FA neurology Flashcards

1
Q

Differential for circling

A

Asymmetrical cortex lesion

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2
Q

Differential for falling over

A

Cerebellar lesion

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3
Q

Differential for headpressing

A

Raised intracranial pressure, encephalitis

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4
Q

Differential for tremors

A

BVD/ cerebellar dysfunction

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5
Q

Differential for spasticity

A

Increased muscle tones -> brainstem, spinal cord lesion

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6
Q

Limbs dragged or carried would indicated a neurological problem

A

Dragged

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7
Q

Increased step length or shortened step length would indicate a neurological problem

A

Shortened

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8
Q

Crossing over front legs without correction indicates a problem where?

A

Unconscious proprioception

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9
Q

Optic nerve lesions would yield what clinical signs?

A

Blindness, no menace, reduced PLR,

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10
Q

Trigeminal nerve lesions would yield what clinical signs?

A

Jaw drop, x palatal reflex

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11
Q

Facial nerve lesions would yield what clinical signs?

A

Cannot close eyelid, lower lip hangs (unilateral)

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12
Q

Vagal nerve lesions would yield what clinical signs?

A

Dysphagia, cough, disturbed rumenal contraction

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13
Q

Hypoglossal nerve lesions would yield what clinical signs?

A

Tongue hangs out

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14
Q

Name three spinal reflexes.

A

Tail reflex, anus reflex (contaction of sphincter), scrotal reflex (wrinkles), patella reflex, radio-carpal extensor reflex,

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15
Q
  • Ataxia
  • Proprioceptive deficit
  • Blindness
  • Nystagmus
  • Circling
  • Behavioural/ consciousness changes
  • Head pressing

Which area of CNS is affected?

A

Cortical disease

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16
Q
  • Imbalance
  • Wide base stance
  • Head tilt
  • dysmetria
  • Nystagmus
  • Tremors
  • Hyperaesthesia

Which area is affected?

A

Cerebellar disease

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17
Q

Differentials for acute cortical signs.

Which are notifiable

A
  • Meningo-encephalitis
  • CCN - thamine deficiency
  • Lead toxicity
  • Nevous ketosis
  • Hypomagnesemia
  • IBR/ MCR
  • Pseudorabies
  • Rabies
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18
Q

Differentials for chronic cortical signs.

Which are notifiable?

A
  • CNS abscess
  • BSE
  • Hypovitaminosis A
  • Brain tumour
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19
Q

Outline three aetiological causes of meningitis in cows.

A
  • Low colostrum in calves
  • Haematogenous spread - joint ill, mastitis, liver abscessation
  • Locally invasive infection - sinusitis
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20
Q

What clinical signs are associated with meningitis in FA?

A
  • Diarrhoea
  • Fever
  • Anorexia
  • Stiff neck
  • Hyperaesthesia
  • Spasmodic extension of limbs
  • Lack of suck reflex
  • Head pressing
  • Cranial nerve deficiency
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21
Q

What antibiotic properties would be desirable for treatment of meningitis?

A
  • Active against gram -ves
  • Inflammatory penetration - acidity
  • IV
  • Bactericidal
  • Long acting or give for 10-14 days
  • BBB penetration

Choice: FQ, TMPS, Doxycycline

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22
Q

Cerebro-cortical necrosis is caused by a deficiency in which vitamin?

A

Thiamine - vit B1

Caused either by a primary deficiency or due to bacterial thiaminases (high concentrate diet)

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23
Q

What clinical signs are indicative of CCN?

A

Early: Star gazing, blindiness, diarrhoea, hyperaesthesia, muscle tremors

Late: Opisthotonus (+++extension), headpressing, miosis, excitement, repetitive chewing, facial twitching, nystagmus, head tilt, convulsions

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24
Q

A carcass is presented with brain tissue which is markedly pale and swollen. It has patchy discolouration (lipofuscin) and fluoresces under UV light.

What aetiology may be suspected?

A

CCN

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25
Q

Name a toxin which can cause acute encephalopathy in the cow.

What are potential sources which could be found on farm?

A

Lead toxicity

Old batteries, paint, industrial pollution, roofing!

26
Q

Outline the progressive clinical signs seen with lead toxicity in cattle.

A
  1. Depression, hyperaesthesia, muscular fasciculations
  2. Ataxia, blindness, head pressing, episodic mania, convulsions, coma
  3. Sudden death or acute death within 12-24 hours
27
Q

What treatment plan should be instigated with lead toxicity in cattle?

A
  • Pentobarbitone to control fits
  • CaEDTA chelates the lead
  • Theiamine mobilises intracellular lead in blood
  • Oral magnesium sulphate precipitates lead from the GI tract
28
Q

Weight loss/decreased condition/milk production

Bizarre behavior – licking, chewing, pica, bellowing, aggression;

Circling, staggering, trembling

These clinical signs may indicate what aetiological cause?

