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Equine Final Year > Equine Neurology > Flashcards

Equine Neurology Flashcards

1
Q

How do horses with CNS disorders often present?

A

–Ataxia

–Seizures/collapse

–Blindness

–Autonomic dysfunction (bladder, GIT, other)

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2
Q

What are the common disorders of peripheral nervous system (2)

A

–Weakness

–Autonomic dysfunction (dysphagia, bladder, GIT)

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3
Q

What is the most common and important CNS disease in the UK?

A

Ataxia caused by cervical vertebral disease

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4
Q

What is tthe most clinically important (and relatively UK specific) neurological disease of the peripheral nervous system in the UK?

A

Equine grass sickness

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5
Q

What are the 2 degnerative central causes of neuro disease?

A

•Cervical Vertebral Malformation

–Type 1: Juvenile onset

–Type 2: Adult onset osteoarthritis

•Equine Degenerative Myeloencephalopathy

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6
Q

Name 2 anomalous Central causes of Neurological Disease (5)

A
  • Benign epilepsy of Arabian foals
  • Narcolepsy
  • Hydrocephalus
  • Occipitoatlantal malformations
  • Cerebellar Abiotrophy
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7
Q

What should you not do in benign epilepsy of arabian foals?

A

Euthanse - they grow out of it

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8
Q

Name 2 metabolic Central causes of Neurological Disease (4)

A
  • Hepatic encephalopathy
  • Perinatal asphyxia syndrome
  • Hypoglycaemia
  • Electrolyte abnormalities
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9
Q

Name a nutritional Central causes of Neurological Disease

A

•Equine Degenerative Myeloencephelapoathy

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10
Q

A) Name a common neoplastic Central causes of Neurological Disease

B) Name 2 rare (3)

A

A)

•Pituitary Pars Intermedia Dysfunction

B)

–Hamartoma

–Cholesterinic granuloma

–Epidural lymphosarcoma

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11
Q

Name infectious central causes of neuro disease:

A) Bacterial

B) Viral (4)

C) Spirochete

D) Other

A

A) Bacterial meningitis (foals), Abcessation

B) Equine Herpes Virus

  • *Togaviridae (Eastern, Western and Venuzuelan equine encephalitis)
  • *Flavivirus (West Nile Virus, Japanese encephalitis)
  • *Hendra virus, Borna, Rabies

C) Borrelia Burgdoferri

D) Equine Protozoal Myeloencehpalitis

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12
Q

Name an inflammatory Central cause of Neurological Disease

A

•Polyneuritis equi

–Cranial nerves and cauda equiina

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13
Q

Name 2 idiopathic central casues of neuro disease (4)

A
  • Idiopathic hypersomnia
  • Idiopathic epilepsy
  • Narcolepsy
  • Idiopathic headshaking
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14
Q

Name 3 toxic Central causes of Neurological Disease (5)

A
  • Rye Grass Staggers
  • (Lead – more in cattle)
  • Ivermectin/Moxidectin

–Usualy lipid bound but a lack of body fat means you can over dose

  • Fluphenazine
  • *Yellow star thistle
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15
Q

Name a vascular Central causes of Neurological Disease

A

•Postanaesthetic myelopathy

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16
Q

Define ataxia

A

•Lack of order, inconsistency

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17
Q

What is the grading of ataxia?

A

–Grade 0: Normal

–Grade 1: Minimal deficits noted, requires provocative testing to identify

–Grade 2: Mild abnormality seen at walk

–Grade 3: Easy to see at walk

–Grade 4: Very ataxic, may fall with provacative testing (circling)

–Grade 5: Recumbent (cannot stand)

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18
Q

What is wobblers syndrome?

A

Cervical vertebral malformation (CVM)

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19
Q

What are the 2 types of CVM and where do they occur?

A

–Type 1: Juvenille onset (C3-5 compression)

  • They might not present until 5 yo! As they were not worked
  • Fast growing
  • Common in yearlings/2 yo

–Type 2: Mature onset

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20
Q

A) Which breed is at risk of CVM?

B) Which gender?

A

A) Thoroughbred/ WB

B) Male

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21
Q

What are the 2 presentations of CVM and which one is ataxic at all times?

A
  • Functional (dynamic)
  • Absolute (static)

–Ataxic at all times

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22
Q

What are the clinical signs of CVM?

