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Year 4 Livestock and One Health > Neurology: Cattle Neurology > Flashcards

Neurology: Cattle Neurology Flashcards

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1
Q

What should be inspected of surroundings for neurological disease?

A
  • Lead
  • Ration- proprotion of conc, silage quality
  • Poisonous plants
  • Cadavers
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2
Q

What are the following observations signs of?
1. Circling
2. Falling over
3. Head-pressing

A
  1. Asymmetrical cortex lesion
  2. Cerebellum lesion
  3. ICP/encephalitis
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3
Q

What can be observed about stance and locomotion at a distance?

A

Stance
* Tremors- rapid contractions
* Spasms- sudden, contractoins of muscles- tetanus
* Spasticity- increased muscle tone- brain stem, spinal cord lesion

Locomotion
* Decreased coordination
* Weakness- paresis or paralysis

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4
Q

What can be inspected on hands on clinical exam of skull and vertebrae?

A
  • Inspection- symmetry, muscle atrophy
  • Palpation- pain, crepitus
  • Percussion- finger (head), fist (neck)
  • Passive movement- bend head/neck in all directions

Reflexes- cerebellum, brain stem, spinal reflex

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5
Q

What is the normal function of the brain stem/cranial nerves
Cerebellum
Spinal cord/peripheral nerves

A

Brain stem/CN
* cranial nerve functions

Cerebellum
* unconscious control of proprioceptive functions- coordination and smoothing of movements

Spinal cord/peripheral nerve
* Limb strength and movement

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6
Q

What are the 6 steps to neurological exam?

A
  1. Mental status
  2. Cranial nerves
  3. Gait and posture
  4. Postural reactions
  5. Spinal reflexes
  6. Response to pain
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7
Q

What does mental status tell us?

A
  • Helps differentiate between intracranial and extracranial lesions
  • Brainstem- arousal, appear sedated but aware of surrondings
  • Thalamocortex- cognititive function, fail to react to environmental stimuli, seperates from herd- head pressing, tilt, circling, blindness

Check for menace response, nasal septum stim (absent if cortical involvement)

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8
Q

What does nasal septum stimulation test?

A

Tests CN V and thalamocortex

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9
Q

What are the 12 cranial nerves?

A

Olfactory
Optic
Oculomotor
Trochlear
Trigeminal
Abducent
Facial
Vestibulo-cochlear
Glossopharyngeal
Vagal
Accessory
Hypoglossal

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10
Q

What does the menace response test?

What does the PLR test?

A

Menace- CN II, VII, cortex, cerebellum

PLR- CN II and III

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11
Q

What is responsible for eye position and movement?

What is responsible for physiological nystagmus?

What is responsible for palpebral reflexes and facial symmetry?

A

Eye position and movement
* CN III, IV, VI

Physiological nystagmus
* CN III, IV, VI, VII

Palpebral reflex
* CN V, VII

Facial symmetry
* CN VII

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12
Q

What would caus head tilt and pathological nystagmus?

A

CN VII

  • Assess animal facing you- eye should be horizontal
  • Check for pathological nystamus- fast phase away from side of lesion
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13
Q

What CN are responsible for food prehension and chewing?

What CN dyfunctions can cause dysphagia and laryngeal problems?

A

Food prehension and chewing
* XII and V
* Unilateral XII- tongue falls from side of mouth toward lesion

Dysphagia and laryngeal- CN IX and X

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14
Q

What are the three types of ataxia?

A
  • Vestibular
  • Cerebellar
  • Proprioceptive
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15
Q

How can vestibular ataxia be identified?

A
  • Always head tilt
  • Hypermetra
  • Hypertonia
  • Unilateral cerbellar- animal will lean towards head tilted side
  • Bilateral vestibular dysfunction is more subtle
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16
Q

How can cerebeller ataxia be identified?

When is proprioceptive ataxua usually observed?

A

No proprioceptive defecits or weakness as pathways to and from the limbs to cerebrum are ok

Proprioceptive
Spinal cord disease
Look at foot placements

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17
Q

What spinal reflexes can be used?

A

Extensor reflex of front limb
* radial nerve dysfunction- dropped elbow

Patellar reflex
* tap patellar tendon and observe extension of stifle

Flexor
* front limbs axillary, median, ulnar,

Musce tone- passively flex and look for symmetry

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18
Q

How is the perineal reflex tested and what does it test?

A

Gently touch under the tail- downward contraction of the tail and anal sphincter contraction

Pudenal and caudal nerves

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19
Q

How can CSF fluid be taken and analysed?

A
  • Lumbosacral space
  • 4 inch spinal needle
  • Protein and cytology
  • Clear and colourless
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20
Q

What are common clinical signs localisable to cerebrum?

A
  • Opisthotonos- stargazing
  • Apparent blindness- intact PLR
  • Abnormal mentation
  • Change in behaviour
  • Aimless wandering
  • Seizures
  • Abnormal vocalisation
  • Ataxia without weakness
  • Absent menace
  • Hypermetria
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21
Q

What are clinical signs localisable to the vestibular system?

