy, myotonia congenita

what are clinical signs of uveitis? what can develop after chronic cases?

ACUTE: 1) ocular pain/blindness 2) aqueous flare (tyndall effect) - humour is clear in normal conditions. blood aqueous barrier is disrupted. 3) miosis 4) conjunctival/episcleral hyperaemia (red eye) 5) corneal oedema (blue) 6) hypopion (WBC) /hyphema (RBC, 8 ball eye) 7) synechia - posterior = iris to lens - anterior = iris to cornea, repairing a hole CHRONIC - cataracts due to poor nourishment of the lens. can also cause uveitis due to irritatoin. - retinal detachment - glaucoma - lens luxation (cats)

how are cataracts classified?

AETIOLOGY: 1) PRA (secondary to retinal disease, Cocker spaniels, retina releases toxins) 2) METABOLIC (diabetes, sorbitol, dogs) 3) congenital (always nuclear) or inherited (breed-related, juvenile or adult onset) - afghans, cocker spaniels, retrievers, shepherds, poodles, staffies/bulldogs 4) nutritional 5) secondary to intraocular disease (uveitis) 6) senile 7) traumatic: FBs, cat scratches - phacoclastic uveitis STAGES OF MATURITY: - incipient: less than 10-15%. dog has "normal" vision - monitor - immature: involves nuclear + cortex. decreased vision - mature: complete opacity of the lens (surgery) - hypermature: small, glistening, crystalline particles - morgagnian: avanced lysis and liquefaction

what is "loading therapy" and what are the doses for AED?

AIM: rapidly elevate serum conc to achieve therapeutic levels (high doses within short timeframe). PB: up to 20mg/kg IV in 24 hrs LEVETIRACAM: 60 mg/kg IV KBR: 600 mg/kg over 1-5 days (PO or PR) then continue at normal daily dose rate. SE: severe ataxia, sedation, disorientation, vomiting, diarrhoea. may require hospitalisation, careful nursing care, IVT/

what do you look for on a gait analysis? how can that help you neurolocalise?

ATAXIA: - cerebellar ataxia: complete uncoordination - vestibular ataxia: leaning towards one side - general proprioceptive ataxia: knuckling, crossing legs LOSS OF MOTOR fUNCTION: - paresis (tetra/para/mono) - partial loss of motor function: ambulatory or non-ambulatory -plegia: complete loss of motor function if ONLY paresis: neuromuscular/lumbosacral if ONLY ataxia: cerebellar, vestibular ATAXIA + PARESIS: spinal, brainstem problem

what is ankylosis and what is it a common sequelae of in horses?

Ankylosis = stiffness of a joint due to abnormal adhesion and rigidity of the bones of the joint, which may be the result of injury or disease. often result of trauma, or severe arthritis causes CVM-2. image: bone scintigraphyy showing hotspot of cervical vertebrae from the side.

what are the most common causes of inflammatory diseases affecting the CNS in rabbits?

BACTERIAL: middle ear (p. multocida) or central vestibular (listeriosis) VIRAL: perpesvirus PARASITIC: toxoplasmosis FUNGAL: encephalotizoon cuniculi

which diseases can cause cerebellar hypoplasia in ruminants?

BVDV (if < 180 days) lambs: bluetongue, border disease vrus (BDV, hairy-shaker) or cache valley (NA)

cattle spinal cord/PNS lesions: what is the most common cause?

BY FAR trauma nerve injury due to parturition/trauma, prolonged recumbency, etc can also get elso heel (cattle, spastic paresis, progressive extension of hindlimb), swayback

what are the segments of the spinal cord?

C1-C5 C6-T2 T3-L3 L4-S3

1.5 year old jack russel, peracute presentation. no postural replacements. tetraplegic. mental status normal, spinal reflexes normal, nociception normal.

C1-C5 spinal cord segments. if acute: trauma, bleeding. diagnosis: cervical spine fracture. (atlanto-axis subluxation, C1-C2. cast on head, neck and chest or pins/screws.

what is a cataract vs nuclear sclerosis?

CATARACT: - prevents visualisation of fundus. - interfere with sight, but only complete ones cause blindnesss NUCLEAR SCLEROSIS: - NOT a cataract. ageing change of the lens. generally does not cause blindness. - the fibres in the periphery compress the nucleus of the lens, causing it to become more dense. you can see the lens but you CAN see through it with direct/indirect opthalmoscopy. - not pathlogic

Ddx for adult cattle with cerebrum/forebrain vs. brainstem vs. spinal cord lesions? what about small ruminants?

CATTLE: cerebrum/forebrain: polioencephalomalacia, other shit (infectious/toxic stuff mostly, BSE) brainstem: listeria (CN V-XII) spinal cord: parturition, trauma associated nerve injury SMALL RUMINANTS cerebrum/forebrain: Coenurosis (gid) - surgical - also caprine arthritis, maedi visna, polioencephalomalacia, scrapie, border disease brainstem: listeria, coenurosis - also get louping ill (ovine encephalomyelitis)

what is atypical myopathy? what causes it?

CAUSES: ingestion of plant toxin (Hypoglycin A) - seasonal pasture myopathy - USA: seeds of boxelder tree - UK: Sycamore tree CS: acute onset severe myopathy in horses at pasture - SEVERE myoglobinuria. so weak they can barely move. DIAGNOSTICS: - CK, AST massively increased - marked increase lipids in the muscle (vacuoles) Muscle biopsy pre/post mortem - triceps/intercostal/diaphragm

What are causes of circling/head turning?

CIRCLING: - doesn't have to come from the brain (vestibular) if tight circles. wide circles would be forebrain. - lesion on same side of the direction of circling. the brain is contralateral to the muscles. a LEFT forebrain lesion means you can't perceive the RIGHT stimuli, so you ignore the right side and go towards the LEFT. head turning: forebrain issue (same principle as circling, hemi-neglect syndrome)

how does CK and AST in the blood change during an episode of equine rabdo?

CK: peaks around 6 hours. AST peaks around 24 hours, remains days/weeks. can use to time episode and rule out other diseases.

what are clinical signs, diagnostics, and treatments of polioencephalomalacia? how can you prevent it?

CLINICAL SIGNS: MILD: lethargic, obtunded. - develops hours to days. - appear blind, slow but present PLR. miosis, strabismus, - opisthonous, hypermetric gait, hyperaesthetic progress to depression, head tilt. - symmetrical (metabolic) SEVERE: sudden death/found recumbent/comatose, convulsions, hypertonic between seizures. grave prognosis. DIAGNOSIS - response to thiamine tx over 24 hrs - CSF normal (w or w/out mononuclear pleocytosis) - blood thiamine levels are not reliable - erythrocyte concentration of thiamine/transketolase activitiy - PME: cortical swelling, softening, flattening of gyri PME: lesions in cortex extending to other regions of brain, diffuse laminar necrosis Tx: - thiamine supplementation - cerebral oedema reduction - seizure mgmt - get rid of source of SULFUR in WATER prevention: - avoid access to high-sulfur feed/water, supplement in diet w outbreaks

summarise the clinical signs and neurological signs of lumbosacral disease (cauda equina syndrome)

CLINICAL SIGNS: - decreased exercise, unwillingness to jump - unilateral/pelvic limb lameness - paresis WITHOUT ataxia: short strided pelvic limb gait, dropped hock in dogs, plantigrade stance in cats - flaccid tail (decreased tail tone) +/- urinary incontinence Neuro exam: can be normal, can also have sciatic nerve defects - can have proprioceptive deficits - can have decreased withdrawal reflex (hock flexion), muscle tone (distal from hock) - PAIN: extension on hips, lumbosacral palpation, dorsal extension of tail

what are clinical signs of acute glaucoma?

CLOUDINESS due to oedema. VERY PAINFUL. - episcleral congestion - conjunctival hyperaemia - epiphora - mydriasis (dilated pupil due to presusre) - aqueous flare (tyndall effect) - absent menace REVERSIBLE: remove pressure and CS go away.

what is the trochlear nerve? what is it responsible for? how can you tell there is a CN IV issue?

CN IV. - dorsal obliques - extraocular muscles only CN that is CONTRALATERAL AND IN DORSAL part of brainstem. like a pulley system. strabismus leaning away would be a sign.

guttural pouch in the horse - innervation. how does this affect the horse?

CN IX, X, XII. other side: at the end of the stylohyoid, other side of petrous temporal bone: VII, VIII in dogs, VIII in horses. Horses with GP lesions that affect the CNs will cause dysphagia. test to see if they swallow. in dog: we use the gag reflex but it is difficult to interpret. horses don't have.

what is the function of the facial nerve? where is it? what are causes of a facial neuropathy? what are signs?

CN VII. motor and sensory, parasympathetic. causes of a neuropathy: - infection of the middle/inner ear - trauma - neoplasia - polyneuropathy (hypothyroidism in dogs) - idiopathic in up to 75% of dogs and 25% of cats droopy face on one or two sides. can also have vestibular + facial signs together because they are both in the inner ear. other signs: no parasympathetic innervation = dry eye, dry nose.

how do you differentiate between conjunctival hyperaemia and episcleral hyperemia? what do they indicate?

CONJUNCTIVAL: dichotomous division. tortuous, branching, and bright red. vessels move with the conjunctiva. most evident at fornices. - indicates ocular disease EPISCLERAL: rare. no dichotomous division, straight and deep red. vessels stationary. most evidence closer to the limbus. - indicates deeper ocular tissues (including intra-ocular)

what is decerebellate rigidity?

CONSCIOUS animals but increased muscle tone on all four limbs. often pelvic limbs are flexed and forward.

how do you define the location of a corneal lesion vs. iris lesion?

CORNEA: axial - paraxial - peripheral IRIS: pupil - peripupillary - peripheral

where is the grey matter in the cerebellum? what are the three layers?

CORTEX has grey matter (outer part) molecular layer: AXONS axons of granular neurons, dendrites of purkinje cells. purkinje layer: single cell layer of large pyramidal neurons. axons of pukinje cells project OUT of the cerebellar cortex, synapse on deep cerebellar nuclei. large, flat cells, that feed cortex (release GABA). travel out of cortex and into deep nuclei. granular layer: dense layer of small granular lesions AFFERENT FIBRES: mossy, climbing fibres (in granule and purkinje). come in from CNS and talk to cerebellar systems. EFFERENT: axons of purkinje cells.

how do the receptors work in the semicircular ducts and what do they detect?

CRISTA AMPULLARIS in 3 ducts detect ANGULAR ACCELERATION. in cupula. - ducts located at right angles in XYZ to detect all types of movement. - left/right ducts are paired

clinical signs, diagnosis, treatment of listeria?

CS: fever, anorexia, depression, proprioceptive defects, headpressing, compulsive circling CRANIAL NERVES V-XII dysfunctional: - V: dropped, asymmetric jaw, facial analgesia - VI: medial strabismus on lesion side - VII: ptosis, loss menace response, absent palpebral, drooling, etc - VIII: nystagmus, head tild, circle to lesion side - IX/X/XII: stertor, dysphagia, paresis of tongue, may protrude MOST COMMON: dysphagia (IX, X), mentation, circling, maybe nystagmus - monoparesis - progress to recumbency, lie in lateral, torticollis, opisthonotonus -QUICKLY in ruminants compared to cattle Diagnosis: suspicion + CSF tap. increased protein/wtv Tx: high doses penicillin +/- oxytet. PUBLIC HEALTH concern - cont of milk prodcts (raw milk, cheese)

an animal presents with weakness (generalised): how do you define the system between cardio, systemic, or neuro?

CVS: might have cough, murmur/arrhythmia - blood pressure - ECG - thoracic radiographs - echo - troponin 1 systemic: might have pale mm, pyrexia, distended abdomen - haematology - biochem - electrolyte analysis - blood gas - abdominal US Neuro: based on neuro exam (neurolocalisation)

what are non-ulcerative causes of corneal opacity?

Cats: corneal sequestration - acute bullous keratopathy (looks like melting ulcer) from herpes (image) Both: immune-mediated keratitis (like feline herpes). - scar/fibrosis - mineralisation dogs: - german shepherd keratitis (pannus) - pugs: pigmentary keratitis. optimmune.

a goat has a right head tilt, obtunded, no right hopping reflex (postural deficits). where is the location of the lesions?

Central vestibular (brainstem) on the RHS.

what are the signs of a tibial nerve dysfunction?

Clinical signs: - dropped hock, plantigrade stance in cats - decreased tarsal innervation - characteristic gate with overflexion of tarsus, decreased muscle tone distal from tarsus NEURO EXAM: - LOSS OF HOCK FLEXION during withdrawal - patellar pseudohyperreflexia (due to decreased innervation of antagonistic flexor muscles). note PASSIVE character of patella. floppy. typical of LUMBOSACRAL disease - sciatic nerve is affected due to mobility of this area

what is CRISPR/Cas9? what is it used to treat?

Clustered regularly interspaced short palindromic repeats. CRISPR is originally a bacterial adaptive immune system used in genetic editing techniques. Specific guide RNA can target any given sequence, Cas9 CUTS the genome at any specific site. used to treat DUCHENNES MD - IM. remarkable increase in dystrophin. but need systemic treatment (I/V).

what are some ddx for a central vestibular dysfunction?

D - some neurodegenerative diseases A - epidermoid/dermoid cyst, arachnoid diverticulum N - neoplastic (brain tumours: meningioma, choroid plexus, lyphoma), nutritional (thiamine deficiency) I - inflammatory/infectious (meningoencephalitis: viral (distemper, FIP - dry form), bacterial, protozoal (toxo, neospora), fungal (crypto) T - metronidazole or head trauma V - cerebrovascular accident

what is the most common cause of reduced drainage? what test can you do?

DACRYOCYSTITIS: Inflamed/blocked nasolacrimal duct, often FB present. idiopathic. JONES test: fluorescin drop on eye, wait for stain to come through nose. can also do MRI/CT scan. (above pointer in image) can also get nasal masses that grow into the lacrimal duct.

what is the focal light examination? what does it use? what reflexes do you test (3)?

DIRECT OPTHALMOSCOPE (pen torch/finoff transiluminator) REFLEXES (IN DIM LIGHT) - Dazzle reflex (squinting/blinking) - PLR (pupillary light response). can be DIRECT or INDIRECT and make sure you specify. - SWINGING: to test RELATIVE AFFERENT PUPILLARY DEFECT. might dilate on direct PLR after constricting from indirect PLR. RETROILUMINATION: reflection of tapetum (b/w choroid and retina on DORSAL aspect). - assess pupillary size/shape, presence of opacity

what is articular process joint DJD?

DJD of the synovial joints at the articular processes is a form of vertebral malformation-malarticulation that can result in spinal cord compression. This osteoarthropathy is more common in older horses but has been seen in yearlings. it can compress spinal nerves and lead to lameness. thought to be the result of chronic malarticulation at these joints that represents the effects of osteochondrosis when these patients were young or an injury followed by malarticulation. occurs secondary to severe arthritis of joints (several years). CVM-2.

what are common spinal diseases in dogs, cats?

DOGS: - intervertebral disc disease (IVDD) type I vs type II - ischaemic myelopathy - acute non-compressive nucleus pulposus extrusion - neoplasia - syringomyelia - immune-mediated inflammatory CATS: - infectious inflammatory (FIP) - Neoplasia (Lymphoma (young), osteosarcoma, meningioma (older) - Trauma (Fracture/luxation) over 91% of spinal cases represented by 10 specific diseases.

how does the cornea heal? epithelium vs. endothelium? also, what is the process of superficial corneal neovascularisation and where does it originate?