Include which limbs are worse and why

A

–Bilateral ataxia

•Hindlimbs worse than forelimbs

»Spinocerebellar tracts supply HL Sit superficial so more llikely to be affected by compression

  • Flexor weakness (toe dragging)
  • Extensor weakness (walking tail pull - UMN)

–Dysmetria ( lack of coordination) and spasticity

–Onset

•Usually gradual, may fluctuate with acute exacerbation

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23
Q

When are FL the same or worse than HL in CVM?

A

C5-T1 lesion

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24
Q

What are the 3 predispositions to type 1 CVM

A

•Affects young animals

–Less than 2 years of age

–Complex of developmental orthopaedic disease

•Nutritional

–High energy and protein

  • Never seen in wild equidae
  • Genetic
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25
Q

What is type 2 CVM in older horses?

Where is it typically seen in the horse?

A

–Osteoarthritis of cervical articular articulations

•Typically C5, C6, C

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26
Q

How can we diagnose CVM?

A

–Plain radiographs

  • Stenosis, OA
  • Minimal Saggital Diameter and sagittal ratios

–Suggestive of CVM

–Myelography

  • Required if contemplating surgery
  • Premortem confirmation

–Otherwise of little value

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27
Q

How do you calculate saggitial ratios?

A

•Divide the width of the spinal canal by the width of the corresponding vertebral body at the cranial aspect of the widest point

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28
Q

What does it mean if the saggital ratio is <50% ?

A

There is an 80% chance that a compressive lesion will be observed on a myelogram

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29
Q

What does it mean If the saggital ratio is > 50%?

A

then there is a 20% chance that the horse is a “Wobbler”

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30
Q

How do you definitively diagnose CVM? How is it done?

A

Myelogram:

–General anesthesia

–Plain radiographs

–Inject radiographic contrast media into intrathecal space (NOT epidural)

–Radiographs in neutral, flexion, extension

–Minimum 12 films

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31
Q

What is seen on CSF with CVM?

A

Normal

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32
Q

What is occasionally seen on EMG with CVM?

A

Cervical denervation

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33
Q

What are the 3 sites for CSF and which is the common one?

A

–Common site: Caudal at LS space

–Alantico occitpial

–Atlanto axial joint

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34
Q

How can we manage CVM? Indicate which is best in each type

A
  • Intra-articular glucocorticoids common in type 2
  • Exercise and nutritional restriction

–Help stabilize cases and occasional improvement in type 1 disease

•Surgical stabilisation

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35
Q

Name 4 factors to consider prior to surgery (7)

A
  • Duration of ataxia
  • Age of horse
  • Severity
  • Co-existing conditions
  • Intended use
  • Owner commitment
  • Sites affected (complete myelographic study) & dynamic vs static
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36
Q

How does CVM surgery work?

A
  • Allows fusion of vertebra over time
  • Fusion resolves vertebral instability
  • Bone remodeling
  • Prevents spinal cord

Compression

•Gradual improvement

in neurologic function

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37
Q

A) What condition looks similar to CVM?

B) What signs are seen?

A

A)

•Equine Degenerative Myeloencephalopathy (EDM)

B)

  • Symmetric tetraparesis and ataxia
  • Worse in rear limbs
  • Hyporeflexia
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38
Q

A) What horses does EDM affect?

B) How do we diagnose?

A

A) Young

B)

–CSF, blood, spinal radiographs and EMG normal

–Euthanise –confirm at PM

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39
Q

What is the pathophysiology of EDM?

A

•Neuroaxonal dystrophy

–Spinal cord (cervical)

–Brain stem sensory and proprioceptive nuclei

•Fibre degeneration

–Ascending and descending pathways

•Vit E/Se deficiency

–Antioxidants

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40
Q

What is seen on necropsy of an EDM horse?

A

•No gross lesions

–Neuroaxonal degeneration of brain stem, cervical and especially in thoracic and lumber spinal cord

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41
Q

What is the cause of EDM?

A

Unknown

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42
Q

How can you treat EDM?

A

–Generally valueless

–High doses of vit. E occasionally useful

–Not curative

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43
Q

How do you prevent EDM?

A

–Decrease incidence in siblings or on farms with history of disease

–Vit. E daily for 2 years

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44
Q

What are the signs of EHV 1?

