neuro and muskuloskeletal Flashcards

Question

Radiography – “Hip Series”

Answer 1

includes VD extended VD flexed (frogleg) and lateral

Answer 2

Hip subluxation Dorsal acetabular cover Norberg angle Distraction index- DI < 0.3 – good prognosis DI > 0.7 – poor prognosis- not gennarally used in uk but usefull. involved radiograph exposure however- limb must be positioned in a way to measure how much femoral head is moved out of joint

Answer 3

Start with identifying the treatment goals Know the current therapies and the evidence for/against them Understand the client’s expectations- Age of dog, intended use, stage of disease Consider the financial implications of treatment selections goals- Pain Joint ROM Limb function Muscle mass and strength Activity level Quality of life treatment- Conservative management (see CAM seminar for more details)- Weight management, exercise control, nutraceuticals, physio, medication Surgical management: Pain reduction, mechanical realignment Excision arthroplasty Joint replacement Excision Arthroplasty Joint Fusion (Arthrodesis) Joint Replacement (Arthroplasty)- good results

Answer 4

functions of the ccl- Prevents cranial translation, internal rotation of the tibia Prevents hyperextension of the stifle clinical presentation- Very common injury in the dog Usually a “non-contact” injury (cf. human) Often bilateral (10% at presentation/50% within 2yrs) Breed predispositions Changes often exist before the rupture Partial tears are common

Answer 5

Identified in up to 75% of dogs with CCLR Medial meniscus typically affected Most often evident at surgery, but can also occur later as a complication Poor residual healing capacity, so partial or complete removal indicated

Answer 6

meniscal injury- Identified in up to 75% of dogs with CCLR Medial meniscus typically affected Most often evident at surgery, but can also occur later as a complication Poor residual healing capacity, so partial or complete removal indicated surture- Externally rotates and limits cranial tibial translation Suture will fail but ideally after fibrosis has stabilised the joint Inexpensive and simple to do Low risk of complications will eventaally fail but goal is to encorage fiborous tissue growth to reduce draw and reduce pain osteotomy- Tibial Plateau Levelling Osteotomy- rotaits tibia to flatten it and loading is straight down, improving patient pain or tibial tuberosity advancment- tibial crest teperated and wedged forwart

Answer 7

Most common cause of FL lameness in medium- and large-breed dogs Young dogs (primary disease) to older dogs (DJD) Commonly bilateral (80%) so always check both legs Genetic component – IEWG scheme Osteochondrosis of the humeral condyle Ununited anconeal process Fragmented coronoid process Radi-ulnar incongruity Can occur concurrently cs- Lameness Often shortened (“choppy”) FL gait Commonly bilateral, often asymmetric Effusion (best detected on the lateral aspect of the joint between the lateral epicondyle and olecranon) Pain +/- crepitus, reduced ROM

Answer 8

Growth plate normally fuses by 5 mths GSDs, BMDs, Wolfhounds, M>F Surgery offers best prognosis Reattachment if possible Fragment removal if not

Answer 9

Labradors, GSDs, BMDs 6-14 months Medial coronoid fragments due to sub-surface fissuring Hard to see on X-ray - CT preferred Arthroscopy is definitive- not generally done, refferal Untreated, will lead to DJD…but benefits of surgery not clear

Answer 10

Medial humeral condyle Failure of endochondral ossification Subsurface failure and cartilage lifts Inflammation, pain, DJD Surgical management - arthroscopic debridement +/- osteoarticular graft Similar approach for shoulder OCD

Answer 11

Step between the radius and ulna Short radius > short ulna Hard to diagnose on X-ray, CT better Surgical management usually involves ulnar osteotomy to allow the ulna to “find a new position”

Answer 12

Heritable condition Developmental but not congenital Several theories, none proven Abnormal hip development Hormones (estradiol) Abnormal muscle growth (quadriceps) Muscle imbalance leads to bone deformity signalment- Small breed dogs: terriers, Chihuahua (medial) Medium breeds: Spaniel, SBT (medial) Large breeds: flat coat retriever (lateral), Labrador (medial) Cats: unusual (British short hair) cf- Pelvic limb lameness If intermittent, owner may report a ”skipping gait” May be unable Inability to fix the stifle when weight-bearing May be bilateral (50-64%) small breed dogs generally medial luxation- percentage shifts to lateral as dog gets bgger

Answer 13

Surgical vs. conservative care Medial or lateral release and/or imbrication Wedge recession Block recession Abrasion Tibial tubercle transposition (TTT) grade 1 and 2 often managed with conservative care

Answer 14

Cause of fracture – intrinsic vs. extrinsic, muscle action, etc. Communication with external environment (open vs. closed) Extent of bone damage Number and position of fragments Direction of fracture lines Location Forces acting on the fracture/displacement Stability Degree of complexity and involvement of other tissues Age of fracture (recent, old)

Answer 15

Most common appendicular fractures in small animals Surgical access from lateral IM pin, plates and ILNs are all good options Avoid ESFs (large muscle mass) except when used as pin tie

Answer 16

Distal diaphyseal fractures most common Plate + screw repair cranially and/or medially recommended Can consider repairing repairing both the radius and ulna in select cases External coaptation only for simple transverse fractures with stability and good apposition – case selection very important!

Answer 17

Dependent on fracture assessment, all options for fixation can be considered. Remember to assess whether fibula is intact when assessing fracture Medial side is tension side of bone and gives best surgical access for plate fixation ESF excellent for comminuted and/or open fractures

Answer 18

method used to grade fractures that occur in young animals and involve the growth plate, which is also known as the physis or physial plate type I- slipped 5-7% fracture plane passes all the way through the growth plate, not involving bone cannot occur if the growth plate is fused cit good prognosis type II- above ~75% (by far the most common)fracture passes across most of the growth plate and up through the metaphysis good prognosis type III- lower 7-10% fracture plane passes some distance along with the growth plate and down through the epiphysis poorer prognosis as the proliferative and reserve zones are interrupted type IV- through or transverse or together intra-articular 10% fracture plane passes directly through the metaphysis, growth plate and down through the epiphysis poor prognosis as the proliferative and reserve zones are interrupted type V- ruined or rammed uncommon <1% crushing type injury does not displace the growth plate but damages it by direct compression worst prognosis

Answer 19

Femur - 46.5% Humerus - 19.8% Tibia - 13.5% Radius - 11.8% Fractures are 4 x more common in the distal physis compared to the proximal physis

Answer 20

Early management is recommended Always warn the owner about the risk of complications due to GP compromise Avoid devices that compress/restrict bone lengthening at the physis Recognise difference between tension and compression GPs Smooth K-wires, typically <10% the width of the physis, are preferred whenever feasible

Answer 21

Operate early - delayed management worsens prognosis Generally heal quickly FHNE or THR for chronic cases or in cases with non-union

Answer 22

tension groth plate- patellar ligamebt

Answer 23

Very common, particularly in cats Not usually a challenging diagnosis – can range from minimal displacement to a gaping chasm! Repair technique involves simple materials – hypodermic needles (16-21G) and cerclage wire (18-24G) Tweak the repair to get perfect occlusion Be careful not to overtighten wire and crush tissues Straightforward and often no need for post-operative X-rays as reduction and stability are apparent Wire is removed after 4-6 weeks under sedation or GA Heavy-gauge PDS can be an alternative to wire and avoids the need for repeat sedation/GA If there is caudal instability or comminution, consider intraoral splinting

Answer 24

conserns- diaphramatic hernea, heamoragge, nerve damage Box shape, so usually >1 fracture Abundant soft tissues Rarely open fractures Good healing potential Surgical access can be tricky Indications for Surgery- Fractures along the weight-bearing axis- SI joint (not always), ilial body and acetabulum Articular fractures (acetabulum) Significant (>30%) narrowing of the pelvic canal Severe pain Nerve entrapment Concomitant ipsilateral fractures Working/athletic/breeding dogs where function must be optimal

Answer 25

Manage conservatively if unilateral and <50% displacement Lag screw repair (>60% sacral width) or trans-ilial bolt or pin (easier)

Answer 26

Usually result in pelvic canal narrowing On the weight-bearing axis Lateral approach with lateral plating (can do dorsal Post-op Management- Repeat neuro exam post-op to confirm integrity Stool softeners, plenty of water or fluids Crate confinement Lead exercise only for bathroom Re-evaluate at 4-6 weeks (X-ray)

Answer 27

osteosarcoma- makes bone myeloma lymphoma chondrosarcoma

Answer 28

locally invasive- squamous cell carcinoma metastisis to bone- metastatic tumour

Answer 29

Osteosarcoma is the most common primary bone malignancy in the dog Middle aged - older dogs (but not exclusively) Large & giant breeds (> 30kg) Males > females Distal radius Proximal humerus Proximal tibia Distal femur (distal tibia) Away from the elbow, towards the knee managment- amputation + cisplatin/ carboplatin/ doxorubin (some sort of chemo) amputation alone gives dogs 3 months- ok for pain releif but not atdiquate alone diagnosis- Usually, metaphyseal location Bone destruction Poorly defined margin Cortical destruction May see periosteal new bone disorganised / sunburst Pathological fracture BONE BIOPSY at diagnosis- 90% will have micro-metastasis if metastasis seen in lung there is no reason to treat

Answer 30

Highly specialised connective tissues Both are composites of collagen type I (98%) in a proteoglycan matrix produced by fibroblasts Mechanical and biological properties defined by their composition, structure and blood supply Tendon blood supply is more resilient as it comes from multiple sources, not just the insertion sites

Answer 31

Poor blood supply Heal by formation of scar tissue Requires initial protection (3 weeks) Followed by controlled mobilisation Regain around 60% strength by 6 weeks Susceptible to re-injury Orthotics can be invaluable in managing these injuries

Answer 32

Cruciate ligaments Collateral ligaments Round ligament of the femoral head (luxation) Plantar ligament injuries Carpal ligament injuries

Answer 33

These injuries are usually traumatic, commonly road traffic accident May be open or closed Collateral ligament ruptures are seen in the shoulder (glenohumeral ligaments), elbow, carpus, stifle, hock and interphalangeal joints May attempt primary repair of the ligament but usually reinforced with a prosthetic repair Suture, fibre wire or tape Suture anchors

Answer 34

Commonly major trauma – e.g. dragged by car Soft tissue management critical, not just repair or replacement of collaterals Post-operative focus needs to be on protecting soft tissue cover over the ligaments and any associated implants May not be possible to repair these, and stabilisation by arthrodesis may be indicated

Answer 35

Commonly major trauma – e.g. dragged by car Soft tissue management critical, not just repair or replacement of collaterals Protect soft tissue cover over the ligaments and any associated implants If impossible, may need to stabilise by arthrodesis

Answer 36

Remove residual cartilage (saw, burr, curette) Placement of cancellous bone graft Direct compression of bone surfaces Rigid stabilisation at at functional angle Indications for Arthrodesis- Chronic pain from DJD that is not treatable Untreatable fractures, esp. comminuted, intra-articular Chronic joint luxation Partial neurological injuries Ligament injuries or instability that cannot be surgically stabilised outcomes- Carpus: Good to excellent function Hock: Good to excellent Shoulder: Fair to good Elbow: Poor Stifle: Poor Digits: Unpredictable

Answer 37

Congenital Developmental (e.g. patellar luxation ) Traumatic (motor vehicle, fall)

Answer 38

Usually traumatic (RTA or fall) - 60% are craniodorsal Can be ventral too managment- Acute cases may be closed reduced Immobilisation with Ehmer sling Open reduction may be required Luxations that cannot be closed reduced Luxations that recur following initial closed reduction open tratment- Prosthetic capsule Toggle pin Transarticular pin

Answer 39

(Developmental) Acquired Trauma Iatrogenic Degenerative Drug related: corticosteroids, fluroquinolones

Answer 40

Infraspinatus Supraspinatus Quadriceps Gracilis/ST

Answer 41

Shifting leg lameness Severe cases can be systemically ill Typically 5-8 months Breeds - large especially GSDs Male > female Pain on direct bone palpation Aetiopathogenesis Viral, excess nutrition, genetic? Histopathology Degeneration of medullary adipocytes Stromal cell proliferation, Intramembranous ossification Management Analgesics Usually self-limiting

Answer 42

Ischaemic necrosis Small breeds From 5 months of age Pain on hip extension & flexion Muscle wastage Radiographic Features of AVN- Lucent areas initially Distinct from OA Collapse & mushrooming Articular surface is then destroyed

Answer 43

Signalment Breeds – Terriers, esp. WHW, Scotties, Bostons and Cairns Age 3-8 months Male = Female Genetic basis – autosomal recessive in WHWT Viral? Nutritional? Physical examination Palpably enlarged mandibles Limited mouth opening Pain on opening mouth or palpation Radiography Proliferative new bone on mandibles Sometimes on TMJs On bullae

Answer 44

hilights the sorsomedial aspect and the l ateral palmar aspect

Answer 45

to prevent the natural clefts and ridges from appearing as fractures (and artefacts) on radiograph

