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Equine > Neurological exam of the horse and neuro diseases > Flashcards

Neurological exam of the horse and neuro diseases Flashcards

1
Q

What does hypermetria, intetion tremors and weakness point towards

A

Cerebellar lesion

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2
Q

What is the first question to ask during neurological exam

A

Are there are cranial nerve signs present

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3
Q

What virus can have neurological and respiratory presentations

A

Equine herpes virus

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4
Q

What localisation would blindness, dementia, seizure, mild ataxia point towards

A

forebrain

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5
Q

What location would gait CN signs, gait deficits, tetraparesis and altered consciousness point towards

A

Brainstem

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6
Q

If we see tail/bladder paralysis, perineal hyperalgesia what localistion of lesion does this point towards

A

Sacral

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7
Q

What behavioural abnormalities might we see with forebrain disease

A

Yawning
Wandering
Psychosis
Circling
Head pressing
Seizures

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8
Q

What are some possible causes of forebrain dysfunction

A

Trauma to head
Hyponatraemia, hypoglycaemia
Hepatic encephalopathy hyperammoniaemia
Toxicity
Space occupying lesions
Intracarotd drug administration

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9
Q

How quickly will a horse react to an intra carotid drug injection

A

Immediately off the needle

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10
Q

How can we classify seizures

A

Either generalised or focal
Then focal split into simple focal or complex focal +/- secondary generalisation

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11
Q

Difference between simple focal and complex focal seizures

A

Complex focal has impaired consciousness

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12
Q

Signs of a generalised seizure

A

Loss of consciousness
Tonic clonic contraction
Limb paddling
Loss of continenance
Jaw clamping

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13
Q

WHen might strabismus be normal

A

NEwborn foals

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14
Q

What CN dysfunction causes a ventrolateral strabismus

A

CN III oculomotor nerve

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15
Q

What CN dysfunction causes a medial strabismus

A

CN VI

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16
Q

What CN dysfunction causes a dorsal strabismus

A

CN IV

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17
Q

Pathway for pupillary light response

A

Photoreceptors –> optic enrve –> optic chiasm with 90% decussation –> contralateral optic tract –> visual cortex + some to pretectal nuclei to prasymp CN III nuclei for pupil constriction (some crossing back here hence consensual response)

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18
Q

Which nerve is responsible for pupil constriction in PLR

A

CN III

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19
Q

Difference between dazzle response and PLR

A

Dazzle response uses a higher level of response with rostral colliculi but sitll subcortical
ONly gone in very bad disease

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20
Q

What do we expect to see with the swinging light test

A

Both pupils constrict with more constriction when light moved to contralateral eye

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21
Q

PAlpebral reflex

A

Touch medial canthus; stimulates CNV trigeminal sensory branch
Get blink response via Facial nerve motor

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22
Q

What is important to remember about the menace response

A

IT is learned; absent for a few days

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23
Q

What might a slow, abnormal menace indicate

A

cerebellar disease since cerebellum has a role in coordination and smoothing the menace response

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24
Q

What nerve controls head position and if there is a lesion which way does it go

A

VEstibulocochlear
Fall towards side of lesion

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25
Q

What are classic signs of facial nerve paralysis

A

Ear droop on that side
Eyelid droop
Muzzle twisted towards normal side

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26
Q

What is the cervicofacial reflex

A

Tap neck at C1-C2 and look for grimace from the corner of the mouth; tests C1/C2 nd CNVII

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27
Q

What would an animal with proprioceptive defects look like when walked; esp with head raised to move line of sight

A

Excessively floaty forelimbs

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28
Q

What disease would be shown up when horse blindfolded and asked to move

A

Proprioceptive defects with vestibular disease

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29
Q

What does it mean about deficits if proprioception is abnormal at rest vs when moving

A

If abnormal at rest = conscious deficits
If when moving = unconscious proprioceptiv deficits

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30
Q

Grades 0-5 ataxia

A

0 = normal
1 = mild neuro deficits only under special circumstances e.g walking in circles
2 = mild neuro deficits at all times/giats
3 = moderate deficits at all times
4 = severe deficits with tendency to buckle, stumble, trip, fall
5 = recumbent

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31
Q

Basic signs with UMN lesion

A

Paresis
Hyperreflexia

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32
Q

Basic signs with LMN lesion

A

Paralysis/paresis
Neurogenic muscle atrophy
Loss of reflexes

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33
Q

What would we see with gait at C-C5 lesion

A

UMN signs in fore and hindlimbs with hindlimbs looking worse

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34
Q

Wha would we see with C6-T2 lesion

A

LMN signs in forelimbs
UMN signs in hindlimbs

So forelimbs look ‘worse’

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35
Q

What would we see with T3-L3 lesion

A

Normal forelimbs, UMN signs to hind lims

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36
Q

What would we see with L4-S1 lesoni

A

Normal forelimbs
LMN signs to hindlimbs

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37
Q

What would we see with sacral/caudal lesions

A

Normal forelimbs
Normal or LMN signs in hing limbs
Cauda eqiune sign e.g bladder issues

