Equine neurology, toxicology, myopathy Flashcards

Question

What is cranial nerve XI? What is its function? What is seen with dysfunction?

Answer 1

``` Accessory nerve Function: - trapezius - part of sternocephalicus Dysfunction: trapezius atrophy ```

Answer 2

``` Hypoglossus nerve Function: motor to tongue Dysfunction: - tongue deviation/atrophy - problems with prehension Evaluation: - tongue size, tone and symmetry ```

Answer 3

Orthopaedic problem Neurological: 1. Loss of spatial awareness - conscious proprioceptive deficits at rest, abnormal posture when stop/not correcting (don't manipulate limb) 2. inability to move limb

Answer 4

Subconscious proprioceptive deficits seen as irregular and unpredictable movement Lood for poor coordination, swaying, limb moving excessively during swing phase (weaving, abduction, adduction, crossing limbs, stepping on self) Exaggerated by tight circles, sudden stopping, backing, hills, raising head

Answer 5

``` Cerebellar: - no weakness - hypermetric ataxia - other signs of cerebellar disease e.g. tremor, lack of menace response Vestibular: - loss of balance - hypometric ataxia - wide based - other vestibular signs e.g. head tilt, nystagmus Spinal (most common in uk): - dysmetric ataxia - +/- weakness ```

Answer 6

Subtle: deficits barely detected at normal gait, occur during backing, stopping, turning, swaying, neck extension etc Mild: detected at normal gait, exaggerated by above manoeuvres Moderate: prominent at normal gait, tend to buckle and fall with above manoeuvres Severe: tripping and falling spontaneously at normal gait to complete paralysis

Answer 7

``` Interruption to general somatic efferent pathways (motor pathways) Extensor weakness: - sinking/buckling - weak when pulling tail Flexor weakness: - toe drag/delay in picking up - swinging movement ``` ``` Motor tract lesion (UMN): tail pull during movement Motor neuron (LMN): tail pull at rest ```

Answer 8

Epidemiology: - replicates in birds = reservoir - mosquitoes (Culex) transfer virus from birds to a number of species (horses and humans) - human and horses are terminal hosts Pathogenesis: 1. Initial virus replication at site of inoculation 2. Viraemia -> signs of uncomplicated infection (fever, depression, anorexia) 3. In some horses virus enters CNS: - diffuse or multifocal encephalomyelitis - involvement of spinal cord common (unlike EEE / WEE) Neurological signs: - muscle fasciculations over entire body (particularly head and neck) - weakness, ataxia, dysmetria - cranial nerves may be affected - mentation may be affected (indirectly due to intracranial oedema) - sudden death in some horses Treatment: - hyperimmune plasma specific to WNV available in USA - supportive care - NSAIDs - DMSO? Mannitol? to reduce oedema - corticosteroids? Prognosis: - few cases gradually resolve -> long term neurological deficits

Answer 9

``` Wild: - Ragwort - Giant hogweed - Water hemlock - Foxglove (Digitalis) - Deadly nightshade - Bracken fern - Oak/acorn - Rhododendron - Houndstongue Garden: - Sorghum - Oleander - Lantana Fungal/toxin elaboration: - Endophytes e.g. ryegrass, fescue toxicoses - Contamination e.g. mouldy corn ```

Answer 10

Ragwort - pyrollizidine alkaloid Houndstongue - pyrollizidine alkaloid Lantana - triterpene acids, lantadene A, lantadene B

Answer 11

= Senecio jacobaea Toxic at all stages of growth and when dried Biennial: - spring: Small rosettes (commonly ingested) - summer: up to 1.5m tall with distinctive yellow flowers and ragged leaves (rarely ingested except in preserved forage) Unpalatable when fresh - usually ingested in preserved state Toxicology: - hepatotoxic pyrrolizidine alkaloids or triterpene acids cause liver failure - pyrrolizidine alkaloids alkalate DNA, stop hepatocyte cell division, causing megalocytosis and liver failure

Answer 12

``` Weight loss Jaundice Dullness and depression Muscle tremors and weakness Frequent yawning Inappetance and difficulty swallowing Respiratory noise/laryngeal paralysis Compulsive walking/incoordination/head pressing Photosensitisation Colic Encephalopathic signs: classic signs are quiet, dull, head press ```