Answer 46

pecial senses- e.g. vision, hearing, taste, smell (processing not collection- crainial nerves Behaviour

Answer 47

Midbrain, and hindbrain (pons and medulla) Cranial nerves Autonomic activity - Parasympathetic outflow cranial nerves III (eye), VII (lacrimal, mandibular and submandibular glands), IX (parotid and mucosal glands), X (vagus – to cardiorespiratory, gastrointestinal systems) Reticular activating formation/system (RAS)- Controlling and activating centreMaintains central processing areas in state of activity

Answer 48

 Fine movement control - Abnormality causes loss of fine control  Exaggerated, coarse, abrupt movement  Worse for voluntary MUST be intact for normal menace response- Complex response NOT simple reflex

Answer 49

 Behaviour - may indicate forebrain disease e.g. seizures in foals, head pressing, compulsive wandering, circling, changes in voice depression/obtundation +/- coma, +/- seizures, +/- circling, +/-blindness (central) gaiut- mild ataxia no crainil nerve involvment

Answer 50

Mental Status - RAS and forebrain= level of awareness of consciousness Depression/obtundation +/- circling, +/- head tilt (if caudal lesion) ataxia?- None ataxia/weakness +/-quadruparesis crainial nerve involvment?- Yes Rostral lesion CN II; mid-brain CN IIIIV; caudal lesion V-XII Vestibular disease - peripheral or central -Basisphenoid fracture Facial nerve paralysis (vii&viii may occur together) Ocular abnormalities e.g. horner’s Pharyngeal/laryngeal deficits – dysphagia Trigeminal neuritis - headshaking

Answer 51

Head posture- however could also be peripheral vestibular, central, musculoskeletal, neuromuscular Intention tremor, +/- menace reflex gait?- Dysmetria/spasticityNo weakness no crainial nerve involvment

Answer 52

The three step cranial nerve exam: I - olfactory – smell (can’t test for unilateral lesions – ignore) STEP 1. THE EYE: II, III, IV, VI, (plus V+VII with palpebral)  Menace, eye position & movement including different head positions, normal positional nystagmus, PLR and palpebral reflex  parasympathetic innervation to the eye Step 2. "ears" Vestibular VIII - head posture, induced eyeball movement/normal vestibular nystagmus, normal gait, blindfold, hearing Step 3. "mouth" Swallowing and tongue IX, X, XI, XII Pull out tongue, assess for tone and symmetry, replace and observe swallow

Answer 53

 I - olfactory - smell  II - optic - sight, menace (note neonates), PLR, swinging light test, cerebellum III - occulomotor - PLR & eye position & movement  IV, VI - trochlear and abducens - eye position & movement -note normal responses -sympathetic & parasympathetic innervation to the eye  V - trigeminal - sensation to face, motor to muscles of mastication -facial reflex vs. sensation - look for behavioural response VII - facial - muscles of facial expression - may be subtle asymmetry -palpation may be useful  VIII - vestibulocochlear - head posture, induced eyeball movement, normal vestibular nystagmus, normal gait, blindfold, hearing IX, X, XI - glossopharyngeal, vagus & accessory - sensory & motor to pharynx & larynx - swallowing, endoscopy - XI motor to trapezius, cranial part of sternocephalicus XII - hypoglossal - tongue size, tone & symmetry

Answer 54

Assessment of spinal cord and peripheral nerve and muscle function Which limbs are abnormal? What are the abnormalities? Grade (1-4)?  Is there concurrent or primary lameness? Ataxia - General body Conscious proprioception deficits Weakness - paresis, hypometria, postural deficits, recumbency (tetraparesis) Hyper-reflexia/increased muscle tone-Hypermetria Hypo- reflexia/decreased muscle tone-Hypometria (note spasticity can also appear hypometric) atophy

Answer 55

Cell bodies in motor centre of brain- series of synapses from cortex through brainstem (NB motor cortex itself Afferent fibres travel down spinal cord- inhibitory or modulating function Synapse with lower motor neurone

Answer 56

Cell bodies in ventral horn (grey matter) of spinal cord - cervical and lumbosacral intumescence (thickening) LMN final common pathway whether voluntary or reflex motor response (and also sensory in efferent fibres)

Answer 57

 With increasing compression more functional deficits occur:  loss of proprioception- ataxia- wide based stance  motor weakness- narrow based stance  loss of sensory perception - touch  loss of pain- very rare and only with sever traumatic leasions

Answer 58

UMN – spinal cord and brainstem- Increased muscle tone Increased reflexes No atrophy Variable weakness and sensory loss depending on depth of lesion LMN – spinal cord Grey matter and peripheral nerves Decreased muscle tone Decreased reflexes Muscle atrophy Weakness Sensory loss

Answer 59

Whole body or limb look for poor co-ordination, swaying, limb moving excessively during swing phase - weaving, abduction, adduction, crossing of limbs, stepping on themselves- exaggerated by tight circles - pivoting, circumduction, serpentine, sudden stopping, backing, hills, raising the head visual compensation Concurrently observe for reflexia and muscle tone

Answer 60

look for hoof wear - dragging toes, low arc of flight of the hoof (hypometria) tail pull - at rest (LMN) and during walking (UMN able to reflexly resist while standing still) hopping, circling, slope - trembling, buckling of weak limb, knuckling over generalised weakness ‘walk better than they stand

Answer 61

generalised weakness, no ataxia - neuromuscular disease localised weakness - LMN or peripheral nerve disease weakness and ataxia - UMN - descending motor pathway ipsilateral and caudal to the site of the lesion weakness’ associated with vestibular disease - tend to fall towards the side of the lesion

Answer 62

UMN signs in both fore and hindlimbs

Answer 63

lower motor neurone signs in forelimbs upper motor neuron signs in hindlimbs

Answer 64

normal neurone signs in forelimbs upper motor neuron signs in hindlimbs

Answer 65

normal neurone signs in forelimbs lower motor neuron signs in hindlimbs

Answer 66

normal in all limbs

Answer 67

1 (+) subtle- deficits just barely detected at normal gait, occur during backing, stopping, turning, swaying, neck extension etc. 2 (++) mild)- detected at normal gait, exaggerated by above manoeuvres 3 (+++) moderate- prominent at normal gait, tend to buckle and fall with above techniques 4 (++++) severe- tripping falling spontaneously at normal gait to complete paralysis Forelimbs may be a grade less than the hind limbs with focal cervical spinal cord and brainstem lesions

Answer 68

For horses with signs localised cranial to T2 - confirmation and localisation Observation and palpation of neck- muscle atrophy, asymmetry, sweating Range of movement of the neck sensory perception - two-step technique local cervical and cervicofacial reflexes sway reaction

Answer 69

Observation and palpation- muscle atrophy, asymmetry, sweating Sensory perception Tail - voluntary movement, tone Perineal reflex/tail clamp Male external genitalia Rectal examination - assess lumbar, sacral or coccygeal vertebrae, bladder volume, tone

Answer 70

Decide on anatomical location- good use of thoracic limbs? - caudal to T2 weak use of thoracic limbs? - caudal cervical lifts head only? - cranial cervical Reflexes, tone, voluntary effort can be used- as with small animals Reflexes, tone, voluntary effort can be used -as with small animals Often awkward, emergency situation, insufficient info. or time adrenaline/autonomic domination for first 1-2 hours after trauma make every effort to make the animal stand after this time (unless fracture is suspected) best to delay final decision 24 hours

Answer 71

Brain disease in Adults: Trauma (meningitis) Hepatic encephalopathy Uncommon - Abscess Cholesterol granuloma Verminous Infectiousmeninigitis and meningoencephalomyelitis Neoplasia Toxins (mouldy corn etc) DDx: Other e.g. Intracarotid injection Sleep Disorders – hypersomnia- occurs when horses cannot coplete full sleep cyle by lying down- muskuloskeletal? fear fo being cast? Previous term ‘narcolepsy’ less accurate Rapid raising of head old horses- carrotid bareoreceptor- dx for seasures Metabolic e.g. hypoCa/Mg, ammonia

Answer 72

(dummy foals, hypoxia ischaemic encephalopathy) Ischaemia, oedema and reperfusion injury to foal’s brain, kidneys, intestine and other organs due to lack of oxygen In utero hypoxia Interruption of oxygen supply during birth May not be apparent until the foal is 12- 24 hours old Severe cases may have central respiratory depression Mild - Unable to attach to mare, poor suck reflex Moderate -Aimless wandering Abnormal phonation (barkers) Blind Severe- Seizures, coma

Answer 73

Prognosis good if sepsis score <11 (not septic) with good nursing Can take up to 2 weeks Expensive Rare long term effects e.g. cerebellar injury Still need basic care for neonate Antibiotics (short term), +/- gastric ulcer meds, nutrition, care of eyes, stop damage to self Oxygen

Answer 74

Trauma Sepsis- less common manifestation Secondary neurologic disorders- ANAEMIA Hypoglycemia Metabolic - e.g. hypo Na+ Developmental abnormalities & malformations Cerebellar ‘fits’ Portocaval shunt Benign epilepsy of foals esp. Arabs, up to 12 months of age low seizure threshold during development

Answer 75

 Signs usually at birth, may develop in 1st 6 mths Developmental abnormality Arabian foals intention tremors loss of fine motor control ataxia, basewide stance no treatment

Answer 76

trauma and otitis media/interna are the

Answer 77

 temporohyoid/stylohyoid osteoarthropathy predominantly peripheral VIII rarely an extension from otitis externa- usually haematogenous infection of middle ear low-grade infectious process- rarely results in rupture of tympanic membrane DDx idiopathic neoplasia Parasitic (including EPM in USA) diagnosis- clinical signs, lesion localisation Radiography/Computed tomography guttural pouch endoscopy - for evidence of stylohyoid bones changes or rarely drainage from middle ear, NOT for guttural pouch disease

Answer 78

uttural pouch mycosis and empyema disease is more common than neurological presentation CN’s IX, X, XI, and XII and internal carotid artery are in the dorsomedial aspect of the medial compartment Lead poisoning

Answer 79

Facial nerve paralysis is commonly iatrogenic due to halters left on during field anaesthesia injury- Prolonged/permanent deficits Eye injury, keratitis, dry eye Dysphagia, feed pouching Poor performance - nostril collapse

Answer 80

Note most common cause of Horner’s syndrome is iatrogenic due to extra vascular injection of irritant. Miosis, enophthalmus, and protruding nictitating membrane as for other spp. Hyperaemic mm of head & face, sweating of the head & face due to interruption of sympathetic supply to blood vessels & sweat glands of the head

Answer 81

Headshaking Abnormal rapid usually vertical flicking of the head e.g. "bee up the nose May rub the nose on objects or on the ground- nostril clamping during exercise Horses may seek shady areas, or put his face right under the tail of other horses (photic) Severe cases strike at face grading system in horses Abnormal trigeminal nerve function – reduced threshold for stimulation- No pathology or abnormal potentials once triggered Similarities to human trigeminal neuralgia Diagnosis by exclusion of other causes Treatment – trial in order of: nose nets, medical therapy, percutaneous electrical nerve stimulation (PENS)

Answer 82

0/3 = no headshaking 1/3 = headshaking at exercise but insufficiently severe as to interfere with ridden exercise 2/3 = headshaking at exercise, of a severity sufficient to make riding impossible or dangerous 3/3 = headshaking even at rest, in the stable and/or field

Answer 83

Spinal cord trauma  Cervical Vertebral Malformation (CVM)*  >90% equine spine lesions are trauma and CVM (nonEPM areas)  Others include neoplasia, osteomyelitis, AO malformation in Arabian foals

Answer 84

History of sudden onset of ataxia or recumbency, sometimes an observed incident No progression, frequently improvement, although later progression due to callus formation may occur Trauma may play a role in the acute exacerbation of CVM Sites of predilection: 1. Occipitoatlantoaxial region 2. caudal cervical 3. mid-back, but requires considerable force - usually u Signs - vary from ataxia and paresis to recumbency  no or short-lived spinal shock / Schiff-Sherrington  may be focal of diffuse sweating with C1-T2 lesions  horses may panic

Answer 85

Aetiology is multifactorial but includes congenital, familial esp. TB’s and Warmbloods, dietary and managemental (including exercise) factors mares that produce a lot ofmilk might predispose their foals Is related to developmental orthopaedic disease (DOD) Assessment: Lesion localisation Note: neck pain is rarely seen in CVM versus trauma Radiography, CT +/- contrast Plain radiography may be all that is required Minimum sagittal diameters etc. can aid in diagnosis MSD: the narrowest diameter form the dorsal aspect of the vertebral body to the ventral border of the dorsal laminae Types of lesions: a) stenosis of vertebral canal - dynamic or static b) abnormal articular processes (incl. OC lesions) c) subluxation of vertebrae on flexion (C2-C6) or extension (C6-T1) of the neck d) enlarged vertebral physeal growth regions e) overriding of the vertebral arch and next caudal vertebral body causing dynamic stenosis during flexion or extension f) proliferation of articular and periarticular soft tissuesm