EPITHELIUM: good regenerative power, basal cell turnover in about 7 days for a superficial ulcer/scratch (to regenerate from the bottom up) - very small cell epithelial defects heal within 24 hours - cell migration. - corneal vascularisation: takes over a week of inflammation until vessels grow. it's a GOOD thing. ENDOTHELIUM: - not regenerating. SINGLE LAYER. - can become complete cloudiness in both eyes if endothelial damage. LIMBUS: between cornea and sclera. protective ring. they are on guard, and if something happens to the cornea, they shoot blood vessels and pigmentation. this can be a good thing because it promotes healing. - QED lesions in center of cornea take longer to heal

what's the most common cause of multicentric, asymmetrical neuropathies in horses?

EPM - equine protozoal myeloencephalitis. sarcocystis neurona.

describe how the brain receives vestibular information in semicircular canals in a normal and abnormal animal using an example of turning the head to one side.

EXAMPLE: TURN HEAD TO ONE SIDE - endolymph flows towards ampulla on that side, away from ampulla on opposite side - endolymph displaces cupula which distorts stereocilia - stimulates hair cells on moving side, inhibits on opposite - UNEQUAL input received by VESTIBULAR NUCLEI in MEDULLA DISEASE: compromises input from one side, which is perceived as movement. results in reflex changes in posture, eye movement that create clinical signs of vestibular disease.

FA Neurology

Emil Olson

where is the vestibulocerebellum? what does it do and how does it affect the brain?

FLOCCULONODULAR LOVE which receives afferent input from vestibular nuclei + some axons DIRECT to cerebellum from CN VIII axons enter via caudal cerebellar peduncle efferent output: INHIBITORY to the vestibular nucle by releasing GABA!!!!

Listeriosis/Listeria monocytogenes: pathogenesis/transmission? which species are most at risk? what type of bacteria is it?

G+ve anaerobic - survives long periods in environment, multiplies in low temps. causes ACUTE MENINGIOENCEPHALITIS, multifocal microabscesses in brain tissue. PATHOGENESIS: - unclear pathogenesis but possible up CN or microabscess in brainstem, trigeminal ganglion from ingesting silage. esp 5th or 7th trigeminal SHEEP GOATS - more acute, higher fatality rates than cattle (individuals) Risks: - poorly preserved silage (but other stuff too, like soil) - risk of cont higher if there is soil BRAINSTEM ISSUE.

how can you classify a seizure? (general vs. focal, self-limiting/vs clusteed/continuous)

GENERALISED: bilateraly involvement (both sides of body/cerebral hemispheres). lose consciousness, salivation, urination, defecation. FOCAL: lateralised/regional signs. can be sensory, motor, autonomic, or behavioural signs. - can ALSO have focal seizures with SECONDARY bilateral cerebral involvement. starts with facial twitch and ends with generalised seizure. Self-limiting: any single event, 1-2 minutes Clustered: 2 or more in 24 hours. Continuous: status epilepticus. no recovery of normal consciousness.

how might you differentiate a GMA from an SRMA on a microscope?

GMA: granulomatous meningioencephalomyelitis. - MONONUCLEAR cells SRMA: - NEUTROPHILS - pleiocytosis. both high cellularity.

What is caprine arthritic encephalitis virus?

GOATS (kind like goat HIV) - leukoencephalomyelitis - ataxia, paresis, head tilt, nystagmus, opisthotonus, decreased PLRh - usually young goats - symmetric or asymmetric neurolocalisation older animals: - paralysis (enlarged joints, shifting lameness, wt loss, mastitis, ill thrift)

causes of headpressing?

HEADPRESSING: encephalopathies - often metabolic because it's symmetric, bilateral, forebrain. - renal, hepatic, etc. diffuse forebrain.

how do abnormal (1st/2nd) eyelids affect the cornea? what does this lead to?

HOW: loss of protective effect, loss of oily component of tears, abnormal contact with hairs/masses contacting ocular surface LEADS TO: CONJUNCTIVAL and CORNEAL irritation - corneal neovascularisation/ulceration

what are the intracranial vs. extracranial causes of seizures? some ddx for each?

INTRACRANIAL: 1) structural: - anomalous (hydrocephalous, lissencephaly, arachnoid cyst) - neoplastic (meningioma, ependymoma, astrocytoma) - infectious (rickettsial, viral, fungal, etc) - inflammatory (granulomatous or eosinophilis meningioencephalomyelitis) - traumatic - vascular (ischaemic, haemorrage) 2) functional: idiopathic epilepsy. suspected genetic cause (ion channels) 3) cryptogenic: e.g. head trauma years previously with normal imaging EXTRACRANIAL: reactive 1) environmental: toxins 2) intrinsic: - electrolytes: hypocalcaemia, hypernatraemia, hyponatraemia - energy (hypoglycaemia, thiamine) - organ failure (hepatic, uraemic) - vascular perfusion (hypertension, hyperviscosity, polycythaemia)

how do you differentiate a neuropaty, junctionopathy, and myopathy based on diagnostics?

In order: - CK/AST/ALT/Myoglobinuria = myopathy - electromyography: silent = junctionopathy, sponaneous activity = neuropathy, myopathy - nerve conduction studies: decreased/slowed = neuropathy, decremental response = junctionopathy, normal = myopathy.

What are the 7 causes of cataracts?

Inherited: - breed related (genetic) - most common Traumatic: needs REFERRAL - foreign bodies - cat scratches. - damages lens capsule and subjects it to immune cells. might need to remove lens. Metabolic: diabetic dogs. develop quickly and bilateral. Nutritional: uncommon PRA: progressive retinal atrophy. Senile: generally cortex, wedge shaped, might not occlude vision. if blinding, should operate.

what is stringhalt? aetiology?

Involuntary hyperflexion of the hock towards the abdomen. (equine). can be so severe that the fetlock hits the underbelly. goes away at a trot often. often confused with fibrotic myopathy, but those have feet that are SLAPPED down on the floor, not hyperflexed. often due to traumatic injury to distal limb, affecting SENSORY nerves and therefore reflex arc of that limb. if bilateral - toxic plants.

where does the sciatic nerve exit? what about pelvic/pudendal?

L7-S1. common place to have disease because it's such a mobile area. pelvic (detrusor of bladder) and pudendal (eternal/urethral sphincters) and coccygeal/caucal (motor/sensory to tail) are S1-S3.

what is imepitoin? how does it differ from PB for seizure treatment? what is the dose?

LOW affinity partial agonist for the benzodiazepine binding site of GABA(a) - licenses: idiopathic epilepsy (not cluster seizures) - reduced SE than Phenobarbitol: less sedation/ataxia, less PU/PD/PP DOSE: 10-30 mg/kg PO every 12 hours. - time to steady state: 1-2 days. - no established target serum levels, therefore no need for asst - no contraindication in hepatic compromise jury's out about effectiveness but good for concerned owners.

What are the 3 parts of tears?

Lipid: reduces evaporation. produced by meibonian/tarsal glands (yellow) Aqueous: Nourishes ocular surface (no bVS) - lacrimal gland + accessory or lacrimal of nictitating membrane (blue) Mucin: helps aqueous part adhere to corneal surface. goblet cells (orange)

how is glaucoma managed?

MEDICALLY: - reduce aqueous production (carbonic anhydrase inhibitors, affects ciliary body, other diuretics) - increase outflow (PG analogues) SURGICAL: - laser cyclophotocoagulation (reduce production of aqueous) - aqueous shunt placement - enucleation

how is degen. lumbosacral stenosis treated? what is the most important prognostic indicator for surgical tx?

MILD: medical. restrict exercise, control movement, avoid jumping, NSAIDS, gabapentin. 55% effective. "ADVANCED" = local + corticosteroids in epidural space. "pain clinic". SURGICAL: urinary incontinence. 80%. - decompressive (dorsal lumbosacral laminectomy +/- annulectomy) - neurologist. from L7, lamina is removed. can manipulate cauda equina unlike spinal cord. annulectomy = removal of disk. - lateral foraminotomy for very lateralised compressoins - distraction/stabilisatoin surgery (orthopedics) PROGNOSTICS: urinary incontinence >30 days, not going to get better. can resolve quickly.

what is the function of the mandibular branch of the trigeminal nerve?

MOTOR to the muscles of mastication (masseter, digastricus, temporalis, pterygoids)

what are cell signalling defects?

MYOSTATIN: TGF beta protein. limits growth of muscle. mutations: - belgian blue, piedmontese cattle - "bully whippets" - heterozygous puppies run faster - baby superman - racehorses

how does the spinal cord control bladder function? what part does this?

Mesenteric Ganglion (cats: L2-L5, dogs: L1-L4) - B-receptors: detrusor muscle relax when activated, allow filling - a-receptors: sm. muscle of urethral internal sphincter to contract, close the sphincter pudendal nerve (S1-S3) is motor/sensory from external urethral sphincter bladder dysfunction is often the most important thing to maintain. most often bladder is so big that they cannot urinate.

how do you differentiate a neuropathy, a junctionopathy, and a myopathy based on CLINICAL signs?

NEUROPATHY: reduced to absent spinal reflexes - plantigrade/palmigrade stance - reduced to absent muscle tone - +/- neurogenic muscle atrophy (as opposed to disuse atrophy) JUNCTIONOPATHY: - normal to reduced spinal reflexes - exercise intolerance (may be normal on exam prior to exercise) - no denervation atrophy. might get disuse atrophy tho. MYOPATHY: a little bit in between. - often normal spinal reflexes (unless severe + specific conditions) - exercise intolerance - cervical ventroflextion (CATS) - +/- myalgia, muscle atrophy/hypertrophy DIAGNOSTICS: - increased CK/AST/ALT/MYOGLOBINURIA = myopathy - electrodiagnostics

T3-L3 spinal cord myelopathy clinical signs?

NORMAL thoracic limbs - paraparesis and ataxia pelvic limbs - paraplegia possible - intact or INCREASED spinal reflexes PELVIC limbs (and muscle tone) - URINARY DYSFUNCTION common (UMN bladder) - schiff-sherrington posture possible (disinhibition of thoracic limbs)

unconscious proprioception: what are the two neurons involved?

Neuron 1: rostral spinocerebellar tract (C1-T1) Neron 2: centrobasilar nucleus to cerebellum

describe the mentation, gait, posture, rxns, spinal reflexes, CNs, palpation of animals with a neuromuscular disorder. other clinical signs?

OTHER CS: - regurgitation/dysphonia - focal/generalised muscle atrophy mentation: unaffected gait: weakness/paresis, NO ataxia posture: palmigrade/plantigrade postural reactions: may be normal. spinal reflexes: typically reduced if NEUROPATHY CN: reduced palpebral if weak facial nerve, dropped jaw.

what are ocular and systemic causes of uveitis? how can you differentiate them?

Ocular: more common UNILATERAL signs of uveitis. - ulcers ( reflex uveitis) - penetrating trauma (FB) - cataracts - intraocular tumours Systemic: BILATERAL - Vascular: hypertension, anaemia, vasculitis, etc - Infectious: Viral, FeLV, FIV, others. - Parasitic: Toxoplasma, leishmania, other. - Fungal: cryptococcus, others. - Bacterial: pyometra, other. - Immune-mediated: uveodermatological syndrome, other - Neoplasia: lymphoma, carcinoma, others.

describe the pathway of the PLR and indirect PLR and which nerves are involved.

PLR: optic nerve (CN II), oculomotor nerve (CN III). pre-ganglionic. ciliary ganglion is short (parasympathetic). - pretectal nucleus: small nucleus where they cross (75%??) - all on BRAINSTEM level light--optic nerve--optic chiasm--optic tract--pretectal nucleus--oculomotor nucleus-- CN III--ciliary ganglion -- short ciliary nerves. indirect PLR: Ciliary canglion--short ciliary nerve.

how does AED differ in cats?

Phenobarbitol: 1-3 mg/PO every 12-24 hours. recommended 1st line tx, longer half-life than in dog. can start with once a day dosing. therapeutic levels: 10-20 ug/ml. LEVETIRACETAM: 20 mg/kg PO every 8 hrs. IMEPITOIN: not yet licensed. early studies shown safe to use in cats. KBr CONTRAINDICATED!!! causes allergic PNEUMONITIS!

what are the types of mental statuses? what part of the brain affects the mental status of the dog?

RETICULAR FORMATION: meshwork of neurons that go rostrally, ascend the forebrain. (ARAS ascending reticular activated system) - wakes up, bright/alert/responsive. BRAINSTEM + FOREBRAIN Conscious: - Normal - obtunded (due to forebrain or brainstem): slowed responses Unconscious: - stuporous: reflexes + conscious response b/c reached forebrain - comatose: no conscious response, cannot be aroused

what re the different lobes of the brain and their function?

RHINENCEPHALON (olfactory bulbs) = smell, limbic system. "silent" part of the brain because no clinical signs from a tumour there except seizures/headaches. TEMPORAL LOBE = auditory, vestibular conscious perception. PYRIFORM lobe = olfactory + limbic. FRONTAL lobe = motor, corticospinal/corticonuclear tracts PARIETAL lobes = sensory-motor OCCIPITAL LOBES = visual conscious perception

an animal with a turn to the right and postural deficits on the left side has a lesion in what part of the brain?

RIGHT forebrain. forebrain is ALWAYS contralateral.

what is SARDS and IMR?

SARDS: sudden acquired retinal degeneration syndrome. - acute/subacute vision loss, +/- PLR. - exam otherwise unremarkable - Diagnostic test: ERG (electroretinography) negative IMR: immune-mediated retinopathy - similar changes to SARDS, not well characterised

what are the SE of potassium bromide? how is it excreted and how does that inform treatment/lifestyle?

SE: - sedation, ataxia, weakness, PU/PD/PP - GI irritation - vomiting, diarrhoea. reduce by dividing daily dose and giving /w food - necrotising pancreatitis EXCRETION: unchanged in the urine - IVFT diuresis can increase renal excretion and decrease serum conc. of potassium bromide. - use in CAUTION in dogs with renal disease. - undergoes renal tubular reabsorption in competition with chloride, so high dietary CL- can increase excretion of KBr - maintain CONSTANT DIET (CL-, salt intake) to prevent fluctuations.

what is an absolute stenosis (CVM type 2)? what is the signalment? location?

STATIC. - osseus changes in vertebrae that cause spinal cord compression, or stenosis in spinal canal - usually affects older horses (>8 y, warm bloods/large horses) at C5-C7 - osteoarthritic changes in the articular process joints (facets) as a result of congenital osteochondrosis? (OCD) - thought to be the case. severe sclerotic case - other malformed vertebrae can be seen IMAGES: left- new bone grows, puts pressure on spinal cord between two articular joint surfaces. right: myelogram. loss of dorsal contrast and ventral column due to sclerotic new bone. (middle)

how is IVDD treated? medical vs. surgical?

SURGICAL: THORACOLUMBAR SPINE: Hemilaminectomy. Removal of half the lamina, articular facet joint, and pedicle allowing access to the vertebral canal from a lateral approach CERVICAL SPINE: Ventral Slot. it's burred thru the centre of the disc and adjacent vertebral endplates to gain access to the vertebral canal from a ventral appch. MEDICAL: urinalysis, cage rest, pharamcologic. can lead to muscle atrophy, obesity. NSAID/GABA/opioids +/- other things, massage, acupuncture, laser therapy, electromagnetic fields, transcutaneous electrical nerve stimulation.

what 3 structures make up the third eyelid and what can cause it to become reddened?

Structures: 1) CARTILAGE: (t-shaped): holds third eyelid up against eye. can CURL and cause OUTWARD fold. 2) LYMPHOID TISSUE: large amts. - very prominent in some cases (young animals, allergies, certain infections in cats) - mainly present in the inner side, usually accompanied by hyperaemia 3) ACCESSORY LACRIMAL GLAND: - produces up to 30% of the aqueous component of the tears - can prolapse and become inflamed Causes: - PIGMENTATION: variable, can be poorly pigmented which causes it to be redder. - hyperaemia/swelling: ocular surface disease, orbital disease, TEL neoplasia. - follicular proliferation: young animals, allergies/infections, inner side. - scrolled cartilage/prolapsed nictitans gland.

schiff-sherrington posture is localised to where? what does it indicated about the duration of the lesion? what would the gate be? prognostic?

