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19- FA- Lameness > Neurological conditions of ruminants > Flashcards

Neurological conditions of ruminants Flashcards

1
Q

List 3 spinal reflexes that can be performed in ruminants

A

flexor reflex
patellar reflex
perineal reflex

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2
Q

List 6 things to assess in neuro exam in ruminants

A
  1. Assess mental status
  2. Assess cranial nerves
  3. Assess gait and posture
  4. Assess postural reactions as far as possible
  5. Assess spinal reflexes as much as possible
  6. Assess responses to pain
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3
Q

DEcsribe a primary neurological condition

A

Conditions directly affecting the neurological system (e.g. brain abscesses, spinal cord injuries)

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4
Q

Describe a secondary neuological condition

A

Conditions that present with neurological signs but are not of neurological origin (e.g. hypomagnesaemia, twin lamb disease)

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5
Q

List the steps to approaching a farm animal neuro case

A
  1. is the disease primary or secondary origin
  2. Is the brain affected
  3. Further localise the lesion
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6
Q

what do you see with forebrain lesion

A

whole body affected
abnormal mentation

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7
Q

what do you see with cerebllum lesion

A

whole body affected
normal mentation

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8
Q

Describe what is seen with brainstem lesion

A

Face/head only.
Mentation usually normal mentation (can be depressed

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9
Q

if lesion is C1-T2 what do you see

A

All 4 limbs affected
Not head/face/mentation

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10
Q

what do you see if lesion is T3-L6

A

hindlimbs affected only

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11
Q

what do you see if S1-S3 lesion

A

tail/ perineum only

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12
Q

what do we see with central vestibular lesion

A

head tilt
nystagmus
proprioceptive deficits
depression (if brainstem involvemetn)

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13
Q

what do we see with peripheral vestibular lesion

A

head tilt
Falling/leaning/circling (towards lesion)
Nystagmus (slow phase to lesion

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14
Q

How can biochemistry and haematology help when diagnosing neurological conditions

A

only useful if secondary neuro condition suspected: e.g. Mg, Ca, Na, acid-base balance, specific assays (e.g. toxins)

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15
Q

where do obtain CSF from in ruminants

A

midpoint of lumbosacral space

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16
Q

Describe nervous ketosis

A

Is a secondary neurological condition
Increased ketones and decreased glucose = negative effects on brain function

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17
Q

Describe pregnancy toxaemia in sheep

A

Energy demands of foetus(es) in late gestation > energy obtained from diet
Primarily seen in ewes carrying twins/triplets in more intensive systems during last 2 weeks of gestation

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18
Q

List the clinical signs of early stages of pregnancy toxaemia

A

separation from group
apparent blindness

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19
Q

List the clinical signs of later stage of pregnancy toxaemia

A

marked drowsiness
star-grazing and ataxia
facial twitching
ketone breath
seizures

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20
Q

List the clinical signs of the final stages of pregnancy toxaemia

A

recumbency develops after 3-4 days
develops a comatose state

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21
Q

Describe how to treat pregnancy toxaemia

A

IV glucose
oral propylene glycol
supplement with calcium and potassium
supportive IV fluids?

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22
Q

Describe how to prevent pregnancy toxaemia in sheep

A

ensure rising plane of nutrition in 2nd half of pregnancy
scan and feeding singles/ twins/ triplets separately

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23
Q

List the clinical signs of nervous ketosis

A

sudden onset neuro signs
circling and aimless wandering
apparent blindness
crossing limbs and ataxia
hyperaesthesia
mild tremors

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24
Q

Describe how to diagnose nervous ketosis

A

clinical signs with BHB> 3.0mmol/L

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25
Q

Describe how to treat nervous ketonsis

A

IV glucose
oral propylene glycol
glucocorticoids - given with glucose

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26
Q

What causes CCN

A

thiamine (vitamin B1) deficiency/ inadequacy

But can get sulphur induce CCN - rarer

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27
Q

Descrieb the presentation in of CCN

A

sudden onset blindness
aimless wandering and circling
head pressing
star-grazing

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28
Q

Describe how to diagnose CCN

A

history and clinical exam
generally by response to treatment

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29
Q

Describe how to treat CCN

A

Thiamine (vit B1) treatment - needs high conc
ensure roughage in diet

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30
Q

Describe swayback (sheep and goats)