Answer 86

 In the horse surgery can be performed but is costly and may only improve the horse on average one grade An ataxic horse should not be ridden Early detection in young foals (6 m) and dietary restrictions have resulted in resolution of ataxia and successful racing careers Once disease is advanced, prognosis for suitable riding animal is poor

Answer 87

Sacrococcygeal spinal cord segments, cauda equina, sacral plexus and peripheral nerves to the bladder, rectum, anus, tail and perineum May or may not involve lumbosacral nerve roots to the lumbosacral plexus - gait abnormalities Clinical signs: degrees of hypotonia, hyporeflexia and hypalgesia of the tail, anus and perineal region, urinary bladder paresis, rectal dilation, penile prolapse may also see LMN weakness and paresis of pelvic limbs can be difficult to distinguish UMN disease with urinary retention and 20 contusion of tail, anus from recumbency causes- Trauma: sacrocccygeal fracture and luxation, avulsion of the cauda equina Infectious, inflammatory, immune inflammatory e.g. polyneuritis equi viral/immune? e.g. EHV-1 verminous e.g. EPM Toxic: cystitis and ataxia associated with Sorghum spp. ingestion Miscellaneous congenital anomalies Neoplasia

Answer 88

Cauda equina signs are a result of vasculitis and thrombosis of arterioles in brain and spinal cord (viral endotheliotrophism) Can occur in outbreaks – biosecurity essential! diagnosis: lesion localisation r/o other causes look for history of respiratory inf. or abortion CSF - xanthochromic, +/- antibodies to EHV1 isolate virus from affected or in-contacts (nasopharyngeal swabs or buffy coat) high antibody titres (rising titres may not be demonstrated)

Answer 89

*isolation should be employed* prognosis reasonable with good nursing care better if not recumbent - rapid recovery over days to weeks, although full recovery may take > 1 year if recumbent > 24 hours, poor prognosis (but not hopeless) recurrence of neurological disease in recovered horses has not been documented

Answer 90

Localised weakness: - Peripheral nerve injuries Diffuse weakness:  Equine motor neurone disease  -others including botulism, grass sickness, VitE/Se def, post anaesthetic myoneuropath Abnormal hind limb gait:  Shivering and stringhalt Generalised tetany  tetanus prognosis- neuropraxia (loss of function only)  may resolve within 14 days axonotomesis (severance of axons)  6 months for recovery  should be the worse scenario for closed lesions to the side of the face (i.e. iatrogenic) neurotmesis (severance of entire nerve fibre)  prolonged to permanent loss of function scarring, fibrous tissue or callus formation may lead to (permanent) worsening of nerve injury Hindlimb: sciatic, femoral & obturator forelimb- brahceal plexis, radial nerve paralysis

Answer 91

Treatment: initial stages: anti-inflammatories support other limb surgery? physiotherapy not > 12 inches of nerve re-growth EMG may help in monitoring

Answer 92

Equine Motor Neuron Disease (EMND) Botulism: Clostridium botulinum Abnormal hindlimb gait: stringhalt Tetanus

Answer 93

EMND Clinical signs:  acute onset of trembling, excessive recumbency, shifting of weight, reluctance to stand still/confined and muscle atrophy (esp. hindquarters), elevation of tail head appetite normal to ravenous no ataxia Diagnosis: clinical signs and history mild increases in muscle enzymes low serum vitamin E muscle biopsy of the tail head muscle retinal lipopigment deposits Treatment  Vit E supplementation Physiotherapy prognosis poor

Answer 94

 ingest preformed toxin (8 types - B, C, D): toxin source:  contaminated feed (Big Bales), grass/corn silage  water (dead waterfowl)  UK: associated with poultry litter & carcasses  toxicoinfectious route (horse) type B grows in ingesta of suckling foals, Kentucky, eastern USA  infected wounds (gastric ulcers) (rare) blocks acetylcholine exocytosis at presynaptic membrane of neuromuscular junction- failure of muscle contraction => weak abrupt progressive onset flaccid paralysis of skeletal muscle (tetraplegia)

Answer 95

Another peripheral neuropathy Uni (classical- biomechanical problem secondary ot injury) or bilateral (pasture associated, toxic condition occuring in australia and new zealand- pature assosiated)

Answer 96

poor prognisis Clostridium tetani (soil, gi flora)  wounds, metritis, omphalitis, tooth loss spores may remain dormant for months anaerobic: sporulate, releases toxins tetanospasmin inhibits presynaptic inhibitory neurons (Renshaw cells) in intermediate grey column inhibits release of glycine disinhibition of gamma motor neurons muscles continuously contract (tetany) tetany elicited by sound, light, touch toxin only circulates and is able to be bound by antitixin for a window of time

Answer 97

Wooden tongue Lumpy jaw Mandibular fractures Tooth root abscesses Obstructions Oral lesions/stomatitis Calf diptheria Laryngeal Chondritis Diseases involving the mouth and jaws will often share clinical picture Unable to eat Weight loss (through lack of food intake or disease process) Pain Excess salivation Visible/palpable lumps Conditions of the throat will often present with other symptoms Increased respiratory noise and effort Exercise intolerance Inappetence Malodourous breath

Answer 98

Common disease of cattle Worldwide distribution Caused by Actinobacillus lignieresii Gram-negative bacteria Commensal of URT and alimentary tract Gains entry through breaks in buccal muscosa Wooden tongue is most common clinical presentation of infection- Can see intestinal and cutaneous forms Most commonly seen as individual animal Clinical Signs; Sudden onset salivation Dysphagia Protrusion of tongue Enlarged LNs Submandibular swelling Firm, swollen and painful tongue Discrete yellow lesions visible beneath tongue mucosa Differentials; Stomatitis Lumpy jaw Dental disease Oral foreign bodies Pharyngeal trauma Diagnosis; Based on clinical signs Bacterial culture (and sensitivity) can be used if appropriate

Answer 99

Management; Isolate Ensure adequate food and water Treatment; 5-7 days streptomycin/dihydrostreptomycin or TMPS Commonly penicillin/dihydrostreptomycin combination used Oral potassium iodide or IV sodium iodide have been used historically Neither treatment licensed in food animals in the UK

Answer 100

Causes pyogranulomatous osteitis/osteomyelitis in adult cattle Can be seen in young cattle when teeth erupting Worldwide distribution Caused by Actinomyces bovis Gram-positive bacteria Commensal of oral cavity Gains access to bony structures via lymphatic system from the oral cavity through breaks in muscosa Clinical Signs; Affected generally BAR Enlargement of horizontal ramus Soft tissue swelling present and painful Swelling is irregular and involves fibrous tissue and bone remodelling- Can lead to tooth displacement or pathological fracture May see discharging sinus tracts Enlargement of ipsilateral subman. LN Pain and physical deformity lead to dysphagia- Results in weight loss Differentials; Tooth root abscess Fracture of mandible Neoplasia Foreign body Feed impaction Diagnosis; Based on clinical signs Impression smears of pus from sinus will demonstrate gram-positive filamentous rods Radiography can be used to analyse extent of bone lysis and remodelling

Answer 101

Management; Ensure adequate food and water Treatment; As per wooden tongue 5-7 days streptomycin/dihydrostreptomycin or TMPS Commonly penicillin/dihydrostreptomycin combination used Long term abx treatment can lead to cessation of lesion growth

Answer 102

Can occur due to trauma- Hit by tractor wheel when head through feed space Kick from adult bovine (more likely in calf) Excessive traction at parturition Clinical Signs; Dysphagia Weight loss Excess salivation Swelling at site of fracture Protruding tongue Differentials; Lumpy jaw Wooden tongue Dental disease Diagnosis; Jaw misalignment at fracture site can typically be palpated Radiography can demonstrate extent of fracture

Answer 103

Treatment; Slight displacement treated conservatively Fracture repair- Wire placement, External fixators Euthanasia/Emergency slaughter Prognosis; Depends on site of lesion ramus vs mandibular symphysis Depends on compromise of local tissues Aftercare is key

Answer 104

Dental disease uncommonly reported in farm animals Inefficient mastication (and rumination) can have dramatic effect on feed intakes and therefore productivity Most frequent diseases include loss of incisors, abnormal occlusal surfaces, diastemata with food impaction between cheek teeth, and third molar overgrowth Tooth root abscess can occur due to infection May originate from periodontal disease or penetration of the crown by oral bacteria Clinical signs; Swelling of jaw Excessive salivation Malodourous breath Discharging sinus tracts Inappetence Weight loss Diagnosis; Examination of the oral cavity External palpation Radiography- multiple views

Answer 105

Treatment; Removal of infected tooth Flush? Suture? Implication? Antibiotics? Conservative treatment- NSAIDS? Antibiotics? Dietary changes?

Answer 106

Common occurrence in cattle Can occur in proximal cervical oesophagus, thoracic inlet on within thoracic oesophagus Most commonly described due to access to root crops ie. potatoes Can also occur with accidental access to fruits such as apples Clinical Signs; Cattle are distressed Characteristic stance with neck extended and head lowered Profuse salivation Repeated attempts to swallow If obstruction is lower than large quantities of clear, viscous saliva accumulate in cervical oesophagus Ruminal bloat occurs over several hours Differentials; Frothy bloat Gassy bloat Tetanus (Rabies) Diagnosis; History of access Cervical oesophageal obstructions may be palpable Visual/manual examination of proximal part of oesophagus Passage of stomach tube to confirm blockage

Answer 107

Treatment; Relieve bloat by trocar/needle if needed (respiratory distress) Hyoscine butylbromide 4.0mg IV to relax oesophagus Manually remove obstruction (first 20-30cm of oesophagus) Massage obstruction cranially Pass stomach tube (Selekt pump tube) to dislodge and push into rumen Use of Probang to dislodge or slice obstruction

Answer 108

Stomatitis is a common clinical sign of several diseases Some are zoonotic (Bovine Papular stomatitis) some are notifiable (FMDV) Can be caused by trauma or contact with chemical irritants

Answer 109

Caused by parapoxvirus virus Worldwide condition Zoonotic Spread by direct contact, entry through mucosal abrasions Clinical Signs; Most common in calves 1-12m old Anorexia Salivation Mild pyrexia Expanding popular lesions on muzzle, nostrils and buccal mucosa Severe form can lead to raised lesions and sloughing of mucosa Differentials; FMDV BVDV Vesicular stomatitis BHV BTV Clinical Signs; Most common in calves 1-12m old Anorexia Salivation Mild pyrexia Expanding popular lesions on muzzle, nostrils and buccal mucosa Severe form can lead to raised lesions and sloughing of mucosa

Answer 110

Caused by picornavirus Endemic in many parts of world Most of Europe, North America, Australia and New Zealand are free from disease. Notifiable in the UK; can affect most farmed species (cloven hoofstock) Extremely contagious Clinical Signs; Incubation 2-10 days Anorexia Depression Pyrexia Excessive salivation Milk drop Vesicles develop on tongue, dental pad and hard palate Quickly rupture to from shallow ulcers Submucosa hyperaemic

Answer 111

Caused by Fusobacterium necrophorum Causes a necrotic stomatitis Often seen as outbreak in young calves in unhygienic conditions Lesions can be caused by trauma to buccal mucosa Clinical signs; Lower jaw wet due to excess saliva Infections of cheek lead to large firm swellings May see/feel loss of mucosa within mouth- Advanced cases develop necrotic plug in centre of lesion Malodourous breath Swelling of submand. LN May have pyrexia Clinical signs; If infection involves larynx can lead to; Anorexia Pyrexia Coughing Inspiratory stridor Dyspnoea Death due to asphyxia can occur

Answer 112

Daily procaine penicillin 7-10 consecutive days Can use TMPS and oxytetracycline Corticosteroids during acute stage NSAIDs thereafter Tracheotomy can be performed in severe cases

Answer 113

Upper respiratory tract disease of sheep Unknown aetiology but certain breeds are predisposed Health and welfare implications Can have economic implications for flock Infection of mucosal abrasions leads to abscesses forming in larynx- Texel breed may be predisposed due to short head and neck affecting laryngeal anatomy Clinical Signs; Severe dyspnoea Acute onset respiratory distress Marked inspiratory effort and stertor Animals stand with neck extended, head lowered and nostrils flared Often show open mouth breathing Diagnosis; Based on clinical signs Breed predisposition Can evaluate with endoscope, ultrasound or radiographs Due to oedema of cartilages -> narrowing of airway

Answer 114

Treatment; Steroids in acute case to reduce swelling NSAIDs longer term Long term antibitoics to prevent abscess formation Often recurs after ‘successful’ treatment Unlikely to fully resolve so euthanasia often preferred Tracheotomy can be used in severe cases

Answer 115

a week to 2 weeks after it was caued during the remodling phase of healing

Answer 116

Manual therapies Massage Passive Range of Motion (PROM) Stretching Electrotherapies and Electrotherapeutic Agents Remedial Exercise Prescription

Answer 117

Joint mobilisation Massage Myofascial release Trigger Point release Stretching importance- Biofeedback – use in assessment and for treatment Availability- everyone has hands Owner action and involvement- Little and often yields better results Evidence based results- Decades of published scientific results to explain how and when techniques work Following the palpation element of the clinical work-up Tissues and areas within the tissues that require treatment are identified These will feel ‘abnormal’ as a result of the stress cycle in the muscle This starts as muscle shortening Manual techniques positively affects the following muscle components; Golgi Tendon Organs Muscle Spindles Joint mechanoreceptors

Answer 118

Pain causing muscle spasm / guarding Altered joint mechanics Conformation Overuse or inappropriate repetitive patterning - irreversible changes can occur after just 8 weeks Disuse e.g. immobilisation of a fractured limb (splinting or plaster casts), box / cage rest etc.

