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NEU2 > Equine neurology: central > Flashcards

Equine neurology: central Flashcards

1
Q

Identify the signs of central and peripheral disorders of the nervous system in horses

A
  • Central: ataxia, seizures/collapse, blindness, autonomic dysfunction (bladder, GIT, other)
  • Peripheral: weakness, autnomic dysfunction (bladder, dysphagia, GIT)
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2
Q

List the common disorders of the nervous system in horses

A
  • Botulism
  • Equine herpesvirus
  • Equine degenerative myeloencephalopathy (EDM)
  • Peripheral neuropathies
  • Equine Grass Sickness
  • Idiopathic hypersomnia
  • Hepatic encephalopathy
  • Perinatal asphyxia syndrome
  • Idiopathic headshaking
  • Vestibular disease
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3
Q

List the uncommon, but important disorders of the nervous system in horses that should always be placed on the differentials list

A
  • Viral encephalitidies
  • Polyneuritis equi
  • Horners syndrome
  • Epilepsy incl. benign epilepsy of Arab foals
  • Narcolepsy
  • Rye grass staggers
  • Bacterial meningitis
  • Equine protozoal myeloencephalitis
  • Toxicities
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4
Q

List the uncommon disorders of the equine nervous system that can be managed independently

A
  • Cervical vertebral malformation

- Tetanus

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5
Q

What is the most important central nervous system disease of horses in the UK?

A

Ataxia due to cervical vertebral disease

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6
Q

What is the most important peripheral nervous system disease of horses in the UK?

A

Equine grass sickness

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7
Q

List the differentials for central neurological disease of horses that fall into the “degenerative” category

A
  • Cervical Vertebral malformation (type 1 juvenile onset, type 2 adult onset osteoarthritis)
  • Equine degenerative myeloencephalopathy
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8
Q

List the differentials for central neurological disease of horses that fall into the “Anomalous” category

A
  • Benign epilepsy of Arabian foals (not just Arabs)
  • Narcolepsy
  • Hydrocephalus (foals, severe ataxia, intention tremor)
  • Occipitoatlantal malformations
  • Cerebellar abiotrophy (progressive cerebellar degeneration)
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9
Q

List the differentials for central neurological disease of horses that fall into the “metabolic” category

A
  • Hepatic encephalopathy
  • Perinatal asphyxia syndrome
  • Hypoglycaemia, Electrolyte abnormalities (both uncommon)
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10
Q

List the differentials for central neurological disease of horses that fall into the “nutritional” category

A

Equine Degenerative Myeloencephalopathy

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11
Q

List the differentials for central neurological disease of horses that fall into the “neoplasia” category

A
  • Pituitary Pars Intermedia Dysfunction

- Others rare: hamartoma, cholesterinic granuloma, epidural lymphosarcoma

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12
Q

List the differentials for central neurological disease of horses that fall into the “inflammatory infectious” category

A
  • Bacterial: bacterial meningitis (foals), abscessation
  • Spirochete: Borrelia burgdorferi
  • Viral: EHV, togaviridae, Flavivirus, Hendra virus, Borna, Rabies
  • Other: Equine protozoal myeloencephalitis
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13
Q

Which of the viral infectious that cause neurological signs in horses are notifiable?

A
  • Togavirus (Eastern, Western, Venezuelan equine encephalitis)
  • Flavivirus (West Nile virus, Japanese encephalitis)
  • Hendra virus
  • Borna virus
  • Rabies
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14
Q

List the differentials for central neurological disease of horses that fall into the “idiopathic” category

A
  • Idiopathic hypersomnia
  • Idiopathic epilepsy
  • Narcolepsy
  • Idiopathic headshaking
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15
Q

List the differentials for central neurological disease of horses that fall into the “toxic” category

A
  • Rye grass staggers
  • Lead
  • Ivermectin/moxidectin
  • Fluphenazine
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16
Q

List the differentials for central neurological disease of horses that fall into the “vascular” category

A

Post anaesthetic myelopathy

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17
Q

List the differentials for central neurological disease of horses that fall into the “inflammatory inflammatory” category

A

Polyneuritis equi

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18
Q

What is polyneuritis equi?