T3-L3 Myelopathy (forelimbs work fine) lost innervation in BORDER cells which go cranial to innervate cerivico-thoracic extensors. Causes: severe and acute. gait: paraplegic or severely non-ambulatory paraparetic. NO prognostic value.

what are the 3 tiers of idiopathic epilepsy confidence?

Tier I: - history of >2 unprovoked seizures at least 24 hrs apart, - age of onset be 6 months and 6 years, - unremarkable neuro exam in between, no abnormalities (blood, urinalysis, etc) - can be supported by family history Tier II: factors in 1 + - MRI of brain - fasting/post-prandial bile acids (rule out HE) - CSF analysis Tier III: - tier I + II, ictal or inter-ictal EEG done

agents of optic neruitis? how would you treat?

UK: more likely non-infectious, immune-mediated - immunosuppressants (dexamethasone + cytosine arabinose, prednisolone) - acting quickly is important, they can recover in a few months. infectious: DVC, tick-born, toxo, fungal, rickettsia (erlichia canis).

how can you differentiate between a UMN and LMN bladder dysfunction?

UMN - thoracolumbar. INCREASED tone detrusor/urethral muscle. so hard, like a rock. - large and full, turgid - resistant to manual expression - inconsistent leakage, overflow incontinence. risk of rupture/wall damage, - can persistent atonic bladder wall, where the animal can walk but loses continence forever LN - Sacral (S1-S3) - DECREASED tone. very soft. - easily expressed - can leak spontaneously - URINE SCALD (skin irritation) and persistent UTI. - can get ulcers BOTH cause RETENTION. up to 38% develop UTI.

what is the difference in function and location of UMN and LMN?

UMN: CONTROLS muscles (via LMN) - primarily in WHITE matter or VENTRAL funiculus of spinal cord. LMN: CONTRACT muscles (orange) - VENTRAL horn of GRAY matter throughout spinal cord. most peripheral nerves are a combination of sensory and motor neurons.

which CNs run through the internal acoustic meatus?

VII

when should you suspect an animal has neuromuscular disease? what are the clinical signs/Physical exam?

WEAKNESS without ATAXIA (stiff/stilted gait) EXERCISE INTOLERANCE other findings: - dysphagia/dysphonia - regurgitation/megaoesophagus (dogs, more striated muscle there) - dyspnoea (laryngeal paralysis, aspiration pneumonia) - gait abnormality/lameness PEx: - muscle atrophy or hypertrophy - myalgia - cervical ventroflexion (CATS)

what three questions should be asked when examining a red eye? how do you answer them?

WHERE: ocular/adnexa, iris hyperaemia, or intraocular bleeding? WHAT: almost every structure in the eye can be the cause of redness. HOW: consider whole globe, examine from outside to inside. make sure it isn't normal variation for the patient

what are two main causes of red eyelids?

WHERE: red periocular tissue WHAT: skin, muscles, meibomian glands, conjunctiva HOW: hyperaemia, swelling, ulcers, crusts, loss of hair, etc. 1) periocular dermatitis: several causes. can be systemic or severe. - allergies - mange/ringworm - leishmania - hepatocutaneous syndrome 2) meibomian glands can become infected, inflamed, or neoplastic.

what is a melting corneal ulcer? what are causes (4)? how is it treated?

YELLOW - MMPS (matrixmetalloproteinases) break down collagen and cause it to droop. complication of any ulcer. BRACHYCEPHALIC eyes can lead to melting ulcers very frequently. CAUSE: - bacteria (pseudomonas, staph, strep) - fungi - neutrophils - cornea (epithelium, stroma, tearfilm, etc) Medical tx: - antibiotics (topical/systemic) - mydriatic cyclipegic (atropine) - anti-collagenase (Serum from horses/your own) - treat with NSAIDS surgical: - conjunctival graft - corneo-conjunctival transposition - corneal grafting (frozen/fresh cornea from donor or biologic collagenous grafting material)

what is cauda equina syndrome? what is the clinical presentation? how can it be differentiated from an orthopaedic problem?

a COLLECTIVE term to describe animals with clinical signs of cauda equina dysfunction. includes all disorders VAGUE, UNSPECIFIC - paresis WITHOUT ataxia (cauda equina is PERIPHERAL NERVES, not spinal cord) - pelvic limb lameness that is worse with exercise - spinal hyperaesthesia can be present DIFFERENT: - pain on EXTENSION of hips (compresses the nerve) and DORSAL extension tail. - decreased tail tone - urinary/faecal incontinence often NO neurological deficits.

what is horse "shivers"?

a bizarre condition that affects draft horses. horse cannot pick up hind leg(s). sometimes you try to lift one and it lifts the other. if you do lift it, it "shivers"/shakes, and the tailhead rises. causes difficulty backing up.

what is polioencephalomalacia? what is the aetiology?

a cerebrocortical necrosis. worldwide, common in ruminants, treatable. thiamine deficiency (VITAMIN B1) /altered thiamine metabolism, which is a co-factor for transketolase and provides glucose to the brain. - loss of transketolase = increase lactate, pyruvate, oxoglutarate = intraneuronal swelling = increased ICP/NEURONAL NECROSIS - ANY condition that inactivates thiamine in rumen or synthesis RAPIDLY causes thiamine def. - pre-ruminants: dependent on thiamine ingestion. - ruminants: produce thiamine via bacteria but this can be interrupted sulphur: inhibitors: - SULFUR (inhibits mitochondrial CCO): found in beef feed, cruciferous vegetables, molasses. reduced and incorporated. NEUROTOXIC. - BRACKEN FERN - HORSETAIL - NARDOO FERN (thiaminease)

how do cats get d- shaped pupils? what is this associated with?

a defect in one of the short ciliary nerves (either nasal or malar) affect constriction on one side. FELV-ASSOCIATED LYMPHOSARCOMA INFILTRATION

what is electromyography and what is it used for?

a functional test for muscles. to differentiate between disuse (orthopedic) and denervation atrophy. mapping distribution of disease. electrically SILENT at rest - normal muscle or disuse atrophy (junctionopathy) spontaneous electrical activity = neuropathy or myopathy.

what is the MDR-1 gene (ABCD1) and what drugs does if affect?

a gene for an ATP-dependent efflux pump. - sits on luminal surface of brain capillary endothelial cells and excludes important drugs from the CNS: - ivermectin - antibioitics - dexamethasone SOME dogs are defective (border collies, ivermectin toxicity). upregulation of p-glycoprotein found in some EPILEPTIC drugs, malignant GLIOMAS (chemo resistance).

What is centronuclear myopathy? ("Labrador myopathy")

a hereditary myopathy of labradors - internalised myofibre nuclei. typically type II myofibre atrophy mutation in the PTPLA gene. signs around 3-4 months old, exacerbated by cold. CS: weakness, short-strided gait, kyphotic posture, muscle atrophy often with reduced tendon reflexes. - usually stabilises around 6-12 months of age with mild disabilities. tx: dietary carnitine, coenzyme Q10, B vitamins.

paradoxial cerebello-vestibular lesions

a lesion in the cerebellum - no inhibition of muscles - extensor tone INCREASES. that causes a contralateral head tilt/circle.

what is ovine encephalomyelitis?

a parasitic disease (louping ill) - sheep. ixodes ricinus - togavirus. fever, depression, tremors/ataxia, hypermetria, hyperexcitable, bunny hopping. yearling sheep, spring.

what is wallerian degeneration associated with CVM/S?

a post-mortem diagnostic of the spinal cord to try to determine precisely where it was occurring. - DEGENERATION of ascending proprioceptive tracts ROSTRAL to the lesion (dorsal funiculus, dorsolateral funiculus) - white matter and grey matter change AT the site of the lesion - descending (motor) tracts CAUDAL to the lesion (ventral funiculus). pathologist will segment the spinal cord all the way up to the neck to neurolocalise.

Horses that undergo repeated episodes of tying up: what should you investigate?

acquired cases should be considered, and if possible ruled out - certain "acquired causes" may precipitate an attack on a genetically-susceptible animal (overexertion) - inherited causes more likely. 2 forms of genetic disorder are recognized - recurrent exertional rhabdomyolysis of thoroughbreds - pollysaccharide storage myopathy

what are the aetiologies of exertional rhabdo (acquired vs. inherited) in the horse?

acquired: - overexertion (eccentric contraction: happens while muscle is lengthening, metabolic exhaustion, oxidative injury - hot weather, lack of vitamines) - electrolyte imbalance - hormones - infectious causes INHERITED: - recurrent exertional: defective calcium regulation. might not be the same defect. - polysaccharide storage myopathy.

what is the use of potassium bromide for seizures? what is the dose/time to steady state? target concentrations? mechanism of action?

adjunct therapy to PB/imepitoin if they are at the max dose but still inadequate seizure control. Dose: 10-15 mg/kg q12 hrs or 20-30 PO q 24 hrs time to steady state: 120 days!!!!!! asses serum conc. then. target: 1000-3000 mg/ml suspected MoA: act at GABA-gated Cl- channels, causing neuronal hyperpolarisation.

what is the mechanism of c. botulinum? what are the 3 aetiologies?

aetiologies: 1) "forage" - ingestion of feed material with preformed toxin. commonly from poorly made "big-bale" silage that had soil contamination or air. 2) toxico-infectious - seen most commonly with young foals. GIT c. botulinum. 3) wound - anaerobic wounds contaminated. LEAST common, most easily missed. MECHANISM: acts at NMJ by inhibiting AcH release at presynaptic membrane. no signal passed - flaccid paralysis.

what are the 3 presentations of entropion? how/when is it treated?

after eyelid opening at 14 days: - can't go under surgery. tacking sutures (temporary) which might resolve - if not, definitive surgery when fully grown. acquired: due to eyelid/skull extreme conformations, elderly dogs/cats (loss of retro-orbital fat and laxity) - > 10 techniques depending on type - Holz-Celsus: versatile. incision made in a smile-shape (image). blepharospasm: eye closed due to pain. apply proxymetacaine to investigate source of ocular pain.

Seizures and Epilepsy

alberta de stefani [email protected]

what is equine rhabdomyolysis syndrome? what are the two presentations, the diagnostics, and the treatments?

also called "monday morning" and "tying up", because they worked out over the weekend and then stopped, built up glycogen. muscle cramping/pain during, following exercise. lysis of muscle fibres. presentations: - acute (may require emergency trx) - stiff mvmts, pain, swelling, tachycardia, myoglobinuria. some can't move, become recumbent. - b/w episodes in a horse w/ several or multiple episodes. requires investigation of cause. DIAGNOSTICS: ACUTE: - plasma CK, ASK activities - rule out other diseases - urine: dark, frothy. - image: renal tubular cast. damages renal tubular epithelium, can cause renal failure. BW: - 20 minutes of lunge exercise (trot/canter) pre, 6 hr post exercise CK measurement. rise in CK is significant. TX: - analgesics (NSAIDS, opiates because myoglobin is nephrotoxic) - IV/oral fluids - diuretics to maintain urine output, minimise nephrotoxic effects of myoglobin

what is symbleraphon? when is it most common?

an eyelid issue: partial or complete adhesion of palpebral conjunctiva of eyelid to bulbar conjunctiva of the eyeball. that can interfere with passage of light. - most common in CATS - neonatal ocular infection secondary to FHV-1. - can also b trauma

a horse presents with acute onset paresis in all 4 limbs and signs suggesting a central vestibular lesion. what test should you do in the field?

an upper airway endoscopy to assess the skull base and guttural pouch. horse vets have an advantage because you can endoscope the region of the skull that might be involved. radiography in the field is difficult.

neural causes of what is a "nerve root signature"?

animal holds up affected leg. indicates entrapment of spinal nerve (peripheral).

what should animals be treated with for life after cataract surgery?

anti-inflammatories to prevent lens-induced uveitis.

what is prochlerperazine?

antiemesis for rabbits.

what is a cataract? sequelae?

any opacity of the lens that impedes light transmission. SEQUELAE: - uveitis: phacolytic (intact lens capsule) or phacoclascic (rupture of lens capsule - trauma) - blindness

what are specific tests you can do for testing neuromusculare diseases?

aquired m. gravis - nicotinic AcH antibody titre (very specific but takes a few weeks) masticatory myositis: type 2M muscle fibre antibody infectious agents: toxoplasma, neospora, FeLV, FIV ADDITIONAL: - metabolic screening (urine, blood lactate/pyruvate like mitochondrial diseases or storage disorders) - Genetic testing for inherited diseases

what is the forebrain? what is the function (generally speaking) of the two parts?

area of the brain ROSTRAL to the TENTORIUM CEREBELLI. telencephalon/CEREBRUM - sensory input, information integration, voluntary motor control, memory, behavior, CONSCIOUS PERCEPTION - olfactory bulbs, frontal, parietal, temporal, and occipital lobes and thalamus (diencephalon) - gateway to forebrain (relay center) - alertness/arousal, awareness - autonomic, homeostatic control - pineal gland (circadian/seasonal) - parts of UMN system

what is the ARAS? where is it? what is it's function?

ascending reticular activating system in the BRAINSTEM. part of the reticular formation, and activates awake state, affects level of consciousness. OTHER THINGS - respiration + cv function - voluntary excretion, swallowing + vomiting - muscle tone + voluntary movement

how can you differentiate pelvic limb lameness and ataxia in horses?

assymmetric spinal cord lesions can produce signs similar to certain lameness. ataxia: irregular irregularities. also circumduction, pacing, hypermetria. lameness: regularly irregular. bilateral susp. ligament desmitis/sacroiliac pain common causes of ataxia-like, but regular.

how can extent of muscle atrophy help differentiate between a LMN and UMN or acute/chronic disorder when looking at neuromuscular disease?

atrophy: LMN that is 10-14 days old no atrophy: acute, LMN or UMN. only disorders that involve LMN will have muscle atrophy,

how is a corneal abscess treated?

atropine to dilate the eye.

what is the vestibulo-ocular reflex and what is it used for? what tracts does it use?

axons from vestibular nuclei -- MEDIAL LONGITUDINAL FASCICULUS of brainstem-- to motor neurons of CN III, IV, VI. physiological nystagmus: enables the animal to maintain useful visual input during head mvmt and prevent blurring. eyes remain focused on original target and then JERK in the DIRECTION OF HEAD movement. abnormal nystagmus in event of lesion anywhere along tract (involving vestibular receptors, CN VIII, vestibular nuclei, MLF of brainstem, or CN III, VI, VI. )

how does the forebrain receive input from the vestibular system?

axons from vestibular nuclei to a THALAMIC NUCLEUS and to a contralateral vestibular cortex enabling conscious proprioception of balance, body position

what fractures often occur when horses flip over backwards?

basisphenoid bone fracture - stike the pole on hard ground. damages the brainstem. also, damage to optic nerves (stretched by brain as it catapults). often sudden onset (permanent) blindness uni or bilaterally.

a 7.5 female spaniel has acute onset blindness. absent menace response, absent pupillary reflex (PLR). where is the neurolocalisation/what do you do next?

bilateral optic nerve/optic tract because that is the only part that both pathways cross over. optic nerve -- optic chiasm. do an optic exam. the optic disk was protruding - inflammation of optic nerve or brain oedema (but would be obstunded). bilateral optic neuritis - can still have normal fundus.

a 5 y-o femal whippet has a 2-3 week history of lethargy, acute onset blindness. absent menace, absent PLR, palpebral is present. normal fundus. what is your neurolocalisation?