A
  • Abortion, stillbirth, weak foals
  • Respiratory disease

–Neurological disease – Myeloencephalopathy

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45
Q

What disease do you get with EHV 4?

A

•Upper respiratory tract disease

–Abortion

–(? Myeloencephalopathy)

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46
Q

A) How are EHV 1 cases seen?

B) What signs are shown?

A

A) Sporadic

B)

–Other horses affected

•Oedema (scrotal, distal limb), pyrexia, respiratory

–Hind limb ataxia – symmetrical

•Urinary bladder paralysis (dribbling urine)

–Sacrococcygeal spinal cord

–May progressively ascend the CNS

–Decreased tail tone

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47
Q

What is the pathogenesis of EHV 1?

A

•Inhaled pathogen

–Nasal secretion, fetal or placental tissues

  • Cell associated viraemia
  • Vascular endothelial disease

–Vasculitis and thrombosis

•Secondary CNS necrosis

–Due to antigen-antibody complex formation

•Latency

–Persistence (trigeminal ganglia) with reactivation

48
Q

How can you diagnose EHV 1?

A

•CSF

–Xanthochromia

  • Low cellularity
  • Serology

–4 fold increase

–Very high titre and ataxia

•Virus isolation

–Nasal swab, buffy coat

•VIRAEMIA! –

–Heparinised whole blood!!

•Response to treatment

49
Q

How can we treat EHV 1?

A

•Corticosteroids

–Dexamethasone (0.1mg/kg IM BID) **

–Immune complex disease causing the diesease

•?Acyclovir/ Other cyclovirs/ Interferon(v exp)

–Viraemic stage has passed

–Acyclovir has poor bioavailability

•Nursing care

–Urinary bladder catheterisation

–Management of the recumbent horse

•Dimethylsuphoxide

–Anti-inflammatory, free radical scavenger

50
Q

How can we control EHV 1?

A

•Isolation of affected animals

–21 days after no new cases

51
Q

What is the prognosis of EHV 1?

A
  • Good if mild (able to stand and walk)
  • Guarded if recumbent
52
Q

How likely is a horse to have vestibular disease?

A

Uncommon

53
Q

Perrenial Rye grass staggers:

A) What causes it?

B) What disease is caused?

A

A) Mycotoxin (Neotyphodium Lolii)

B)

•Spinovestibulocerebellar disease

–Ataxia, muscle tremor, Dysmetria

»Worsens with exercise

»Tremor includes eye muscles

54
Q

What disease is currentl exotic to UK, common the in the US and caused by Sarcocytis neurona (and Neospora hughesi)?

A

•Equine Protozoal Myeloencephalitis (EPM)

55
Q

Why may equine protozoal myeloencephalitis be over diagnosed?

A

Non specific neurological disease with diffue signs

56
Q

What are the classic sign of Equine Protozoal Myeloencephalitis (EPM)?

A

–Classic signs – Unilateral Gluteal atrophy, paresis, horners syndrome, mastecatory atrophy

57
Q

How can we diagnose Equine Protozoal Myeloencephalitis (EPM)?

A
  • Blood serology – Exposure NOT disease
  • CSF antibodies– variable (western blot)
  • Many FALSE POSITIVES
  • Definitive diagnosis requires

–Neurological deficits

–Antibodies in CSF

–Lesions on PM

•lymphoid perivascular cuffing, macrophages and eosinophils

58
Q

How can we treat EPM?

A

•FOLIC ACID INHIBITORS:

–Pyrimethamine/Sulfamethoxazole (Daraprim® and sulfa)

–Trimethoprim/sulfadiazine

  • Synergistic
  • Coccidiostatic,
  • Rx 3- 5 months
  • Ponazuril (Marquis®)
  • Toltrazuril (Baycox®)
  • Diclazuril
59
Q

How can we prevent EPM?

A
  • Elimination of opossums??
  • Prevent access of opossums to feed
  • Remove carrion
  • Vaccine
60
Q

Vrial encephalitidies:

A) What are they all in the UK?

B) Name 2 (3)

A

A) Exotic and notifiable

B)

•Arborviruses

–Arthropod-borne

  • Large scale losses
  • Zoonotic

–Flaviviridae – West Nile Virus (less severe)

–Togaviridae – Severe

61
Q

Togaviruses:

A) What do they all produce?

