Equine Neuro Flashcards

1
Q

Give some viral causes of neurological disease

A
  • EHV-1
  • Borna disease
  • Eastern, Western and Venezuelan encephalitis
  • West Nile Virus
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2
Q

Give some bacterial causes of neurological disease

A
  • Meningitis

- Encephalitis

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3
Q

Give a protozoal cause of neurological disease

A

EPM (equine protozoal myeloencephalitis; caused by Sarcosytsis)

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4
Q

Give some toxins that can cause neurological disease

A
  • Botulism

- Tetanus

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5
Q

Give some neurodegenerative diseases of horses

A
  • EDM (equine degenerative myeloencephalopathy)
  • EMND (equine motor neurone disease)
  • EGS (equine grass sickness)
  • Cerebellar abiotrophy (kills off Purkinje cells in cerebellum)
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6
Q

Give some metabolic neurological diseases of horses

A
  • HE (hepatic encephalopathy)
  • Intestinal hyperammoniaemia
  • HYPP (hyperkalaemic periodic paralysis disease)
  • Electrolyte imbalances (eg Ca, Mg, Na)
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7
Q

What is CVSM?

A

Cervical vertebral stenotic myelopathy (‘Wobblers’)

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8
Q

Give some neurotoxins that can cause neurological disease in horses

A

-Avermectins
-Lead
-Amitraz (tick and mite tx)
-Bracken
-Rye grass (staggers)
Mouldy corn -> leukoencephalomalacia

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9
Q

Give a vascular cause of neurological disease in horses

A

Thromboembolic meningoencephalitis

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10
Q

What is stringhalt?

A
  • Sudden, involuntary, exaggerated flexion of one or both hindlimbs during attempted movement
  • Leg jerks in an unnatural, quick movement before dropping back down
  • Seen mostly and walk and when walking backwards
  • Cause unknown
  • Digital extensor muscle contracts excessively
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11
Q

What is shivers?

A

-Reflex hypertonia of flexor muscles of pelvic limbs
-Initially horse snatches up the hindlimb when being picked up
-Accentuated when turning or backing horse and
if excited
-Pelvic limbs are flexed and held in a spastic space
for some time
-Draft breeds
-Always progressive.
-No effective tx

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12
Q

Give some neuromuscular diseases that can cause an abnormal gait

A
  • Shivers

- Stringhalt

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13
Q

Which type of neuromuscular diseases cause localised weakness?

A

Peripheral nerve injuries

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14
Q

Give some neuromuscular diseases that cause diffuse weakness

A
  • EMND (equine motor neurone disease)
  • Botulism
  • EGS (equine grass sickness)
  • HYPP (hyperkalaemic periodic paralysis disease)
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15
Q

Give a neuromuscular disease that causes excessive activity

A

Tetanus

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16
Q

Give some clinical signs of forebrain disease

A
  • Disorders of behaviour and personality: aggression, compulsive walking, loss of learnt behaviour, yawning
  • Seizures (not common)
  • Blindness
  • Altered states of consciousness
  • Head posture (head and neck turn, head pressing)
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17
Q

What is the cauda equina?

A
  • Bundle of spinal nerves and spinal nerve roots: 2nd-5th lumbar nerves, 1st-5th sacral nerves, coccygeal nerve
  • Located at base of spine
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18
Q

Give some causes of forebrain disease

A
  • Trauma
  • Abscess
  • Cholesterol granuloma (can get cholesterol crystals in CSF with old age)
  • Verminous
  • Infectious meningoencephalomyelitis
  • Neoplasia
  • Toxins
  • Intra-carotid injection
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19
Q

What kind of brain lesions cause narcolepsy and sleep deprivation?

A

Forebrain

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20
Q

Give some metabolic causes of forebrain disease

A
  • HE (hepatic encephalitis; altered mentation, central blindness)
  • Intestinal hyperammoniaemia
  • Electrolyte imbalances
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21
Q

What are the most common causes of seizures and epilepsy in neonates?

A
  • PAS/NMS/HIE
  • (Perinatal Asphyxia Syndrome/Neonatal Maladjustment Syndrome/Hypoxic Ischaemic Encephalopathy)
  • ‘Dummy foal’
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22
Q

Give some other causes of seizures and epilepsy in neonates

A

-Metabolic (hypoNa, hypoglycaemia), drug-associated, idiopathic (grows out of)
-Juvenile idiopathic Arab epilepsy: benign, up to 12
months of age

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23
Q

Give some clinical signs of brainstem disease

A

-Vestibular disease: peripheral or central (ataxia, head tilt, nystagmus, ventral strabismus)
-Facial nerve paralysis (VII and VIII frequently affected together)
-Pharyngeal/laryngeal deficits: dysphagia
-Other cranial nerve deficits
-Severe brainstem lesions: gait abnormalities,
coma

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24
Q

What is the best way to assess ataxia in the horse and why?