A

Copper deficiency of ewes/does in mid-pregnancy

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31
Q

List the 3 presentations of swayback

A
  1. congenital cerebrospinal swayback
  2. progressive spinal swayback - most common
  3. cerebral oedema - only wales
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32
Q

Describe congenital cerebrospinal swayback

A

Lambs born dead or weak and unable to stand
Liveborn lambs are recumbent with spastic paralysis of all limbs
Movement is uncoordinated and erratic

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33
Q

Describe progressive spinal swayback

A

Stiff staggering gait, hindlimb ataxia (swaying gait)
Signs develop at 3-6 weeks of age
Most common form

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34
Q

Describe how to diagnose swayback

A

history and clinical signs
treatment trial

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35
Q

Describe how to treat swayback

A

Treatment involves oral supplementation of copper

36
Q

Describe how to prevent copper swayback

A

Ensure ewes/does have adequate copper supplementation in diet during mid pregnancy

Care for copper toxicity

37
Q

Describe primary vitamin A deficiency

A

associated with diets insufficient in vitamin A

38
Q

Describe secondary vitamin A deficiency

A

associated with chronic liver or enteric disease

39
Q

List the clinical signs of vitamin A deficiency

A

night blindness
skeletal muscle paralysis
Corneal keratinisation, mucoid ocular discharge, photophobia

40
Q

Describe how to treat vitamin A deficiency

A

vit A supplementation
response to treatment is rapid- blindness doe snot improve

41
Q

Describe the acute form of hypomagnesium

A

hyperaesthesia, ataxia, collapse, seizures

42
Q

Describe the signs of subactute hypomagnesium

A

wild facial expression, hypermetric gait, muscle tremors, spasmodic urination and defecation

43
Q

how can you test for hypomagnesaemia in dead animal

A

vitreous humour

44
Q

Describe how to treat hypomagnesaemia

A

sedate if seizuring
SC magnesium
IV calcium with magnesium added- DON’T GIVE WHOLE BOTTLE OF MAGNESIUM IV

45
Q

what is CCN

A

Cerebrocortical necrosis

46
Q

what is hydrocephalus

A

brain ventricle distension with fluid
hereditary in some breeds- holsteins, herefords and suffolks

47
Q

what generally causes cerebellar hypoplasia and atrophy

A

Commonly secondary to BVDv infection in utero (100-200 days gestation)
Hereditary in some breeds- hereford, shorthorn, ayrshire, aberdeen angus

48
Q

List the clinical signs of Cerebellar hypoplasia and atrophy

A

vary from recumbency and opisthotonos to generalised ataxia with hypermetric gait

49
Q

Name 2 inherited neurological conditions in ruminants

A

Hydrocephalus
Cerebellar hypoplasia and atrophy - only cattle

50
Q

List infectious diseases that can cause neurological signs(11)

A

BVDV
Borders disease
Listeria
Louping ill
Transmissible spongiform encephalopathies- scrapie and BSE
Nervous coccidiosis
Coenurus cerebralis (Gid) (parasitic)
tetanus
Botulism
Brain abscess
Neuro maedi-visna

51
Q

what causes listeriosis

A

Listeria monocytogenes
All ruminants affected but especially seen in sheep

52
Q

List the 3 most common syndromes of listeria

A

Encephalitis/meningitis
Abortion
Keratoconjunctivitis/uveitis (associated with ring/big bale feeders)

53
Q

How do animals get listeria

A

Typically associated with feeding poorly made/poorly stored silage
Bacteria is ingested and ‘accesses’ trigeminal nerves through abrasions of buccal mucosa or gum lesions

54
Q

List 3 risk factors of listeriosis

A

Poor nutritional status
Suppressed immunity (e.g. pregnancy/parturition)
Sudden weather changes (typically dry to very wet)

55
Q

Decsribe how to diagnose listeriosis

A

clinical exam and history
ante-mortem confirmation not currently possible

56
Q

List the clinical signs in initail stages of listeriosis

A

Depressed, separate selves from flock
When approached try to run away but are ataxic and fall easily
Pyrexia >40 °C in very early stages

57
Q

List the clincal signs seen in later stages of listeriosis

A

Progression to recumbency and severe depression (appear sedated) – rapid in sheep/goats
Facial paralysis and hyperalgesia – drooling and flaccid tongue common
Absent palpebral reflex may lead to exposure keratitis

58
Q

Describe how to treat listeriosis

A

early treatment needed
penicillin- 10-14 days
supportive care
NSAIDs?