A

Peripheral and Central:
* Head tilt to lesion side
* Falling/circling/leaning

Just central:
* Nystagmus
* Proprioception defecits on side of lesion
* Depresion/Anorexia

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22
Q

How are the following CN assessed?
1. II
2. V
3. VI
4. VII
5. VIII
6. IX and X
7. XII

A
  1. Optic- blindness and abscence of PLR, dilated pupils
  2. Trigeminal- loss of sensation to head and cornea
  3. Abducens- ventromedial strabismus, inability to retract globe
  4. Facial- motor muscles to face- droopy ears/eyelids/lips, unable to blink
  5. Vestibulo-cochlear- head tilt, circling, leaning/falling
  6. Glossopharyngeal and vagal- can’t swallow
  7. Hypoglossal- cannot retract tongue
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23
Q

What clinical signs show reticular activation system, thalamus lesions?

A
  • Depression, altered mentation
  • Difficulty regulating body temp
  • Depressed respiration
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24
Q

How can clinical signs be localised to spinal cord:
1. C1-C5
2. C6-T2
3. T3-L3
4. L4-L6
5. S1-S3

A
  1. Altered head and neck movements- no CN defectits- FL and HL reflexes exaggerated
  2. Depressed or absent reflexes with reduced muscle tone in the FLs and exaggerated HL reflexes with normal muscle tone in the HLs
  3. Reflexes in FL normal- HL exaggerated, proprioceptigve defectits in the HLs with ataxia
  4. Absence of HL reflexes and decreased muscle tone
  5. Decreased anal tone, loss of sensation to perineal region
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25
Q

What are the signs of cerebrum diseases?

A
  • Circling
  • Blindness
  • Mania
  • Aggressive behaviour
  • Head pressing
26
Q

What could cause acute cerebral cortex signs?

A

Acute:
* CCN
* Lead poisoning- contact APHA
* Nervous ketosis
* Hypocalcaemia
* Hypomag
* Salt poisoning
* IBR
* Pseudorabies- contact APHA
* Rabies- contact APHA

27
Q

What could cause chronic cortical signs?

A
  • Brain abscess
  • BSE
  • Hypovitaminosis A
  • Brain tumour
28
Q

What cattle most commonly are affected by meningitis?

A

Calves 1 week of age without enough colosturm

May present like staggers
* lack of suck reflex
* Head pressing

29
Q

How is meninigitis diagnosed and treated?

A

Diagnosis
* CSF- increase in protein and WBC

Treatment
* Poor
* Consider euthanasia
* Can give IV ABs

30
Q

What ABs penetrate the brain?

A
  • B-lactams- do not diffuse well into the CSF but have high safety margin so can achieve therapeutic conc
  • Potentiated sulphonamides
  • Aminoglysides- high conc
  • Fluoroquionolones- protected
  • Pot Sulphonamides
31
Q

What normally causes a brain abscess?

What are the initial signs and later signs?

A

Truperella pyogenes often extension of sinus infection

Initial: vision loss/mydriasis in contralateral eye, compulsive walking, head pressing, circling, head tilt, depression, mania

Later: hypertonicity, hyperflexia, opisthotonus, coma, convulsions

ABs- prognosis poor

32
Q

What is hydrocephalus

A
  • Failure of drainage of CSF therefore increased intracranial pressure
  • Domed cranium
  • Diffuse cerebral signs-mania, head pressing, muscle tremors
33
Q

What is hydrocephalus

A
  • Failure of drainage of CSF therefore increased intracranial pressure
  • Domed cranium
  • Diffuse cerebral signs-mania, head pressing, muscle tremors
34
Q

What causes cerebrocortical necrosis?

When is it most common?

What are the clinical signs?

A

Thiamine- vit B1 deficiency
Necrosis of greay matter

Most common in cattle 6-18 months old

CS
* dead
* early- head in air, appear blind, PLR present, disorientates
* late- opisthotonos, head pressing, strabismus, miosis, exitement, recumbent

Blindness and stargazing

PM- brain pale and swollen

35
Q

How is CCN treated and controlled?

A
  • 10-15 mg/kg thiamine repeated every 4 hours for 24 hours

Identify and rectify underlying cause

36
Q

What are the clinical signs of lead poisoning?

A

First
* stand alone and depressed
* hyperaesthesia, muscular fasiculations

Progress
* ataxia
* blindness
* head pressing
* episodic manic behaviour
* convulsions
* abdominal pain, rumen atony
* diarrhoea

37
Q

How is lead poisoning treated?

A
  • Controls fits- IV pento
  • Chelate lead CaEDTA
  • Thiamine
  • Oral MgSO4
38
Q
  1. What are the clinical signs of nervous ketosis?
  2. How is it treated?
A
  1. Obsessive licking, circling, staggering, head pressing, pica, aggression
  2. 40% dextrose IV, propylene glycol BID, corticosteroids
39
Q

When is staggers most common?

A

Especially in pastured lactating beef cows in first months after calving

40
Q

What are the clinical signs of staggers?