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38
Q

What is coup and contrecoup

A

Where the brain is shaken inside the skull causing acceleration decelleration injuries which cause bruising and swelling to cranial and caudal aspects of the brain

39
Q

What effect can be seen over 1-2 weeks after coup contrecoup with head trauma

A

Loss of vision due to optic nerve twang during swinging and slow degeneration

40
Q

What happens in a rectus capitus muscle avulsion

A

caused by hyperextension of neck
Muscle can rip off temporal bone causing huge haemorrhage, nose bleed

41
Q

Why might we choose to take CSF from the lumbosacral space after a head injury

A

Because there is a risk of cerebellar herniation if the ICP is raised and atlanto-occipital puncture is done

42
Q

Things to consider in approach to head trauma (treatment)

A

CT best
Manage seizures
Reduce intracranial pressure if needed; hypertonic saline
NSAIDs
Vit E
Steroids
O2 if needed

43
Q

How to manage seizures in a horse

A

Diazepam, phenobarbital, KBr

44
Q

Signs of hyperammonaemia causing cerebral oedema

A

Yawning
Dullness
Wandering
Head pressing
Aggression

45
Q

What two things can cause hyperammonaemia

A

Liver disease
Intestinal disease

46
Q

Approach to dealing with hyperammonaemia

A

Deal with underlying disease
Add lactulose to convert ammonia to ammonium salt so less is absorbed
Antimicrobials to change gut slora

47
Q

Why do horses with equine motor neuron disease look worse when standing than walking

A

Because the postural type 1 muscles are most affected since these have higher oxidative requirement

48
Q

Aetiology of equine motor neuron disease

A

Vitamin E deficiency causing oxidative neuronal damage and neurogenic muscle atrophy

= neurodegenerative disease causing LMN signs

49
Q

What things can lead to vitamin E deficiency in equine motor neuron disease

A

Dietary: lack of access to fresh pasture
INability to absorb vit E due to GI tract disease
Excess dietary copper

50
Q

Treatment and prognosis of equine motor neuron disease

A

Treat with non-synthetic vitamin E suppleentation
40% improve a lot, 40% stabilise and 20% deteriorate
= guarded prognossi

51
Q

Diagnosis of equine motor neuron disease

A

Muscle biopsy for neurogenic atrophy
Can measure vitamine E serum concentration but this is not specicifc

52
Q

Clinical signs of equine motor neuron disease

A

Weakness and muscle atrophy
Narrow base stance
WEight shifting
Pigment retinopathy

53
Q

What is polyneuritis equi

A

Granulomatous infiltration of extradural cauda equina
Signs = tail/anus/perineum/bladder/rectum paralysis as with caudal equine syndrome
+ cranila nerve signs
Poor prognosis

54
Q

What cranial nerve signs are esp common with polyneuritis equi

A

facial nerve, trigeminal, vestibular signs

55
Q

What is temporohyoid osteoarthropathy

A

Degenerative change at the temporohyoid articulartion; due to osseous proliferation at the joint and then pathological fractures of petrous temporal bone

–> Causes damage to vestibulo-cochlear (+/- facial nerve)

56
Q

What are some possible aetiologies of temporohyoid osteoarthropathy

A

Spread of infection from middle/inner ear
Non-septic degenerative joint disease
Trauma

57
Q

Clinical signs of temporohyoid osteoarthropathy + diagnosis

A

Vestibulocochlear nerve dysfunction: head tilt, nystagmus, dizziness, ataxia, dysphagia

Facial nerve dysfunction: asymmetry, corneal ulcers from exposure keratopathy

Diagnosis = seeing endoscopic thickening of articulation of sytohyoid bone in dorsal guttural pouch
[+ could do CT; or DV plain X-ray and compare the two sides]

58
Q

Treatment of temporohyoid osteoarthropathy

A

Anti-inflammatories
+/- antibiotics
Surgical ceratohyoidectomy

59
Q

What is Horner’s syndrome and what are the signs

A

Interruption of the sympathetic innervation to face
Lesion can be anywhere on pathway e.g neck, guttural pouch, cranial thorax
Signs = sweating, miosis, ptosis

60
Q

What is shivers

A

Muscular condition of unknown origin where limbs with shivering flexed hindlimb posture
Progressive with no treatment; can progress to forelimbs

61
Q

3 post-anaesthetic neuro complications and their signs

A

Facial neve paralysis: muzzle deviated away from lesion, may see corneal ulcers due to exposure keratitis (reduced saliva and tear production)
Radial nerve paralysis: dropped elbow and unable to bear weight
Spinal cord malacia; dog sitting with flaccid paralysis caudal to lesion after GA

62
Q

Whta is the cause of cervical vertebral stenotic myelopathy in young vs old horses and which areas are affected

A

Young horses: malformation of vertebral canal/ligaments/cervical vertebrae
–> Affects mid cervical spine

Old horses: osteoarthritic change of articular process joints
-> Affects caudal cervical spin