bilateral optic nerves, optic chiasm. both VISION and LIGHT defects. she had a meningitis that was compressing the optic chiasm, compressed both nerves. was idiopathic - responded to steroids. (idiopathic hypertrophic pachymeningitis)

how can you differentiate between entropion and blepharospasm?

blepharospasm: eyelid closed tightly, can lead to SPASTIC entropion. apply 1 drop of PROXYMETACAINE (topical anaesthetic). if entropion persists: needs surgical correction. if disappears: investigate source of opthalmic pain.

what do different corneal colours signify? what are some ddx for each colour?

blue: oedema - corneal ulcer - vascularisation (they leak) - intraocular disease: uveitis, glaucoma, lens luxation red: neovascularisation - irritants (eyelid abnormalities, burns) - chronic diseases (pannus, dry eye, immune mediated keratitis) - corneal ulcers - slceritis/episcleritis - granulation tissue - neoplasia brown: pigmentation - irritants - sequestrum - pigmentary keratitis - melanoma - FB yellow: cellular infiltrate - abscess, pus, etc white: deposits - lipid deposits (cushings/hyperlipidaemia, etc) can build in the eye - calcium - scar/fibrosis

why is it important to use high doses of antibiotics when treating brain disesases?

brain has low antibody levels, few phagocytics. penicillins, cephalosporins, and aminoglycosides are polar, hydrophilic: poor BBB penetration. need high doses to facilitate diffusion.

thiamine diphosphate (TDP): what pathways rely on it? what can a deficiency cause?

brain uses it as a substrate a lot. TPP: used as a co-factor for carbohydrate metabolism Krebs cycle, pentose-phosphate pathway (PPP), etc., etc. no thaiamine = POLIOENCHEPHALOMALACIA

a horse has ataxia in all 4 limbs, possibly paresis, and obtundation. there is vertical nystagmus but no head tilt. where might you localise the lesion?

brainstem problem affecting vestibular nuclei b/c central vestibular + ataxia + paresis + obtundation (reticular activating system). mentation deficits CAN be cerebral but would not explain the vestibular. gait deficits likely combo of vestibular system + proprioceptive. paresis = upper motor neurones that pass through brainstem. no head tilt = bilateral.

a horse presents with an ACUTE, progressive, generalised, neuromuscular syndrome. He is trembling, sweating, circling, and has other cranial nerve dysfunctions (dilated pupils, dysphagia/dysphonia) as well as poor tail/anal tone. what is your most likely ddx? what is the mechanism?

c. botulinum. MECHANISM: acts at NMJ by inhibiting AcH release at presynaptic membrane. no signal passed - flaccid paralysis. explains poor tail/anal tone, dilated pupils, muscle fasciculations.

what is acute canine polyradiculoneuritis? what is the pathogenesis?

called "coonhound paralysis" . (after racoon bites in NA) stimulus still unknown. immune-mediated inflammation of VENTRAL NERVE ROOOTS (guillan-barre sydrom) ACUTE onset, PROGRESSIVE weakness (days) then plateau (days-weeks) then gradual recovery (weeks/months) more severe cases: affect resp. muscles leading to hypoventilation. tx: - human IV immunoglobulins - plasmapheresis

how can you differentiate between scrolled cartilage and prolapsed nictitans gland (cherry eye) on the TEL?

can be very similar clinically - may be required to manipulate the TEL under topical anaesthesia to differentiate

strabismus in horses: how to assess?

can't lie them down like a dog. Look UP along the nose and move the head upwards to tease it out. IMAGE: ventral strabismus on left eye.

what are clinical signs of chronic glaucoma? how is it treated?

can't treat anymore, doesn't respond. - PERMANENT corneal oedema - optic nerve head cupping - habschestriae (stretch marks on cornea) - buphthalmia - absent menace, BLINDNESS + signs of acute - lens subluxation/luxation - episcleral congestion - conjunctival hyperaemia - epiphora - mydriasis - aqueous flare

what are clinical signs of lens disease?

cataracts - decreased transparency phacodenesis - wobbly lens iridodonesis - trembling iris (means lens is gone) aphakic crescent - lens subluxation

what are possible complications of of chronic uveitis?

cataracts: poor nourishment of the lens. can also CAUSE uveitis (lens induced uveitis) due to irritation others: retinal detachment, glaucoma, lens luxation (cats)

where is the cerebellum? what is the anatomy - lobules, folia?

caudal cranial fossa, separated from forebrain by osseus tentorium. comprises 50% of the brain's neurons. two hemispheres, 9 lobules. PRIMARY FISSURE: rostral, caudal lobe UVULONODULAR FISSURE: flocculonodular lobe. FOLIA: folded surface. outer gray matter inner WHITE MATTER/LAMINA (darker on MRI) extends into each folia, making ARBOR VITAE. - central medulla.

interaction b/w cerebellar and vestibular system.

cerebellum has an inhibitory effect on the extensor muscles. a lesion on the vestibular system that disconnects from the cerebellum, you will have an increased ACTIVATION of the EXTENSOR muscles. lesion to right side of vestibular nerve, tension in muscles is decreased, head tilts.

what is the mechanism of paradoxical vestibular disease?

cerebellum is INHIBITORY to vestibular nuclei. acts to suppress vestibular nuclei activation of extensor muscles. CAUDAL CEREBELLAR PEDUNCLE: carries afferent info to cerebellum and efferent info from cerebellum to brainstem. lesions in THE CCP interfere with descending cerebellear INHIBITORY drive. (or the flocculonodular lobe) QED on the side of the lesion, there is LESS INHIBITION of vestibular nuclei and the brain perceives this as the animal TURNING TOWARDS the lesion (as opposed to away). all the signs are PARADOXICAL

causes of wide-based stance?

cerebellum/vestibulocerebellar.

what are some ddx for calves with a cerebrum/forebrain vs. brainstem vs. spinal cord lesion?

cerebrum/forebrain - meningoencephalomyelitis (CSF) from umbilical infections - polioencephalomalacia (thiamine, MRI, PME) - lots of other things can occur but not very likely brainstem: otitis media/interna spinal cord: uncommon. neospora caninum (rare), vertebral body abcess, vertebral body fracture

a pony presents with with patchy sweating, fine muscle fasciculations and dysphagia. The pony has been losing weight for the past few weeks. The pony has an unusual stance, with the pelvic limbs further forwards, under the abdomen. Physical examination reveals tachycardia. Temperature and respiratory rate and capillary refill time are normal. The pony has a dried, crusty deposit within each nostril. There is bilateral ptosis. what is your main ddx? what are the 3 main forms?

chronic grass sickness. chronic: wt loss, dysphagia, patchy sweating, muscle fasciculations, variable tachycardia, paretic stance (pelvic limbs adducted) sub-acute: dysphagia, colic (impactions, sweating, fasciculations, tachycardia. acute: sever, sudden onset colic with SI distension, nasogastric reflux. death by gastric rupture. common cause of death in the UK in horses. might be caused by enteric c. botulinum toxin.

what is a SCCED (spontaneous chronic corneal epithelial defect)? causes/predispositions? Tx?

chronic, indolent corneal ulcers with high rate of recurrence. - common with BOXERS - SPECIAL form of superficial ulcer with an abnormal thin hyalinised layer of acellular stroma underneath missing BM - abnormal corneal nerve plexus - initiating event likely corneal trauma. Tx: take off epithelium: scratch cornea (debridenement) - if THAT doesn't work - keratotomy/burring, contact lens placement. - can also close with third eyelid flap. DO NOT DO IN A CAT (scratch) because it can SPREAD herpres

what is ectopic cilia? what are presenting signs?

cilia growing in meibomian glands, emerge on INSIDE of eyelids. far more irritation that distichiasis and cause ELLIPTICAL corneal ulcers on dorsal cornea and can pigment cornea (image). - also corneal oedema, vascularisation trying to heal defect in image.

how do you differentiate between a central vs. peripheral vestibular dysfunction?

clinical signs: PERIPHERAL: compromise of CN VII or sympathetic innervation of the eye (close proximity to tympanic bulla). CS: could have horner's syndome, but NO vertical nystagmus and NO nystagmus changing direction CENTRAL: any other cranial nerve, adjacent ascending proprioceptive tracts from spinal cord, descending UMN tracts, ascending reticular formation (mentation) CS: other CN deficits, reduced consciousness, other proprioceptive deficits/paresis.

what are the gait abnormalities involved with spinal disease? what about proprioception?

combo of ataxia AND paresis. OR hyperaesthesia. paresis can progress to plegia, bladder dysfunction. if only paresis: consider neuromuscular or lumbosacral problem if only ataxia: consider cerebellar or vestibular problem ataxia AND paresis: spinal or brainstem problem PROPRIOCEPTION: - very reliable indicator for presence of disease, but not useful for precise localisation - occurs BEFORE gait abnormalities occur NEURO EXAM: - can have intact or abnormal spinal reflexes +/- spinal hyperaesthesia.

what is fibrotic myopathy in horses? causes? CS?

common in QUARTER HORSES. HAMSTRING muscles (semitendonosis, semimembranosis). causes: - muscle tears, IM injection, neuropathy. Gait: unusual. asummetry with a firm structure. straight, slapped down leg on the floor. Tx: - rest, NSAIDS, surgical resection of fibrous tissue or tenotomy

what is the diagnostic approach to uveitis?

complete opthalmic exam: check eye pressure, ulcers, cataracts, etc + physical exam. identify underlying cause: - ocular causes may require US. - Systemic: BP, CBC/Haem, Serology, CT

what are 4 main disorders of the lens?

congenital abnormalities: - PHTVL/PHPV (persistent hyperplastic primary vitreous): non-regressed reminants - microphakia (abnormally small lens, elongated ciliary processes) - lens coloboma (rare, piece of lens not formed) cataracts: non-physiologic opacities of the lens. due to diabetes, insoluble proteins, diminished antioxidant activity (vit C, E, Glutathione) lens-induced uveitis: inflammation due to leakage of lens proteins durng cataract formationg lens luxation: aphakic crescent. primary or secondary.

what structures can caused a red conjunctiva? how?

conjunctiva IS: mucous membrane lining eyelids, third eyelid, and sclera. consists of epithelium, mucin cells (goblet cells), lymphoid tissue. blood vessels WITH dichotmous division. appear superficial, move with conjunctiva. most evident in fornixes. how: hyperaemia, swelling, ulcers, lymphoid follicles. sign of OCULAR SURFACE DISEASE.

what are the cerebellar peduncles? what do they do and where are they?

connect cerebellum to brainstem. act as highways/conduits for both afferent and efferent information rostral, middle, caudal from different parts of the brainstem.

define these words: - conus medullaris - filum terminale - cauda equine - dorsal longitudinal ligament - interarcuate ligament/ligamentum flavum

conus medullaris: tapered ending of the spinal cord, most caudal portion before cauda equina filum terminale: filamentas attachment of conus to sacral vertebral column dorsal longitudinal ligament (posterior) ligamentum flavum: between vertebrae. can become degenerate in a lot of processes.

what is enzootic neonatal ataxia (swayback)? what are some clinical signs?

copper deficiency. wallerian degeneration as copper is needed for myelin formation. leads to: - progressive incoordination and recumbency, starting in pelvic limbs and progressing to thoracic limbs - wt loss, diarrhoa, coat changes.

a dog has ptosis, mydriasis, strabismus, absent direct and indirect PLR in the left eye. besides that the animal is neurologically normal. what is your neurolocalisation of the lesion? what muscles are involved?

cranial nerve III. extraocular muscles involved: levator palpebrae superioris, medial, dorsal, ventral rectus, and ventral oblique. also innervates IRIS SPHINCTER ad CILIARIS (PLR). (Superior oblique = CN IV, lateral rectus: CN VI) pathlogical grouping of disease most likely cause: inflammatory/infectious, neoplastic, or idiopathic. dog was diagnosed with idiopathic oculomotor neuritis.

describe all of the prefixes for eye words

dacro = lacrimal kerat = cornea cyclo = ciliary body phac = lens hyalo = vitreous

how do you manage progressive corneal ulceration? what are some sequelae? what mediator is involved?

deep stromal ulcer, often caused by bacterial invasion - PG release for inflammation. - "axon reflex" triggered by corneal nerve endings -- secondary uveitis SEQUELAE: - HYPOPION = anterior uveitis from ulcer. can lead to .. - desmetocele which is NOT treatable medically and leads to iris prolapse (refer quickly) - corneal melting: YELLOW. collagenases DROOP over the eye. t Tx: cytology, culture

what is deep corneal neovascularisation a sign of? how does it present? what are two causes?

deeper ocular tissue disease (including intraocular) CS: short, stright, deep red. usually stay close to the limbus - looks like a bush. 1) UVEITIS: episcleral hyperaemia, DCN. small pupil (MIOSIS), LOW IOP (image) 2) GLAUCOMA: episcleral hyperaemia and DCN. dilated pupil (MYDRIASIS), HIGH IOP

what is the most common cause of cauda equina syndrome in dogs and what structures are involved?

degenerative lumbosacral stenosis. combination of bony + soft tissue structures which causes progressive stenosis. INTERVERTEBRAL DISC PROTRUSION most common also: - ligamentum flavum hypertrophy - articular process hypertrophy - telescoping lamina S1 into vertebral canal L7 - vertebral misalignment - transitional vertebra - lumbosacral osteochondrosis - synovial cysts - osteophyte formation

how do the receptors work in the macula of the utricle and saccule? what do they detect?

detect head position and linear acceleration. glycoprotein layer - dense (or otolithic membrane) with heavy statoconia crystals is displaced by gravity/linear acceleration. - this distorts sterocilia on hair cells - hair cells activate axonal endings of CN VIII to initiate action potential

How do you perform a retroillumination exam on a dog? what should you look for? how do you assess which pupil size is abnormal?

determines OPACITIES in the eye, and pupil SIZE/SYMMETRY via the silhouette. the animal needs to be level/on the table to get the tapetum on the dorsal aspect (shine from under). use DIRECT DISTANT OPTHALMOSCOPY. top: anisocoria (left pupil os smaller) middle: dyscoria (abnormality in pupil shape) bottom: 3rd eyelid protrusion. HOW TO DETERMINE which eye is abnormal: dim lights. if abnormal pupil is LARGER, anisocoria will decrease. if abnormal pupil is SMALLER, anisocoria will decrease. OPACITIES: determined in another flashcard lmao. cataracts cast shadows on retroilumination but are white on direct view.

what is synchronous diaphragmatic flutter "thumps"

diaphragm contracts rhythmically with the heart. phrenic nerve is depolarised by electrical activity of the heart. severe electrolyte abnormalities (hypocalcaemia). sign of an exhausted horse.

what is the function of the thalamus?

diencephalon. has a lot of NUCLEI which organise information and sent it to the correct lobe. - gateway to forebrain (relay center) - alertness/arousal, awareness - autonomic, homeostatic control - pineal gland (circadian/seasonal) - parts of UMN system

husky, 3 years old, acute onset after a walk. obtunded, swinging to the right and left. inconsistent in proprioception of all four legs.

diffuse intracranial, conscious. high likelihood for toxic cause due to acute, after a walk, and diffuse. won't DIE because the reflexes are there. option to monitor the dog overnight or just send the dog home and see if dog is okay.

what is close direct opthamalscopy used for? what about indirect?

direct, upright image of fundus/RETINA @ 19.5x magnification. keyhole view. can see the entire diameter of the eyeball depending on which lens you use. can visualise the optic nerve, etc. (distant direct = retroilumination) INDIRECT: virtual, inverted, slightly magnified image. bigger field of view and the pupils need to b DILATED. the light source is close to your eyes and an arm distance away from the patient. the lens is perpendicular to the light. you can see everything on the fundus in LESS detail, as a MIRROR image.

what is a transitional vertebra?