A
  • Blindfolded, as horses can compensate with their eyesight

- Can also assess vestibular signs by walking horse up a ramp

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25
Q

What does the motor cortex control?

A

Fine movement (mainly done by mouth in horses)

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26
Q

Where do seizures tend to start in the horse?

A
  • Around the mouth/lips/tongue

- Can see excessive chewing movements

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27
Q

Give some causes of vestibular disease

A

-Trauma: central or peripheral (petrous portion of
temporal bone)
-Idiopathic
-Otitis media/interna (temporohyoid osteoarthropathy) (peripheral vestibular disease)

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28
Q

What should be your first differential in cases of acute-onset vestibular dysfunction with facial nerve paralysis?

A
  • Temporohyoid osteoarthropathy
  • Chronic bony proliferation of the petrous temporal bone and stylohyoid bone -> ankylosis of the temporohyoid joint -> fracture of petrous temporal bone -> direct trauma to vestibulocochlear and facial nerves and hemorrhage into the middle and inner ear
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29
Q

Give some causes of facial nerve injury

A
  • Commonly iatrogenic due to halters left on during field anaesthesia
  • Trauma (± vestibular)
  • THO (± vestibular)
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30
Q

Give some clinical signs of facial nerve injury

A
  • Drooping of ear, eyelid (ptosis), lip

- Nostril deviation

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31
Q

Give some prolonged/permanent signs of facial nerve injury

A
  • Poor performace (due to collapsed nostril)
  • Exposure keratitis
  • Dysphagia
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32
Q

What causes Horner’s syndrome?

A

Interruption of the sympathetic innervation to the head (and neck)

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33
Q

What is the most common cause of Horner’s syndrome in horses?

A

Iatrogenic due to extravascular injection of irritant substance (phenylbutazone, buscopan)

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34
Q

Give some clinical signs of Horner’s syndrome

A
  • Miosis (constricted pupil), enophthalmos, ptosis, protruding nictitating membrane
  • Hyperaemic membranes, sweating
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35
Q

Give the clinical signs of cauda equina syndrome

A

-Degrees of hypotonia, hyporeflexia and hypoalgesia
of the tail, anus (ie no anal tone) and perineal region, urinary bladder paralysis (incontinence), rectal dilation, penile prolapse
-May also see LMN weakness and paresis of HLs

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36
Q

Can a horse be ridden if it has ataxia?

A

No-too dangerous

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37
Q

Give some causes of cauda equina syndrome

A
  • Trauma: sacrococcygeal fracture and luxation, avulsion of the cauda equina
  • Infectious, inflammatory, immune:
    • Inflammatory: polyneuritis equi (± cranial nerve signs)
    • Viral/immune: EHV-1 (± ataxia, ± cranial nerve signs)
    • Verminous: EPM (equine protozoal myeloencephalitis)
38
Q

Give some effects of EHV-1

A
  • Resp signs
  • Abortion
  • Occasionally myeloencephalopathy (sudden onset and early stabilisation of signs including ataxia, paresis, urinary incontinence, very rarely cranial nerve signs)
39
Q

Why does EHV-1 myeloencephalopathy occur?

A

-Result of vasculitis and thrombosis of arterioles in spinal cord (and brain) -> viral endotheliotrophism

40
Q

How can you diagnose EHV-1 myeloencephalopathy?

A
  • CSF sample: xanthochromic (yellow colour that occurs several hours after bleeding) +/- antibodies to EHV-1
  • Detection of virus in affected or in-contact horses (nasopharyngeal swabs or buffy coat)
  • High antibody titre
41
Q

How do you manage EHV-1 myeloencephalopathy?

A
  • Isolate
  • Recovery takes days to weeks
  • Vasculitis -> anti-inflammatories: NSAIDs, corticosteroids, aspirin (anti-thrombotic)
  • Antivirals: acyclovir, valacyclovir
42
Q

Give some diseases that affect the spinal cord

A
  • Cervical vertebral malformation (CVM)
  • Cervical vertebral stenotic myelopathy (CVSM)
  • Wobbler syndrome
43
Q

How would a horse with spinal cord trauma present?