Answer 119

Use within sub-acute and chronic phases of tissue repair Improves circulation to muscle Improves lymphatic drainage Desensitises facilitated areas Release of endorphins = pain relief and reduction in muscle hypertonicity / spasm Facilitates normal interchange of fluid and gases between tissues Bonding Effleurage massage- Reduces muscle spasm that is secondary to pain Increases circulatory flow Reduces oedema Calming effect Before exercise = warms muscles After exercise = removes metabolic waste hacking and cupping- Increases circulation Relieves muscle spasm Removes lung secretions

Answer 120

Range of motion (ROM); active (AROM), active assisted (AAROM), active resisted (ARROM), passive (PROM), joint accessory mobilisation techniques Essential for the maintenance of synovial joint nourishment in the recumbent patient, or the patient with reduced physical activity (chronic pain management) Focal or local : global approach

Answer 121

Elongates pathologically shortened tissues sarcomeres are added to lengthen muscle tissue increased resting length Increases flexibility and joint ROM and reduces tightness in normal & abnormal tissues

Answer 122

Or more specifically – Electro Physical Agents (EPAs) Electrical stimulation modalities Thermal agents Non-thermal agents H-Wave TENS NMES LASER Therapeutic Ultrasound Pulsed Electromagnetic Field Therapy In combination with other therapies, there is a strong evidence base that these therapies effect a positive physiological change in cells / tissues. Right choice Right time Right level Right frequency The ability to influence the tissue healing process to effect a better or quicker repair is a fundamental interest to Vet Physios Select the best agent to use- Determine nature of the pathology Decide on the desired physiological response or outcome Select a modality that can effect those changes Arndt-Shultz Law- Therapeutic window – will move as patient’s condition alters- healing Apply- Introduce slowly Build intensity Reduce / remove if necessary do not push if not well tolerated

Answer 123

We transfer / confer energy on the cell, in various forms and at various levels Sound Heat Light This encourages cellular activity either by; Delivering so much energy the cell membrane is forced to change activity Delivering a smaller amount of energy and exciting the cell membrane; this leads to upregulation – doing more of what they normally do, harder and faster The latest evidence points to the latter approach as being more effectiv So, it’s the cells themselves that effect the change, not the therapy.

Answer 124

Active Targeted Tailored Improves strength and endurance- Injury prevention Improves range of motion of joints Corrects gait patterning Improves proprioception Mood enhancing Immediate effects of exercise- Muscle contraction Increased blood flow to muscles Rise in muscle temperature Long-term effects of exercise - Increased bone density Stronger muscle, tendon and ligament tissue Increased joint stability Increased joint ROM Muscular hypertrophy Higher fatigue threshold Plus correct gait patterning Improve proprioception no exersise results in- Bone density and modelling Joint capsule and soft tissue contracture Muscle mass and strength Cardiovascular fitness Proprioceptive capability

Answer 125

Relates to how the animal moves. This informs the active rehab. plan Observe in a straight line, and on small circles Observe from cranial, caudal and lateral views In walk and trot On firm and soft surfaces Consider- Gait pattern- breed?- paso fino Limb placement Joint flexion Harmonious use of the body To develop an effective rehabilitation programme we need to fully understand the animal’s functional anatomy, locomotion and biomechanics- Muscle antagonists, synergists Joint ROM, and bones as levers Gait patterning And most importantly Understand what Normal looks like, so we know when and where something isn’t right and how to develop effective exercises to restore function….. plus recognise when this has been achieved

Answer 126

Baited stretches Poles Labrynths Proprioceptive tracks Inclines, declines and steps Gadgets and gismos

Answer 127

Sit to stand Wobble cushion / board Peanut and gym ball

Answer 128

Balance Increased muscle tone and strength Improved ROM Better limb loading Increased stride length reduced- Muscle fatigue Painful joints Soft tissue injury Muscle soreness Tailor to the individual Little and often Start small and build

Answer 129

Behaviour – circling/headpressing/blind? Consciousness – Overexcited/ response to stimuli / depressed/ stupor / comatose? Stance Tremors – rapid contractions of muscle groups and their antagonists Spasms – sudden intense contraction of muscle groups Spasticity – Increased muscle tone; occurs from brain stem/ spinal cord lesions (spastic paresis) Locomotion Reduced coordination / ataxia Weakness (dysmetria) – Paresis or paralysis, uni/bi-lateral Orthopaedic or Neurological? – is the limb being carried or dragged? Is the step shorter or longer than normal?

Answer 130

Percussion – Tap the face with your fingertips, use your fist over neck vertebrae and percussion hammer over vertebrae/pelvis Test the reflexes - to localise the lesion Cerebrum, cerebellum and vestibular labyrinth Brain stem Spinal reflexes Coordination – Cerebrum Cerebellum and v labyrinth; can it correct? Eye movement Head movement Cross one leg over the other Walk towards obstacle on floor i.e. conscious proprioception Repeat obstacle test but blindfolded i.e unconscious proprioception Can the animal rise normally? (Cattle HL first!) Brain stem- Optical nerve. Blindness (no menace response): defect in retina, optical nerve, or cortex? First look at retina; then iris reflex (if blindness in cortex then reflex normal) Trigeminal nerve. Jaw drop. Palate reflex – press palate and mouth should open Facial nerve. Cannot close eyelid, lower lip hanging off (one-sided failure to close mouth) Vagal nerve – animal not able to swallow (tube) or cough (pinch larynx/trachea); disturbed rumen contraction patterns (‘vagal indigestion’) Hypoglossal nerve – tongue cannot be retracted and hangs out of mouth Spinal reflexes - Pinch the withers Tail reflex (touch perineum or perineal side of tail) Anus reflex (thermometer – contraction sphincter) Scrotal reflex (wrinkling of the scrotal skin when it is touched) Patella reflex (calves) Radio-carpal extensor reflex (calves) Pinch skin between claws – animal will bend leg

Answer 131

Haematology - Differential WBC Biochemistry Hepatic Enzymes -(GLDH GGT), BHB, NEFAs (nervous ketosis/fatty liver) Mg, Calcium in blood, Lead (post mortem) ZST assess colostrum transfer CSF – protein, WBC, bacterial growth

Answer 132

Ataxia, proprioceptive deficit, blindness, circling, nystagmus, changes in behaviour/ conciousness, head pressing Acute or chronic? forebrain disease Acute- Meningitis Cerebro-Cortical Necrosis (CCN) Lead poisoning - APHA Nervous ketosis Hypomagnesemia (Grass staggers) Salt poisoning IBR / MCF (sporadic) Pseudorabies (Aujesky’s) - APHA/DVM Rabies - APHA/DVM Chronic- Brain abscess Bovine Spongiform Ecephalopathy (BSE) AHVLA/DVM Hypovitaminosis A Brain tumour (very rare)

Answer 133

imbalanced, wide based stance, head tilt, dysmetria, nystagmus, tremors, hyperaesthesia

Answer 134

Extension of local infection (sinusitis) or haematogenous – Look for another lesion (septic arthritis, E. coli and Salmonellae in calves, Pseudomonas mastitis in adult cattle, liver abcess, endocarditis etc.) Calves ~ 1 week of age which have not had enough colostrum Diarrhoea, fever, anorexia, stiff neck, hyperaesthesia; spasmodic extension of limbs (when stimulated), muscle fasciculations; depression or ‘mania’, signs of pain when neck extended, tetraparesis, hyperflexia, circling, falling over; cranial nerves may be involved (nystagmus, facial palsy, blindness etc.); coma/fitting. May present like hypomagnesemia (‘staggers’) Early treatment essential; poor prognosis Blindness and ‘Star gazing’ Seizure (shortly before death)

Answer 135

Permeability- inflammation Preferably IV Preferably bactericidal Penicillin (on its own) no activity against gram negatives so not a good choice Continue for 10-14 days Concomitant Dexamethasone GOOD (NORMAL & INFLAMED)- Trimethoprim/sulfonamide chloramphenicol, metronidazole, doxycycline, fluoroquinolones POOR (NORMAL)- Tetracyclin, penicillin, streptomycin GOOD (INFLAMED)- cephalosporins, penicillin

Answer 136

‘Necrosis of the grey matter’ caused by Thiamine (Vit B1) deficiency. absolute deficiency in preruminant calves relative deficiency – large amount of bacterial thiaminases produced when overindulging on concentrates; bracken? Most common in cattle 6-18 months old. Early signs: head up in the air and appear blind; diarrhoea (concentrates?); hyperesthesia and muscle tremors also possible. Late signs: opisthotonus, headpressing, strabismus, miosis, excitement, repetitive chewing, facial twitching, nystagmus, head tilt, convulsions. Good response to treatment if diagnosed early. Blindness and star gazing High head carriage Head pressing Diagnosis: History, Clinical Signs + Response to Treatment Blood thiaminase assay PME - Brain Pale and Swollen; patchy yellow discolouration (accumulation of lipofuscin pigments in lipophages) fluoresce under U.V light

Answer 137

10-15mg/kg thiamine vit B1repeated every 4 hours for 24hrs Respond in 3-6 hours Corticosteroids and mannitol Identify and rectify underlying cause Thiamine-supplemented ration; introduce concentrates slowly

Answer 138

Any age of cattle but especially young cattle due to curious nature Access to old car batteries, engine oil, old lead paint, asphalt roofing, environmental pollution from industrial works Acute encephalopathy (as opposed to horses). Cerebral and GI signs Clinical signs: First stages: stand alone and depressed; hyperaesthesia, muscular fasciculations Progresses to ataxia, blindness (pupillary reflexes present), head pressing, episodic manic behaviour, convulsions, coma Also abdominal pain, rumen atony (bloat), diarrhoea, frothing at the mouth Severe will die 12-24 hrs; sudden death may also occur

Answer 139

Control fits with I.v pentobarbitone (dose to effect) Chelate lead CaEDTA slow drip 110mg/kg I.v every 2nd day for 3 treatments Thiamine 20-100mg/kg subcut daily (mobilises intracellular lead into blood) Oral magnesium sulphate 500-100g to precipitate lead from GI tract Prognosis poor!! Consider whether meat or milk is suitable for human consumption estimated 6-7 months for blood and milk levels to return to normal – Get APHA involved

Answer 140

Aetiology as ketosis (acetonaemia itself a chronic disease; ‘slow fever’) Acute onset of obsessive licking, circling, staggering, head pressing, pica, aggression Signs last 1-2 hours; recur at ~ 10-hourly intervals Diagnosis – clinical signs or ketones in blood Treatment - 40% dextrose i.v, propylene glycol BID, corticosteroids - examine management NEB > FAT MOBILISATION FROM ADIPOSE TISSUE > FFA FFA + ALBUMIN > LIVER > GLUCOSE OR TRIGLYCERIDES TG XS ACCUMULATE IN LIVER FATTY LIVER SYNDROME IMPAIR LIVER FUNCTION

Answer 141

Especially in pastured lactating beef cows in first months after calving (but also non-lactating animals); Occasionally in 3-6 month old ruminants (on poor diet; little Mg in milk, less able to resorb from bones > 3 m) Classically in spring but also autumn/winter Mg stored in body not readily available If uptake disturbed (Na:K ratio in rumen, stressors, not enough in diet or) levels rapidly dangerously low Adverse weather conditions may predispose Excretion of Mg in milk; - fresh cows most at risk cs- Hyperexcitable, may charge Erect ears, ear twitching, hyperaethesia Muscle fasciculations / tremors Frenzied running turning into staggering Lateral recumbency with violent episodes of ophistotonus and convulsions (can be triggered by any stimulus... also by vet!) Dead within an hour of the seizure episodes

Answer 142

Either water containing too much salt or water deprivation. Sodium deposition in the brain blocks anaerobic glycolytic pathways; increased intracranial pressure may also occur (attracts water) Mostly during summer; normally a clear clue in the history Dehydrated, depression, diarrhoea and colic, star-gazing, blindness, aggressiveness, hyperexcitability, vocalisation, head pressing, teeth grinding . Poor prognosis; rehydrate first then hypertonic saline (otherwise intracranial pressure increased).