Answer 13

``` Examine hay for ragwort leaves Clinical signs Test blod: - non specific signs of liver damage - specific alkaloid detection (definitive) PM ```

Answer 14

Spraying herbicide (blanket or spot): - cannot use land for grazing for weeks to months - leaves bare patches where ragwort can easily re-establish Uprooting and burning (manual or mechanical): - labour intensive - wear gloves to prevent skin irritation Cutting: - less effective as roots remain and can re-establish - only done when field not in use to prevent flowering, seeding and spreading - ensure cuttings removed ?Grazing land with sheep which may be resistant to toxicity before turning horses out: - controversial

Answer 15

Myotoxins: - sycamore: hypoglycin A Enterotoxins: - oak/acorns: tannins

Answer 16

Toxicology: - hypoglycin A? - acquired multiple Acyl-CoA dehydrogenase deficiency - causes atypical myopathy Clinical signs: - weakness, fasciculations - recumbency - red urine (myoglobinuria) - marked elevations in serum muscle enzymes (CK, AST) PM: widespread myonecrosis (skeletal and cardiac) Spring and autumn - sudden weather change? - horses at pasture

Answer 17

Toxicology: - oak leaves and acorns contain tannins - highest tannin content of sap in spring Acorns Sept-Oct Pathology: - gastroenteritis - haemorrhages in abdominal cavity over GIT and beneath endo and epicardium - subcutaneous oedema over pelvic limbs and along ventral body wall Clinical signs: - parachute/acute/sudden death - colic - tenesmus - haemorrhagic diarrhoea But poisoning rare in horses - some unaffected Diagnosis: - acorn husks/shells in faeces - urinary phenolic content to differentiate from other colics Treatment: - as medical colic (IVFT, analgesia, oral laxatives, diuresis, acid/base balance, serum calcium levels) Control: - fence off oak trees in autumn when acorns are abundant - pick up acorns from pasture

Answer 18

Oleander Rhododendron Fox glove Contain cardenolides or cardiac glycosides which interfere with electrical conductivity of the heart -> arrhythmias/sudden death

Answer 19

``` All parts very toxin Cardiac glycosides Signs: - Diarrhoea/melaena - Disruptive cardiac arrythmias - Death often within minutes Necropsy: - Nil findings - Plant? ```

Answer 20

St John's Wort | Giant Hogweed

Answer 21

Hedgerows and gardens Slow expansion, perennial Primary photosensitisation Hypericin - therapeutic agent?

Answer 22

No specific signs | Oral irritation/ulcers

Answer 23

``` Deadly nightshade Yew Hemlock Sorghum Flatweed Singletary Pea Ryegrass Mouldy corn ```

Answer 24

'Milo'/'Sudan' grass Chronic cyanide poisoning? - cyanogenic glycosides Bladder paralysis

Answer 25

``` Common wild plant in stable yards and poorly maintained pastures (dandelions) Widespread Ingested in low amounts normally Stringhalt (but not really in UK) Persistent neurologic deficits ```

Answer 26

``` Atropine related signs (parasympatholytic): - mydriasis - shivering/muscle spasms - tachycardia - dry mucous membranes - colic (ileus/obstipation) Treatment: - neostigmine? (but may be worse than the poisoning!) - activated charcoal - fluids etc ```

Answer 27

Overstated effects - heavy/persistent ingestion? Not very common Contains thiaminase -> vitamin B1 (thiamine) deficiency Carcinogenic? Clinical signs (bracken staggers): - anorexia - cardiac dysrhythmia - crouched stance, arched neck, feet wide apart - incoordination - convulsions - clonic spasms and opisthotonus then death Diagnosis: - low blood thiamine (not pathognomonic) - elevated pyruvate - bracken on pasture or in hay - known ingestion Treatment: - thiamine every 12h IM or slow IV for up to 7 days - avoid IV if possible (anaphylactic reaction) Prognosis: - therapy usually highly effective if early

Answer 28

Thiaminase CNS signs predominate Treatment: thiamine

Answer 29

Flowers/leaves similar to cow parsley Distinct irregular purple blotches on stem Hemlock flowers and fruits contain most toxic alkaloid Water hemlock roots and leaves Especially poisonous in dry, hot summers Toxicology: - hemlock: alkaloid coiine (nicotine like action) - water hemlock: cicutoxin and cicutol - first stimulating and then depressing autonomic ganglia - curare-like effect - paralysing skeletal muscle motor nerve endings Clinical signs: - agitation, nervousness - twitching - seizures - excess salivation - dilated pupils - skeletal muscle weakness - cardiac abnormalities - difficulty breathing - death from respiratory paralysis May develop following ingestion of only small quantities Treatment: activated charcoal and/or lavage

Answer 30

