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Farm Animal Final Year > Ovine Neurology > Flashcards

Ovine Neurology Flashcards

1
Q

What are the 6 classifications of neurological disease by cause. Give an example for each.

A
  • DEVELOPMENTAL eg Swayback, DandyWalker malformation - hydrocephalus, ’Daft Lamb’ cerebellar hypoplasia
  • INFECTIOUS

–Bacterial eg meningitis, abscesses

–Viral eg. Border disease

–Parasitic eg. Gid

  • METABOLIC/NUTRITIONAL – eg CCN
  • TOXIC eg. Lead poisoning
  • INJURY eg. cervical subluxation (rams)
  • PERIPHERAL NERVE eg. Radial (kangaroo gait) or sciatic damage
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2
Q

Name the 2 most common neuro diseases in sheeps

A

Pregnancy Toxaemia

Hypocalcaemia

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3
Q

What type of disease is scrapie?

A

Transmissable encephalopathy

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4
Q

What is the main source of infection of scrapie?

A

Placenta in lambing

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5
Q

What is scrapie caused by?

A

An accumulation of an altered host protein – protease-resistant prion

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6
Q

Name Clinical signs of scrapie?

A
  • Paresis and ataxia, especially hindlimbs
  • Quadriplegia and recumbency
  • Separation from the rest of the flock
  • Depression, anxiety or hyperexcitability
  • Head tremor & low head carriage
  • Pruritus (“nibble” response)
  • Weight loss, bruxism, cud-dropping
  • No menace response
  • Usually sheep above 2 years old
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7
Q

How do we diagnose scrapie?

A

Detection of the PrPsc in brain on post-mortem

Isolation of PrPsc in biopsy of lymphoid tissue (tonsillar tissue or rectal mucosa)

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8
Q

Why is scrapie rare?

A

Testing and eradication programme! So has gone from very common to rare. Slecting and extinguishing VRQ and HRQ genotype

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9
Q

Which scrapie is still seen?

A

Atypical

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10
Q

What are clinical signs of maedi visna?

Visna virus (also known as visna-maedi virus, maedi-visna virus and ovine lentivirus) from the genus Lentivirus and subfamily Orthoretrovirinae, is a “prototype”retrovirus that causes encephalitis and chronic pneumonitis in sheep.

A
  • The sheep may be ataxic, paretic and drag a leg. Hind legs are often affected more than the front but all 4 can be involved.
  • They may also have depression, head tilt and fine tremor of the lips. Occasionally they may also appear to be blind.
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11
Q

Name 2 differentital for maedi visna (3) How do you distinguish?

A

Listeriosis, aberrant larval migration, spinal abscess/mass and scrapie, and so a diagnostic PM should be performed

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12
Q

What is the neuro component of maedi visna accompanied by?

A

Cachexia (no appetite) and chronic wasting.

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13
Q

What are the 2 forms of swayback?

A
  • Congenital
  • Delayed
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14
Q

What is congenital swayback caused by?

A

•Copper deficiency little extra feed in mid-late pregnant hill ewes (susceptible breeds and on deficient pasture)

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15
Q

What is seen in sheep with swayback?

A
  • Lots of stillbirth, small weak lambs with fine head tremors.
  • Lambs bright but weak on hind legs ->stumbling/swaying gait. Fine boned & dull coats.
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16
Q

How can we diagnose congenital swayback?

A

Diagnosis - do histopath on brain & spinal cord.

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17
Q

When is delayed swyback seen and what is the cause?

A

Normal at birth but progressive weakness of pelvic limbs at 2-4 month old

Demyelination & reduced myelin synthesis in spinal cord. So only becomes apparent when the lamb grows

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18
Q

How can we prevent delayed swayback?

A

Inject chelated copper or CuO needle or give glass bolus in mid pregnancy BUT NOT to Texel or other continental breeds and primitive native breeds as highly susceptible to copper toxicity

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19
Q

What is acute coenurosis and what is seen?

A

Seen 10 days after turning onto land HEAVILY contaminated with dog faeces. Pyrexia, listlessness & head aversion. Death 4-5 days after neurological signs.