A

Nervious ketosis - treat by improving pre-calving nutrition & steroids/ dextrose in acute cases

29
Q

Grass staggers

A

Hypomagnesemia

30
Q

Hyperexcitibility, hyperaesthesia, muscle fasciculations, staggering gait, lateral recumbency and sudden death in newly calved suckler cow may be suspect of what aetiology?

A

Hypomagnesemia

31
Q

Outline the pathogenesis of salt poisoning in cattle.

A

Sodium depositation blocks anaerobic glyolysis and increases intracranial pressure via osmosis

32
Q

This notifiable disease which is transmitted to cows via contact with pigs can lead to depression, ataxia, proprioceptive deficit, severe pruritis of the head and death within 2 days of infection.

A

Pseudorabies

33
Q

Brain abscessation is usually due to which bacterial agent

A

Arcanobacterium pyogenes

34
Q

Vacuolisation of brain tissue is characteristic of which prion mediated disease?

35
Q

Outline the clinical signs presented with BSE.

A

3-6 years

Wt loss

Hyperaesthesia, fasciculations of the head and neck, teeth grinding

Apprehensive, reluctant for contact (milking)

Ataxia

Aggression

36
Q

What differentials should also be considered with clinical signs of BSE?

A
  • Nervous ketosis
  • Focal abscessation
  • Listeria encephalitis
  • Hypomagnesaemia
  • CCN
37
Q

In which husbandry situation would hypovitaminosis A be more likely?

A

Cereal fed housed animals

38
Q

Night blindness

A

Hypovitaminosis A

39
Q

Differentials for cerebellar hypoplasia.

A
  • Inherited - Hereford guernsey, holstein etc
  • BVD
40
Q

Aetiology for brain stem and cranial nerve dysfunction.

Clinical signs.

A

Listerial monocytogenes - Poor quality silage or soil contamination

  • Febrile
  • Dull
  • Loss of cranial muscle tone - lip and cheek
  • Dysphagia
  • Ptosis
  • Circling, head pressing
41
Q

Differentials for spinal cord or peripheral nerve signs.

A

Spinal fracture

Spinal abscess

Spastic paresis

Tetanus

Botulism

Peripheral neuropathy

42
Q

Asymmetrical spasticity and hypertonia of the extensor muscles of rear limbs.

A

Spastic paresis - unable to flex the hocks

43
Q

Tetanis

A

Clostrifium tetani

44
Q

Transmission of tetanus

A

Soil/ GI tract

Wounds

Directly from GI tract

45
Q

Incubation period of tetanus

A

2-4 weeks

Disease progresses over 4-5 days

46
Q

Stiffness, reluctance to move, tremors

Prolapse third eyelid, Rumen tympany, elevation of the tail.

Rocking horse position

Recumbency, convulsions and death

These progressive signs are seen in a calf that has been recently castrated. What might you suspect?

47
Q

What treatment options are utilised with mild tetanus infection?

A

Antitoxins (only if early)

Irrigation of infection site

Keep in a quiet and dark area

High dose penicillin

ACP - muscle relaxation until resolution

48
Q

Botulism

A

Clostridium botulinum

49
Q

Obturator neuropathy usually occurs during what?

A

Calving - nerve damage due to fetal pressure through the pelvic canal

Shackles and steroids

50
Q

How can peroneal neuropathy occur?

A

Falling/ prolonged recumbency - the nerve runs over the lateral stifle joint

Affected animals show hyperextension of hock, fetlock and digital flexion. Also lost sensation over dorsal fetlock distally

51
Q

Sciatic nerve damage may occur in what situation?

A

Prolonged recumbency - struggling to rise

52
Q

How can CCN be treated?

A
  1. Thiamine course for 5 days
  2. Dexamethasone to reduce cerebral oedema

Should see initial response within 1-2 days - blindness may take longer

53
Q

What risk factors are associated with development of CCN?

A

Changes in diet

Bracken ferm poisoning

Corn/ sugar cane byproducts

54
Q

Which parasite causes GID?

Describe its lifecycle.

A

Taenia multiceps multiceps.

Sheep ingests taenia eggs from dog faeces. Eggs develop into onchospheres, these penetrate GI mucosa and travel to brain and spinal cord in blood. Onchosphere develops into metacestode which develops into a cyst, destroying brain tissue.

Cycle is complete when dog eats sheep brain/ neural tissue and ingests cyst.

55
Q

Why is shooting in nearby fields and leaving batteries lying around in fields a risk to farm animals?

A

LEAD POISONING

56
Q

What treatment options are there for cases of lead poisoning?

A

EDTA given BID for three days

Magesium sulphate precipitates lead in gut

57
Q

What bacterial toxicity is associated with spoiled silage?

A

Listeriosis

Penicillin G treatment for 7-14 days

High dose dex

POOR PROGNOSIS

58
Q

What risk factors are associated with copper toxicity?

A

RF: Stress, housing, low forage diets, texel

CS: Weakness, headpressing, jaundice, rumen stasis, death

59
Q

What clinical signs are associated with organophosphate poisoning?

What treatment options are available?

A

CS: Profuse salivation, colic and diarrhoea are followed by muscle tremors, stiffness progressing to paralysis

T: Atropine