Common Equine Neurological Diseases 1 + 2 Flashcards

1
Q

Describe how a horse would present with forebrain disease?

A
  1. Disorders of behaviour and personality - aggression, compulsive walking, loss of learned behaviour, yawning
  2. Seizures
  3. Blindness
  4. Altered state of consciousness (alert -> quiet -> depressed -> obtunded -> comatose)
  5. Altered head posture (head and neck turn, head pressing)
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2
Q

What are the causes of forebrain disease?

A
  • Trauma: ↑↑
  • Metabolic: HE, intestinal hyperammonaemia
  • Intracarotid injection
  • Cholesterol granuloma
  • Infectious meningoencephalomyelitis
  • Neoplasia
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3
Q

How can forebrain disease be diagnosed?

A

If safe:
* Whole clinical exam
* Imaging head

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4
Q

How is forebrain disease treated?

A
  • Oxygen supplementation
  • Fluid therapy
  • NSAIDS
  • Elevate head
  • Steroids?
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5
Q

What is hepatic encephalopathy?

A

Ammonia that is normal detoxified in the liver, isn’t - check liver parameters

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6
Q

How does hepatic encephalopathy present?

A

Central blindness - no menace, PLR still present

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7
Q

What is the cause of intestinal hyperammoniaemia?

A

Enteritis / Colitis
↑ permeability

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8
Q

Describe sleep disorders in horses

A

True narcolepsia: Rare
Sleep deprivation:
* Inability to lie down
* Musculoskeletal pain!
* Fear?
In true narcolepsy they wont wake up if you try to wake them, but they will in sleep deprivation

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9
Q

Describe seizures in adult horses

A

Rare in adults
* High seizure threshold – takes a lot for a seizure to occur
* Trauma, encephalitis, metabolic, neoplasia

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10
Q

Describe neonatal seizures and epilepsy

A
  • Low seizure threshold
  • Most common: PAS (dummy foal) (NMS/HIE), sepsis, trauma
  • Also: metabolic Juvenile idiopathic Arab epilepsy: benign, up to 12 months of age
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11
Q

How would a horse with brainstem and cranial nerve disease present?

A
  • Vestibular disease: peripheral or central
  • Facial nerve paralysis (VII and VIII frequently affected together)
  • Pharyngeal/laryngeal deficits: dysphagia
  • Other cranial nerve deficits
  • Severe brainstem lesions: gait abnormalities, coma (RAS)
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12
Q

What are the clinical signs of vestibular disease?

A
  • Head tilt
  • Nystagmus
  • Ventral strabismus
  • Ataxia: wide based stance
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13
Q

How can you test for ventral strabismus in a horse?

A

Tilt head back, eyes drop severely, more than normal (remember prey species)

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14
Q

What are the causes of vestibular disease?

A
  • Trauma: central or peripheral (petrous portion of temporal bone)
  • Idiopathic
  • Otitis media/interna (temporohyoid osteoarthropathy)
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15
Q

What is the most common cause of facial nerve injury?

A

Iatrogenic due to halters left on during field anaesthesia

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16
Q

List the clinical signs of a horse with facial nerve injury

A

Dropped ear
Ptosis
Nostril deviation

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17
Q

What are the long term/secondary effects of a facial nerve injury?

A
  • Exposure keratitis
  • Corneal ulcers
  • Dysphagia: feed pouching
  • Poor performance due to nostril collapse
  • Hyposalivation
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18
Q

What is the most common cause of Horners syndrome in horses?

A

Iatrogenic due to extravascular injection of irritant substance (PBZ, Buscopan)

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19
Q

What are the clinical signs of a horse with Horner’s syndrome?

A
  • Miosis
  • Enophthalmos
  • Ptosis
  • Protruding nictitating membrane
  • Hyperaemic membranes
  • Sweating (opposite to other spp)
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20
Q

What are the clinical signs of a horse with cauda equina syndrome

A

Degrees of hypotonia, hyporeflexia and hypalgesia of the tail, anus and perineal region, urinary bladder paralysis, rectal dilation, penile prolapse
- No anal or bladder tone
- Urinary incontinence
- Weakness of hindlimbs

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21
Q

What are the causes of cauda equina syndrome?

A
  • Trauma: sacrococcygeal fracture and luxation, avulsion of the cauda equina
  • Inflammatory: polyneuritis equi (± cranial nerve signs)
  • Viral / immune: EHV-1 (± ataxia, ± cranial nerve signs)
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22
Q

Describe the feature of EHV-1 myeloencephalopathy

A
  • Uncommon manifestation of EHV-1 infection
  • May occur sporadically or as an outbreak
  • May be a recent history of respiratory disease or abortion
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23
Q

What are the clinical signs of EHV-1 myeloencephalopathy?

A
  • Sudden onset and early stabilisation of signs including ataxia, paresis, urinary incontinence (and very rarely cranial nerve signs)
  • Clinical signs occur as a result of vasculitis and thrombosis of arterioles in spinal cord (and brain) → viral endotheliotrophism
24
Q

How is EHV-1 myeloencephalopathy diagnosed?