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20
Q

What is chronic coenurosis and what is seen?

A

Much more common in growing sheep 6-18 mths. V rare >3yrs old.

Insidious onset with slowly progressive focal lesion.

2-6mths from Larval hatching to migration & onset of neurological dysfunction

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21
Q

What is the larval stage of Taenia multiceps?

A

Coenuris cerebralis

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22
Q

How does Coenuris cerebralis complete its cycle?

A

LC completes when the definitive host (dog) ingests sheep brain (see it more in highlands as don’t have complete clearance of fallen stock)

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23
Q

Name Clinical signs of coenurosis if it is in the cerebral cortex?

A
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24
Q

Name clinical signs of coenurosis in the vestibular?

A

Head tilt towards affected side

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25
Q

Name clinical signs of coenurosis in the cerebellar

A

Dysmetria, ataxia, wide-based stance.

Bilateral postural deficits

Rapid deterioration

26
Q

How can we prevent Coenurosis?

A

Worm dogs every 6 weeks and remove all carcasses

27
Q

How can we treat coenurosis?

A

Surgery

Give cortiosteroids to reduce surgical brain oedema

28
Q

How would you remove coenurosis surgically?

A) Cerebrum?

B) Cerebellum?

A

Cerebrum – trephine 1-2cm lateral to midline & rostral to coronal suture line.

Cerebellum – trephine midline between nuchal line & suture between occipital & parietal bones.

  • Remove 1cm core, incise dura mater & tissue fills hole.
  • Drain & remove cyst wall & protoscolices with forceps.
  • Give post-op analgesia & A/bs.
29
Q

What is the best option if a sheep had coenurosis?

A

Euthanasia

30
Q

What is the cause of louping ill?

A

The cause is a a tick-transmitted Arbovirus belonging to the tick-borne encephalitis (TBE) complex

31
Q

What are the clinical signs of louping ill?

A

Affects the brain and causes varying signs of in-coordination, paralysis, convulsions and death.

32
Q

What are the host species of louping ill?

A

The disease is primarily associated with sheep, but Humans, cattle, goats , pigs, horses, farmed red deer, llamas, dogs and (wild)red grouse can all be affected.

33
Q

How can we diagnose louping ill?

A

serology for antibody to the virus

34
Q

Louping ill:

A) What is the mortatlity in naive animals?

B) How do we treat?

C) How do we prevent?

D) How can we reduce risk?

A

A) 100%

B) None

C) Vaccine

D) Dip in organophosphate

35
Q

What is seen in Plant poisoning?

A

Affected sheep are permanently blind and adopt a characteristic alert attitude.

The pupils respond poorly to light, and ophthalmoscopic examination of sheep with advanced disease reveals narrowing of arteries and veins and a pale tapetum nigrum with fine cracks and spots of gray.

36
Q

What is seen diagnostically with poisoning?

A

Histologically, the lesion is seen as severe atrophy of the retinal rods, cones, and outer nuclear layer that is most pronounced in the tapetal portion of the retina. Affected animals often have many of the other bracken fern–associated lesions such as bone marrow suppression, hemorrhage, immunosuppression, and urinary tract neoplasia.

37
Q

What is seen clinically as tapetal hyperreflectivity?

A

Plant poisoning esp Bracken in hill flocks causes ‘Bright Blindness’ ptaquiloside toxicity.

38
Q

How can oxalate poisoning come about?

A

All beet crops concentrate oxalate in their leaves so grazing the top as well as the bulb can be dangerous.

39
Q

What are the symptoms of oxalate poisoning the same as?

A

Hypocalcaemia

40
Q

How can we prevent oxalate poisoning?

A

Prevention by limiting the % of the diet that is leaf by strip grazing or lifting the crop to feed just the bulb.

41
Q

Name signs of cerebellar syndrome

A

Ataxia & hypermetria – high-stepping

Head tremor & high head carriage

Jerky movement & intention tremors

Usually bilateral proprioceptive defects or ipsilateral & circle towards.