A

Abnormalities of cranial nerves and cauda equina

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19
Q

Describe the signs of rye grass staggers in horses

A
  • Wide based stance
  • Signs of cerebellar ataxia
  • Muscle tremors
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20
Q

Explain how toxicity due to ivermectin/moxidectin can develop

A

Needs to be lipid bound to easy to overdose horses with lipid avialable e.g. foals, skinny horses

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21
Q

What is fluphenazine typically used for and what is the potential effect?

A

Used by trainers to calm horses, can cause seizure like activity

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22
Q

Define the grades of ataxia in horses

A
  • Graded 0-5
    0: Normal
    1: Minimal deficits noted, required provocative testing to identify e.g. tight circling
    2: Mild abnormality seen at walk
    3: Easy to see ataxia at walk
    4: Very ataxic, may fall with provocative testing
    5: Recumbent, cannot stand
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23
Q

What is cervical vertebral malformation also known as?

A

Wobbler syndrome

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24
Q

What are the 2 types of cervical vertebral malformation in horses?

A
  • Type 1: juvenile onset

- Type 2: mature onset

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25
Q

In which groups of horses if Cevical vertebral malformation commonly seen?

A
  • Young, fast growing
  • Weanlings, yearlings
  • TBs and WBs
  • Males
  • Often seen earlier in racehorses as start training earlier, in others not until 4-5yo
  • Horses given excess concentrate
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26
Q

Where is the compression from Cervical vertebral malformation in horses typically located?

A

C3-C5 typically

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27
Q

What does it mean when CVM is described as being functional or absolute?

A
  • Functional: position of head can exacerbate the degree of ataxia
  • Absolute: static lesions causing static spinal cord compression
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28
Q

List the clinical signs of Cervical vertebral malformation in horses

A
  • Bilateral ataxia
  • Dysmetria and spasticity
  • Gradual onset
  • Often associated with trauma
  • May flare up
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29
Q

Describe the ataxia seen in CVM of horses

A
  • HL worse than FLif lesion C3-C5
  • FL similar/worse than HL if lesion C5-T1
  • Flexor weakness leading to toe dragging
  • Extensor weakness (walking tail pull)
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30
Q

What are the predisposing factors for CVM type 1?

A
  • Young horses <2yo
  • Nutritional: high plane of energy and high protein
  • Genetic: more common in certain breeds
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31
Q

Describe the development of CVM type 2

A
  • Old horses
  • Osteoarthritis of cervical articular articulations (new bone covering intervertebral space, extends into spinal cord, initially soft tissue then bony compression of spinal cord)
  • May be traumatic in origin
  • Typically C5, 6, 7, may be asymmetrical
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32
Q

List the tests used in the diagnosis of CVM of horses

A
  • Radiography
  • Myelography
  • CSF
  • Electromyelography
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33
Q

Describe the radiographic findings that are suggestive of CVM

A
  • Stenosis, osteoarthritis
  • Minimal sagittal diameter and sagittal ratios
  • Changes in caudal epiphysis of vertebrae (processes, ski-jump appearance)
  • Sagittal ratio: divide width of spinal canal by width of corresponding vertebral body at cranial aspect of widest point, <50% ratio = 80% chance of compressive lesion on myelogram. >50% ratio = 20% chance horse has CVM
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34
Q

When is myelography indicated in the diagnosis of CVM in horses?

A

If contemplating surgery

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35
Q

Describe the method for myelography of suspected CVM in horses

A
  • Standing or GA
  • inject radiographic contrast media into intrathecal space
  • Radiogrpahs in neutral, flexion and extension
  • Minimum of 12 films
  • May not always find lesions
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36
Q

What findings would be indicative of CVM on myelography?

A
  • Compression of dye column
  • 25% reduction of dye column at site that is affected
  • May not always find lesion
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37
Q

Describe the CSF of a horse with CVM

A

Usually normal

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38
Q

What are the sampling sites for CSF in horses?

A
  • Caudal sample from lumbosacral space
  • Atlantoaxial joint
  • Atlantooccipital joint
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39
Q

What may be found on EMG in a horse with CVM?