A
  • History of sudden onset ataxia or recumbency, sometimes an observed incident
  • No progression, frequently improvement, although later progression due to callus formation may occur
  • May exacerbate CVM (cervical vertebral malformation)
44
Q

In which sites are spinal cord trauma more likely to occur?

A
  • Occipito-atlanto-axial region
  • Caudal cervical
  • Mid-back: usually unstable fracture, paraplegia and recumbency (dog sitting position)
45
Q

Give some clinical signs of spinal cord trauma

A

Vary from ataxia and paresis to recumbency

46
Q

What should you give to sedate horses when assessing spinal cord trauma?

A

Xylazine

47
Q

How should you assess spinal cord trauma?

A
  • Complete physical exam (check for unstable fractures)
  • Neuro exam to localise lesion
  • Plain radiographs to look for fractures (may see callus formation in follow-up cases)
  • CSF analysis may rule out other causes
48
Q

How would you treat a fracture of the spinal vertebrae?

A
  • Neck brace
  • Box rest
  • Don’t ride again
49
Q

How would you manage spinal cord trauma?

A
  • Early aggressive anti-inflammatory therapy: corticosteroids (?), NSAIDs, DMSO (?)
  • Surgical therapy?, Neck brace?
  • Box rest if standing
  • Nursing care if recumbent
50
Q

Delayed callus formation on a spinal fracture may lead to what?

A

Compression of the spinal cord

51
Q

What is CVM?

A

Cervical vertebrae malformation

52
Q

What is the most common cause of ataxia in horses in the UK?

A

Cervical vertebrae malformation

53
Q

What are the 2 types of cervical vertebrae malformation?

A

Type I:

  • Young horses
  • Compression as a result of developmental abnormalities
  • Dynamic stenosis
  • Any site

Type II:

  • Older horses
  • OA of articular processes
  • Static stenosis
  • C5-C6 and C6-C7 most common
54
Q

Give the clinical signs of cervical vertebrae malformation

A

Ataxia in all 4 limbs, HLs worse than FLs

55
Q

How do you diagnose cervical vertebrae malformation?

A

Radiography

56
Q

Which changes occur with cervical vertebrae malformation?

A

-Stenosis of vertebral canal: dynamic or static
-Abnormal articular processes
-Subluxation of vertebrae on flexion or extension of
the neck
-Enlarged vertebral physeal growth regions
-Overriding of the vertebral arch and next caudal
vertebral body causing dynamic stenosis during
flexion or extension
-Proliferation of articular or periarticular soft tissues
-Is possible to not see any changes on radiography - could do myelography

57
Q

Give some risks associated with myelography of the spine

A
  • Anaesthetic risks (esp if ataxic)
  • Iatrogenic damage to spine (need radiographic guidance)
  • Risk of diffusion of contrast material into brain
58
Q

How do you manage type 1 cervical vertebrae malformation?

A

-Early detection in young foals and dietary
restrictions have resulted in resolution of ataxia
and successful careers
-Poor prognosis once advanced

59
Q

How do you manage type 2 cervical vertebrae malformation?

A

Intra-articular corticosteroids

60
Q

Give some clinical signs of neuromuscular disease and the diseases that cause them

A
  • Abnormal gait: shivering, stringhalt
  • Localised weakness: peripheral nerve injuries
  • Diffuse weakness: EMND, botulism, EGS, HYPP
  • Excessive activity: Tetanus
61
Q

What are the 2 types of stringhalt?

How would you treat each one?

A

-Australian or plant associated: dandelion, flat
weed? Treatment: remove from pasture
-Sporadic stringhalt: aetiology not fully understood. Treatment: myotenectomy of lateral digital extensor

62
Q

Anecdotal improvements in Shivers has been noted with what kind of diet?

A

-Increased fat, decreased carbohydrates

63
Q

How do radial nerve injuries typically occur?

A
  • External blows

- Following lateral recumbency in anaesthesia

64
Q

What are the clinical signs of radial nerve damage?

A

-Unable to flex shoulder, extend limb, flex elbow

65
Q

What is Sweeny?

A
  • ‘Shoulder slip’- shoulder is pushed laterally as leg is put down
  • Due to suprascapular nerve damage
66
Q

How does suprascapular nerve damage occur?

A
  • External blows

- Poorly fitted collars in draft horses

67
Q

Give some clinical signs of suprascapular nerve damage

A
  • Atrophy of supra-and infraspinatus muscles
  • Abduction of limb
  • Unable to advance shoulder
68
Q

How do you treat peripheral nerve injuries?

