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Musculoskeletal dysfunction > Large animal neurological conditions > Flashcards

Large animal neurological conditions Flashcards

1
Q

Name three spinal cord diseases in equines

A

Cervical vertebral stenosis myelopathy

Equine Herpes Virus

Occipito-atlantoaxial malformation

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2
Q

Name four peripheral nerve diseases in equines

A

Stringhalt

Shivers

Head shaking

Horner’s syndrome

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3
Q

What are the three types of ataxia?

A
  1. Proprioceptive - abnormal limb placement,limb paresis, weakness
  2. Vestibular - Head tilt, rolling/falling to one side
  3. Cerebellar - wide base stance, intention tremors
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4
Q

Define paresis

A

Reduction in voluntary movement

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5
Q

Define monoparesis

A

affecting one limb

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6
Q

Define hemiparesis

A

affecting both limbs on the same side of the body

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7
Q

Define paraparesis

A

Affecting either both forelimbs or both hindlimbs

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8
Q

Define tetraparesis

A

Affecting all four limbs

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9
Q

Name three diseases affecting the spinal cord

A

Cervical vertebral stenotic myelopathy

Equine Herpes Virus

Occipito-atlantoaxial malformation

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10
Q

Describe cervical vertebral stenotic myelopathy

A

Cervical vertebral malformation

‘Wobblers’ syndrome – care with use of this term

Compression of the cervical spinal cord due to changes in the vertebral column

Males > females

Type I and II

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11
Q

Describe type I CVSM

A

Younger horses – Thoroughbred, Warmblood

Compression due to excess movement of the vertebrae

Dynamic

Normally affects C3-C5

Causes:

Genetics

Nutrition

Rapid growth

Trauma

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12
Q

Describe type II CVSM

A

Older horses

Due to arthritic changes on articular process joints

Traumatic

Acquired

Normally affects C5-7

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13
Q

What are the clinical signs of cervical vertebral stenotic myelopathy?

A

Progressive then plateau (unless traumatic)

Hindlimb ataxia +/- forelimb dysmetria

Dragging of the toes

Wide based stance

‘Sway’ at walk

Neck pain/stiffness (C2-4)

Circumduct hindlimbs when circling

All made worse by neck flexion

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14
Q

What are the 6 stages of the mayhew ataxia grading system?

A

0- no neurological deficits

1 - Neurological deficits just detected at walk. Worsened by turning, backing or extension of the neck

2 - Neurological deficits easily detected at walk. Exaggerated by turning, backing or extension of the neck

3 - Neurological deficits prominent at walk with a tendency to buckle or fall when turned, backed or neck extended

4 - Stumbling, tripping and falling at walk

5 - Recumbent

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15
Q

How would you diagnose CVSM?

A

Clinical signs

Radiography

Measure canal to vertebra ratio

Myelography

CT?

Difficult to get lower neck.

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16
Q

How would you medically treat CVSM?

A

Anti-inflammatories

Box rest

Type 1:

Reduced carbohydrate and protein

Vit E and selenium for nervous system health

Type II:

Glucocorticoid injection into the joint

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17
Q

How would you surgically treat CVSM?

A

Very specialist surgery – only a handful of surgeons in the UK

Rarely carried out as most horses still unsafe to ride

Fusion of the vertebrae:

Bagby basket technique

Kerf Cut Cylinder

Locking compression plate

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18
Q

Describe the equine herpes virus (EHV-1)

A

Many strains of Equine Herpes Virus – 1, 3, 4

1 – most common to cause neuro disease

4 – occasionally causes neuro disease

Causes inflammation of the blood vessels ‘vasculitis’  ischaemia

INFECTIOUS – air-borne virus

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19
Q

How can equine herpes virus present?

A

Respiratory disease

Abortion

Neonatal disease

Thought to be infected within weeks of birth

Incubates for 2-10 days but can cause latent infection – lymph nodes

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20
Q

How do you diagnose EHV-1?

A

CSF sample

Virus isolation

Antibodies

Post mortem

Histopathology

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21
Q

How do you treat EHV-1?