A

Occasionally cervical denervation

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40
Q

Describe the management of CVM in the horse

A
  • Intra-articular glucocorticoids
  • Exercise and nutritional restriction
  • Surgical stabilisation
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41
Q

Outline and evaluate the use of surgical stabilisation in the treatment of CVM

A
  • Decompression and cervical stabilisation
  • Remove soft tissues, drill Bagby basket into affected joint space
  • Bone graft and fuses joint
  • Likely to generate only 1 grade of improvement
42
Q

Outline the factors that should be considered prior to surgery for the treatment of CVM

A
  • Duration of ataxia
  • Age of horse
  • Severity
  • Co-existing conditions
  • Intended use post surgery
  • Owner commitment (horse likely to still have some ataxia after)
  • Sites affected and whether this is dynamic or static
  • Poor prognosis for trotters vs pacers
  • Patience required, will take 1 year for results
  • Management of owner expectations
43
Q

How does surgery for CVM work?

A
  • Allows fusion of vertebra over time
  • Fusion resolves vertebral instability
  • Bone remodelling takes place
  • Prevents spinal cord compression
  • Gradual improvement of neurological function
44
Q

Describe the clinical presentation of Equine Degenerative Myeloencephalopathy

A
  • Similar to CVM
  • Symmetric tetraparesis and ataxia
  • Worse in HL
  • Hyporeflexia
  • Young horses (birth to 2yo)
45
Q

How is EDM diagnosed?

A
  • Diagnosis of exclusion - CSF, blood, spinal radiography and EMG all normal
  • Once everything ruled out, euthanase and confirm diagnosis at PM
46
Q

Describe the pathophysiology of EDM

A
  • Neuroaxonal dystrophy of cervical spinal cord and brain stem sensory and proprioceptive nuclei
  • Fibre degeneration of ascending and descending pathways
  • vit E/selenium deficiency allowing free radicals to cause damage
47
Q

What are the main differences between CVM and EDM?

A
  • CVM: abnormalities seen on radiography, myelography and sometimes EMG, no abnormalities in EDM
  • EDM can be seen in wild equidae, CVM is not
48
Q

What would these findings on necropsy be indicative of in a young horse with symmetric ataxia and hyporeflexia?
Neuroaxonal degeneration of brain stem, cervical and thoracic and lumbar spinal cord

A

Equine Degenerative Myeloencephalopathy

49
Q

Outline the treatment of EDM

A
  • Generally valueless
  • High doses of vit E occasionally useful
  • Not curative, once damage done, will not recover
50
Q

How can EDM be prevented?

A
  • Vitamin E supplementation daily for 2 years
51
Q

Describe the clinical signs of EHV-1

A
  • Abortion, stilbirth, weak foals
  • Respiratory disease
  • Neurological disease - myeloencephalopathy
  • Ataxia, acute recumbency usually seen
  • Oedema of scrotum, distal limb, pyrexia
  • Symmetrical HL ataxia
  • Urinary bladder paralysis (dribbling urine)
  • Decreased tail tone
52
Q

Describe the pathogenesis of neurological disease by EHV-1

A
  • Causes vascular endothelial disease due to antigen-antibody complex formations
  • Vasculitis and thrombosis with secondary CNS necrosis
  • Cell associated viraemia
53
Q

Describe how horses can contract EHV-1

A
  • Inhaled pathogen from nasal secretion, fetal or placental tissue
  • Direct spread between individuals most important
  • Humans can act as fomites
  • Can persist in trigeminal ganglia and be reactivated
54
Q

What methods are used in the diagnosis of EHV-1?

A
  • CSF
  • Serology
  • Virus isolation
  • Response to treatment
55
Q

What findings on CSF would indicate EHV-1?

A

Xanthochromia, low cellularity

56
Q

What findings on serology would indicate EHV-1?

A

4 fold increase - 80% of UK herd exposed to EHV previously so serology may be positive even if not currently infected

57
Q

Outline the method of viral isolation for diagnosis of EHV-1

A
  • Nasal swab
  • Heparinised whole blood
  • Thick buffy coat and viraemia
  • Need to be in chronic phase of infection in order to get results
58
Q

Describe and justify the treatment of EHV-1

A
  • Corticosteroids: dex 0.1mg/kg
  • Acyclovir (poor bioavailability in the horse)/other cyclovirs/interferon
  • Nursing care e.g. urinary bladder management, turning recumbent horses
  • Dimethylsulphoxide (DMSO)
59
Q

Why are corticosteroids important in the treatment of EHV-1?