dogs/cats have 7 cervical, 13 thoracic, 7 lumbar, 3 sacral vertebrae. - vertebrae of different region have specific anatomical characteristics - occurs at that the "transition" of two separate regions and has anatomical characteristics of both regions. first sacral vertebra with characteristics of a lumbar vertebra. most caudal lumbar vertebra with characteristics of a sacral vertebra. - often not assoc w/ clinical signs - can alter spinal biomechanics, promote degenerate changes

how do you grade corneal ulcers?

don't have to memorise. one case could have all of those grades. grade 5 is iris prolapse.

how does the location of the disorder of a spinal cord affect the clinical signs? (dorsal vs. lateral vs. ventral funiculi)

dorsal/lateral funiculi: sensory and proprioceptive. ATAXIA. ventral/lateral funiculi: MOTOR/UMN PARESIS LMN cell bodies (ventral horn grey matter): LMN PARESIS spinal disease often a combo of ataxia and paresis.

what are muscular dystrophies?

duchenne muscular dystrophy, golden retrievers: - protein dystrophin. shock absorber for muscle during contraction. mutations in this protein can cause MD. sphynx: dystroglycans. muscle damage is severe. fibrosis, infiltration of muscle cells.

what is dysautonomia? CS?

dysregulation of autonomic system. CS: - TEL protrusion - decrased tear production - mydriasis - megaosophagus - megacolon - atonic bladder difficult to reach diagnosis. usually relies on multiple CS no specific treatment except symptomatic based on clinical signs

what are the types of persistent pupillary membranes? what causes them?

embryologic membrane which gives blood supply to the lens as it develops. should REGRESS after birth, but can cause corneal/lens opacity. originates from the IRIS COLARETTE - often assoc w other ocular congenital defects - type 1: least severe. little dots on the surface of the lens - type 2: iris to iris - type 3: iris to lens - type 4: most severe, iris to cornea

what is the probable pathogenesis of atypical myopathy? how can you treat it?

energy deficit within the muscle, related to fat metabolism. Hypoglycin A (boxelder, ackee, broken down into MCPA). LCFA are shuttled across membranes into mitochondria and via Acyl-CoA dehydrogenase become ketones/TCA/steroids. - metabolite MCPA: potent INHIBITOR of Acyl-CoA dehydrogenase tx: - ribovflavin (B2) - used as a cofactor - carnitine - support carbohydrate metabolism (insulin/glucose)

what is EMND? how is it diagnosed?

equine motor neurone disease (EMND) - there is often severe weight loss caused by the generalised neurogenic muscle atrophy. - Unlike with grass sickness and botulism, these horses have a good appetite and they are not dysphagic. - "elephant on a drum" stance - as below. They don't like standing still - preferring to keep moving. - aetiology: uknown, assoc w/ lack of green pasture and free radical damage - often have raised tail head DIAGNOSTICS - electromyography (referral) - biopsy of the sacrocaudalis dorsalis (SDCM) muscle: most common/practical, easily done in standing horse with local. neurogenic muscle atrophy. IMAGE: atrophied and angular Type I (slow) fibres. - fundoscopy: characteristic ∆ on retina assoc w/ lipofuschin pigment - biopsy of accessory spinal nerve (CN XI): rare

what is tonometry? what can it be used for? when should it be done?

estimation of IOP. can differentiate b/w glaucoma (high), uveitis (low), and keratitis/conjunctivitis/scleritis/cellulitis. do it BEFORE dilating pupils. difference b/w eyes should be <20%

how does corneal oedema cause opacity?

example: image of dog with canine hepatitis/adenovirus. called "blue eye" (endothelium). If the aqueous is infection, the endothelium will be affected. SWELLING causes DISORDER and MISALIGNMENT of collagen fibrils. can be reversible depending on extent of damage.

what is a seizure?

excessive + hypersynchronous neuronal activity in the rain - excitation > inhibition due to abnormal cerebrocortical connectivity. cells lose their normal connectivity and can excite themselves (image)

how does the sciatic nerve split upon exit? what is the clinical presentation of a sciatic nerve dysfunction?

exits: L7-S1 intervertebral foramen splits: - peroneal nerve (dorsal part distal limb) - tibial nerve: plantar side distal limb. MOST obvious in dogs with lumbosacral disease (dropped hock etc)

what would be we a work-up for extracranial vs. intracranial seizures?

extracranial: - CBC/Biochem/Cytology - glucose, calcium, sodium, potassium, ammonia - Resting bile acids (in small animals, dynamic) - urinalysis (not common in horses) - BP in mature animals (cardiac workup, cats) intracranial: - imaging (MRI/CT) - Clinpath: CSF - WBC, differential cell count, protein content

what is an intrinsic vs. extrinsic myelopathy?

extrinsic: extradural, intradural (intervertebral disk disease) intrinsic: intramedullary (diffuse or focal). tumour/contusion. myelopathy = disorder of spinal cord.

what is an intention tremor?

failure to coordinate activity of agonist + antagonist. -they fight each other, causing the joint to oscillate. -classically fine head/neck. -increasingly apparent during goal-oriented movement (reaching for food/toy), ergo intention tremor

which disease can cause cerebellar hypoplasia in kittens? (targets rapidly dividing cells, causes diarrhoea, reduced WBC in adult cats)

feline parvovirus/feline panleukopenia

how can uveitis lead to glaucoma? how is it prevented?

fibrin, etc can mechanically obstruct the outflow pathways and constrict the pupil. this leads to "bundt cake" iris where the aqueous accumulates and pushes the iris foreward. prevention: atropine to dilate the pupil.

what is the first-line treatment for a dog with meningoencephalitis of unknown aetiology?

first line: immunosuppressive therapy (Dex intravenously, then oral prednisolone) +/- cytarabine, azathioprine, or cyclosporin odansetron for nausea requires long-term immunosuppressive therapy and careful monitoring for signs of disease recurrence.

medical mgmt of contusion /traumatic brain injury?

fluids, mannitol to prevent raised intracranial pressure.

when might advanced imaging be used for neuromuscular lesions?

focal presentations. (CT/MRI) left: peripheral nerve sheath tumour right: masticatory myositis

3 YR border collie, 3 month history GTC seizures. occur every 2-3 weeks. normal in between. what is your diagnosis? what should you do next?

forebrain. idiopathic epilepsy. chronic, non-progressive, non-painful, etc. can do blood test but not likely for toxic or metabolic. without testing, you can start treatment with a tier 1 level of confidence. if the seizures don't reduce - might be a structural disease.

what is the function of glycogen synthase?

forming 1-4 links between glucose monomers to make glycogen.

How do tears flow?

from 1-5. Part can flow retrograde and be swallowed. Lacrimal puncta -- canaliculus -- lacrimal sac -- nasolacrimal duct -- nasal punctum.

describe the pathways of the menace response? what can give a "red herring" absent menace response?

from eyeball to occipital lobe. from lobe, to association fibres to motor cortex (frontal lobe) motor cortex goes to the pontine nucleus in the cerebellum/pons, to cerebellar cortex, to facial nuclei and facial nerve (brainstem) QED ABSENT MENACE CAN BE AN ISSUE WITH ANY OF THE ABOVE THINGS (motor cortex, cerebellum, vision, brainstem facial nerves) ABSENT IN - first 10-12 wks - stressed - lethargic - disorientated

what is the typical shape of senile cataracts?

from the outside - in (wedge-shaped). dense nucleus of the lens and spoofs?? in the periphery.

what are breed dispositions to seizures?

generalised: beagles, GSD, Labradors, Golden retrievers, Bernese mountain dogs, Belgian tervuerens, Keeshonds, Irish Wolfhounds Partial seizures w/out 2nd gen: Viszlas, English Springer Spaniels, Danish Labadors, Lagotto Romagnolo, standard poods, finnish spitz

what are the opthalmic findings with systemic hypertension?

generally insidious/chronic disease. - intraocular haemorrhages (hyphema in ant chamber, vitreal/retinal haemorrhages) - bullous retinal detachment - irideal haemorrhages - tortuous retinal vessels

what is nucleus ambiguous? what is the function of these?

glossopharyngeal (IX), vagus (X), accessory nerve (CN X) motor, sensory, and parasympathetic. - gag reflex (IX-X): CAN HAVE ASPIRATION PNEUMONIA GLOSSOPHARYNGEAL - motor pharynx and palatine structures - sensory (caudal 1/3 of tongue, pharyngeal muscles) - parasympathetic (Parotid, zygomatic glands) VAGUS nerve (CN X): - motor larynx (RLN), pharynx, oesophagus - sensory (larynx, pharynx, thoracic, abdominal viscera) - parasympathetic (thoracic + abdominal viscera)

how do you examine an animal to see if they have primary glaucoma? (normal vs. fancy)

gonioscopy to assess iridocorneal angle. the little windows are pectins where the aqueous goes in. if they are abnormally shaped, there is an issue. (referral) tonometry: - applanation tonometry: requires topical anaesthetic needed - rebound tonometry: small rounded probe is rapidly expelled from a fixed distance to contact the cornea. no topical anaesthetic, easy.

what is the grey vs. white matter of the spinal cord?

grey matter: nerve cell bodies white matter: axons (tracts) - dorsal funiculus - lateral funiculi - ventral funiculus

how might you define a neuromuscular lesion, broadly?

haematology, CBC, urinalysis - if suspect endocrine: ACTH, T4/TSH - if suspect systemic or if regurgitation: Thoracic/abdominal imaging. 80% of dogs with acquired M. gravis have megaoesophagus and aspiration pneumonia - CSF: disease affecting NERVE ROOTS (acute canine polyradiculoneurositis) THEN: more specific testing, advanced imaging (CT/MRI) and finally nerve/muscle biopsy if necessary

what are the receptors of the vestibular system? how do they work?

hair cells = specialised epithelial cells. - lined by fine, hairlike processes STEROCILIA, one lage KINOCILIA - distorted by movement (towards) synapse onto endings of CN VII fibres

what is border disease virus?

hairy-shaker: infects NAIVE ewes in pregnancy - abortion, infertility, derformities. - lambs infected in FIRST half: immunotolerant (PI) - adults develop short viraemia, immunity SPREAD: vertical and horizontal CS: lambs <60 days gestation - skin: steel wool coat, hyperpigmented - skeletal: short legs, domed forehead, small orbits, arthrogryposis - nervous system: ataxia, tremours, hop on rear legs - CNS: disappear at 20 weeks testing: antibody for flock status

how can you neurolocalise a spinal cord lesion in the horse?

harder in the horse because no withdrawal reflex able to be tested. have to use a few pieces of information.

what ABS can cause retinal toxicity?

high dose enrofloxacin in CATS, even at recommended doses. can also cause neurologic clinical signs. Also with Marbofloxacin.

what is a hypermature vs. morgagnian cataract?

hypermature: small, glistening, crystalline particles from degraded lens fibrers and proteins - wrinkles anterior lens capsule - lens may decrease in size morgagnian: advanced lysis and liquefaction of lens fibres - solid nucleus may gravitate ventrally or float around

most common causes of reactive seizures in dogs?

hypoglycaemia, intoxication, electrolyte disorder, HE

what is pueperal tetany/eclampsia?

hypokalaemia/hypocalcaemia hyperkalaemia/hyperkalcaemia hypermagnesamia electrolyte imbalance. weakness + tremours, going through labour.

what is the horner's pathway in horses?

i am sympathetic that you are horny. horses SWEAT on their NECK with a HORNERS lesion: only species.

how can you differentiate between a seizure and any other inappropriate movement of the body?

if a patient has an inability to regulate the entire limb movement/body movement but does NOT lose consciousness is unlikely to have a seizure, because generalised seizures would involve loss of consciousness. autonomic signs like salivation, pupil dilation, etc with a specific part of the body are more likely to be a focal seizure.

how can you recognise a paradoxical vestibular lesion?

if it disrupts the CCP, it also disrupts ascending proprioception to the cerebellu. there would be delayed postural reactions in the IPSILATERAL limbs. RIGHT paradoxical lesion would cause LEFT head tilt , RIGHT SIDED postural reaction deficits.

how should you remove an eyelid mass?

if its <1/3 of margin: wedge resection - >1/3rd: referral WEDGE RESECTION/INVERTED HOUSE: shape of removal. close in 2 layers, skin with figure 8. do NOT penetrate conjunctiva/cornea.

how do you determine WHERE an opacity is on the globe on retroilumination? how do you describe it?

if the lesion moves WITH you when you move to the left or right: it's in the posterior pole (vitreous) and if it moves away from you - it's in the anterior pole (aqueous). if it doesn't moves: lens.

how is diagnosis made of muscular dystrophy?

immunohistochemistry. absence of dystrophin (right images).

what is cervical ventroflexion? what is it a sign of?

important clinical sign suggestive of neuromuscular disease in CATS (not dogs) particularly suggestive for a myopathy ( HYPOKALAEMIA v. common) not seen in dogs with NM disease due to nuchal ligament passively holding their heads up.

what is the neurolocalisation of decreased/exaggerated spinal reflexes? what is the mechanism behind this?

important for identifying which segment is affected. DECREASED: LMN sign - lesion in reflex arc - C6-T2 or L4-S3 EXAGGERATED: UMN sign, which tells LMN what to due (in VENTRAL horn of GREY matter) - usually they INHIBIT LMN but when they are off, they DISINHIBIT - CRANIAL from reflex arc - C1-C5 or T3-L3 if there's a lesion in the middle (UMN) you can get spastic paresis, increased muscle tone, etc. too rigid.

how do perform a focal light exam? what structures are you looking looking at? what is the tyndall effect?

in a DARK room, look at the eyelids, ocular surface, iris, anterior chamber, and lens. EYELIDS: meibomian glands (tear film), pigments, and nasolacrimal duct (can swell). look for hairs. OCULAR SURFACE: CLEAR (no vasculature). - want it to be smooth and an exact replica of light. dry eyes can be dull, disrupted. (purkinje reflex) - look for corneal lesions (clock description). ANTERIOR CHAMBER: can get hyphaemia, hypopion, keratic precipitates, fibrine, lens luxation. - TYNDALL EFECT: aqueous flare. marker of inflammation. "fog in headlights". look for the gap of black going through the eye.

what drugs can be used to tx seizures? what is the cascade? which ones have the worst side effects?

in chronological order: phenobarbitol or imepitoin (not 4 cluster) first, then potassium bromide (if not sufficient response or contraindicated like hepatic disease), then levetiracetam. safety: lev most safety, then imepitoin, then pheno, then potassium bromide.

where do reflexes synapse?

in the BRAINSTEM, not FOREBRAIN (conscious)

what is the function of the red nucleus? where is it?

in the MIDBRAIN - mesenchephalon. responsible for GAIT GENERATION rostral midbrain leads to CONTRALATERAL postural rxn deficits.

what is meningoencephalomyelitis in calves a result of? signalment, clinical signs, diagnosis, and treatment.

inflamation of meninges + brain + spinal cord. aetiology: sequelae to septicemia from umbilica via infections/omphalophlebitis which become embolic and go to the brain. - most common e.coli, K99. - also salmonella, campylobacter, klebsiella, staph signalment: - <30 days, neonatal with FPT of immunity (need IgG) clinical signs: NEURO dull/obtunded/comatose, lethargic, lost suckle reflex - can be variable. - extended neck - hypopion - hyperthermia - seizures - DON'T HAVE TO HAVE FEVER DIAGNOSIS: - Clinical signs (basically PEM vs. encephalanolyelitis) - FPTI- other signs of sepsis/sources (umbilicus/joints) - leukocytosis - CSF findings if you can: neutrophilia, increased protein, culture images: A - hypopion, epiphora. B: extended neck. C opisthonos D: torticolis (wry neck) TX: poor prognosis. mortality rate around 100% - beta-lactans don't penetrate - florfenical IV/IM good penetration - Enrofloxacin: restrictions on use - SMZ/TMS/TMPS - seizure control

how is the aqueous volume usually regulated/produced and how does that change with glaucoma? what are the causes of primary/secondary glaucoma?