A

Supportive treatment

Many horses will stabilise rapidly and improve over

a few days

Deep bedding

Sling or scoop if recumbent

Urinary catheterisation

+/- anti-viral medication

+/- glucocorticoids

Full recovery can take up to 18 months.

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22
Q

Describe management of a EHV-1 outbreak

A

Isolate horse as soon as disease suspected - barrier nurse

No movement of horses on or off the yard for at least 3 weeks after last case identified

Burn infected bedding

Disinfect stable, equipment and clothing

Vaccination provides only partial and short-lived immunity

Not appropriate to vaccinate at-risk animals during a breakout

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23
Q

What is occipito-atlantoaxial malformation?

A

Malformation of the vertebra in cranial cervical spine

Compresses spinal cord

Arab breeds

Typically effects from birth  1 year of age

24
Q

What are the clinical signs of occipito-atlantoaxial malformation?

A

Crepitus on movement of the neck

Left or right bony prominence

Scoliosis

Tetraplegia

25
Q

How do you treat occipito-atlantoaxial malformation?

A

Management or euthanasia

26
Q

Describe stringhalt

A

Motor disorder of unknown aetiology

Involuntary hyperflexion of hock whilst moving

Types

Idiopathic

Epidemic / ‘Australian stringhalt’ - ?dandelion / ?flatweed.

Intoxication – sweet pea plants

27
Q

What are the clinical signs of stringhalt?

A

Can be unilateral or bilateral

Worse when backing up

Grade 1 – only mild signs noted when animal starts to move

to

Grade V – reluctant to move and ‘bunny hops’

28
Q

How do you diagnose stringhalt?

A

Diagnosis is based on clinical signs and ruling out other diseases.

29
Q

How do you treat stringhalt?

A

Remove toxins

Tenotomy or tenectomy of the lateral digital extensor tendon

Phenytoin (muscle relaxant)

30
Q

Describe radial nerve damage

A

Provides innervation to the extensor muscles of the forelimb

Causes extensor paresis

Can be seen following:

Lateral recumbency during GA

Kick injury

31
Q

What are the clinical signs of radial nerve damage?

A

Location of injury can alter clinical signs

Near the elbow joint  ‘high’

Dropped elbow

Toe scuffing

Distal injury  ‘low’

Knuckling of carpus, fetlock and pastern joints

Over time leads to atrophy of the extensor muscles`

32
Q

Describe femoral nerve damage

A

Has motor and sensory functions

saphenous branch

Most commonly occurs due to extended HL position during GA

Leads to:

Loss of weight support

Inability to extend or fix stifle

Sensory deficit to medial thigh

33
Q

Describe sciatic nerve damage

A

Uncommon

Mostly caused by poor injection technique

Limb often dropped with stifle dropped and extended

Commonly seen in post-partum cow

34
Q

Describe treatment of peripheral nerve injuries

A

Can take weeks  months to recover

Anti-inflammatories

Support limb

Bandages

Splints

Support the horse if required (slings)

Aim to slow down muscle atrophy

Passive movement

Regular stimulation

Deep, comfortable bedding

IVFT

Sedation if distressed

35
Q

Describe idiopathic head shaking

A

‘Abnormal condition when a horse shakes it’s head in the absence of obvious external stimuli’ Mair (2013)

Unknown aetiology

? trigeminal neuritis

? photophobia

Seasonal variation – late spring/summer

36
Q

What are the clinical signs of idiopathic head shaking?

A

Most commonly occur during ridden exercise

Rapid vertical head flicking

Sneeze/snort at walk or trot

‘Nudging’ owner at walk

?Engorgement of superficial facial vessels

37
Q

How do you diagnose idiopathic head shaking?

A

Extensive – rule out all other causes

Ears

Eyes

Cervical spine

Respiratory

CNS

Teeth

Oral cavity

Can block infra-orbital nerve

38
Q

How do you treat idiopathic head shaking?