B) What are the clinical signs?

C) Who are reservoir?

D) Who is the vector?

A

A) Cerebral disease

B)

  • Fever, colic, anorexia
  • Acute / peracute CNS signs

–Dementia, ataxia, seizures, blindness

C) Bird

D) Mosquito

62
Q

How can we prevent togaviruses?

A

Vaccine

63
Q

West Nile Virus:

A) What are the clinical signs?

B) How do we diagnose?

C) How do we treat?

A

A)

–Caudal spinal cord involvement

–Ataxia, hyperaesthesia, muscle fasiculations, weakness

–Milder clinical signs than EEE, VEE, WEE

B) Antigen/antibody in CSF/blood

C) Nursing, anti-inflammatory treatment

64
Q

What are the signs of rabies?

A

–Aggression – quite rare

–Hyperaesthesia

–Paresis/Paralysis

–Fever

–Ataxia

–Seizures

65
Q

What does hepatic encepalopathy occur due to the effects of?

A

–Ammonia and other false transmitters

•Liver failure

–Unable to breakdown intestinal NH3

•Congenital abnormality

–Portosystemic shunt (rare)

•Gastrointestinal disease

–Overproduction of NH3

–Exceeds rate of metabolism

66
Q

What are the signs of with hepatic encephalopathy?

A

•Signs of cerebral dysfunction

–Seizures, circling, head turn.

–Covered in more detail in other species

67
Q

Perinatal Asphyxia Syndrome (PAS):

A) What is it?

B) What is dysfunctonal?

C) What causes it?

D) What are they like for first 12-24 hours?

A

A) Multisystemic condition of newborn foal due to hypoxia at birth?

B) Neurological system, GI, Urinary dysfunctions

C) Caused by perinatal asphyxia

  • Unobserved foaling
  • Red bag delivery

D) Normal for first 12-24 hours

68
Q

What are the clinical signs of PAS?

A
  • Loss of suckle reflex
  • Recumbency, lethargy, wandering, head pressing, vocalisation, dysphagia
  • Seizures, head tilt, blindness
  • Apnea
69
Q

What are the non neuro signs of PAS?

A
  • Hypotension
  • Reduced GI blood flow, necrotizing enterocolitis, ileus, reflux, colic
  • Renal - oliguria
  • Respiratory – apnoea
  • Pulmonary artery hypertension

–Hypoxia and acidaemia

–Maintains fetal circulation

•Endocrine

–Glucose metabolism

•Secondary: Sepsis – due to recumbency

–Respiratory / umbilical

70
Q

How can we treat PAS?

A

•Anticonvulsant

–Diazepam

•Respiratory, circulatory, renal support

71
Q

A) What is narcolepsy?

B) Name 2 common breeds (6)

A

A) Excessive daytime sleepiness

B) Suffolk, Appaloosa , miniature horse, Shetland, Fell, Welsh Pony

72
Q

What are the mechanisms of collapse?

A

–The brain is not keeping the animal upright (or conscious)

•Vestibular disease, cerebellar disease, metabolic disease, pressure, epilepsy, narcolepsy

–The nerves are not working

  • Motor neurone disease, myasthenia gravis
  • Electrolyte abnormalities interfering with conduction

–The muscle are not working

  • Exercise induced collapse
  • Other metabolic disorders of muscles
  • Electrolyte abnormalities interfering with conduction
73
Q

What are the 3 systems of collapse?

A

•Cardiovascular and respiratory causes

–Collapse during exercise / excitement

•Metabolic causes

–Rest, (during) or after exercise

•Neurological causes

–At rest (during or after exercise)

–Exercise may make some worse

74
Q

What causes:

•Inappropriate sleep in standing ADULT

–No REM

–Rapid or slow onset of recumbency

  • Wake spontanously
  • May cause trauma
  • May be triggered by specific stimuli
A

Idiopathic hypersomnia

75
Q

Name 2 reasons an animal will have recumbent sleep deprivation (3)

A
  • Thoracolumbar pain
  • Bilateral lameness
  • Behavioural (herd dynamics)
76
Q

What nerves are affected by injuries involving the head?

A

Vestibuar and facial nerves

77
Q

How can we manage head trauma?