inflow: aqueous produced by ciliary body via carbonic anhydrase into the anterior chamber. outflow: irido-corneo angle or unconventioual pathways (iris, ciliary body, vitreous) back into the veins glaucoma = no OUTFLOW Causes: PRIMARY: malformation/malfunction of outflow pathways. genetically predisposed via gene issue. must examine IRIDO-CORNEAL ANGLE. HEREDITARY. SECONDARY: any concurrent ocular disease. uveitis, lens luxation, intraocular tumour, cataracts.

what is collie eye anomaly?

inherited disease that can cause retinal detachment, hyphaemia/vitreal haemorrhage.

what is retinal dysplasia? what are 3 main types? sequelae?

inherited in certain breeds (CKCS, ESS). abnormal arrangement of the retina 3 main types: - folds (less severe) (bottom left): grey lines, some y or v-shaped that are the folds. - geographic - bottom right - the circular lesion. - retinal detachment (severe) sequelae: blindness

what are the objective assessments of vertebrae that help diagnose CVM/S? when is it most useful?

inter-vertebral ratio: b/B or c/B. intra-vertebral ratio: minimal distance across spinal canal / maximal distance across vertical process. (a/A) - <52% = spinal cord compression SOMEWHERE in its neck. HIGH sensitivity AND specificity in young horses. less so in older horses (because they are often assoc/with arthritis of joints, less so stenosis of spinal canal.)

what is an ICLE? what is it for?

intracapsular lens extraction. whole lens is removed, treatment of lens luxation. dog can see but is far-sighted

how can you differentiate between a disorder involving the spinal cord and one involving an adjacent structure (meninges, intervertebral disc, periosteum)?

intrinsic spinal cord disorders (degenerative myelopathy) will NOT be painful. gait abnormalities + neuro deficits occur only when spinal cord affected. meninges, intervertebral discs, and periostem have abundance of pain receptors but will not result in ataxia or paresis.

when should you do a workup (MRI/CSF) for an animal with seizures?

investigating a suspected structural epilepsy. - age <6 months or > 6 years - interictal neurological abnormalities consistent with neurolocalisation - status epilepticus or clusture seizure - not responding to treatment

how should you deal with an outbreak of EHV-1?

it's very complicated, there's a lot of quarantine. handled similarly to a notifiable disease.

what is telescoping lamina into vertebral canal L7?

lamina of S1 (transitional vertebrae) under vertebral canal L7 (arrow). compression caused by IVD protrusion. obstructs canal during dorsal tail displacement.

what are the short ciliary nerves?

last step of the PLR - iridal sphincter muscles. in cats: nasal and malar (only 2) in dogs: 5-8 all around.

what are the UMN spinal cord tracts? where do they travel and what do they do?

lateral and medial VESTIBULOSPINAL: travel in VENTRAL FUNICULUS of spinal cord activate LOWER MN that innervate IPSILATERAL EXTENSOR muscles inhibit LMN that innervate contralateral extensor muscles overall effect: increase ipsilateral extensor tone, decrease contralateral extensor tone (HEAD TILT)

a horse has ataxia in all 4 limbs ( L>R), left sided Horner's syndrome, and sweating on LHS of body. where is the lesion and what can explain these signs? (where..is..the body?)

left cervical spinal cord. HORNERS SYNDROME: a lesion in the neck anywhere along the pathway will cause horner's syndrome. they sweat due to peripheral vasodilation. their sweat glands are controlled by the bloodflow to them. a loss of sympathetic tone in the neck would cause parasympathetic vasodilation. the regional sweating can tell you where the lesion is. (just neck = axons in vagosympathetic trunk, whole body is spinal cord)

- 3 day history of progressive abnormal behaviour - 2 years old cat - lethargy, circling towards left upon physical exam: obtunded, no menace on right, no facial sensation on right, no replacement response on right (decreased postural reactions). where would you neurolocalise?

left forebrain (contralateral). Diagnosis: cystic mass in left forebrain. could have been parasitic, congenital, or metastatic neoplasia. very high intracranial pressure - be careful manipulated cats with forebrain issues.

differential diagnoses for spinal cord lesions in the horse?

lesions in the neck is the most common reason for ataxia. VASCULAR INFECTIOUS

what is the slit lamp exam? what is it used for?

less common - referral. Illumination system can rotate from the observer, regulate intensity/shape of light. at an ANGLE so not to block view, helps locate OPACITIES. shows the layers of the cornea and a lesion would decrease the slit width. bottom right: endothelial surface keratic precipitate, on RIGHT of slit.

when to discontinue AEDs?

life threatening adverse effects or remission achieved (no seizures for 1-2 years). must TAPER 20% every 4 months.

describe the pathway of the PLR.

light enters thru optic nerve. 75% cross in dog and goes thru PRETECTAL nucleus (in front of the tectum). direct will be stronger, because it crosses again in the OCULOMOTOR NUCLEUS in the brainstem. CILIARY GANGLION then sends nerve to eye via short ciliary nerve.

what can cause red reflexions on some animals?

lightly pigmented animals (white cats, bunnies, etc) can lack pigmentation in the posterior uvea/retinal pigmented epithelium. can be confused with bleeding in the posterior uvea/retina.

what does the crista ampullaris look like histologically

like this

what are the mechanisms of the two types of GABA receptors?

main treatment for seizures. GABA(a): - ligand-gated Cl- ion channel - GABA binding opens the Cl- ion channel, which increases Cl- influx into neuron - HYPERPOLARISES neuronal membrane, reduces likelihood of AP occurring - BARBITUATES + BENZODIAZEPINES bind this receptor. GABA(b): - Metabotropic (G-protein linked) - Increases K+ conductance (K+ moves out of cells, hyperolarising membrane)

a dog comes in with a 24 h history of a dropped jaw. what is your neurolocalisation? what might other CS be?

mandibular branch of the trigeminal nerve. other CS: - hypersalivation - difficulty drinking/eating - abnormal facial sensation - can get horner's syndrome

what nerves can you assess on the horse by looking at facial symmetry? what about nasal septum?

masseter + Temporalis : CN V Ears + Eyelid/eyelash + muzzle: CN VII nasal septum: CN V

the STT1 measures what? it should be performed before....(3). what is a normal reading in dogs?

measures AQUEOUS portion of PRECORNIAL tea film. perform before: - topical solutions - manipulating the eye - bright lights wait 1 minute per eye. normal: >15 mm

what is the function of the abduscens nerve? where is it? whats the clinical signs?

medulla. motor (abduscent) of extraocular muscles ( LATERAL RECTUS) , retractor bulbi. CS: medial strabismus, enopthalmia

Principles of Brainstem Disease: what are the three parts of the brainstem?

midbrain (mesencephalon), pons, and medulla. pons + medulla = rhomboencephalon

what is decerebrate rigidity? where does it come from?

midbrain lesions and UNCONSCIOUS mental status. increased muscle spindle sensitivity to stretch leads to rigidity of muscles due to blocking ANY inhbition to GAMMA MOTOR neurons VERY RIGID. serious.

what are diagnostic tests for an opaque cornea?

most important structure to look at. STT1 (basal and reflex tearing). 10-15mm is suspicious. Fluorescein - paper strips are better (won't stain lipophilic descemet's membrane, only hydrophilic stroma). Ideally with blue light Seidel Test - to detect leaks in the eye (diluted fluorescin) Cytology: cytobrush +/- culture

what are the most common diagnostic findings in animals with degenerative lumbosacral stenosis?

most often type II intervertebral disk protrusion. - TRANSITIONAL VERTEBRAE common in dogs with DLSS, which can complicate surgery if not recognised

review the physiology of muscle contraction.

motor end plate synapses with muscle fibre membrane. AcH released, leading to AP in the motor end plate and across T-tubles, activating the DHP receptor that interacts with RYR which causes Ca release from SR. then goes back in via Ca- ATPase pump. each of these things are important and can have deficiencies.

what is the function of the hypoglossal nerve? how can you detect a CN XII neuropathy?

motor to the tongue. can cause hemiparesis/asymmetry of the tongue if lateral.

What is "sweeney" in horses

muscle atrophy of the scapula, etc. cause of a damage to the suprascapular nerve. often due to kick/trauma of shoulder/scapula. commoner in draft horses due to pressure on nerve.

what is the final way to define a neuromuscular lesion if exhausted all costs?

muscle/nerve biopsy.

cattle otitic media/interna: causes, CS, DG, Tx?

mycoplasma bovis most common, can also get H somni, etc CS: - CN VII, VIII: ear droop, ptosis, exposure keratitis, epiphora, head tilt - rarely: regurgitation of milk/rumen fluid, dysphagia DG: CS, CT, UT, Xray PME: destruction/sclerosis around ear, granulation tissue

what are the CNS signs of EHV-1?

myeloencephalitis due to ascending paresis/ataxia. pyrexia, depression. starts in the pelvic limbs and heads towards the thoracic limbs. initial presentation: weakness in back end. sitting like a "dog" others: - bladder incontinence/urine scalding, tail paresis - occasionally CN signs due to latency in the trigeminal ganglion.

a horse has it's neck stuck in a weird position and doesn't want to move it (acute). what is the most likely ddx?

neck fracture.

how should you do a PLR on a horse? Palpebral?

need a really good light source. can use your phone. pen torch not that helpful. PLR: CN II in, + III out (oculomotor) Palpebral: V (trigeminal) + VII (eyelid)

what are the infectious causes of cerebellar disease in dogs?

neospora, toxoplasma, cryptococcus

what is retinal detachment and what are two types? how is it visualised on exam?

neuro-retina detaches from retinal pigmented epithelium. 1) Inflammatory: retina pushed by fluid (bullous). image. also caused by systemic hypertension. 2) disinsertional: retina loses peripheral attachments (rhegmatogenous). can see a veil hanging down behind the lens. most often after intraocular surgery. on opthalmic exam: - HYPOreflective tapetum - retinal vasculature remains VISIBLE, CLOSER to the lens - retina always remains attached to optic nerve.

what is the way to approach a blind dog?

neurologic + ophalmic investigation. if NEUROLOGIC ISSUES: - take IOP to rule out glaucoma - otherwise further neuro/opthalmic investication to look for central blindness, MUA, retina, hypertension, cataracts IF NO SIGNS: - look for ERG (test photoreceptors) - negative: SARD/IMR (exclusion) - positive: advanced imaging (MRI/CSF) - central blindness

what are ddx for a dropped jaw?

neurological (mandibular branch of CN V) - inflammatory, trauma, toxic (botulism), itiopathic, neoplasia (lymphoma) non-neuro: bilateral luxation of TMJ, mandibular fracture, oral foreign body

what is the most important clinical indicator for prognosis of a spinal disease? When should you test it?

nociception. only necessary in paraplegic animals. do NOT confuse with withdrawal reflex. an animal can feel pain without a withdrawal reflex. be careful with stoic dogs, analgesia, systemic shock, or decreased mentation. consider re-evaluating after systemic stabilisation or evaluation in unaffected limb for "comparison"

what are vitreal diseases?

non-unions: toy breed distal radius/ulna. - DON'T cast them. bone can whittle away/disappear. soft tissue complications: - tell owners to monitor carefully. sighthounds more likely to develop soft-tissue injury. 2/3 will develop injury but most very mild. malunions: length discrepancies, etc. from casting in the wrong position. swelling: don't wrap the toes over, only to the tips of the claws. use sequential layers. be vigilant. advice: - daily check by owners: weight bearing, smells, swelling (toes), colour, discharge. - weekly check at vet. - keep covered when going outdoors (plastic bag)

what is the mechanism of the blood brain barrier? why do we have it? pros/cons?

normal capillaries: fenestrated basement membrane with clefts between cells BBB: tight junctions between endothelial cells, basement membrane without fenestrations, and an external ring of pericytes (sm. muscle-resembling) and astrocyte end feet. PROS: - maintaints CNS env. for brain function, exclude toxic substances, protects from excessive levels of circulating NTs CONS: - hinders drugs - limits passive diffusion of water-soluble substances (metabolites which need active transport)

what is lens-induced uveitis? what are clinical signs? what are sequelae and what type of cataracts are more predisposing?

normal immune tolerance or anterior chamber to lens protein. they leak through the capsule during cataract maturation. subtle inflammatory response. anything that injures the lens can subject to inflammation (Cat scratch, cataracts) clinical signs: - low IOP - resistance to pharmacologic dilation - dark iris color cataracts in the mature or hypermature stage need anti-inflammatories to prevent lens-induced uveitis and subsequently PHACOLYTIC UVEITIS (shrunken eyeball) or the lens can rupture. diabetic cataracts at higher risk.

how do the spinal cord and the vertebral column differ? how is the spinal cord divided?

not the same length. - VERTEBRAL longer than SPINAL CORD which ends around L6-L7 in most dogs and then extends as cauda equina - SC located cranially from corresponding vebrae - (L7-S1 will terminate at L6 they don't correlate) 4 segments: based on whether they contain "functional" LMN.

how can lens luxation lead to glaucoma?

obstructs outflow tract of vitreous.

what is the congenital spinal malformation of arabian foals?

occipitoatlanto-axial malformation (OAAM). genetic, other breeds as well. young foals, ataxic, stiff neck. cause of CVM type-2

describe the optic pathway

optic nerve -- optic chiasm (crossover 75% in dogs, 66% in cats)-- optic tract -- lateral geniculate nucleus (in the thalamus) -- optic radiation -- occipital lobe/cortex. blindness can be anywhere along that lesion. medial retina crosses. lateral retina does not cross (not very much lateral view.

what are the five components of the fundus that are are examined on close direct opthalmoscopy?

optic nerve, retinal vasculature/tapetum, tapetal-non tapetal junction, non-tapetal fundus, periphery fundus

what is a synovial cyst?

originates from articular facet degeneration. indicated by arrow on CT images. happens with degenerative lumbosacral disease.

what is idiopathic epilepsy? what breeds are most predisposed?

overarching term for both genetic and non-genetic causes of seizures. can be genetic (ADAM23, LGI2) , suspected genetic (breed), or unknown cause. breeds: shepherds, border terrier, irish wolfound, labs, finnish spitz

what is a muscle strain injury?

overstretching of muscle - disruption of fibres. inflammation + healing with fibrosis. - can be mild to severe (complete rupture) - recovery: rapid with low-grade, but fibrous injury can predispose to re-injury or conracture palpation, US can help diagnose.

TSE in cows vs sheep. sheep: aetiology, clinical signs, etc

pathophys: accumulation of abnormal prion proteins (PrPsc) in cNS, deposited as amyloid plaque within lymphoreticular and nervous tissue. SLOW PROGRESSION, infectious. SCRAPIE: sheep and goats 1-5 years old (takes time to show up - CS: behavioral (separate from flock, restless, nervous) wt. loss - PRURITIS: wool loss, dermatitis, excoriation, nibble reflex (LIP SMACKING = SURE SIGN) - ataxia, weak, tremours, pytalism, seizures, collaps testing: all fallen stock >18 months tested. SPREAD: colostrum, milk, placenta, faeces, urine. bred for genetic resistence. DIAG: IHC, western blot. BSE (Mad cow): 4-6 years old. CS: behavioral changes similar to scrapie, hyperaesthesia, aggression, ataxia, tremours - NO genetic component identified - possible cause of crutzfield-jacob disease in humans PREVENTION: - don't feed them stuff - risk material control (brain, eyes, spine, ilium, tonsils don't enter food chain) - cattle >48 month that is killed needs to go into a monitoring program or any emergency slaughtering needs ante-mortem inspection.

what are the main ddx for a vestibular lesion in a horse?

petrous temporal bone issues. infectious: viral encephaliditis, etc trauma: skull fractures, etc degenerative: temporohydoid osteeoarthropathy

what is recurrent exertional rhabdomyolysis? how is it prevented?

possible defect in calcium regulation, studied in a small group of thoroughbreds. not too much information on it. - most common in young, nervous fillies - 5% TB affected PREVENTION: - oral dantrolene - calcium release channel blocker for TB with presumed problem. can't race on this. - high FAT, low CARB diet: rice bran, veg oil, commercial - regular exercise/turn out (don't confine)

what is a precocious vs. altricial animal? what are their structural differences?

precocious: well developed cerebellum at birth. herbivores. ambulatory within hours altricial: carnivores, rabbits. not ambulatory for first few weeks +. cerebellar development continues after birth.