``` Evergreen - hedges and gardens Toxicology: - alkaloid taxines - all parts of tree poisonous Pathology: - distended stomach - inflammation if death occurs after several hours - liver, spleen and lungs engorged with dark blood Clinical signs: - trembling - ataxia - bradycardia - hypothermia - weak - dyspnoea - rapid death ```

Answer 31

Mouldy corn toxicity Rye grass staggers Fescue toxicosis

Answer 32

``` Mycotoxin = fumonisin B1 Infected corn/commercial foods Can be fatal to horses Pathology: liquefactive necrosis of brain Signs 2-4 weeks after ingestion: - anorexia - blindness - ataxia - head pressing - circling - hyperexcitability - seizures - recumbency/death ```

Answer 33

Associated with endophyte infected plant - produces toxin Lolitrem B Signs: - trembling, unsteadiness and poor muscle coordination - erratic and anxious behaviour - milder cases may display some trembling of head, neck, shoulders - signs worsen if exposure increases Treatment: - get better quickly if take off pasture

Answer 34

``` Perennial tufted grass, related to ryegrass 10cm - 2m tall Toxicology: - toxicity due to endophyte Acremonium coenophialum - most significant alkaloid substance produced is the ergo peptide ergovaline Affects pregnant mares and unborn foals Clinical signs: poor reproductive function: - prolonged gestation - abortion - premature separation of chorion - dystocia - thickened and retained placenta - lack of milk let down - reduced pregnancy rates - immature foals born - poor foal immunity ```

Answer 35

``` Aspergillus 5 major toxins: - B1, B2, G1, G2, M1 - B1 most important Mostly stored feeds Poorly recognised clinically Clinical signs: 1. Sudden death: - no premonitory signs 2. Neurotoxic syndrome: - incoordination, aimless walking - lethargy -> mania, convulsions - delirium - sweating - death 3. Hepatotoxic syndrome: - head swelling, jaundice - depression, signs of liver failure - coma -> death No effective treatment Management: - remove contaminated feed - supportive therapy - high dose vitamin B - vitamin B1? - sedation if required - mannitol/DMSO - laxatives/activated charcoal? ```

Answer 36

Natural water courses - looks like algae but isn't Cyanobacteria Highly toxic

Answer 37

Ca/Po4 imbalance | Secondary nutritional hyperparathyroidism

Answer 38

``` Peripheral nerve dysfunction: - motor nerves worse -> weakness - minimal sensory loss Depression Weight loss Laryngeal/pharyngeal paralysis -> dysphagia, aspiration pneumonia Facial paralysis Anal/bladder paralysis Colic Diarrhoea Hepatic failure Blindness Seizures Coma -> death Lead crosses placenta: - premature/weak/still born foals ``` (can look like rabies or botulism)

Answer 39

``` Remove source Chelation therapy Ca disodium EDTA - binds out bone lead Fluids Nursing support High dietary calcium ```

Answer 40

``` Supplement overdose - care with cattle licks as horses need less selenium per day than ruminants Seleniferous plants Signs: - hair loss (mane, tail) - laminitis ```

Answer 41

Chicken feed often contains monensin (coccidiostat for poultry but highly toxic to horses) Acute - sudden death, diarrhoea Chronic - cardiac failure DCM

Answer 42

Foal dies suddenly Poor body condition Muscle biopsy - PAS staining unusually absent

Answer 43

Pathogenesis: - accumulation of glycogen = storage disease on exercise Poor performance Becomes stiff and reluctant to move after short period of exercise Raised muscle enzymes Semimembranosus muscle biopsy – abnormal accumulation of PAS positive material and evidence of cell degeneration/regeneration, amylase resistant inclusion bodies Treatment: low carb, high fibre diet (oil to replace carbs for energy)

Answer 44

Stress Intermittent muscle cramping and stiffness Poor performance Mild elevation of CK and aspartate aminotransferase Muscle biopsy – cellular degeneration/regeneration but normal PAS staining

Answer 45

``` Well muscled (Sire impressive) Periods of sweating and muscle fasciculations over shoulder, flank and neck Lasts 30 minutes and is weak Seems to happen when excited or stressed ```

Answer 46

Acute: pain relief, fluids, ACP Chronic: warm up, avoid stress and high energy feeds

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Equine neurology, toxicology, myopathy Flashcards

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