A
  • Lesion location
  • Rule out other causes
  • History of respiratory disease and/or abortion
  • CSF sample: xanthochromic ± Abs to EHV-1
  • Detection of virus in affected or in-contacts (nasopharyngeal swabs or buffy coat)
25
How is EHV-1 myeloencephalopathy managed?
- Isolate - Prognosis reasonable with good nursing care - Recurrence of neuro signs not reported - Vasculitis → anti-inflammatories: NSAIDs, corticosteroids, aspirin (anti-thrombotic) - Antivirals: acyclovir, valacyclovir
25
How does spinal cord disease present?
History of sudden onset ataxia or recumbency, sometimes an observed incident No progression, frequently improvement, although later progression due to callus formation may occur
26
How is a horse with spinal cord disease managed?
- Early aggressive anti-inflammatory therapy: corticosteroids (??), NSAIDs, DMSO (??) - Surgical therapy?, Neck brace? - Box rest if standing - Nursing care if recumbent - Time!
27
Name the most common cause of ataxia in horses
Cervical vertebral malformation
28
Describe the physiology of cervical vertebral malformation
Narrowing of the cervical vertebral canal causing compression of the spinal cord, often in combination with malalignment and malformation of the cervical vertebrae
29
Describe type 1 CVM
- Young horses - Compression as a result of developmental abnormalities - Dynamic stenosis - Any site
30
Describe type 2 CVM
- Older horses - OA of articular processes - Static stenosis - C5-C6 and C6-C7 most common
31
How would you assess a horse for CVM?
Lesion location: ataxia all 4 limbs, hindlimbs more severely affected than forelimbs (by a maximum of 2 degrees of ataxia) Neck pain rarely seen Radiography
32
Describe the type of lesions seen on radiography of a horse with CVM
- 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
33
What is it not uncommon to see on the radiographs of a horse with CVM
No radiographic abnormalities - this does not rule out CVM
34
What can be used to aid diagnosis of CVM when there are no radiographic changes?
Myelography BUT - Most of the times it does not provided any additional information - Has risks of anaesthesia: Induction and recovery of ataxic animal - Has risk associated with technique - Not performed very often
35
How should horses with CVM be managed, based on type 1 vs type 2
Surgery can be performed but it is costly and may only improve the horse on average one grade An ataxic horse should not be ridden Type I: Early detection in young foals and dietary restrictions have resulted in resolution of ataxia and successful careers. Once disease is advanced prognosis is poor Type II: intraarticular corticosteroids (US guided)
36
List some neuromuscular diseases of horses
Abnormal gait: shivering, stringhalt Localised weakness: peripheral nerve injuries Diffuse weakness: EMND, botulism, EGS, HYPP Excessive activity: Tetanus
37
What is Shivering (shivers)
- Reflex hypertonia of flexor muscles of pelvic limbs - Initially horse snatches up the hindlimb when being picked - Accentuated when turning or backing horse and if excited - Always progressive
38
What is stringhalt?
Sudden, involuntary, exaggerated flexion of one or both hindlimbs during attempted movement
39
What are the two types of stringhalt?
1. Australian or plant associated: dandelion, flat weed? → treatment: remove from pasture 2. Sporadic stringhalt: aetiology not fully understood. Treatment myotenectomy of lateral digital extensor
40
Which nerves are most susceptible to peripheral nerve injuries?
Radial nerve Suprascapular nerve
41
When is radial nerve damage most likely to occur and how does it present?
- Most common from external blows or following lateral recumbency in anaesthesia - Inability to flex shoulder, extend the limb and fix the elbow
42
When is suprascapular nerve damage most likely to occur and how does it present?
- Most common from external blows or poorly fitted collars in draft horses - Atrophy of supra- and infraspinatus, abduction of limb and inability to advance shoulder
43
How are peripheral nerve injuries treated?
Anti-inflammatories, DMSO?, physiotherapy, vit E? Return of function may take days to months (or may never return)
44
What is the cause of equine motor neuron disease?
Degeneration of motor neurons in spinal cord due to low vit E concentration. Normally history of horse stabled with no access to pasture for a period of time
45
What are the clinical signs of equine motor neuron disease?
- Weight loss (muscle wasting), muscle fasciculations, prolonged recumbency - Elevated tail head - Ocular signs in 30-40% cases: brown pigment accumulation in retina
46
How is equine motor neuron disease treated? What is the prognosis?
Vit E supplementation Prognosis: 40/40/20 - 40% stabilize - 40% will progress - 20% rapid deteriation, cant do anything
47
What are the toxic sources of clostridium botulinum?
* Contaminated feed (big bales), grass/corn silage * Water (dead waterfowl) * UK: associated with poultry litter and carcasses
48
Why is clostridium botulinum toxic?
Blocks Ach release at presynaptic membrane of neuromuscular junction failure of muscle contraction → weak - Abrupt progressive onset flaccid paralysis of skeletal muscle
49
What are the clinical signs of Botulism in horses?
- 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 - Die in 10 days (respiratory muscle paralysis)
50
What is the cause of shaker foal syndrome?
Clostridium botulinum 1-3mo, initial episodes of trembling
51
How is botulism Tx?
Penicillin (not procaine!) Supportive, fluids
52
What are the sources of clostridium tetani?
Soil GI flora
53
How is clostridium tetani toxic?
Gram +, anaerobic: sporulates with right conditions (wounds!) and releases toxins
54
What are the clinical signs of Tetanus?
- Elevated tail head - Stiff gait - Anxious: ears back, eyelids wide open, nostrils flared, head extended - Lock jaw: drool, can’t swallow - Prolapse 3rd eyelid - Recumbency, rigidity - Secondary ulcers, trauma
55
How is a horse with tetanus managed?
1. Support: quiet, dark, low stimulation room. 2. Hydration, deep bedding 3. Eliminate source: open, flush wound. Treat with metronidazole (penicillin not recommended any more!) 4. Neutralize unbound toxin: antitoxin 5. Muscle relaxation: Acepromazine, Diazepam
56
What must be given to a horse with tetanus?
Toxoid * Separate site from antitoxin * Administer ALWAYS * If previously vaccinated use only toxoid