A

Is an autoimmune caused condition

60
Q

Discuss the use of DMSO in the treatment of EHV-1

A
  • Anti-inflamm
  • Free radical scavenger
  • Some evidence, but poor, for effects in CNS in large animals
  • Unlikely to do harm
61
Q

Outline the control of EHV-1

A
  • Isolation of affected animals

- Follow HBLB code of conduct

62
Q

Discuss the prognosis of a hrose with EHV-1

A
  • Good if mild (able to stand and walk), can return to normal function
  • Guarded if recumbent, some do recover, others die (lots of comorbidities if recumbent e.g. anorexia, msucle damage, inability to urinate)
63
Q

Which equine herpes viruses cause neurological signs?

A

EHV-1 and EHV-4

64
Q

What causes Perennial Grass staggers in horses?

A

Mycotoxin Neotyphodium lolii

65
Q

Explain how horses become affected by perennial rye grass staggers

A
  • Mycotoxin taken up by plants and concentrated in leaves, esp. old leaves
  • Heavily grazed pasture is risk factor
  • Ingestion of leaves or imported rye-grass hay commonly causes disease
66
Q

Describe the signs of perennial rye grass staggers in horses

A
  • Spinovestibulocerebellar disease
  • Ataxia, muscle tremor, dysmettria
  • Worse with exercise
  • Tremor incl. eye muscles
  • Tends to occur in outbreaks
  • Recover spontaneously
67
Q

Where is perennial rye grass staggers more commonly seen?

A

Uncommon in UK, more in Southern Ireland (wetter)

68
Q

Describe the prevalence of Equine Protozoal Myeloencaphalitis (EPM)

A

Exotic to UK, common in USA (50% of horses in USA seropositive) - may be seen in UK in horses shortly after import from USA

69
Q

What causes Equine Protozoal Myeloencephalitis?

A
  • Sarcocytis neurona
  • Neospora Hughesi
  • Single protozoan, migrates through CNS and spinal cord causing very focal disease, can sit in single spinal cord tract
70
Q

Describe the clinical signs of EPM

A
  • Often unilateral disease, very bizarre signs (pretty much anything)
  • Asymmetrical ataxia, head tilt, hyperaesthesia
  • Unilateral gluteal atrophy
  • Paresis
  • Horner’s syndrome
  • Mastecatory atrophy
  • Is multifocal, necrotic and non-suppurative
71
Q

How is EPM diagnosed?

A
  • Blood serology (only shows exposure)
  • CSF antibodies (Western blot, variable, suggestive but not diagnostic)
  • Definitive requires neurological deficits, antibodies in CSF, lesions in PM (lymphoid perivascular cuffing, macrophages and eosinophils)
72
Q

What is the treatment for EPM?

A

Folic acid inhibitors

73
Q

Describe the prevention of EPM

A
  • Elimination of opossums (important vectors)
  • Prevent access of opossums to feed
  • Remove carrion
74
Q

Name the Arboviruses that cause neurological disease in horses and state how they are spread

A
  • Arthropod borne
  • Flaviviridae (West Nile Virus)
  • Togaviridae
75
Q

Discuss the importance of the neuropathy causing Arboviruses

A
  • Zoonotic, cause large scale losses
  • Flaviviridae less severe than Togaviridae
  • Both exotic to Uk and notifiable
  • Flavi unlikely to be risk to Uk as mosquitoes required for spread not present in UK
76
Q

Name the 3 types of Togavirus and state their prognosis

A
  • Eastern Equine Encephalitis: very poor prognosis
  • Western Equine encephalitis: Fair prognosis
  • Venezuelan Equine encephalitis: very poor prognosis
77
Q

Describe the disease caused by Togavirus

A
  • All 3 types cause diffuse cerebral disease, are neutrotropic
  • Clinical signs: fever, colic, anorexia
  • Acute/peractue CNS signs: dementia, ataxia, seizure, blindness
78
Q

How can Togavirus be controlled?

A

Vaccination

79
Q

Give the reservoir and vector for Arboviruses

A
  • Reservoir: birds

- Vector: mosquito

80
Q

Describe the clinical signs of West Nile virus in horses

A
  • Caudal spinal cord involvement
  • Ataxia, hyperaesthesia, muscle fasciculations, weakness
  • Milder clinical signs than Togavirus
81
Q

What is the prognosis for West Nile Virus in horses?