What is the function of the vestibular system?

primary sensory for balance. eye, neck, trunk, limb position. detects head mtion, regulates lower motor neurons innervating muscles throughout head/body

what is the difference between primary and secondary lens luxation? what is a key symptom of lens subluxation?

primary: terrier breeds, anomalous zonules (genetic defect in zonules - collie, GSD, shar pei). sudden onset @ younger age. secondary: chronic inflammation/uveitis, glaucoma, bupthalmia, tumours, trauma symptom: aphakic crescent. edge of the lens is seen due to being shifted.

how can you differentiate between acute spinal cord disease and bilateral cruciate ligament disease?

proprioceptive deficits = spinal cord disease no proprioceptive deficits = cruciate. make sure to hold up dog's weight.

what is the sequence of progressive neurological deficits?

proprioceptive deficits FIRST -- paresis + ataxia -- plegia -- bladder dysfunction -- tail dysfunction -- pain sensation/nociception -- recovery

what are the 3 deep cerebellar nuclei (function, how are they affected)?

purkinje neuron axons travel to the deep cerebellar nuclei. they are INHIBITORY to the deep cerebellar (release GABA) DEEP CEREBELLAR - output to other regions of brain, regulate all centres involved in voluntary movement. don't need to know: fastigial: vestibular nuclei, reticular formation of brainstem interposital: red nucleus, reticular formation lateral (dentate): basal nuclei, thalamus

how to assess CN VIII in the horse?

put a blindfold on them. makes it very difficult to self-correct a vestbular issue.

which dogs get rhabdo? signs?

racing greyhounds, sled dogs. myoglobinuria, elevated CK, hyperthermia, renal failure.

1 yr old x-breed, peracute onset of body tremors and tonic seizures. hyperthermic, tachycardic, tachypnoeic, mildly dehydrated. continuous seizure activity prevented neuro exam. diagnosis?

reactive seizure. went scavenging in compost heap a few hrs prior. high risk of developing status epilepticus.

what is levetiracetam? onset of action? excretion? administration? SE? how is it used to treat cluster seizures?

recent anti-seizure drug: reduces excitatory neurotransmitter release. - RAPID onset of action (can use in emergency situation) but possible honeymoon effect after 4-8 months of tx - consider pulse therapy for dogs w/ cluster seizures: start, continue 72 hrs, stop. - EXCRETION: renal - ADMINISTRATION: 20 mg/kg PO every 8 hrs. increase dose or dosing frequency if concurrent PB administration due to induction of cP450. decrease if impaired renal function. - SE: very well tolerated, can cause sedation/ataxia

what is the function of the cerebellum? what info does it receive and what does it do with it? what does it NOT do?

regulates RATE, RANGE, FORCE of movement. coordination, posture, equilibrium. AFFERENT: - PROPRIOCEPTIVE from muscle spindle, golgi tendon organs, vestibular system - MOTOR cortex: voluntary movements EFFERENT: ipsilateral. - modulates motor activity of MOTOR CORTEX, other nuclei that activate UPPER MOTOR NEURONS - postural, ensures proper movement NO DIRECT cnxn to cerebellum and LMN. CANNOT INITIATE movement.

Intracorneal haemorrhage: what is it? causes?

relatively uncommon. always associated to corneal neovascularisation. can be associated w/systemic disease (systemic hypertension).

what is epileptogenesis?

result of an initiating event like trauma, febrile seizure, stroke, infection, gene defect. chronic seizure disorder but not all animals end up with epilepsy. brain has enduring predisposition to generate seizures. epilepsy defined as 2 unprovoked epileptic seizures >24 hrs apart. 1-5% of dogs, 2% of cats.

a dog has absent PLR, absent menace, ventrolateral strabismus, and ptosis on the right eye. what is your neurolocalisaton?

right oculomotor neuropathy (motor/parasympathetic) had an enlargement of oculomotor but didn't look like a tumour. responded to prednisolone/azathioprine.

what is the decerebellate posture?

rostral lobe of cerebellum - inhibitory to UMN. - lesion there causes marked rigid EXETENSION of thoracic limbs, opisthonous (head/neck extension) - pelvic limbs can be flexed forward under the body (hypertonia of hypaxial muscles that flex the hips) - conscious mental status

what is the horse "pain face?"

rotate ears back, half closed eye, lifted nostrils. can also head-press.

What can cause redness of the episclera/sclera? what structures are affected?

sclera: the fibrous tunic of the globe. consists of collagen, blood vessels. NO dichotomous division. doesn't move with conjuntiva, most evident close to the limbus. hyperaemia/swelling sign of DEEPER ocular tissue disease (including intraocular)

what are two abnormalities of the trunk/neck? what is scoliosis vs kyphosis vs lordosis?

scoliosis = left-right deviation, kyphosis = raised back lordosis. = raised butt ventroflexion: CATS. losing muscle tone in neck and head flops forward. no nuchal ligament. low head carriage: DOGS. could be cervical hyperaesthesia/ neck pain.

what is progressive retinal atrophy (PRA)? what is the progression? how is it treated?

secondary to retinal degeneration. retina releases toxins during degeneration (glutamate) that lead to cataracts. - NIGHT blindness which progresses to DAY blindness. - often starts at middle age - leads to cataracts (end stage). Diag: - direct opthalmoscopy: vasculature visible, but thinner than normal, tapetum brighter than normal due to thinning of overall retina (hyperreflective) - genetic and there are specific genetic tests. controversial. Tx: - not painful, some gene therapies developed in the last few years: some viruses introduced into the retina that place the gene into the photoreceptors that produce proteins needed to stay alive.

12 year old: 2 month history of focal seizures, recently circling. obtunded after his focal seizures. upon neuro exam: circling to left, absent menace in right eye. what is the localisation? what is your ddx?

seizure = FOREBRAIN. LEFT forebrain. circles TOWARDS the lesion in the brain, and menace is contralateral. INTRAcranial because there are LATERALISING signs, which imply a STRUCTURAL BRAIN issue. not idiopathic seizures because those would require the animal to be normal at all times. structural epilepsy.

what is status epilepticus? why is it an emergency?

seizure > 5 min or recurrent seizures with incomplete recovery of consciousness. 59% of dogs with idiopathic epilepsy will have >1 episode of status epilepticus. EMERGENCY: increased autonomic discharge leads to hypertension, tachycardia, hyperglycaemia, cardiac arrhythmias. - continuing activity leads to hyperthermia, rhabdomyolosysis, lactic acidosis, hyperkalaemia. - can lead to organ failure - death.

what is a "dropped elbow" ?

severe brachial plexus damage caused by running into a fence post leading to paresis of the triceps muscle.

describe the nerves/pathway of vision that are shared with the PLR and the rest.

shared: retina--optic nerve (CN II) -- optic chiasm --optic tract not shared: lateral geniculate nucleus -- occipital lobe. 75% on contralateral cortex. PLR goes to pretectal nucleus

what is coenurosis?

sheep gid. intermediate/larval stage of taenia multiceps - tapeworm that infects carnivores that can migrate into the brain. need to know about for the NAVLE. CS: 80-90% migrate into one hemisphere - ascending paresis starting with the pelvic limbs. space occupying cranial lesion. causes ataxia, unilateral vision loss, head tilt, circling, hypermetria, coma. - forebrain/cerebellar, depends on neurolocalisation EPI: adult worms shed in dog/cat faeces, ingested on pasture. eggs hatch in SI and migrate to CNS via blood, mature into C. cerebralis. Tx: praziquantel, prevent dog/cat access or worm them.

Maedi Visna Virus: clinical signs, transmission, aetiology, testing?

sheep: ovine progressive penumonia. prevalence increasing in UK TRANSMISSION: aerosol (colostrum, milk, transplacental) CS: diffuse encephalitis, ataxia, proprioception, circling, blindness, coma, seizure. - sometimes just emaciation AETIOLOGY: immunosuppressive: secondary bacterial infections (mastitis, pneumonia, etc) -diffuse non-suppurative inflammation TESTING: accreditation testing scheme (premium sheep and goat health) - Ab ELISA

what is superficial corneal neovascularisation?what does it look like? what are two major causes of it? what are clinical signs?

sign of OCULAR SURFACE disease. growth of new blood vessels from the pericorneal plexus into avascular corneal tissue as a result of oxygen deprivation. LOOKS LIKE: dichotomous division, long and branching (look like trees), may occur with or without corneal neovascularisation. 1) ulcerative keratitis: conjunctival hyperaemia, SCV and fluorescin stain +VE (STT1 variable) 2) Keratoconjunctivitis sicca: conjunctival hyperaemia and ocular discharge, and SCV. F stain VARIABLE, STT1 LOW.

What is the 5 finger rule?

signalment, onset, clinical course, lateralisation, pain, neuroataonomical localisation. in that order.

what tests should you do for a dog with suspected secondary glaucoma?

small pupil: uveitis big pupil: glaucoma

what is encephalitozoon cuniculi? transmission, pathogenesis, diagnostics

small, intracellular pathogen. one of the most common infectious diseases in pet rabbits n the UK (52% seroprevalence). TRANSMISSION: URINE. - contaminated food or water ingestion PATHOGENESIS: - GI epithelium -- gut associated lymphoid tissue -- bloodstream -- kidneys or CNS in blood or monocytes - can remain hidden or multiply leading to GRANULOMATOUS INFLAMMATION and CS CLINICAL SIGNS: - head tilt, hindlimb paresis, seizures, urine scalding - placenta in-utero goes into the eye, cataracts - can be asymptomatic DIAGNOSTICS: - IgM/IGG for recent exposure - PCR but with caution - Histopath/PCR of organs for definitive diagnosis TREATMENT: - 28 day course fendbendazole, may still have neuro changes - can reaccur CS

what is an acute non-compressive nucleus pulposus extrusion?

specific type of disk extrusion. sudden extrusion of non-degenerated (liquid) nucleus pulposus. causes CONTUSION but no spinal cord compression -- NO SURGERY - occurs typically during strenuous activity - not painful? NOT degen disk disease

which structures of the spinal cord can lead to clinical signs?

spinal cord surrounded by meninges and spinal nerves. vertebrae surround spinal cord and between each vertebrae is an intervertebral disk (most common structure that leads to a disorder).

boxer, 3 y o acute onset. - monoplegic on left pelvic limb. - spontaneous knuckling. no replacement on either hind limbs. small reflexes on l1. - normal spinal reflexes on all 4 legs. what is the neurolocalisation and most likely ddx?

spinal reflexes: L4-S3 answer: T3-L3 myelopathy (UMN, reflexes intact) diagnosis: acute, non-compressive nucleus pulposis extrusion (ANNPE) = slipped disc. on the left. more likely to lateralise than ischaemic myelopathy. treatment: caged rest, physio. annulus has to heal. 4-6 weeks.

how do you calculate/decide dose for phenobarbital? how long does it take to achieve steady state?

starting dose: 2.5-3 mg/kg PO every 12 hrs. - assess haem, CBC, BAST b4 treatment serum therapeutic range: 15-35 ug/ml. CHECK LEVELS to ensure SAFE, EFFECTIVE blood conc. high risk of toxicity above 35. steady state: 10-14 days. check levels if poor seizure control. once stable: check every 3-6 months. NEW DOSE: desired conc/actual conc x current daily dose

what is SRMA? clinical signs, causes?

steroid-responsie meningitis- areritis. young animals. certain breeds: beagles, boxers, bermese, weimeraners. CS: - Spinal pain and Elevated Temp - severe in the neck but can also be present in lower back, most severe on cervical ventroflexion - also can affect joints CAUSE: - young animals DIAGNOSTICS: - excluding other causes of spinal pain - CSF: inflammatory cells, neutrophils, high cellularity, marked pleiocytosis Tx: pred

which disease can cause nystagmus, seizuring, and fatal meningitis in piglets?

strep suis - in the brain. suckling and weaning pigs. can also cause polyserositis, peritonitis, polyarthritis, and pleuritis.

9 y o boxer has 2 week history of disorientation, pacing, circling to right side. 3 GTC seizures over past 2 weeks, two of which in cluster. abnormal behaviour between seizures. normal physical exam. no menace response on left side. absent proprioception left pelvic limb. diagnosis for type of epilepsy?

structural epilepsy.

differentiate between the appearance of superficial and deep corneal neovascularisation and their causes. how can you tell the main ddx apart?

superficial: dichotomous division, long and branching causes: 1) ulcerative keratitis: variable STT1, Florescin +ve, conjunctival hyperaemia 2) keratoconjunctivitis sicca: low STT1, Florescin -ve, ocular discharge deep: sign of deeper ocular tissues (including intraocular). short, straight, and deep red. usually stay close to the limbus (looks like a bush) causes: 1) uveitis: episcleral hyperaemia, miosis, low IOP 2) glaucoma: same, mydriasis, high IOP.

how is congenital obstructive hydrocephalus treated?

surgicallly: ventriculoperitoneal shunt. catheter with an away valve into the abdomen. longterm complications but prognosis is good.