A
  • Hyperexitable, may charge
  • Erect ears, ears twitching, hyperaesthesia
  • Muscle fasiculations/tremors
  • Lateral recumbency with violent episodes of ophistotonus and convulsions
  • Dead within hour of seizure
41
Q

What can cause salt poisoning?
Why does it cause p

A
  • Too much salty water or water deprivatoin
  • Sodium deposition in the brain blocks anaerobic glycolytic pathways- increased intracranial presure may also occur

Poor prognosis- rehydrate first then hypertonic saline

42
Q

How can pseudo and pseudorabies be distinguished?

A

Pseudo- pruritis- mad itch

Rabies- depression

43
Q

What are the clinical signs of BSE?

A

3-6 years
* Weight loss
* Hyperaesthesia, fine fasiculations of head and neck, shoulder flank, teeth grinding
* Apprehensive when approached
* Ataxia
* Aggression

44
Q

What is the action of BSE case?

A
  • Inform APHA
  • Visit to inspect animal to decide to PTS as suspect
  • Farmer compensated and trace put on the offspring
45
Q

When is hypovitaminosis A most commonly seen?

What causes the clinical signs?

A

Straw/cereal based diet in housed animals

Signs from thickening dura mater/abnormal bony growth in the brain cavity- increase CSF
Retina degeneration- absent PLR

Plenty of vitamin A in green forages and feeds

46
Q

What are the signs of hypovitaminosis in calves to deficient dams and older cattle?

A

Calves to deficient dam- blindness, weakness, domed forehead, thickened carpal joints

Deficient calves- blindness, anorexia, diarrhoea, pneumonia

Older cattle- blindness, start gazing, nystagmus, ataxia, convulsions, diarrhoea, thickening and whitening of cornea

47
Q

How is hypovitaminosis treated?

A
  • Vitamin A daily
  • Older cattle with ocular form often do not respond
48
Q

What are the signs of cerebellar hypoplasia?

What can cause it?

A

Balance- ataxia, falling, unable to stand, tremor, hypermetria, nystagmus

Acquired BVD- 90-170d of gestation
Inherited

49
Q

What diseases present principally with brain and cranial nerve dysfunction?

A
  • Listeriosis
  • Environmental pathogen- infectious sporadic and usually associated with feeding poor quality forage
  • Infection travels upto brain stem from conjunctiva via trigeminal
  • Forms microabscesses in brain stem/cerebellum/spinal cord
50
Q

How is lepto treated?

A
  • Stop disease worsening and hope defecits resolve
  • High dose penicillin 7-14d or oxytet
51
Q

What can cause spinal cord or peripheral nerve signs?

A
  • Spinal fractures
  • Spinal abscess
  • Spastic paresis
  • Tetanus
  • Botulism
  • Peripheral neuropathies
52
Q
  1. When are spinal fracutures common?
  2. What are spinal abscesses normally secondary to?
A
  1. 3-6mo investigate underlying cause- VitD, calcium or copper deficiency
  2. Oestomyelitis- T. pyogenea, staph aureus, P. haemolytica, F. necrophorum
53
Q

What are the signs of spastic paresis?

A

Asymmetric spasticity and hypertonia of extensor muscles of rear limbs
* Continuous when stand, not when it lays down
* Excessive tone of gastrocnemius
* Hyperextended hock
* Unilateral or Bilateral

54
Q

How is spastic paresis treated?

A

Neurectomy of tibial nerve rootlets innervating the gastrocnemius

55
Q

What are the clinical signs of tetanus?

A
  • Incubation period variable
  • Normally 2-4 weeks
  • Progression of 4-5 days
  • Stiffness, reluctance to move, muscle tremors
  • Prolapsed 3rd eyelid
  • RUMEN TYMPANY
  • Recumbancy, convulsions, death
56
Q

What can cause botulism?

A

Clostridium botulinum
* Ensiled poultry waste as food
* Poultry litter to pasture
* Carcasses in pasture or feed

57
Q

What are the signs of botulism?

A
  • Muscle weakness
  • Progresses to ataxia and paralysis
  • Excessive drooling
  • Droopy expression, tonggue hanging out of mouth
  • Decreased rumen motility, bloat, constipatoin
  • Resp failure leading to death
58
Q

How is botulisim diagnosed?

A
  • History
  • Clinical signs
  • Toxin serum ELISA
  • Samples of feed
59
Q

When does obturator neuropathies occur?

A
  • Following dystocia- especially heifers
  • Obturator nerve damaged by foetal pressure
  • Unable to adduct limb
  • Treatment- chain between hindlimbs, soft bedding, steroids
60
Q

What are the signs of peroneal neuropathy?

A

Hyperextension of hock, fetlock, digits flexed
Loss of skin sensation below fetlock
Self cure- bandage over fetlock to prevent damage

61
Q

When does sciatic damage occur?

What is the signs?

A

When recumbent and struggling to rise

Non-weight bearing, no sensation distal to stilfe

DDX- femoral fracture

Year 4 Livestock and One Health (58 decks)

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