Answer 143

Pseudorabies (Aujesky’s disease, Mad Itch) Depression, ataxia, conscious prioprioceptive deficit, circling, nystagmus, strabismus, aggression, pruritus (of the head), dead within 2 days. Contact with pigs. APHA/ DVM Rabies Hyperexcitability, fear, rage, depression, flaccid paralysis. APHA / DVM

Answer 144

Holstein, Jersey, Friesan, Guernsey Result from failure of drainage of CSF and therefore increased intracranial pressure Domed cranium Diffuse cerebral signs mania head pressing muscle tremor, convulsions blindness weakness Increase in intracranial pressure defect drainage of CSF holsteins hereford ayrshie jersey Sometimes domed cranium Diffuse cerebral signs, Mania, head pressing, muscle tremor convulsions blindness weakness

Answer 145

Normally Arcanobacterium pyogenes, often extension of sinus infection (so initially in front cortex); slower onset and more asymmetric signs than meningitis. Initially vision loss/mydriasis in contralateral eye, may progress to compulsive walking, head pressing, circling, head tilt (towards lesion), depression or mania, coma. When extending to base of the brain may give ‘cranial nerve signs’. Later stages: hypertonicity, hyperflexia, opisthotonus, coma, convulsions. Treatment antibiotics (see meningitis); Prognosis poor.

Answer 146

Agent unknown Current theory Prion Hypothesis infectivity caused by a struturally modified form of the host protein PrP. Normal membrane associated protein found in the CNS . Modified PrP promotes the conversion of other PrP molecules which accumulate within the affected neurones. Virino –core of nucleic acid and host proteins Filamentous virus Epidemiology points to extended common source epidemic. No evidence of cattle to cattle transmission Only common feature use of commercially produced compound feed containing meat and bone meal Offspring of infected cows 10% more likely to develop BSE Infectivity is caused by a struturally modified form of the host protein PrP . This is a normal membrane associated protein found in the CNS . The modified PrP promotes the conversion of other PrP molecules which accumulate within the cells Multiple individual disease outbreaks which can be traced back to a common source First recorded 1986 Outbreak peaked 1992 Total over 180,000 cases in U.K so far 2003 approx. 600 cases detected either from clinical cases on farm or compulsory testing of 1) fallen stock (over 24 months) 2) casualty animals over 30 months 3) sample of OTM 4) cattle over 30 months for HC (v few) 5) all cattle born after 31 July 1996 aged over 42 months Recent case! – March 2023 Now virtually zero cases cs- 3-6 years Initial signs often subtle but always progressive, rate of progression variable 2-3 weeks to several months Weight loss Hyperaesthesia, fine fasciculations of head and neck shoulder flank, teeth grinding, Apprehensive when approached, reluctant to be milked or moved through gate ways Ataxia Aggression Differential Diagnosis : Nervous ketosis Focal abscessation (Listeria encephalitis) (Hypomagnesaemia) (CCN) Notifiable Disease Inform DEFRA VO visit inspect animal decide whether to PTS as BSE suspect or not Farmer will be compensated and trace put out on the offspring of animal If disease confirmed offspring will also be culled Long incubation Period of BSE makes diagnostic and screening tests difficult Current tests for PM. No test for live animals. Histopathology Western Blotting (PrPSC) Immunocytochemistry (PrPSC) Contact DEFRA, VO slaughter suspects Confirmed cases offspring cull Feed ban no mammalian protein in feed for food producing animals , fishmeal is allowed for pigs/poultry but strict production/ storage/ to prevent cross contamination with ruminant feed. Regular inspections of animal feeds carried out by DEFRA

Answer 147

Deficiency VitA or precursor carotene Plenty in green feeds and forages Deficiency seen usually straw/ cereal based diet in housed animals Clinical Signs: caused by thickening dura mater/ abnormal bony growth in the brain cavity, increase CSF pressure Congenital or acquired Also retina degeneration - absent pupillary light reflex important diagnostic tool Calves born to deficient dams – blindness, weakness, domed forehead, thickened carpal joints Deficient calves – blindness, anorexia, diarrhoea, pneumonia (‘ill thrift’) Older cattle – blindness, star gazing, nystagmus, ataxia (hind limbs first), convulsions; also diarrhoea and occasionally thickening and whitening of cornea. Treatment = 400iu/kg vitamin A daily Response even in fitting animals often good (48hrs) Older cattle with ocular form often do not respond Check diet 40iu/kg BW per day (green feed) Ophthalmoscopic photograph of the fundus of a steer with hypovitaminosis A. Optic disc is pale and enlarged, with indistinct edges (papilledema).

Answer 148

Inherited Hereford, guernsey, holstein, shorthorn, ayrshire) Acquired (BVD) – infection dam 90-170 days gestation Severity varies Balance (ataxia, falling backward) or unable to stand, tremor, hypermetria, nystagmus Severe opisthotonus

Answer 149

Hansen Type 1(bursting) and Type 2 (bulging) intervertebral disc disease (IVDD) Cervical myelopathy (Wobbler’s disease) IVD degenerates with age but chondrodystrophoid breeds are at higher risk Dachshund Bassett hound Pekingese French Bulldog Beagle Shih Tzus Cocker Spaniel IVD degeneration occurs earlier in CD breeds than NCD breeds In CD breeds, pathological changes seen in >75% of Ce, T and L discs by 12 months of age Degeneration of the NP is followed by changes in the AF (dorsal >> ventral AF) more symptomatic in thoratic vertebra as less room in vertebral collum Type 1 are more explosive and cause concussive damage to the SC, rather than compressive and chronic with Type 2 Pain (neck pain may be more obvious than lower back pain) Reduced proprioception (check knuckling) Weakness or paralysis - Ce lesions can affect all four legs, TL lesions affect hind limbs, bladder pathophysiology- SC concussion – acute haemorrhage, necrosis, infarction SC compression Nerve root compression Irritation and inflammatory changes For Grade 1 and 2, medical management is recommended Grade 3 – transitional Grade 4 and Grade 5 – outcome with surgery are certainly superior to those with medical management Slow and unpredictable return of function – critically important to provide nursing support (e.g. bladder) and rehab

Answer 150

Usually acute and explosive in onset Ce or TL spine in CD breeds Typically, young dogs (2 yrs of age) Often multiple sites affected – 75% cases involve T12 to L2 Can be accompanied by calcification of the IVD

Answer 151

Much more common in NCD breeds (Terriers, Dalmatians, GSDs) More usually caudal Ce and LS spine Older dogs (>5 yrs) Single level more common

Answer 152

1-Painful but no neurological deficits 2-Painful, wobbly but ambulatory 3-Non-ambulatory but intact motor 4-No motor function, but intact deep pain 5-No motor function and deep pain gone

Answer 153

Usually grades 1 and 2 Strict cage rest for 3-4 weeks Anti-inflammatories plus analgesics Urinary bladder management

Answer 154

Fenestration - no penetration of vertebral canal Decompressive surgery Removal of extruded material Relief of compression Prevention of further damage May be hemilaminectomy (TL) or ventral slot (Ce)

Answer 155

Removal of the nucleus pulposus Performed through one or more annulotomy incisions Does not decompress the canal Prophylactic (Ce or TL junction)

Answer 156

Ventral midline approach Remove bone from one vertebral body to the other (across the disc) Does enter the canal, so removal of extruded material is possible Take care to avoid venous sinuses

Answer 157

Cervical spondylomyelopathy Cervical vertebral instability Cervical vertebral malformation-malarticulation Cervical spondylopathy Seen in humans, dogs and in horses Cervical spondylomyelopathy Cervical vertebral instability Cervical vertebral malformation-malarticulation Cervical spondylopathy Seen in humans, dogs and in horses Pathophysiology- Disc- associated; Middle-aged Dobermanns Dorsal annulus hypertrophy and protrusion Dorsal ligamentum flavum hypertrophy Ce5/6 and Ce6/7 Bone- associated: More likely in young Gt Danes Bone malformation and OA of the articular facets Multiple levels affected, most often cranial Ce spine

Answer 158

Medical and surgical management have been described Approximately 50% improve with medical management, 30% stay the same and 20% get worse >20 different surgical procedures have been described! Most focus on a combination of decompression and stabilisation

Answer 159

Giant and large breed dogs but also common in Min Schnauzers and Shetland Sheepdogs Vocalization (acute pain often subsides quickly) Knuckling, weakness or collapse of one or more limbs (lateralised) Lameness Usually not progressive beyond 24 hours

Answer 160

Conservative/supportive care Non-steroidal anti-inflammatory drugs (NSAIDs) and steroids Prognosis can be variable, even with aggressive treatment Absence of deep pain is considered a poor prognostic sign

Answer 161

Chronic, progressive myelopathy that has both UMN and LMN involvement Most common in older dogs (> 8 yo) from breeds such as GSD, Boxer, Chesapeake and Ridgeback Similar to ALS in humans (Lou-Gehrig’s Disease) Veriable signs – wobbling, loss of proprioception, scuffed toes Important to rule out other important causes of spinal disease Disc disease LS disease Spinal tumours Discospondylitis X-rays, CT and MRI Genetic testing available – SOD1 as a risk factor only manangment- Supportive care only Hydrotherapy and regular exercise can be helpful to keep animals moving and maximise QoL Progression to non-ambulatory within 12 months is common May well end up being a PM diagnosis

Answer 162

Diseases of the Vertebral Body Toy or small-breed dogs <2 yo Cervical pain – if you suspect it, take care not to flex the neck Neurologic deficits map the lesion to C1-C5 UMN Highly variable clinical picture ranging from mild pain through to tetraplegia/respiratory distress diagnosis- Major differential is Ce trauma so take care of the neck! Radiography, CT and/or MRI Congenital hypoplasia or complete absence of the dens

Answer 163

Conservative- Good option for mild casesAt least 6-8 weeks of neck bracing, strict rest Surgical- Best outcomes with mild disease Risky surgery – respiratory 20% risk of death in first 48 hours

Answer 164

Primary Meningioma Glioma Nerve sheet tumour Lymphoma Neuroepithelioma Secondary (metastatic)

Answer 165

Seen most often with excessive intake of liver or cod liver oil Acute toxicity can cause nausea/vomiting, but chronic exposure is more common Clinical signs include lethargy, poor hair coat, constipation, anorexia, stiffness/reluctance to move May see neurological deficits in the forelimb First priority is to manage pain and stiffness Change diet immediately to remove Vitamin A source Prognosis depends on degree of involvemenet

Answer 166

Infection of the disc and vertebral endplates Most often Staph. pseudintermedius or Staph. aureus Haematogenous, bite wounds, FBs, surgical site infection Most often middle-aged dogs of large breeds – rare in cats May be multifocal Typically, gradual onset Spinal pain, stiffness, ataxia and sometimes paresis Pyrexia In chronic cases, may see muscle atrophy

Answer 167

Risk of fracture – so rest the animal (confine to cage or room) Antibiotics (based on C&S) for >8 weeks (check – FUNGAL?) Anti-inflammatories (NSAIDs) and analgesia Surgery to decompress, debride and collect samples for culture Prognosis is fair to good (guarded to poor if fungal)

Answer 168

(Listeria monocytogenes) Environmental pathogen, infections sporadic and usually associated with feeding poor quality silage, fermentation and soil contamination Infection travels up to brainstem from conjunctiva, face/mouth via trigeminal nerve. Forms microabscesses in brain stem/cerebellum/spinal cord; may progress to meningoencephalitis Clinical Signs: Febrile Dull; loss of lip and cheek muscle tone: difficulty in eating chewing, accumulation cud in cheek, salivation, tongue protrude Ptosis, drooping of ear on the deviant side, circling Headpressing, propulsive walking

Answer 169

Aim is stop disease getting worse as neurological deficits may not resolve. High doses of penicillin 44,000iu/kg BID 7-14 days followed by 22,000iu/kg BID 7-14 days High doses of oxytet. Remove underlying cause ie silage

Answer 170

Spinal fractures – 3-6 month old calves: investigate underlying cause; VitD, calcium or copper deficiency?

Answer 171

– normally secondary to osteomyelitis (vertebrae); often cervical; haematogenous or injections; A. pyogenes, Staph. aureus, P. haemolitica, F. necrophorum Pain, heat, swelling; animals stiff, reluctant to eat from the ground; if close to brain hyperaesthesia, spasmic muscle contractions, recurrent profuse sweating. Treatment: antibiotics (see meningitis).