42
Q

Name 2 things causing generalised cerebellar syndrome (3)

A

Daft lamb (hypoplasia)

Border disease

Scrapie

43
Q

Name a localised cause of cerebellar syndrome (2)

A
  • Gid
  • Abscess
44
Q

Name clinical signs of cerebral syndrome

A

Mental state/behaviour change - (compulsive walking, circling, jaw movements)

Stupor, depression, hyperaesthesia, opistotonus, head-pressing, head deviation

Contralateral proprioceptive defects

Contralateral blindness (but normal pupillary light reflex)

Circling towards superficial lesions & away from deeper

45
Q

Name 2 causes of generalised cerebral syndrome (4)

A
  • CCN/PEM
  • Bacterial meningitis
  • Pregnancy toxaemia
  • Scrapie
46
Q

Name a localised cause of cerebral syndrome (2)

A
  • Gid
  • Abscess
47
Q

Name clinical signs of vestibular syndrome

A

Head tilt with falling, rolling or circling

Nystagmus

48
Q

Name a cause of vestiblar syndrome

A

Middle or inner ear infection

49
Q

Name clinical signs of pontomedullary disease

A

Depression & cranial nerve deficits

Ipsilateral hemiparesis, circling (VIII), facial paralysis (VII), cheek muscle paralysis & decreased sensation (V)

Abnormal respiratory patterns (resp centre in medulla)

50
Q

Name a disease which causes pontomedullary lesions

A

Listeriosis

51
Q

Name clinical signs of midbrain lesions

A

Depression, coma, limb rigidity, opistotonus

Normal vision with strabismus & mydriatic pupil

52
Q

Name a cause of midbrain lesions (2)

A

Hepatic encephalopathy, cranial trauma (not common in sheep)

53
Q

Name clinical signs of hypothalamic lesions

A

Altered behaviour/mental state – hyperaesthesia, aggression, disorientation

Impaired vision, dilated, poorly responsive pupils

Appetite & thermoregulation affected

54
Q

Name a condition causes hypothalamic lesions (2)

A

Pituitary gland tumours & abscesses (not common in sheep)

55
Q

Name 6 tests to examine the cranial nerves (7)

A

Menace response

Pupillary reflex

Palpebral reflex

Corneal reflex

Vestibulo- ocular reflex

Hand clap reflex

Nb gag reflex difficult in sheep

56
Q

A) Why do we examine facial symmetry, ear position and ocular apertue?

B) What does damage cause?

A

A) VII Facial nerve

B) Damage causes drooped ear, eyelid & lips& food packing in cheek

57
Q

A) Why do we examine eye position?

B) What does damage cause?

A

III Oculomotor

(lateral strabismus)

IV Troclear

(dorso-medial strabismus)

VI Abducens

(medial strabismus)

58
Q

A) Why do we examine tongue tone and position?

B) What does damage cause?

A

A) XII Hypoglossal

B) Damage causes tongue paralysis

59
Q

A) Why do we examine the ability to swallow?

B) What does damage cause?

A

A) IX Glossopharyngeal, X Vagus & XI Accessory

B) Dysphagia

60
Q

A) Why do we examine facial sensation and jaw tone?

B) What does damage cause?

A

A) V Trigeminal nerve

B) Damage causes decreased facial sensation, dropped jaw, saliva pooling & food packing in cheek

61
Q

What nerves are tested:

A) Menace response

B) Pupillary reflex

C) Palpebral reflex

A

IA) II (sees) & VII (closes eyelids). Requires visual cortex to process threat

B) II (sees) and III (constricts pupils)

C) V (senses touch) and VII (closes eyelids)

62
Q

What nerves are tested:

A) Corneal reflex

B) Vestibulo- ocular reflex

C) Hand clap reflex

A

A) V (senses touch)

VI (retracts eyeball)

VII (closes eyelids)

B) VIII (senses balance)

III, VI (moves eyes)

C) VIII (hears clap)

VII (moves pinna)

Farm Animal Final Year (131 decks)

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