A

60% recover, worse if <5yo, recumbent, weak. Some may relapse

82
Q

Describe the diagnosis and treatment of West Nile Virus in horses

A
  • Diagnosis: antigen/antibody in CSF/blood

- treatment: nursing, anti-inflammatory treatment

83
Q

Discuss the use of vaccines in the control of West Nile Virus in horses

A
  • Vaccine available

- But mortality and morbidity falls as becomes endemic

84
Q

Describe the clinical signs of Japanese encephalitis (flavivirus)

A
  • Mania

- Hyperaesthesia

85
Q

Describe the clinical signs and control of Hendra virus in horses

A
  • Death in horses (and humans)
  • Some neuro signs
  • Vaccine available for horses
86
Q

Describe the clinical signs of rabies in horses

A
  • Same as other species
  • Aggression (rare)
  • Hyperaesthesia
  • Paresis/paralysis
  • fever
  • Ataxia
  • Seizures
87
Q

What causes hepatic encephalopathy in horses?

A

Toxic effects of ammonia and other false transmitters

88
Q

Explain the mechanisms of hepatic encephalopathy in horses

A
  • Liver failure = unable to break down intestinal NH3
  • Congenital abnormality e.g. portosystemic shunt (rare)
  • Primary gastrointestinal disease (e.g. severe colic, gastritis) leading to overproduction of NH3 by intestinal flora, exceeding rate of metabolism
89
Q

Describe the clinical signs cerebral dysfunction as a result of hepatic encephalopathy

A

Seizures, circling, head turn, head pressing

90
Q

Describe the management of hepatic encephalopathy in horses

A
  • Reduce ammonia production by flora through use of antibiotics
  • Drugs that reduce uptake of ammonia
91
Q

What is Perinatal Asphyxia Syndrome in horses and what is it caused by?

A
  • Aka Hypoxic Ischaemia Encephalopathy, Dummy Foals, Barkers, Neonatal maladjustment syndrome
  • Multisystemic condition of newborn foal: neuro, GI, urinary
  • caused by perinatal asphyxia due to unobserved foaling or red bag delivery
92
Q

Describe the presentation of Perinatal Asphyxia Syndrome

A
  • Appear normal for first 12-24 hours (i.e. stand and suck)
  • Then become recumbent, lose suck reflex, start to seizure, resp centre depressed (apnea)
  • Wandering, head pressing, vocalisation, dysphagia
  • Seizures, head tilt, blindness
93
Q

Describe the non-neurological signs of Perinatal Asphyxia Syndrome in horses

A
  • Hypotension: reduced GI blood flow, necrotising enterocolitis, ileus, reflux, colic
  • Oliguria
  • Apnea
  • Pulmonary artery hypertension: hypoxia and acidaemia (maintains fetal circulation)
  • Glucose metabolism affected
  • Secondary sepsis (due to recumbency)
94
Q

Describe the management of Perinatal Asphyxia Syndrome

A
  • 7-10 days intense 1to nursing, very expensive
  • Anticonvulsant diazepam
  • Respiratory (ventilator for several days), circulatory and renal support
  • Must be hospitalised
95
Q

What is narcolepsy?

A

Excessive daytime sleepiness, with REM sleep occurring +/- cataplexy

96
Q

How does narcolepsy develop and how does i affect the daily life of the horse?

A
  • Pattern of sleepiness
  • Can be roused with stimulation
  • Usually safe to work and will not sleep while ridden but may collapse if stop working for long periods
97
Q

Which horse breeds are predisposed to narcolepsy?

A

Suffolk, Appaloosa, miniature horse, Shetland, Fell, Welsh pony

98
Q

What are the main mechanisms of collapse?

A
  • Brain not keeping animal upright/conscious
  • Nerves not working
  • Muscles not working
99
Q

List diseases of the horse that may cause collapse due to the brain not keeping the animal upright/conscious

A
  • Vestibular disease
  • Cerebellar disease
  • Metabolic disease
  • Pressure
  • Epilepsy
  • Narcolepsy
100
Q

List the diseases of eh horse that may cause collapse to the the nerves not working

A
  • Motor neurone disease
  • Myasthenia gravis
  • Electrolyte abnormalities interfering with conduction

NEU2 (23 decks)

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