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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
Describe how to treat nervous ketonsis
IV glucose oral propylene glycol glucocorticoids - given with glucose
26
What causes CCN
thiamine (vitamin B1) deficiency/ inadequacy But can get sulphur induce CCN - rarer
27
Descrieb the presentation in of CCN
sudden onset blindness aimless wandering and circling head pressing star-grazing
28
Describe how to diagnose CCN
history and clinical exam generally by response to treatment
29
Describe how to treat CCN
Thiamine (vit B1) treatment - needs high conc ensure roughage in diet
30
Describe swayback (sheep and goats)
Copper deficiency of ewes/does in mid-pregnancy
31
List the 3 presentations of swayback
1. congenital cerebrospinal swayback 2. progressive spinal swayback - most common 3. cerebral oedema - only wales
32
Describe congenital cerebrospinal swayback
Lambs born dead or weak and unable to stand Liveborn lambs are recumbent with spastic paralysis of all limbs Movement is uncoordinated and erratic
33
Describe progressive spinal swayback
Stiff staggering gait, hindlimb ataxia (swaying gait) Signs develop at 3-6 weeks of age Most common form
34
Describe how to diagnose swayback
history and clinical signs treatment trial
35
Describe how to treat swayback
Treatment involves oral supplementation of copper
36
Describe how to prevent copper swayback
Ensure ewes/does have adequate copper supplementation in diet during mid pregnancy Care for copper toxicity
37
Describe primary vitamin A deficiency
associated with diets insufficient in vitamin A
38
Describe secondary vitamin A deficiency
associated with chronic liver or enteric disease
39
List the clinical signs of vitamin A deficiency
night blindness skeletal muscle paralysis Corneal keratinisation, mucoid ocular discharge, photophobia
40
Describe how to treat vitamin A deficiency
vit A supplementation response to treatment is rapid- blindness doe snot improve
41
Describe the acute form of hypomagnesium
hyperaesthesia, ataxia, collapse, seizures
42
Describe the signs of subactute hypomagnesium
wild facial expression, hypermetric gait, muscle tremors, spasmodic urination and defecation
43
how can you test for hypomagnesaemia in dead animal
vitreous humour
44
Describe how to treat hypomagnesaemia
sedate if seizuring SC magnesium IV calcium with magnesium added- DON'T GIVE WHOLE BOTTLE OF MAGNESIUM IV
45
what is CCN
Cerebrocortical necrosis
46
what is hydrocephalus
brain ventricle distension with fluid hereditary in some breeds- holsteins, herefords and suffolks
47
what generally causes cerebellar hypoplasia and atrophy
Commonly secondary to BVDv infection in utero (100-200 days gestation) Hereditary in some breeds- hereford, shorthorn, ayrshire, aberdeen angus
48
List the clinical signs of Cerebellar hypoplasia and atrophy
vary from recumbency and opisthotonos to generalised ataxia with hypermetric gait
49
Name 2 inherited neurological conditions in ruminants
Hydrocephalus Cerebellar hypoplasia and atrophy - only cattle
50
List infectious diseases that can cause neurological signs(11)
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
what causes listeriosis
Listeria monocytogenes All ruminants affected but especially seen in sheep
52
List the 3 most common syndromes of listeria
Encephalitis/meningitis Abortion Keratoconjunctivitis/uveitis (associated with ring/big bale feeders)
53
How do animals get listeria
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
List 3 risk factors of listeriosis
Poor nutritional status Suppressed immunity (e.g. pregnancy/parturition) Sudden weather changes (typically dry to very wet)
55
Decsribe how to diagnose listeriosis
clinical exam and history ante-mortem confirmation not currently possible
56
List the clinical signs in initail stages of listeriosis
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
List the clincal signs seen in later stages of listeriosis
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
Describe how to treat listeriosis
early treatment needed penicillin- 10-14 days supportive care NSAIDs?
59
what causes Louping ill
Tick borne (Ixodes ricinus) flavivirus typically seen in sheep with rough hill grazing
60
List the clinical signs of louping ill
Muscle tremors, nibbling, ataxia, drooling, death after 1-3 days
61
Describe nervous coccidiosis
Neurological manifestation of Eimeria infection Typically enteric signs (haemorrhagic diarrhoea) precede neuro signs (cerebral signs) poor prognosis
62
Describe Coenurus cerebralis (Gid)
parasite - intermediate stage of T. multiceps ( dog tapeworm) seen in sheep poor prognosis
63
Decsribe how to prevent Coenurus cerebralis (Gid)
regular worming of dogs with praziquantel don't allow dogs to scavenge carecases
64
List the clinical signs of tetanus
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
Describe how to treat tetanus
tetanus antitoxin high dose penicillin supportive care poor prognosis
66
List the clinical signs of botulism
cow- flaccid paralysis sheep - initially muscle stiffness and ataxia then progress to flaccid paralysis prognosis grave
67
Generally what causes brain/spinal abscesses
Haematogenous spread most common
68
Decsribe how to treat brain/ spinal abscesses
Treatment with antibiotics can be attempted but response often poor
68
Describe Visna (neuro form of Maedi-visna)
very rare in UK Slow onset signs relating to demyelinating encephalitis disease is always fatal
69
Name a inherited disease that affects the peripheral nervous system
spastic paresis
70
describe spastic paresis
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
Describe how to treat spastic paresis
partial tibial neurectomy
72
Describe the clinical signs seen with lead toxicity
acute- tremors, staggering, blindness, twitching of face subacute form- GIT dysfunction, blindness, muscle twitching death occurs in 3-4 days
73
Describe how to treat lead toxicity
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
List 4 cerebral conditions in calves
Cerebral corticonecrosis (CCN) Septic meningitis Hypernatremia (salt toxicity) Brain abscesses
75
Decsribe hypernatremia in calves
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
Describe how to treat obturator nerve injury
Manage conservatively NSAIDs (for concurrent injuries) Deep bed Hobbles/shackles (maintain medial positioning of hindlimbs)
77
Describe sciatic nerve injury
Post-calving (typically dairy cows) and iatrogenic (typically calves and small ruminants) causes dropped hock and knuckled fetlock
78
describe how to treat sciatic nerve injury
NSAIDs Supportive care prognosis good
79
Describe how tibial nerve injury presents
dropped hock with hyper-extended fetlock (cow walk on heels)
80
Describe femoral nerve injury
calves injured during birth Calves are unable to extend stifle or bear weight on affected limb
81
Decsribe how to treat femoral nerve injury
Treatment is conservative --> remember to ensure adequate nutrition
82
What causes brachial plexus injuries
calf- birth injuries sheep- accidents or harness injuries (rams)
83
Describe what is seen with brachial plexus injury
Inability to extend elbow, carpus or fetlock Shoulder muscles atrophy
84
Describe how to treat brachial plexus injury
consevative
85
Describe what is seen with radial nerve injury
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
Describe how to treat radial nerve injury
conservative management Prognosis depends on severity of injury

19- FA- Lameness (15 decks)

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