12 year old staffie. 6 months history of "slowing down". two months ago - facial twitching/jerking, mainly in morning. now focal seizures with 2ary generalised. all normal on examination. what is your suspect and next steps?

suspected genetic/breed epilepsy. possibly waxing/waning because they are mostly in the morning which is suspect metabolic. FOREBRAIN. nothing to indicate if it's intra vs. extracranial. next steps is blood (diabetes, hypoglycaemic seizures - which the dog had). REACTIVE seizures.

what is chemosis?

swelling/oedema of the conjunctiva due to oozing from abnormally permeable capillaries. nonspecific eye irritation

what is the exhausted horse? clinical signs, mechanism, treatment, prevention?

syndrome assoc w/ long rides, often in hot, humid conditions, particularly in relatively unfit animals. - endurance rides, races, three day eventing/x-country, hunting - glycogen depletion from muscles, electrolyte loss from sweat, hypovolaemia clinical signs: - depression, dehydration, anorexia, decreased thirst - increased RR/HR - SYNCRHONOUS DIAPHRAGMATIC FLUTTER "thumps" - poor sweating response, poor jugular distension, increased CRT, decreased pulse pressure - decreased gut sounds - laminitis - muscle pain/stiffness ("tying up") Tx: IV/Oral fluids, rapid cooling, NSAIDS, check CK/ASK for rhabdo Prevention: - training, heat acclimatisation - free access to water/administer electrolytes - frequent vet checks

what are 3 tests you should run for the red eye? what is a contraindication for one of them? what further investigations might one take?

tear production (STT1), fluorescin stain, IOP. HOWEVER: STT1: not for corneal/scleral rupture. should be minimally manipulated, treated as a fragile eye. FURTHER: - infectious keratitis: cytology, C/S - glaucoma: gonioscopy - uveitis: systemic investigations, ocular US - retrobulbar disease: MRI/CT

what are you looking at on the fundus during close direct opthalmoscopy? (from back to front)

the SCLERA you can't usually see. CHOROID: marked pigmentation, large BVS. TAPETUM: surface of choroid. colour/size depends on animal, eye, usually yellowish. RPE: monolayer of cells b/w choroid and retina. heavily pigmented. but sometimes if white coat/blue eyes, it's not, and you can see the BV underneath. (retinal pigmented epithelium) RETINA: most inner layer, with RETINAL vasculature. continuous with optic nerve.

what extends into the optic nerve?

the diencephalon. it's not really a peripheral nerve. it can get all the diseases that the CNS can get.

what is ocular proptosis? predispositions, effects? tx? prognostic indicators? (DOGS)

the eyelids have become trapped behind the globe equator of the globe. usually marked conjunctival hyperaemia, chemosis. CAUSES: - brachycephalic dogs, sometimes only after minor trauma EFFECTS - damage to extraocular muscles, including tearing/avulsion - damage to optic nerve, blindness TX: - ANALGESIA - lubricate cornea to avoid ulceration - LATERAL CANTHOTOMY (full thickness cut at lateral canthus (black arrow) to release, reposition eyelids, then closed - temporary tarsorrphaphy (suture to close eyelids) must then be placed, left for 2/3 weeks PROGNOSTICS - negative: rupture of >2 extraocular muscles - compromises blood supply to eye - hyphaema may indicate retinal detachment, globe rupture (blood in anterior chamber) - dolicocephalic (long skull) breeds even worse then brachycephalic

what is the retrobulbar space? how can it bleed?

the intra and extraconal space. intra = extraocular musculature, nerves, and vessels. extra = lacrimal and salivar glands, bone teeth, roots and other nerves/vessels. how: any growing structure within the space will most likely DEVIATE the globe, compromise vasculature.

what is synechia? what are causes?

the iris adheres to either the cornea (i.e. anterior synechia) or lens (i.e. posterior synechia). CAUSES: ocular trauma, uveitis, iritis or iridocyclitis and - may lead to certain types of glaucoma. in this cat: the OS had red fundus reflexion, OD had corneal neovascularisaion, posterior sychechia, eccentric pupil, bupthalmus. after US the cat had intraocular bleeds and 2ary glaucoma in right eye due to severe systemic hypertension

what is a lens luxation? causes, CS, Treatment?

the lens starts to become detached and moves freely in severe cases. the lens can slip to the FRONT of the eye and become stuck between the cornea and the iris. CAUSES: - primary: genetic defect in zonules - terrier breeds, collie, german shepherd, shar pei - secondary: UVEITIS, GLAUCOMA, TUMOURS, trauma CS: acute pain, vision loss, sore/blue eye, increase IOP, blinding. emergency tx. - On exam: anisocoria (dilated pupil), circle of lens visible - aphakic crescent = key symptom, edge of the lens is seen due to being shifted. Tx: - if stuck - remove lens, usually followed by enucleation, or widen pupil medically + push lens back (50% success), or enuclation - MIOTICS (keep pupil small) 2X DAILY FOREVER to try to maintain

where is CSF collected in the horse?

the lumbosacral space.

what is the oculomotor nuclei responsible for? where is it? what is a sign of a CN III dysfunctoion?

the midbrain. motor and parasympathetic. - extraocular muscles (dorsal, ventral, medial rectus, ventral oblique) - sphincter pupillary muscle consctriction - levator palpebrae superioris muscle. dysfunction: ptosis of upper eyelid, dilated pupil

how does Horner's syndrome manifest in an animal with a lesion localised to the C6-T2 spinal cord segments?

the signals from the brain to the eye go through T1-T3 units in the neck and disrupt it.

can you do postural rxn testing in the horse? why? what can you do instead?

thorough gait analysis. look for ataxia. start walking, then trotting, then cantering, to highlight subtle neurologic deficits. postural (foot-placing) reactions are not useful because neurologically normal horses have quite variable responses.

where are the locations of the hair cells in the inner ear?

three in the semicircular ducts, in the ampulla, in the crista ampullis. 2 in the macula: utricle, saccule

treatment for uveitis?

topical: if ocular disease permits. Steroid/NSAID eye drops to treat inflammation. - cycloplegic eye drop to treat ocular pain: Tropicamide + Atropine to dilate the pupil and prevent glaucoma. Systemic treatment: concomitant disease permits - systemic NSAIDs (carprofen, meloxicam, other) - systemic immunosuppressives (if immune-mediated disease): prednisolone, other

which receptors are involved in proprioception in the horse?

touch (hoof, skin), muscle spindles + golgi tendon organs - enter spinal cord via dorsal root ganglia, into dorsal gray matter. from there, up spinal cord in dorsal + dorsolateral aspects of WHITE matter in the spinal cord (which is primarily white (myelinated) on the outside, grey on inside). DORSAL FUNICULUS, DORSOLATERAL. up to cerebellum.

what is the pathogenesis of an EHV-1 infection and how it progresses to the CNS?

transmission: - droplets (inhalation), fomites (hands, water, feed) replication: nasal epithelium, shedding in nasal secretions + CS w/in 24 hrs and for 7-14 days. within week it usually clears up OR becomes progressive. in CNS: VASCULITIS secondary to viral replication in endothelial cells, immune complex localisation in blood vessel walls. - sharply demarcated haemorrhages/ischaemia throughout the spinal cord secondary to vasculitis and thrombosis big worry for people with lots of horses. if big outbreak, a few of them can die from CNS, abortion (vasculitis within the placenta).

A dog presents with unilateral atrophy, unilateral medial strabismus, lack of palpebral on the lateral side and variable response to facial stimuli. what is your neurolocalisation?

trigeminal nerve - all three parts, one side.

what is the only nerve in the pons? what are the branches?

trigeminal nerve. sensory and motor. maxillary: SENSORY component to all three parts of the face. mandibular: MOTOR to the muscles of mastication (masseter, digastricus, temporalis, pterygoids) opthalmic: SENSORY cornea, inner nose

how is EDM diagnosed? treated?

try to rule out other diseases (CVM/S which is much more common) - signalment (young hourse) - vit E. plasma conce - usually made on PME treatment: not much to do except high dose vitamin e to try to stabilise. poor prognosis, unlikely to be athletic. manage owner.

what is type I, type II, type III IVDD?

type I: chondrodystrophied breeds (daschunds, basset hounds, beagles, corgis) often young to middle aged type II: middle aged or older, often large breeds

what is corneal sequestrum in the cat? aetiology/treatment?

unique in this species. might be related to tear film abnormalities. multifactorial: - brachycephalic breeds (persian), decreased corneal sensation, chronic irritation, feline herpesvirus treatment: surgery. don't let them slough off. - corneal-conjunctival transposition: pull conjunctiva over the cornea.

what are the 3 indicatons for a corneal/conjunctival cytology?

use for purulent conjunctivities, inflammatory infiltrate, and melting ulcers. numb eye with topical al and sample using cytobrush, diffquick

What are nerve conduction studies? what are they used to determine? how are the results interpreted?

used to differentiate between a myopathy and a neuropathy. Test of nerve function. stimulate nerve: look at muscle sign stimulate further down: look again NEUROPATY: decreased amplitude or slowed conduction velocity JUNCTIONOPATHY: myaesthenia gravis - decremental response on repetitive nerve stimulation MYOPATHY: normal

what is ischaemic myelopathy /FCE?

vascular disease of spinal cord. sudden embolisation spinal cord blood vessel by fibrocartilaginous tissue identical to nucleus pulposus. -peracute onset - strenuous activity - non-surgical - can take 2 weeks not lateral, no pain on palpation

describe what part of the nervous system neuromuscular disease involves.

ventral horn of the grey matter of the spinal cord: LMN. meets NMJ + muscle. some neuropathies also affect sensory neurons (motor signs predominate). MOTOR UNIT = LMN + NMJ + muscle. any disease affecting this unit = neuromuscular disease.

how does the CN VII get vestibular information to the brain? what are the vestibular nuclei?

vestibular potion: neronal CELL BODIES in VESTIBULAR GANGLION in PETROUS TEMPORAL BONE. - joins with axons from cochlea (that carry auditory info) to form vestibulocochlear nerve - enters cranium via INTERNAL ACOUSTIC MEATUS - axons enter medulla, synapse on vestibular nuclei 4 VESTIBULAR NUCLEI - rostral, medial, lateral, caudal - also receive afferent info from spinal cord (spinovestibular tracts) for info on NECK POSITION

what are the 3 functional zones of the cerebellum?

vestibulo: flocculonodular lobe. regulates balance, posture spinocerebellum: vermis and paraflocculus, regulates limb movement, gait generation pontocerebellum: hemispheres and mid vermis, regulates fine/skilled movements. more developed in primates/humans.

what are coloured light filters used in direct opthalmoscopy?

white: most commonly usd green: red-free filter, helps distinguish pigment from haemorrhage blue: for viewing fluorescence

where do horse seizures usually start?

with lip quivering.

describe the anatomy of the lens and the aetiology of nuclear sclerosis.

you should NOT see the lens - it's perfectly clear. nucleus in the middle, surrounded by capsule. attached firmly by ciliary body. EPITHELIUM (anterior) produces lens fibres throughout live and become denser in the middle, and eventually get a dense nucleus (nuclear sclerosis). but that does not cause blindness.

what is discospondylitis? which species is particularly susceptible to it?

young alpacas. neonates are susceptible to bacteraemic spread due to partial or complete FPT. young alpaca - spinal cord signs = top differential - then trauma tx: oxytetracycline (penetrates bone), C/S, NSAIDS

12 week old M collie. been with owner for 1 week. always been quiet. over the past 24 hrs - abnormal behaviour, seizures upon neuro exam: round skull. compulsive pacing + deep sleep. all four limbs vestibular ataxia. reduced proprioception in all 4 limbs. absent menace bilaterally. visual impairment. diagnosis/ddx?

young, acute?, progressive, non-painful, non-lateralising forebrain lesion (at LEAST). could be multifocal. ddx: degenerative, inflammatory, neoplastic, anomalous, metabolic. next: CBC, biochemistry (BA + ammonia to assess PSS). it was all normal -- structural lesion. CT: severe hydrocephalus in brain, 4th ventricle.

14 wk old JRT. 4 weeks of behavioural changes, 1 generalised seizure night b4 referral. upon neuro exam: ataxia, visual impairment, no menace response (it's young, but probably still has it). pacing, low head carriage.

young, chronic, progressive, non-painful, non-lateralising forebrain lesion. ddx: inflammatory, neoplastic, degenerative, anomalous, metabolic. CBC: high BA, high ammonia. PSS diagnosed on CT (image).

2 yo DST, one week history of sudden onset generalised tonic-clonic seizures. normal between events. 6 months ago was in a fight with a dog. upon neuro exam: abnormal gait, postural rxn deficits on left side, small asymmetry over right frontal sinus, absent menace on left side. what is your ddx?

young, sudden/acute, non-progressive, non-painful, right forebrain lesion. LATERALISING means structural (intracranial). structural epilepsy. mot likely bite wound/fracture lead to hernia of the brain leading to the swelling on the sinus. forebrain lesions can have completely normal gaits but lack of conscious proprioception. it was managed medically.

what is lymphoplasmacitic infiltrate of the cornea (Chronic superficial keratitis/german shepherd keratitis)? aetiology, tx?

"Pannus" - immune system attacks cornea which causes deposition, blood vessels, pigmentation. will lead to complete corneal pigmentation if untreated. - UV light might initiate/potentiate it. more likely in areas with more sun. - classic pigmentation/vascularised area near the LIMBUS because it's IMMUNE mediated (where the immune cells are) changes in TEL: de-pigmented (plasmoma) and margins are irregular. Tx: contact lenses UV protective, cyclosporine/immunosuppression (optimmune)

what is a coccygeal muscle injury?

"limber tail, cold tail rudder tail" - working breeds: labradors, pointers, etc - cold, exercise, swimming, prolonged caged transportation predispose CS: - pain at tail base - mild elevation in CK Tx: rest, NSAIDS

what happens to the spinal cord at the lumbosacral junction?

"peripheral nerves" - cauda equina. SC stops around L6 in cats and L7 in dogs. it tapers like a conus medullarus and that becomes filum terminale which attaches to the sacrum. most mobile part of the vertebral column and can cause a lot of issues.

what is a sacrocaudal luxation? mechanism, prognosis? prognostic indicator? Tx?

"tail pull" - trauma to sacral spinal cord segments. happensin RTA when tail trapped under tire, cat tries to run away. can be present +/- paresis (possibly transient) - anal sphincter + bladder dysfunction (risk of permanent faecal + urinary incontinence). can become atonic due to reflex dysynegia. VERY difficult to predict if animal will ever urinate again. DIAGNOSIS: clinical sings + radiograph. PROGNOTIC INDICATOR: feeling at tail base. - prognosis for recovery of gait = good - tail function: good if sensation present - 50-60% of cats with absent tail base sensation will still be able to regain ability to urinate, mostly in period of 7 TO 14 DAYS. IF NO URINATE >30 DAYS, EXTREMELY LIKELY TO BE PERMANENT Tx: CONTROVERSIAL to amputate tail. indicated with traumatic damage (skin lesions, "degloving" - bladder mgmt: manual expression, catheterisation, surgically placed cystonomy tubes - maybe + medication to help relax bladder but the side effects are bad (hypotention for example). monitor closely.

what is the CVM/S pathogenesis?

"wobbler's syndrome" 1. Paresis + ataxia (spinal cord in the neck. green fibres are proprioceptive, purple are motor. can get compression of both) 2. Neurologic signs result from progressive spinal cord compression (image) 3. Two main types of osseus malformation/stenosis: - type 1 (dynamic) - type 2 (absolute)

when should you start treatment for seizures?

- CLUSTERS (>2 w/in 24 hrs) - status epilepticus - severe post-ictal signs - worsening frequency or severity - >2 w/in 6 months - underlying structural cause in PEOPLE: no benefit after 1 seizure. evidence after 2nd seizure.

what are the eyelid abnormalities? (4) that can reduce tear drainage?

- Euroblepharon (macroblepharon) - too large opening, you can see a lot of sclera - entropion: lower eyelid rolls inwards, hair touching cornea - diamond eye (eye too big) - eyelid coloboma/agenesis. most common in cats. causes irritation

what are the CN assesments?

- PLR: sensory (optic nerve II), motor (CN III) - Menace response: learned in 10-12 wks. CN II, VII (facial). requires integration from cerebral cortex, cerebellum, rostral colliculi - Fixating response: optic (II), oculomotor (III), trochlear (IV), abduscens (VI) - Vestibulo-ocular: vestibular system. CN III, IV, VI. eye movements opposite to head direction. - Palpebral: V (trigeminal), motor (VII, obicularis oculi) - Corneal: Sensory (V), motor (VII), retractor bulbi (VI) - Facial sensation: poke nose. - Gag reflex: IX, X

what are the Tx, prognosis in equine cervical vertebral malformation/stenosis?

- Pace diet: reduce protein intake to slow down the growth, allow spinal canal to catch up. evidence is POOR. - Articular process joint medication: applies particularly in older, warm-blooded, arthritic in neck. can inject steroids in joint processes to reduce inflammation, therefore reduce pressure on spinal cord. however, if lots of new bone formation, nothing you can do about that. - Ventral stablilisation surgery: horse is anaesthetised, large incision made in ventral part of neck. move important parts, go into ventral spect of vertebrae, get a large drill, and take out a core between the two vertebrae. screw in titanium implant so they won't move on each other anymore. expensive, not done very much. done at RVC. OFTEN EUTHANASED.

what are the goals of seizure treatment?

- REDUCE or ELIMINATE epileptic events - reduce SEVERITY of seizures - avoid the LOTS of adverse effects - minimise morbidity + mortality only 15-30% have no seizures after tx and only 2/3 respond at all. lifelong commitment.