A
  • Control seizures
  • Consider fluid status / nutrition
  • Patience
  • Corticosteroids

–No evidence for good

•DMSO

–Osmotic diuretic > reduces ICP

–Stabilizes lysosomes

–Free radical repair

•Mannitol

–Reduces ICP

78
Q

Name 2 indications for euthanasia in spinal trauma? (4)

A
  • Recumbent for > 5 days
  • Worsening clinical signs
  • Muscle pathology (myoglobinuria)
  • Colic, uncontrollable pain
79
Q

Name a degenerative Peripheral causes of Neurological Disease

A

Equine grass sickness

80
Q

Name an anomalous Peripheral causes of Neurological Disease (2)

A
  • Hyperkalaemic periodic paralysis
  • Polysaccharide storage myopathy
81
Q

Name a metabolic Peripheral causes of Neurological Disease

A

•Synchronous diaphragmatic flutter

82
Q

Name a nutrional Peripheral causes of Neurological Disease

A

•Equine Motor Neurone Disease

83
Q

Name a neosplastic Peripheral causes of Neurological Disease

A

•Mediastinal Neoplasia (Horners syndrome)

84
Q

Name an infectious Peripheral causes of Neurological Disease (2)

A
  • Guttural Pouch Empyaema (CRS)
  • Vestibular disease
85
Q

Name an inflammatory cause of Peripheral causes of Neurological Disease

A

•Polyneuritis equi

86
Q

Name 2 idiopathic Peripheral causes of Neurological Disease (3)

A
  • Equine Recurrent laryngeal neuropathy (CRS)
  • Shivering (MSK)
  • Stringhalt (MSK)
87
Q

Name a toxic cause of Peripheral causes of Neurological Disease (2)

A
  • Botulism
  • Tetanus
88
Q

Name a traumatic Peripheral causes of Neurological Disease (2)

A
  • Postanaesthetic neuropathies (eg radial)
  • Facial nerve damage
89
Q

What is seen with vestibular disease?

A
  • head tilt and circle in ipsilateral direction.
  • nystagmus “fast phase away” from lesion
90
Q

What is vestibular disease usually due to?

A

•Usually due to ear disease

–Trauma (basisphenoid fracture)

–Otitis media/interna

91
Q

Polyneuritis equi
Cauda equina neuritis:

A) Which nerve roots? (3)

B) What signs are seen?

A

A) Proximal spinal, cranial sensory, motor nerve roots

B) Urinary and faecal incontinence

  • Occasionally cranial nerve disease (head tilt)
  • Tail, anal, penile, perineal areflexia, atonia and analgesia
92
Q

Where is demyelination in polyneuritis Equi?

What can be given?

A

A) Sacrococcygeal roots of cauda equina

B) Anti-p2 myelin antibodies

93
Q

What is equine grass sickness?

A
  • A generalised dysautonomia affecting primarily the enteric nervous system
  • Non GI effects aid in its diagnosis
94
Q

What is the epidemiology of grass sickness?

A

–Young male animals

–Pasture

–No previous exposure to EGS

–Change of pasture in previous 2 weeks

–Dry weather

–Previous cases on same pasture

–Cool dry weather, Frost

95
Q

What are the GI clinical signs of grass sickness?

A

•Abdominal pain

–Ileus due to myenteric neuronal degeneration

•loss of parasympathetic control

–Dehydration of colonic contents - impaction

–Liver pathology

•Nasogastric reflux

–Loss of lower oesophageal sphincter tone & ileus

–Horses aren’t usually sick

•Dysphagia

–Loss of parasympathetic control to pharynx (Glossopharyngeal nerve)

96
Q

What are the non GI clinical signs of grass sickness?

A

•Tachycardia

–Loss of vagal control (Perkins et al 2000), increased sympathetic outflow (John et al 2001)

–Heart rate often higher than would be expected for degree of pain

•Ptosis

–Parasympathetic dysfunction to CN III/VII

•Levator palpebrae superioris, levator anguli oculi

–Mullers muscle (sympathetic innervation)

–Non specific - debilitating disease

•Rhintis Sicca - Snuffles

–Loss of parasympathetic supply to mucosal glands of nasal mucosa

–Seen in late subacute/chronic disease

•Muscle fasiculations and weakness (Narrow based stance)

97
Q

How do you diagnose grass sickness?