Answer 172

Asymmetric spasticity and hypertonia of the extensor muscles of the rear limbs Continuous when the animal stands but not when it lays down Most breeds A few weeks to 6 months Genetic predisposition ? Do not breed from affected animals Clinical signs Excessive Tone of Gastrocnemius Muscle Hyperextended hock Unilateral or Bilateral If unilateral the affected leg is thrust out behind during walking and advanced with a swinging motion without touching ground Often spend longer lying down

Answer 173

Neurectomy of the tibial nerve rootlets innervating the gastrocnemius muscle high epidural or GA If bilateral then leave 6-10 weeks inbetween Success rate ~ 60% Inability to flex the hock when walking, the limb is circumducted; ‘pendulum-like motion

Answer 174

Clostridium botulinum Ensiled poultry waste (as food) (illegal), poultry litter applied to pasture or used as bedding, accidentally contain carcasses Poor quality BBS Carcasses in pasture or feed Incubation period variable, normally 2-4 weeks Progression of disease 4-5 days Stiffness, reluctance to move, muscle tremors Prolapse 3rd eyelid, RUMEN TYMPANY, elevation tail Progression to generalized muscular tetany and “rocking horse” position Recumbancy, convulsions, death. Extended head posture, extensive tone in facial musculature, stiff, raised tail, legs held rigidly extended No test; no characteristic PM signs; identify site of infection and attempt to culture. Full blown tetanus prognosis poor PTS Animal well bedded kept in dark and quiet Antitoxin not much help unless very early. 2. Penicillin high doses. 3. Irrigation of infection site penicillin, antitoxin. 4. Muscle relaxants like ACP administer till signs resolve Vaccination

Answer 175

Clostridium botulinum Ensiled poultry waste (as food) (illegal), poultry litter applied to pasture or used as bedding, accidentally contain carcasses Poor quality BBS Carcasses in pasture or feed Clinical Signs Characterised by muscle weakness, progressing to ataxia and then paralysis Anorexia, dilated pupils Excessive drooling Droopy expression, tongue may hang out of mouth Decreased rumen motility, bloat, constipation Respiratory failure leading to death Diagnosis History Clinical Signs No specific PM findings Toxin in serum ELISA (not always) Samples of feed or bedding may help consult with lab. Treatment Supportive, purgatives to remove toxins. Fluids. Prognosis poor but if caught in early stages and source of infection removed the animal may recover

Answer 176

Obturator Peroneal Sciatic Radial Nerve / Brachial Plexus

Answer 177

Following dystocia esp heifers Obturator nerve damaged by foetal pressure Unable to adduct limb (splits) Diff Dx pelvic fracture Treatment: chain between hind limbs (hobbles), soft bedding, coricosteroids

Answer 178

Branch of sciatic nerve damaged as it runs course over lateral aspect stifle joint esp recumbant cow or fall Hyperextension of hock fetlock and digits flexed (knuckled over) Loss skin sensation below fetlock dorsal surface Self cure can bandage or cast to fetlock to prevent self trauma

Answer 179

Damage occurs when cow recumbant and struggling to rise Non weight bearing, no sensation distal to stifle (medial mid tarsal region o.k) Diff diagnosis femoral fracture Prognosis guarded

Answer 180

Excessive traction of a large calf in anterior presentation Inability to extend the elbow, carpus and fetlock and bear weight on the affected limb in severe cases Treatment: Anti-inflammatories + time (guarded prognosis) Prevention/control: Avoid excessive traction during calf delivery. Do not calve cows in a crush There is a loss of muscle over the shoulder with resultant prominent spine of the shoulder blade. There is a dropped elbow, flexion of the distal limb joints and scuffing of the hooves as the leg is moved forward. The foot is knuckled over at rest.

Answer 181

* Border Disease (tremors, hairy shakers) * Congenital Swayback (ataxia) * Drunken Lamb Disease (ataxia, depression star gazing)- treatment see lamb lecture * Bacterial meningitis (collapsed)– Try high doses penicillin * Tetanus

Answer 182

Congenital OR Delayed form (2-4m of age) Ewes were deficient in copper during pregnancy (usually mid – late trimester) Soil issue! Breed pre-disposition in Scottish blackface Stillbirth / weak lambs/ characteristic weakness of pelvic limbs Confirm with a copper assay (blood and liver samples) Congenital form – treatment is hopeless PTS on welfare grounds Delayed form – some evidence that supplementation slows progression of disease, restrict exercise and feed high proportion of concentrates to achieve market weights Swayback is a congenital condition affecting new- born lambs; delayed swayback (enzootic ataxia) most commonly affects lambs aged 2–4 months. The incidence depends upon geographical area, soil type, land and pasture improvements through drainage and lime application, breed and weather conditions during the period corresponding to mid-trimester.

Answer 183

1-3weeks of age Acute onset ataxia and incoordination tending to recumbency Death usually within 24-48 hours after clinical signs appear Biochemistry shows weak azotaemia, hyperphosphataemic, and all have metabolic acidosis (very high D-lactate) PME – Nephrosis observed, relevance to clin signs?? Treatment successful in one study- 50ml of solution of sodium bicarbonate dissolved in tap water (35g sodium bicarbonate in 400ml water to make a stock solution of 8 doses) was given orally Parenteral long acting amoxycillin also given Rapid clinical recovery- Resolution of clinical signs within hours, Lambs return to suckling mothers

Answer 184

spinal abscess – Treat 1mg/kg dexamethasone – Penicillin * Lamb nephrosis – “drunken lamb” * D lactic acidosis * Delayed swayback – ataxia/recumbency * Bacterial meningitis * Listeriosis – circling – facial nerve paralysis) * Louping ill * Tetanus

Answer 185

Tick borne * most infections are slight and give immunity * clinical disease in all ages depending on immunity – colostral antibody – think of exposure periods * can get outbreaks of disease Important in Grouse (80% mortality) * Vaccine available * Variable signs – head pressing – trembling & tremors – nystagmus – lip twitching etc – “louping gait”

Answer 186

CCN * Listeriosis * Gid * Louping ill (tick area)

Answer 187

Younger ewes * Taenia multiceps – Eggs picked up by sheep cysts develop in brain cerebral, cerebellar (Coenoris cerebralis) Gradual onset – circling – unilateral blindness * opposite side to lesion head tilt – skull softening * Precise signs depend on site of lesion – cerebral – good prognosis – cerebellar – poor * Control – worm dogs every 6-8 weeks (praziquantel) – keep away from sheep carcasses

Answer 188

Vitamin B1 deficiency (thiamine) * acute onset in growing lambs (2 –6 months) * sporadic but can get outbreaks * history of diet change or worming – thiaminase production in rumen – PME – brain Clinical signs vary depending on progression of disease – Dull – Disorientated – Blind – Tremors – Recumbency – Opisthotonos – Convulsions

Answer 189

– Vitamin B1 iv (slow 10mg/kg)) – Vit B1 i/m every 12 hours – For 3 days – House quietly – Vision should return 5-7days * Prevention ? – diet changes – Thiamine in food ??

Answer 190

Common!! * Listeria monocytogenes * Associated with feeding poorly preserved silage soil contaminated (mouldy) * 18-24 months old common, but not exclusive changing molar teeth allowing infection of buccal tissues * Ascending infection to brainstem Anorexia, depression * Unilateral hemiparesis * trigeminal nerve paralysis - Salivation, food impacted in cheek * Facial nerve paralysis (drooped ear, lowered eyelid, deviated muzzle, loss of blink)

Answer 191

Diagnosis – Clinical signs – CSF tap – PM * Treatment – Good if caught early – 75kg ewe – 6g benzylpenicillin (Crystapen x 2 vials) i.v – 20ml procaine peniciliin i.m (divided sites) – 1mg/kg dexamethasone i.v – 5ml procaine penicillin daily for 5 days – Supportive care * Remove silage!!

Answer 192

Cervical sub-luxation (paresis, rams fighting) * Gid cyst * Listeriosis * Brain abscess * Louping Ill (tick areas, abnormal gait) Metabolic disease (pregnancy) – Pregnancy toxaemia- * blind, dull – Hypocalcaemia * Collapsed, bloated, flaccid paralysis – Hypomagnesaemia * staggers, hyperaesthesia * Wobbler Texels * Scrapie

Answer 193

* Pregnancy toxaemia – diagnosis – History, clinical signs, ketones in urine, nasal secretion (PME) – treatment – poor prognosis unless very early * Oral propylene glycol + IV glucose * Hypocalcaemia – before lambing – stress factors – treat with 20 – 40 ml Ca Borogluconate I/V – instant and complete response ( 80 ml s/c slower response) * Septicaemic listeriosis – hopeless prognosis - PTS

Answer 194

Diet fed – Energy – Fibre (SARA) – Trough space * Stressors: – movement, – weather, – over-crowding – vaccination – Other disease: * Lameness, pneumonia etc * Housing * Diagnostics – Response to Ca – Ketostix – BOHB * last 3 weeks – group of ewes

Answer 195

Inadequate drainage initially Foreign body Sequestrum Keratoma Laminitis Quittor A non resolving draining tract MUST BE investigated

Answer 196

History Trauma? Twisted shoe, stepped on nail? Injury to hoof/ solar penetration Clinical signs Persistent foot abscess Recurrent draining tract at coronary band diagnostics- RADIOGRAPHS!! Radiographs have a classic appearance- bone surrounded by involuprim (black area) (infection of bone,- treat with Debride and follow the draining tract Surgical debridement dont resolve via antibiotis as cause still presednt Sequalae…pedal osteitis

Answer 197

Benign tumour of keratinised tissue diagnosis- radiographs- Solar keratoma shows circular ‘onion like’ appearance on the sole sat within the white line Radiographs!! Classic appearance – circular radiolucent area in P3. (Care – Crena solar marginalis) Treatment- Surgical removal under GA Prognosis- Good Potential for recurrence

Answer 198

Necrosis of the collateral cartilages- infection Secondary to trauma or infection Uncommon- seen in draft breeds Diagnosis- Non healing wound *Draining tract is above the coronary band not from the coronary band!* Radiographs insignificant abnormalities – irregular active bone? Probe or contrast material to define- put into draining tract and see where it communicates Treatment- Surgical debridement Local and systemic antibiotic therapy

Answer 199

Poor quality hoof horn Separation in the Stratum medium at the junction of the non-pigmented and laminar horn Aetiology- Unknown…BUT Multifactorial: environmental/ nutritional/ mechanical/ infectious Clinical signs- Lameness Hoof wall crumbling Diagnosis- Appearance Radiography Treatment- Debride the affected tissue, stabilise the hoof wall consider trigger factors- shoeing, dampness of enviroment, laminitis? (esspecially when it effects the hoof horn), nutrition effecting hoof quality

Answer 200

Chronic hypertrophic pododermatitis Hypertrophy of the dermis horn Cause- Anaerobic bacteria Fusibacterium necrophorum Bacteroides Aetiology- Infects stratum germinativum Intertubular horn Causes dyskeratosis Causes dyskeratosis Diagnosis- Vegetative, moist, white mass Rarely lame Biopsy? Treatment- Surgical debridement- requires lots of packing post surgery Topical metronidazole and astringents **RECURS** manage enviroment

Answer 201

Most common cause of forelimb lameness 80% of all FL lameness Multiple structures can be affected Requires a systematic approach causes- Foot balance Hoof wall/capsule DIP joint Collateral ligament of the DIP joint Digital cushion Collateral cartilages Navicular bone Navicular bursa DDFT Distal sesamoidean ligament Impar ligament Sidebone Unilateral vs bilateral!

Answer 202

Lameness – chronic and intermittent Inconsistent performance Loss of suppleness Stumbling Unwilling to go forwards Temporary improvement with rest Worse on hard surface Exacerbated with circling Mild to moderate lameness One limb more severely affected Decreased cranial phase of the stride

Answer 203

Minimal to no external signs: Digital pulse Swelling Insiduous or acute onset Improves with rest The order of differential DDx is different between unilateral vs bilateral!! Clinical examination Look at static and dynamic foot balance Diagnostic tests Hoof testers Distal limb flexion Diagnostic analgesia Diagnostic imaging Radiography US Nuclear scintigraphy MRI

Answer 204

Likely contributing factor for all FL lameness Needs addressing before evaluating for other DDx’s Easily identified on clinical examination + radiography

Answer 205

A collection of clinical signs or diagnostic results which together constitute the picture of disease. Our understanding of what we used to call ‘navicular disease’ has massively changed to the development of advanced imaging techniques which can identify specific structures as the cause of lameness. Middle aged horses Hunters/ showjumpers/ eventers/ dressage horses Presentation- Often bilateral shortened stride Worse on a hard surface Intermittent Insidious onset Contributing factors- Upright confirmation Poor foot balance: long toe, low heel Repetitive concussion Etiology- Biomechanical forces Repetitive trauma to the navicular bone causing bursitis Movement between the DDFT and the navicular bone Bone remodelling occurs due to load and pressure (flexor cortex) Pathological changes- Alteration of palmar fibrocartilage Increase force on the subchondral bone causing sclerosis Adhesions of navicular fibrocartilage to the DDFT Radiographic abnormalities- Synovial fossae- lollypop leasions Enlarged Abnormal shape Abnormal location 7-8 normal in middle aged horses Cyst formation Enthesiophytes- Collateral sesamoidean ligament and impar ligament Osteophytes Flexor cortex abnormalities Medullary abnormalities- sclerosis decreased corticomedullary definition Synovial invaginations Progressive disease Not curable Aim: manage pain and progression Prognosis Good in the early stages Poor if lameness persists

Answer 206

Farriery- Balance foot Decrease pressure on heels Maximise weightbearing surface Bar shoe Medical- NSAIDs- not licensed for long term but often used long term for this syndrome Corticosteroids into bursa- wont reduced bony change but relieves inflamationn Stem cells? Polyacrymide hydrogel? Bisphosphonates Surgical- Palmar digital neurectomy (SALVAGE) Navicular bursocopy

Answer 207

Presentation- Unilateral forelimb lameness Acute onset No other abnormalities detected Diagnostic analgesia- PDNB? Navicular bursa block? DIP block? ASNB positive Diagnostic imaging- No radiographic abnormalities +/- US abnormalities MRI!!