A

Unlikely to be effective – inconsistent results

Nose nets can be used short term

Steroids (inhaled or systemic)

Anti-histamines

Bilateral infra-orbital neurectomy

Coils

PENS – percutaneous electrical nerve stimulation

39
Q

Describe horner’s syndrome

A

Loss of sympathetic innervation to the head

Damage to vagosympathetic trunk as it runs through the neck

Clinical signs

Drooping of the eyelid (ptosis)

Retraction of the eye (enophthalamus)  protrusion of third eyelid

Mild dilation of the pupil (mydriasis)

Inappropriate facial sweating

40
Q

Describe downer cows

A

Cow has been down for more than 24 hours

Usually related to calving

Approx ½ develop within 24 hours after calving.

If they are in the same position >6hrs then leads to secondary pressure damage, compartment syndrome etc

41
Q

What are the types of downer cows?

A

‘Alert downer’ – no sign of systemic disease

‘Non-alert downer’ – systemic illness

‘Creepers’ / ‘crawlers’ – cows that can attempt to rise and can move themselves around

42
Q

Name possible causes of downer cows

A

Mineral deficiency

Dystocia

Fractures

Luxations / subluxations

Muscle damage

Nerve damage

Toxaemia – toxins in the blood stream

43
Q

Describe treatment of downer cows

A

Treat underlying cause

Supportive care

Comfortable, clean, non-slip bedding

Provision of food / water

Turning cow every 3 hours

Anti-inflammatories

Assist to rise

Diagnosis

Improve blood supply

44
Q

What lifting aids can be used for downer cows?

A

Hip clamp / Bagshaw hoist

inflatable bags

slings

45
Q

What is the prognosis of downer cows?

A

Approximately half of all downer cows will get up in 4-7 days.

If the cow has been down for longer than 10 days, prognosis is poor.

46
Q

Describe spastic paresis

A

Elso heel’

Asymmetric spasticity and excess extensor tone in hindlimb(s)

Gastrocnemius

Superficial digital flexor tendon

Normal when recumbent

Aetiology unknown – ?genetic

47
Q

What are the clinical signs of spastic paresis?

A

Seen in most breeds

Young animals - 3 weeks  1 year

Progressive

Unable to flex hock

Circumducts affected limb

48
Q

How do you manage spastic paresis?

A

Aim to usually to provide sufficient relief to finish for slaughter

Neurectomy of the tibial nerve rootlets supplying the gastrocnemius

Tenotomy of the gastrocnemius tendon

Partial tenectomy of the two insertions gastrocnemius and calcanean tendon

49
Q

Describe obturator nerve paralysis

A

Motor innervation to adductor muscles of the limb

Well protected in the horse and small ruminants

Seen in cows during dystocia

50
Q

What are the clinical signs of obturator nerve paralysis?

A

Non-slip surface  minimal deficits seen

Slippery surface  splayed legs

May ‘bunny hop’ when moving

Treatment is the same as horses

Hobbles used

51
Q

Define spinal abscesses

A

Often originate from:

Pre-existing osteomyelitis

Haematogenous spread from heart, lung, injection site etc

If remains within vertebral body  myelopathy

If vertebrae fractures  spinal trauma

If erodes through dura mata  septic meningitis

Treatment is supportive and aggressive antibacterial therapy

52
Q

Describe tetanus

A

Equine and farm animals

Clostridium tetani spores found in soil

Release 2 toxins

Contaminate soft tissue injuries

Causes contraction and spasm of muscles

Stiff gait  recumbency with rigidity of neck and limbs

53
Q

Describe treatment of tetanus

A

Treatment

Sedation/muscle relaxants

Anti-toxin

Fluid/nutritional support

Deep bedding

If they can still drink – good prognosis

If recumbent – grave prognosis

Vaccination!

54
Q

Describe botulism

A

Clostridium botulinum

‘Foraged’ – silage

Clinical signs tend to be acute:

Flaccidity

Weakness

Trembling

Drooling

Recumbency

Sudden death

55
Q

What is the treatment for botulism?

A

Anti-toxin

Antibiotics

Deep bedding

Nursing and nutritional support

Musculoskeletal dysfunction (12 decks)

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