59
Q

what causes Louping ill

A

Tick borne (Ixodes ricinus) flavivirus
typically seen in sheep with rough hill grazing

60
Q

List the clinical signs of louping ill

A

Muscle tremors, nibbling, ataxia, drooling, death after 1-3 days

61
Q

Describe nervous coccidiosis

A

Neurological manifestation of Eimeria infection
Typically enteric signs (haemorrhagic diarrhoea) precede neuro signs (cerebral signs)
poor prognosis

62
Q

Describe Coenurus cerebralis (Gid)

A

parasite - intermediate stage of T. multiceps ( dog tapeworm)
seen in sheep
poor prognosis

63
Q

Decsribe how to prevent Coenurus cerebralis (Gid)

A

regular worming of dogs with praziquantel
don’t allow dogs to scavenge carecases

64
Q

List the clinical signs of tetanus

A

inital muscle stiffness
inability to open mouth
tail held away from body
Progresses to recumbency and convulsions + opisthotonos
Death occurs due to respiratory arrest

65
Q

Describe how to treat tetanus

A

tetanus antitoxin
high dose penicillin
supportive care

poor prognosis

66
Q

List the clinical signs of botulism

A

cow- flaccid paralysis
sheep - initially muscle stiffness and ataxia then progress to flaccid paralysis

prognosis grave

67
Q

Generally what causes brain/spinal abscesses

A

Haematogenous spread most common

68
Q

Decsribe how to treat brain/ spinal abscesses

A

Treatment with antibiotics can be attempted but response often poor

68
Q

Describe Visna (neuro form of Maedi-visna)

A

very rare in UK
Slow onset signs relating to demyelinating encephalitis
disease is always fatal

69
Q

Name a inherited disease that affects the peripheral nervous system

A

spastic paresis

70
Q

describe spastic paresis

A

Usually 1st seen from a few weeks old up to 6 months
Very straight hocks, excess tone in gastrocnemius, ‘tin soldier’ gait, tail elevated –> usually one leg worse than other (or unilateral)

71
Q

Describe how to treat spastic paresis

A

partial tibial neurectomy

72
Q

Describe the clinical signs seen with lead toxicity

A

acute- tremors, staggering, blindness, twitching of face
subacute form- GIT dysfunction, blindness, muscle twitching

death occurs in 3-4 days

73
Q

Describe how to treat lead toxicity

A

Sedate animals with severe neurological signs
Provide IV fluid therapy
Remove animal from source of lead
Chelation therapy- calcium EDTA
add thiamine (vit B1)

74
Q

List 4 cerebral conditions in calves

A

Cerebral corticonecrosis (CCN)
Septic meningitis
Hypernatremia (salt toxicity)
Brain abscesses

75
Q

Decsribe hypernatremia in calves

A

Excessive sodium ingestion in absence of adequate water- generally due to home-made electrolyte solutions

difficult to treat- IV fluids but slowly reduce Na concentration

76
Q

Describe how to treat obturator nerve injury

A

Manage conservatively
NSAIDs (for concurrent injuries)
Deep bed
Hobbles/shackles (maintain medial positioning of hindlimbs)

77
Q

Describe sciatic nerve injury

A

Post-calving (typically dairy cows) and iatrogenic (typically calves and small ruminants)
causes dropped hock and knuckled fetlock

78
Q

describe how to treat sciatic nerve injury

A

NSAIDs
Supportive care
prognosis good

79
Q

Describe how tibial nerve injury presents

A

dropped hock with hyper-extended fetlock (cow walk on heels)

80
Q

Describe femoral nerve injury

A

calves injured during birth
Calves are unable to extend stifle or bear weight on affected limb

81
Q

Decsribe how to treat femoral nerve injury

A

Treatment is conservative –> remember to ensure adequate nutrition

82
Q

What causes brachial plexus injuries

A

calf- birth injuries
sheep- accidents or harness injuries (rams)

83
Q

Describe what is seen with brachial plexus injury

A

Inability to extend elbow, carpus or fetlock
Shoulder muscles atrophy

84
Q

Describe how to treat brachial plexus injury

A

consevative

85
Q

Describe what is seen with radial nerve injury

A

Occurs following prolonged lateral recumbency or traumatic injuries
Knuckling of carpus and fetlock but can still weightbear
Decreased sensation of antebrachium, metacarpus and foot

86
Q

Describe how to treat radial nerve injury

A

conservative management
Prognosis depends on severity of injury

19- FA- Lameness (15 decks)

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