Answer 208

Presentation- DDx for DDFT tear Diagnostic analgesia- As for DDFT tear Diagnostic imaging- No radiographic abnormalities +/- US abnormalities MRI!! Remember impar = distal sesamoidean ligament that attaches the NB to P3

Answer 209

Joints? DIP and PIP Presentation- DDx for foot pain Mild lameness/loss of performance Diagnostic analgesia= Block lameness to articular structure depending on severity and subchondral bone involvement Diagnostic imaging +/- radiographic abnormalities Acute joint damage will lead to synovitis developing rapidly. Osteoarthritis is usually a consequence of ongoing damage

Answer 210

Presentation- Worse on a circle Differential for foot pain Diagnostic analgesia- Variable blocking pattern Diagnostic imaging- Minimal to no radiographic abnormalities +/- US abnormalities MRI!

Answer 211

Presentation- Rarely causes lameness Can be lame if fractured Diagnostic imaging- Radiography – variation in radiographic appearance Often incidental finding.

Answer 212

NSAIDs Bisphosphonates Intra-articular therapies- Corticosteroids HA Polyacrylamide gel Regenerative therapies

Answer 213

Commonly used Analgesic and anti-inflammatory Only effective in the face of an inflammatory process Clinically used for myositis, tendonitis, laminitis, osteoarthritis, and surgically induced trauma Timing important! carprofen firocoxib phenylbutazone- main one due to low cost and ease of administration flunixon magluminate ect

Answer 214

NSAIDs Most widely used Low cost Safe at low doses Orally or IV More effective than flunixin in musculoskeletal disease? 4mg/kg lasts 12hours Effective for synovitis Side effects? Renal Hypoproteinamia GI ulceration Reduces inflammation, central analgesic mechanism by decreasing hypersensitivity to pain caused by inflammation

Answer 215

NSAID More effective for visceral pain + anti-endotoxic properties IV/orally – 1.1mg/kg

Answer 216

COX 2 preferential NSAID Indications: alleviation of pain and inflammation associated with OA and reduction of associated lameness in horses 0.1mg/kg once daily Now available in paste and tablet form More expensive than phenylbutazone so most owners will use bute but htis is techniqally more suted to chronic cases due to reduced side effects Licensed

Answer 217

Mechanism of action still not fully understood 20mg/kg orally twice daily adjunctive analgesic for laminitis Not licensed- use human tablets so large quantity effective in lamnitis

Answer 218

Regulate bone activity by inhibiting osteoclastic metabolism without affecting osteoblastic action. Notable side effects- large proportion of horses given this wil colic- NSAIDs contraindicated Licensed for use in spavin (Tiludronate) and navicular disease (Clodronate). Can be tested for in doping tests – detection time 28days FEI/ 30days BHA. Weak evidence for use when navicular bone is primary cause of discomfort and where clinical signs are recent in onset. Statistically significant results to support use in horses with tarsal OA.

Answer 219

Intra-articular medications can be a more targeted approach to joint pathology. Their use remain controversial. However we will cover the most common steroids used in practice and the indications and contraindications for each. The action of corticosteroids is exerted through steroid-specific receptors in the cytoplasm of steroid-responsive tissues. This interaction results in the altered transcription of genes, leading to a wide variety of antiinflammatory effects, as well as other effects on the biology of articular cells that are of variable benefit. Corticosteroids are able to suppress inflammation at virtually all levels. The humeral effects of corticosteroids are due to the inhibition of phospholipase A and the decrease in production of pro-inflammatory mediators by both the cyclooxygenase and lipoxygenase pathways. They also inhibit many of the other inflammatory effects, such as capillary dilation, migration of inflammatory cells and the production and release of degradative enzymes; however, such drugs may have a negative effect on the joint environment, as they can cause suppression of cartilage matrix synthesis, as well as, in rare cases, widespread joint mineralisation1,2 when to use them- When we have made a diagnosis of synovitis Reduce the risk of development of osteoarthritis Reduces inflammation within the joint Two main options: Shorter acting Triamcinolone Acetonide (NOT LICENSED) Longer acting Methylprednisolone acetate (LICENSED) Return to work? Gradual 1-2weeks Be conscious of detection times!- sport horses risks- Iatrogenic synovial sepsis Laminitis Mitigate risk? Intra-articular antibiotics? Must warn owners of the risks! can gie ia antibiotics at same time but not necessary if in clean enviroment and follow ropper hygien

Answer 220

DOSE: 6mg to 18mg per joint. Max total dose 20mg steriod Widely used in joint disease therapy High motion joints: carpus/ fetlock and DIP joints One off vs regularly in the face of clinical signs of joint disease Effective in acute cases of synovitis BUT rule out treatable primary cause prior to treatment Shorter detection time risks- Iatrogenic synovial sepsis Laminitis Mitigate risk? Intra-articular antibiotics? Must warn owners of the risks!

Answer 221

20mg/kg to 40mg/kg Max total dose 200mg Longer acting More detrimental to articular cartilage – therefore low motion joint such as tarsus Longer detection time steriod risks- Iatrogenic synovial sepsis Laminitis Mitigate risk? Intra-articular antibiotics? Must warn owners of the risks!

Answer 222

Improves viscosity of synovial fluid – better lubrication Anti-inflammatory effects Reduced pain no scientific evidence that it is better than steriods alone can be iv but often intrarticularly

Answer 223

Similar action to HA – improves lubrication of the joint Studies in horses showed that intra-articular injection of PAAG supported cellular growth and integration. Further studies needed to explore potential effects on synovial inflammation and pain are needed 100% synthetic, non-soluble – acts a substitute for synovial fluid MCP/MTP and DIP commonly treated Reduced risk of IA infection vs steroids Slower improvement seen vs steroids No proven risk of doping

Answer 224

Aim is to aid tissue healing Restore normal structural architecture and biomechanical function to injured tissue. Not cause harm? Limitations? Inflammation and Osteoarthritis- IL-1 and TNF pro-inflammatory cytokines  Erosion of cartilage and osteoarthritis OA has increased expression of IL-1 receptors IL-1ra protein prevents IL-1 from interacting Provide IL-1ra by conditioning of serum ACS or IRAP

Answer 225

Regenerative therapies lacks evidence Autologous conditioned serum It may contain Interleukin receptor antagonist protein. Plus other things. Theory of action: Interleukin-1 is a major driver of OA and thus blocking it is an objective in the treatment of OA. when?- Most commonly sports horses If identified soft tissue pathology (MRI/arthroscopy) Increasingly used early, often before a definitive diagnosis.- more efffective Mainly coffin joints and fetlocks If IA steroid fail Cost- steriods much cheaper in human case- 376 cases of knee arthritis ACS significantly superior to HA and saline placebo Carpal fracture model 16 horses Significantly improved lameness grade Significantly decreased synovial membrane hyperplasia No adverse effects Ongoing concerns with method of action Low risk Seems to be beneficial- lack control studies Lack of controlled studies and high quality of evidence based medicine. Repeated injections

Answer 226

Arti-cell Forte Allogenic stem cells Authorised by VMD for ‘reduction of mild to moderate degenerative joint disease (osteoarthritis) in horses. Contains chondrogenic induced mesenchymal stem cells that target cartilage evidence?- Assessment of short term effect on a limited number of horses, using an OA model Declaration of interest that one author declares competing financial interests as a shareholder in Global Stem cell Technology - owners of Arti-cell Forte.

Answer 227

Supports the MCP joint Flexes the MCP joint Elastic energy store 16% strain at gallop (rupture at 12-20% in lab) Loads in excess of 1tonne on a structure less than 1cmsq in cross-sectional area Tendon operating close to its functional limit Low tolerance = low safety margin Suggests: Any small degeneration in matrix/structural properties will dramatically increase the risk of tendinopathy Prevention of any such change will dramatically reduce the risk of tendinopathy prognosis- Most treatment suggest 60% BUT re-injury rates lowest with stem cells Re-injury is the primary reason for treatment failure Older horses = poorer prognosis Lesion present in tendon or carpal sheath carry worse prognosis – poorer blood supply.

Answer 228

Types Intrinsic (strain) Extrinsic (percutaneous injury) Displacement Very common! 30-40% of NH horses in training suffer tendonitis 46% of limb injuries on racecourses involved flexor tendons/suspensory ligament SDF tendonitis most common injury in event horses Predisposing/causal factors- Biomechanical reasons- Previous tendonitis Uneven or deep track surfaces Muscular exhaustion Foot imbalance Long sloping pasterns Anatomical reasons- Certain reasons have reduced blood supply (mid SDFT) Decreased cross-sectional area in certain areas of the tendon

Answer 229

Hyperthermia in the centre of the tendon at gallop (45deg) Acute overload of the entire tendon Protein and cellular damage (collagen fibre disruption) Classical ‘core lesions’ – loss of fibre integrity in central region

Answer 230

Tendon accumulates microdamage with age (>3yrs) May manifest as acute overload incident Often may get more generalised severe tendonitis Stages of tendon damage - clinical Tendon matrix degradation - cumulative - ageing Fibrillar slippage - breakage of crosslinks Fibril rupture Complete rupture

Answer 231

History: Acute onset Exercise? Peak performance Clinical evaluation: !Stance? Fetlock sinking !Gait – lameness (mild to moderate) Palpation: whilst weightbearing and with limb lifted Swelling Thickening Pain on palpation Oedema Heat Ultrasonography Diagnosis normal and affected limb Timing 4-7days post injury TRANSVERSE AND LONGITUDINAL Examine for: Cross sectional area – 0-15% mild/ 15-25% moderate/ >25% severe Peritendinous oedema Echogenicity Margination – subtle indicator of changes Fibre alignment – indicates quality of scar tissue Examination too acutely may underestimate true damage

Answer 232

Clinical signs - Lameness Severe -> mild Pain on palpation- palpate weightbearing and non weightbearing Inflammation heat oedema loss of definition Pathology- Haemorrhage !Inflammation -! neutrophils - macrophages and monocytes - increased bloodflow - oedema - proteolytic enzymes

Answer 233

Aims: Limit inflammation: Cold water hosing/ ice packs NSAIDs/ Corticosteroids Bandage – reduce oedema Protect from further damage Firm supportive bandage BOX REST!!! Many treatments have been advocated in the past: Most have no effect Some are deleterious ‘above all do no harm’

Answer 234

Clinical signs- Reduction in lameness Resolution of signs of inflammation Tendon still palpably enlarged and soft Signs of reinjury if exercised too early (usually worse!) Ultrasound: hypoechoic Pathogenesis- Angiogenesis Fibroplasia- - ++fibroblasts - collagen type 3 (normal type 2) - small collagen fibrils formed

Answer 235

Aims: Prevent re-injury BOX REST + mobilisation – controlled!! Promote angiogenesis- Stem cells Promote better quality repair- Intralesional injection of mesenchymal stem cells, platelet rich plasma etc Physiotherapy Therapeutic US Low level laser therapy Hydrotherapy Reduce oedema

Answer 236

Expensive and time consuming - autologous Pluripotent progenitor cells capable of forming tendon tissue rather than scar tissue Re-implantation of mesenchymal stem cells (MSCs) into lesion Expanded in vitro Bone marrow from sternum most commonly SDFT core lesions provide natural enclosure for implantation At the time of implantation the granulation tissue provides a vascularised scaffold After the initial inflammatory phase before fibrous tissue had formed Reduced re-injury rate from 56% to 18% (small study)

Answer 237

Stall side treatment Cheaper than MSC’s Produced and implanted same day Blood plasma with concentrated platelet count Activated growth factors Injected under US guidance Long term results lacking

Answer 238

Clinical signs- Tendon size decreases Tendon is less pliable Reduced fetlock extension Ultrasound: hypoechoic to hyperechoic (heterogenous) Pathology- Collagen type 3 -> type 1 Crosslinking Thicker collagen fibrils

Answer 239

Aims: Promote re-orientation and modelling of fibrils Begin loading –controlled exercise Timing and progress monitored by US - Increased fibre density and improved alignment indicated - Further increase in exercise if appropriate controlled exersise program

Answer 240

**Most important aspect of rehabilitation of SDFT tendonitis** Initially box rest and limb support for 2-4weeks Followed by small amounts of in-hand walking out Progressively increase over 9-12months Rescan every 2-3 months: before and after a change in exercise level

Answer 241

Initial severity – lameness Longitudinal pattern when returns to full work Duration of rehabilitation Nature of work Recurrence Treatment

Answer 242

Usually pastern/foot – P2/navicular level If within the DFTS – usually distended sheath Linear tears seen more commonly in the forelimb- Treated by tenoscopic debridement MRI to diagnose in the foot 50-60% success rate with conservative or surgery

Answer 243

Clinical signs- Swelling proximal 1/3 of the metacarpal region Palmar to the suspensory ligament Lameness can be variable ultrasound- Generalised enlargement Focal abnormalities Fibre pattern disruption Concurrent SDFT tendonitis Check ligament often vestigial in the hindlimb Similar signs to forelimb when present