A
  • Anti-inflammatories
  • DMSO (anti-inflammatory)
  • Physio
  • Vitamin E (fresh pasture= good source)
69
Q

What is equine motor neurone disease and what causes it?

A
  • Degeneration of motor neurones in the spinal cord due to low vitamin E (and selenium?) concentrations
  • Normally history of horse stabled with no access to pasture for a period of time
70
Q

Give some clinical signs of equine motor neuron disease

A
  • Weight loss (muscle wasting)
  • Muscle fasiculations (eg triceps; diffuse muscle weakness)
  • Walk better than they stand
  • Elevated tail hair (muscle atrophy)
  • Legs tucked under body when standing
  • Ocular signs in 30-40% of cases (brown pigment accumulation in retina)
71
Q

How do you diagnose equine motor neuron disease?

A
  • Vitamin E (and selenium) levels

- Muscle biopsy (tail head)

72
Q

How do you treat equine motor neuron disease?

A

Vitamin E supplementation

73
Q

What causes Botulism?

A

Clostridium botulinum

74
Q

Give some sources of botulism toxins

A
  • Contaminated feed
  • Water (eg with dead waterfowl in)
  • Associated with poultry litter and carcasses
75
Q

How does botulism cause weak muscles?

A
  • Blocks Ach release at presynaptic membrane of neuromuscular junction -> no muscle contraction -> muscle weakness
  • Abrupt progressive onset flaccid paralysis of skeletal muscle
76
Q

Give some clinical signs of botulism

A
  • Symmetrical weakness (muscle tremors)
  • Stumble, ataxia
  • Tongue weakness, dysphagia
  • Hang head, nose on ground
  • Eventually recumbent
  • Dyspnoea (intercostal and diaphragm paralysis)
  • GI stasis, urine dribbling
77
Q

What causes shaker foal syndrome?

What age of foal is affected?

A
  • Botulism
  • 1-3 months old
  • Initial episodes of trembling, die in 10 days due to respiratory muscle paralysis
78
Q

How can you prevent shaker foal syndrome and botulism in adults?

A

Vaccinate mare twice in last month of gestation

79
Q

How can you diagnose botulism?

A
  • Identify toxin/spores (expensive)

- Stomach content (+/- faeces or feed)

80
Q

How can you treat botulism?

A
  • Antitoxin (USA, expensive)
  • Penicillin (not procaine)
  • Supportive care, fluids
81
Q

The botulism vaccine is effective against which type of botulism?

A

Type B

82
Q

What is the prognosis like for botulism?

A

Poor, esp if rapid onset tetraplegia

83
Q

What causes tetanus?

A

Clostridium tetani

84
Q

Where may a horse pick up tetanus?

A

Soil, GI flora

85
Q

How would you describe clostridium tetani?

A

Gram +ve, anaerobic, sporulates in correct conditions eg wounds and releases toxins (2 types)

86
Q

Which toxins does clostridium tetani release?

A
  • Tetanospasmin: neurotoxin, migrates along motor neuron to spinal cord and brainstem
  • Tetanolysin: increases tissue necrosis at site
87
Q

Give some effects of tetanospasmin (clostridium tetani toxin)

A
  • Inhibits release of glycine
  • Inhibits presynaptic inhibitory neurons in spinal cord
  • Muscles continuously contract
  • Tetany elicited by sound, light, touch
88
Q

Give some clinical signs of tetanus

A
  • Elevated tail head
  • Stiff gait
  • Anxious: ears back, eyelids wide open, nostrils flared, head extended
  • Lock jaw: drool, can’t swallow
  • Prolapsed 3rd eyelid
  • Recumbency, rigidity
  • Secondary ulcers, trauma
89
Q

How do you treat tetanus?

A
  • Supportive: quiet, dark, low stimulation room. Hydration, deep bedding
  • Eliminate source: open and flush wound. Treat with metronidazole (not penicillin as can make signs worse)
  • If unvaccinated: antitoxin (15 units) plus toxoid. at separate sites
  • If vaccinated: toxoid
  • Muscle relaxation (ACP or diazepam)
90
Q

When should you vaccinate against tetanus?

A

2, 3, 6 months, booster at 1 year

91
Q

What is cervical vertebral malformation?

A

Narrowing of the cervical vertebral canal -> compression of the spinal cord, often with malalignment and malformation of the cervical vertebrae