A

Ileal biopsy

History:

•Young horse at pasture

–Access to pasture within last 7 days

–Most horses 2 - 7 years old

•History of recent movement to new pasture

–Within preceeding 2 months

–Other EGS cases on same pasture

•Seasonal bias

–April to July

•Climatic factors

–Cool dry weather / Frost

98
Q

Name differentials for dysphagia in the horse

A

–EGS

–Botulism

–Lead toxicity

–Anatomical pharyngeal abnormalities

–Sub epiglottic cyst, cleft palate

–Foreign body

–Pharyngeal, oesophageal

–Guttural pouch disease

–Mycosis, empyaema

99
Q

How can we treat/support grasss sickness?

A
  • Nursing care is paramount for a successful outcome
  • Treat each individual problem
  • Analgesia
  • Feeding

–Small feeds every 30 - 60 minutes

–Hand feeding (don’t leave horse to eat)

–Hand grazing

–Varied diets

•Appetite stimulation -

–Diazepam 0.02mg/kg IV BID-TID – not as successful as it cats

•Prokinetics

100
Q

What is Equine Motor Neuron Disease (EMND) associated with?

A

•Vitamin E/ Se deficiency

101
Q

What are the signs of equine motor neurone disease?

A

•Weight loss but ravenous appetite

–symmetrical neurogenic muscle atrophy (LMN sign)

–Triceps, biceps, quadriceps

•Fine fasiculations

and coarse trembling

  • Lie down frequently
  • Weakness
  • Look worse standing than walking
  • Stand with 4 limbs close together

–Elephant on a barrel

–Continuously shift weight on hindlimbs (unable to lock stifles)

  • Excessive sweating
  • Low head carriage
  • Tail elevation
  • Short strided gait,
  • No ataxia
  • Some increase in Creatine Kinase and aspartate aminotrasnferase

–Muscle cell damage

•EMG – see evidence of denervation

–Positive sharp waves or fibrillation potentials

•Black teeth

102
Q

What is seen on retina exam of a horse with EMND?

A

–Mosaic pattern of brown pigment in the tapetal fundus

•Lipofuscin deposition

–Similar retinopathy observed in dogs experimentally fed

103
Q

How do you diagnose EMND?

A
  • Clinical signs
  • EMG changes: denervation
  • Retinal exam (changes present in 80% of cases)
  • Biopsy sacrocaudalis dorsalis medialis muscle
104
Q

What is the pathology of EMND?

A
  • No gross lesions (pale vastus muscles)
  • Neuronal degeneration with depletion of motor neurons in the ventral horns of the spinal cord
  • Axon degeneration in ventral roots and peripheral nerves
  • Neurogenic muscle atrophy of Type 1 muscle fibers

–Passive stay apparatus

•Lipopigment deposition in capillaries of spinal cord

105
Q

What is the treatment of EMND?

A
  • Unrewarding
  • Vitamin E
  • Green grass
  • Possible slow improvement (minimal)
  • Prognosis is poor
  • Always remain weak and thin
  • Euthanasia
106
Q

What are the predisposing factors to EMND?

A

–Vitamin E deficiency

–Oxidative disease

107
Q

What is seen in a horse with Idiopathic Headshaking?

A

•Vertical movements of head in repeated fashion

–May rub nasal areas on legs

–Occasionally strike out

108
Q

What are the possible causes of idiopathic headshaking?

A

–Multifactorial, not consistent between horses

–Behavioral / stereotypical

–Allergic Rhinitis

–Photic

–Trigeminal stimulation

109
Q

What therapies can we initially try ruling out with idiopathic headshaking treatment?

A
  • Cyproheptadine (allergies)
  • Carbemazepine (epilepsy and neuropathic pain)
  • Steroids
  • Sunglasses
110
Q

How can we treat idiopathic headshaking?

A

–Medical therapy

  • Cyproheptadine
  • Carbamazepine
  • Steroids

–Physical therapy

•Nose nets (tights), fly shields

–Surgery

•Nerve compression

111
Q

What view is this?

A

Flexion

112
Q

What view is this?

A

Extension

113
Q

What can be seen here?

A

Left ear paralysis

114
Q

What can be seen here?

A

Droopy Left eyelid

115
Q

What can be seen here?

A

Left muzzle paralysis (nose deviates to Right)

116
Q

What is this?

A

Equine Motor Neurone Disease retina

Equine Final Year (102 decks)

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