Answer 244

Acute: Box rest! (2-3 weeks then controlled exercise) NSAIDs Cold hosing/bandaging Chronic: Controlled exercise program NSAIDs Corrective farriery- foot can make a big difference in how tendon heals become contracted/ DIP flexural deformity Shockwave? Prognosis Acute – fair good Chronic + SDFT involvement = poor

Answer 245

Unilateral (can be bilateral –less common) Lameness Palpation – enlargement/pain deep palpation – care! Ultrasound: Focal or generalised lesions Loss of striated pattern Peri ligamentous fibrosis Entheseopathy Radiography- Sclerosis of proximal MC3 Avulsion fractures Prognosis generally good – (60-80%)

Answer 246

Controlled exercise (6-9months) Stem cells/intra-lesional injection if core Shockwave

Answer 247

Electrohydraulic extracorporeal shock wave therapy (ESWT) Control inflammation, angiogenesis and stimulate cytokine production. Provides immediate pain relief – up to 4days

Answer 248

Usually chronic, bilateral hindlimb lameness (rarely acute/unilateral) Clinical examination often unremarkable BUT.. Associated with conformation- straight hindlimbs Usually worse on soft surface Worsens with exercise Diagnosis- Diagnostic analgesia: deep branch of the lateral plantar nerve. Rule out tarsal joint pain with IA anaesthesia Ultrasonography- DIFFICULT!! Enlargement and irregular margin Poor fibre pattern – reduction in echogenicity Irregular bone surface/fibrosis Compare limbs Radiography- Sclerosis MT3

Answer 249

Controlled exercise (20-30%) Shockwave (50%) Surgery (70%)- Neurectomy/fasciotomy FEI implications…

Answer 250

Older racehorses/event horses Lameness variable May be associated with splint bone exostosis Diagnosis: Based on palpation + ultrasound Treatment: Controlled exercise Shockwave HA? Prognosis- Fair – recurrence common Some horses are managed in work with low grade chronic changes.

Answer 251

Both forelimbs and hindlimbs Conformation  abnormal loading Variable lameness Diagnosis Palpation of branches Occasional fetlock effusion Ultrasonography: Enlarged – reduced echogenicity Occasionally core lesion exists Entheseopathy Periligamentous thickening Prognosis: Poor-fair

Answer 252

Controlled exercise Intra-lesional stem cells/PRP Shockwave?

Answer 253

Synovial fluid within the calcaneal bursa (point of the hock) Cosmetic (lameness rare)

Answer 254

Synovial distension of the tarsal sheath proximal to the hock Cosmetic usually Is the sheath of the larger lateral flexor tendon (DDFT) in the hindlimb Swelling is often clinically insignificant *If the horse is lame, look elsewhere first!*

Answer 255

Synovial distension of the fetlock or tendonsheath May or may not be related to lameness may or may not be related to lameness

Answer 256

Acute tenosynovitis: over extension of the fetlock region/trauma to sheath Tendon lesion in DFTS: DDFT tear in forelimb and manica flexoria tear hindlimb Palmar annular ligament desmitis May be idiopathic PAL desmitis Causes constriction of the DFTS Can be primary or occur secondary chronic tenosynovitis Diagnosis- Clinical exam Lameness assessment: Mild to moderate lameness Minimal response to rest Intrasynovial anaesthesia to confirm Ultrasonography – CARE – see next slide!! Radiography…manica tears…contrast studies Tenoscopy

Answer 257

Manica flexoria: a tendinous ring inserting on the medial and lateral borders of the SDFT at the palmar aspect of MCP region that holds the flexor tendons in position

Answer 258

*rule out sepsis* Rest Ice/cold hosing Systemic NSAIDs Intrathecal medication: corticosteroids/ HA Tenoscopy- Indications: Intrathecal pathology diagnosed or suspected Lack of response to conservative management/medical therapy Flush out inflammatory mediators Lesion ID on MRI or US Chronic tenosynovitis- Many cases respond to rest and controlled exercise + medical therapy as described. Tenoscopy: As for acute tenosynovitis: Remove damaged tendon fibres Chronic cases PAL desmotomy Remove synovial masses/adhesions Early exercise postsurgery helps reduce post-operative adhesions

Answer 259

Treatment: box rest and controlled exercise raised heel to reduce load on DDFT PAL desmotomy? Prognosis: Guarded to poor

Answer 260

Aetiology: Compression of the tendon during overextension of the fetlock Treatment: Tenoscopic debridement –removing loose fibres reduces tenosynovitis Removal of chronic adhesions

Answer 261

Desmitis causes mechanical constriction of the smooth movement of the tendon sheath Desmotomy – divide the ligament Good prognosis if the cause of the desmitis has been controlled.

Answer 262

Constriction known as carpal canal syndrome Secondary to tendonitis of the SDFT and DDFT, intra-thecal trauma/haemorrhage, ALSDFT desmitis, fracture of the ACB or osteochondroma of the caudodistal radius. Removal of any osseous impingement is important resolve clinical signs

Answer 263

Over the carpus most commonly affected Commonly aseptic tenosynovitis in jumping horses that suffer blunt trauma their knees. Congenital condition in foals where the CDE ruptures with the extensor tendon sheath causing tenosynovitis Resolved by box rest Address associated flexural deformity

Answer 264

Subsequent to lacerations to the dorsal aspect of the limb Horse unable to extend joints covered by the affected tendon: Commonly: Common Digital and Long Digital extensor tendon Standard wound care/splint if knuckling forward Do not need to suture: Tendon can be removed without long term sequalae Toe extension on shoe to prevent knuckling during first few weeks Prognosis: Good to excellent Horses adapt well!

Answer 265

Potentially serious and life threatening – major part of the support structure for the distal limb. Over reach injury or sharp/blunt trauma Risk of synovial sepsis if digital sheath, carpal/tarsal sheath involved. Usually severe lameness Attitude of the limb indicative which ligament/tendon is involved Watch horse weight bear, walk a short distance or briefly pick up limb Careful digital examination +/- US exam **site of laceration may differ from the site of the cutaneous wound** Synoviocentesis of the DFTS SDFT Fetlock drops on weightbearing DDFT Toe of the foot comes off the ground on weight bearing SDFT, DDFT and SL Toe comes off the ground, and fetlock drops to the ground

Answer 266

First aid: immobilise limb/splint cast Debride wound under GA Treat any synovial sepsis Repair: - Suture if tendon ends aren’t too macerated -If there is a tendon gap leave by secondary intention or use prosthetic material Immobilise limb in distal limb cast for 8-12weeks

Answer 267

Pass a cotton swab soaked in spirit or a strong smelling treat under the nose and assess for a response Olfactory nerve

Answer 268

making a menacing gesture (moving the hand quickly toward the eye) and assessing for the normal blinking response Optic nerve Facial nerve

Answer 269

Shine a light in one eye to elicit pupil constriction in the contralateral eye Optic nerve Occulomotor

Answer 270

Touch the medial or lateral canthus of the eye to elicit a blink reflex Trigeminal nerve – ophthalmic branch Trigeminal nerve – maxillary branch Facial nerve

Answer 271

Touch the cornea to elicit blink and globe retraction Trigeminal nerve – ophthalmic branch Facial nerve Abducent nerve

Answer 272

Move the head to induce nystagmus Vestibulocochlear nerve Oculomotor nerve Trochlear nerve Abducent nerve

Answer 273

Touch the nasal mucosa with the animals eyes covered to elicit head movement away from the sensation Trigeminal nerve – ophthalmic branch Trigeminal nerve – maxillary branch

Answer 274

Touch the pharynx to elicit contraction/gaging behaviour Glossopharyngeal nerve Vagus nerve

Answer 275

Vestibulocochlear nerve

Answer 276

Percussion of the extensor carpi radialis Radial nerve Spinal cord segments C7-T2

Answer 277

Percussion of the muscle belly of the triceps muscle Radial nerve Spinal cord segments C7-T1

Answer 278

Percussion of the muscle belly of the biceps muscle Musculocutaneous nerve Spinal cord segments C6-C8

Answer 279

Pinch a digit or part of the interdigital web on the front foot to elicit limb withdrawal Thoracic limb nerves Spinal cord segments C6-T2

Answer 280

Percussion of the straight patellar ligament overlying the stifle Femoral nerve Spinal cord segments L4-L6

Answer 281

Percussion of the muscle belly of the cranial tibial muscle Sciatic nerve (peroneal branch) Spinal cord segments L6-S1

Answer 282

Percussion of the muscle belly of the gastrocnemius muscle Sciatic nerve (tibial branch) Spinal cord segments L7-S1

Answer 283

Pinch a digit or part of the interdigital web on the hind foot to elicit limb withdrawal Femoral nerve Sciatic nerve Spinal cord segments L4-S2

Answer 284

Stimulation of the perianal region to elicit contraction of the anus Pudenal nerve Spinal cord segments S1-S3

Answer 285

Use a pair of forceps to pinch the skin of the dorsal trunk and elicit a twitch. The spinal cord segment approximately two vertebrae cranial to the area tested.

Answer 286

The paw is placed in an abnormal position and the animal is observed to see how quickly they correct to normal. Non-specific indicator of nervous system disease

Answer 287

Non-specific indicator of nervous system disease The animal's weight is placed exclusively on one limb and the animal's body is forced in one direction.

Answer 288

Non-specific indicator of nervous system disease The front or rear of the animal is raised so that the animal's weight is placed on either both pelvic or both thoracic limbs. The animal is then forced by the examiner to move the body forward (when testing the thoracic limbs) and backward (when testing the pelvic limbs).

Answer 289

Non-specific indicator of nervous system disease A thoracic and pelvic limb on one side are held up by the examiner and the animal is forced laterally in the opposite direction, making the limbs contacting the ground move laterally to accommodate this new body position.

Answer 290

Non-specific indicator of nervous system disease The animal is suspended in the air by picking it up under the thoracic limbs and then lowering it toward the ground. As the animal is lowered, the pelvic limbs will extend prior to touching the ground, and the animal will begin to walk backwards as it touches the ground.

Answer 291

Non-specific indicator of nervous system disease The animal is held in the examiners arms suspended off the ground with its eyes covered, then moved toward the edge of a table or other edged surface until the dorsal aspect of the animal's paw touches the table. The animal should bring the limb forward to rest on the table-top.

Answer 292

Head tilt Positional nystagmus which can be horizontal, vertical or rotatory Abnormal proprioceptive responses Paired IgM and IgG PCR

Answer 293

Head tilt Horizontal or rotatory spontaneous nystagmus Facial nerve paralysis Horner’s syndrome Clinical exam Radiographs CT scan

Answer 294

Intention tremors Ataxia Hypermetria Menace deficits Head tilt/nystagmus MRI

Answer 295

Neck pain Depression Clinical signs Haematology and biochemistry CSF tap

Answer 296

Generalised seizures Agitation Lethargy/depression Intermittent blindness Clinical signs and history Exclusion of other differentials via bloods, urinalysis, CSF tap, serology, imaging etc.

Answer 297

Generalised weakness Dysphagia Regurgtation/megoesophagus Clinical signs Serum acetylcholine receptor antibody titre Edrophonium chloride challenge test Electromyelography

Answer 298

Miosis Enophthalmos Ptosis (drooping) of the upper and lower eyelids Narrowed palpebral fissure Protrusion of the third eyelid Miosis Enophthalmos Ptosis (drooping) of the upper and lower eyelids Narrowed palpebral fissure Protrusion of the third eyelid

Answer 299

Abnormal behaviour (depression, disorientation, wandering, phantom chewing) Head pressing Ataxia Clinical signs Haematology and biochemistry testing Coagulation tests Radiography (contrast venography). Ultrasonography Scintigraphy MRI of abdomen

Answer 300

Schiff-Sherrington, spinal shock, or kyphosis posture Spinal hyperaesthesia Paraplegia Limb withdrawal may be absent Clinical signs Radiography Myelography

Answer 301

Progressive pelvic limb weakness and ataxia Abnormal pelvic limb proprioceptive responses Behavioural changes (reluctance to jump or climb stairs) Clinical signs Radiography Myelography

Answer 302

Cervical pain (including intolerance of neck collars) Sensory abnormalities (face rubbing, foot chewing) Phantom scratching Tetraparesis Sensory ataxia Abnormal proprioceptive responses Clinical signs Radiography MRI

Answer 303

Progressive ataxia Tetraparesis (pelvic limbs more severely affected then thoracic limbs) Neck pain Clinical signs Radiography Myelography CT/MRI

Answer 304

Tail paralysis Tail anaesthesia Urinary incontinence (flaccid bladder with overflow vs distended bladder which is difficult to empty) Faecal incontinence Plantigrade stance Clinical signs Radiography MRI

Answer 305

Seizures Behavioural changes (depression, hyperexcitability) Hyperesthesia Tremors +/- ataxia Paresis/paralysis Clinical signs Serology CSF PCR

neuro and muskuloskeletal Flashcards

(330 cards)