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FA neurology Flashcards

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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
Name a toxin which can cause acute encephalopathy in the cow. What are potential sources which could be found on farm?
Lead toxicity Old batteries, paint, industrial pollution, roofing!
26
Outline the progressive clinical signs seen with lead toxicity in cattle.
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
What treatment plan should be instigated with lead toxicity in cattle?
* Pentobarbitone to control fits * CaEDTA chelates the lead * Theiamine mobilises intracellular lead in blood * Oral magnesium sulphate precipitates lead from the GI tract
28
Weight loss/decreased condition/milk production Bizarre behavior – licking, chewing, pica, bellowing, aggression; Circling, staggering, trembling These clinical signs may indicate what aetiological cause?
Nervious ketosis - treat by improving pre-calving nutrition & steroids/ dextrose in acute cases
29
Grass staggers
Hypomagnesemia
30
Hyperexcitibility, hyperaesthesia, muscle fasciculations, staggering gait, lateral recumbency and sudden death in newly calved suckler cow may be suspect of what aetiology?
Hypomagnesemia
31
Outline the pathogenesis of salt poisoning in cattle.
Sodium depositation blocks anaerobic glyolysis and increases intracranial pressure via osmosis
32
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.
Pseudorabies
33
Brain abscessation is usually due to which bacterial agent
Arcanobacterium pyogenes
34
Vacuolisation of brain tissue is characteristic of which prion mediated disease?
BSE
35
Outline the clinical signs presented with BSE.
3-6 years Wt loss Hyperaesthesia, fasciculations of the head and neck, teeth grinding Apprehensive, reluctant for contact (milking) Ataxia Aggression
36
What differentials should also be considered with clinical signs of BSE?
* Nervous ketosis * Focal abscessation * Listeria encephalitis * Hypomagnesaemia * CCN
37
In which husbandry situation would hypovitaminosis A be more likely?
Cereal fed housed animals
38
Night blindness
Hypovitaminosis A
39
Differentials for cerebellar hypoplasia.
* Inherited - Hereford guernsey, holstein etc * BVD
40
Aetiology for brain stem and cranial nerve dysfunction. Clinical signs.
Listerial monocytogenes - Poor quality silage or soil contamination * Febrile * Dull * Loss of cranial muscle tone - lip and cheek * Dysphagia * Ptosis * Circling, head pressing
41
Differentials for spinal cord or peripheral nerve signs.
Spinal fracture Spinal abscess Spastic paresis Tetanus Botulism Peripheral neuropathy
42
Asymmetrical spasticity and hypertonia of the extensor muscles of rear limbs.
Spastic paresis - unable to flex the hocks
43
Tetanis
Clostrifium tetani
44
Transmission of tetanus
Soil/ GI tract Wounds Directly from GI tract
45
Incubation period of tetanus
2-4 weeks Disease progresses over 4-5 days
46
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?
Tetanus
47
What treatment options are utilised with mild tetanus infection?
Antitoxins (only if early) Irrigation of infection site Keep in a quiet and dark area High dose penicillin ACP - muscle relaxation until resolution
48
Botulism
Clostridium botulinum
49
Obturator neuropathy usually occurs during what?
Calving - nerve damage due to fetal pressure through the pelvic canal Shackles and steroids
50
How can peroneal neuropathy occur?
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
Sciatic nerve damage may occur in what situation?
Prolonged recumbency - struggling to rise
52
How can CCN be treated?
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
What risk factors are associated with development of CCN?
Changes in diet Bracken ferm poisoning Corn/ sugar cane byproducts
54
Which parasite causes GID? Describe its lifecycle.
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
Why is shooting in nearby fields and leaving batteries lying around in fields a risk to farm animals?
LEAD POISONING
56
What treatment options are there for cases of lead poisoning?
EDTA given BID for three days Magesium sulphate precipitates lead in gut
57
What bacterial toxicity is associated with spoiled silage?
Listeriosis Penicillin G treatment for 7-14 days High dose dex POOR PROGNOSIS
58
What risk factors are associated with copper toxicity?
RF: Stress, housing, low forage diets, texel CS: Weakness, headpressing, jaundice, rumen stasis, death
59
What clinical signs are associated with organophosphate poisoning? What treatment options are available?
CS: Profuse salivation, colic and diarrhoea are followed by muscle tremors, stiffness progressing to paralysis T: Atropine
60
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Neurology (5 decks)

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