63
Q

What is static vs dynamic cervical vertebral stenotic myelopathy

A

Static = where there is compression in a neutral position
Dynamic = compression when the head is flexed/extended

64
Q

Why are hindlimbs affected first in cervical vertebral stenotic myelopathy

A

Because the spincerebellar tracts are more peripherally located so they are compressed first

65
Q

What is the classic history/signalment for young horses with cervical vertebral stenotic myelopathy

A

= after a period of recent rapid growth
First sign is reduced proprioception which progresses to paresis or spasticity

66
Q

Diagnosis of cervical vertebral stenotic myelopathy

A

CT best
Myelography/plain radiographs

Take flaexed and neutral positions because dynamic lesions may only be noticed when neck is flexed

Compression normally visible from dorsoventrally

67
Q

Conservative management of CVSM

A

Anti-inflammatories
Restrict diet in younf horses
Restrict exercise

68
Q

Clinical signs of tetanus

A

Third eyelid protrusion
Saw horse rigid stance
Raised tailhead
Lockjaw
Dysphagia
Miosis
Hyperaesthesa

69
Q

How does tetanus work

A

Clostridim tetani contaminated wounds and produces tetanospasmin and tetanolysin toxins

Tetanospasmin undergoes haematogenous spread then retrograde transport up peripheral nerves to inhibtiory interneuros and prevents synaptic release of GABA

Get spastic paralysi s

70
Q

Treatment of tetanus

A

Give antitoxin
Clean and debride wound, make it aerobic to eliminate C tetani
Antibiotics; use metrnodazole
Tetanus toxoid vaccine (at distal site to anti-toxin)
Control muscle spasm: methocarbamol, diazepam, alpha 2 agonist sedation

Nursing care

71
Q

Vaccine protocol for tetanus

A

Vaccinate at 6 months with 2 vaccines 4 weeks apart
Boost in last trimester to protect foal

72
Q

When might we give tetanus antitoxin as tetanus prevention

A

For risk periods e.g any unvaccinated horse where wound/castration/abscess noticed

73
Q

What are the possible ways to get botulism

A

Ingesting spores so toxin produced in GI tract
Infection of wound with C botulinum
Ingestion of pre-formed toxin in forage (spoiled food)

74
Q

Pathogenesis of botulism

A

Haematogenous spread of toxin, binds to NMJ terminal and blocks ACh release causing flaccid paralysis

75
Q

Pathogenesis of equine herpes myeloencephalitis

A

Ubiquitous EHV1 enters resp epithelial cells –> lymphocytes/monocytes –> lymphatics/blood –> dissemination

Have. background of respiraotry disease then sudden onset of neurosigns

76
Q

Signs with equine herpes myeloencephalitis

A

Ataxia esp in hindlimbs
Bladder distension/incontinence, penile protrusion, flaccid tail and anus

77
Q

Treatment for equine herpes myeloencephalitis

A

Supportive care with NSAIDs, nrusing
Antivirals; valacyclovir, gangiclovir 1

78
Q

Why do we not use acyclovir in horses

A

Low bioavailability and poor effect

79
Q

Prognosis for equine herpesvirus myeloencephalitis

A

50-70% survival
May have neuro deficits for life

80
Q

How does vaccination help with equine herpesvirus myeloencephalitis

A

Decreases overal environmental load of EHV1
BUT does not protect against EHV myeloecenpahtiis

81
Q

What is west nile virus

A

Flavivirus not currently in UK but with potential to come here as we have mosquito vector

82
Q

Which species are amplifier hosts for west nile virus and which are dead end

A

Birds are amplifiers
Horses are dead end

83
Q

Clinical signs of west nile virus

A

Most show no signs
Dullness, facial paralysis, dsphagia, muscle fasciculations, hyperexcitabiltiy. ataxia, recumbency

84
Q

What is neuroborreliosis and what are the clinical signs

A

Disease due to borrelia burgdorgeris which is transmitted by ixodes ticks
Causes muscle atropgy/weight loss, CN dysfunction ataxia, shifting lameness, pyrexia, joint effusio

85
Q

Why must we take care with diagnosing Lyme disease from serology

A

ARound 1/3 of healthy horses are seropositive so may not be relevant to signs

86
Q

As well as antibody titre what can we do to help diagnose neuroborreliosis

A

Use silver stain on joint effusion fluid and look for spirochaetes

87
Q

Treatment of neuroborreliosis

A

MOnths long tetracyclines; starting with IV oxytet and moving to oral doxy

88
Q

What type of virus is rabies

A

lyssavirus

89
Q

Incubation time and clinical signs of rabies

A

INcubation = 2 weeks to several months
Signs: ataxia, pyrexia, colic, lethargy, self-mutilation, aggression
= fatal

90
Q

What is equine protozoal myeloencephalitis

A

Protozoal disease from sarcocystis neurona and Neospora nughesia
affects white and grey matter at any CNS site
See atypical lameness, can get seizures, ataxia, dyphaia
NOT in UK

91
Q

Why is monitoring horses important to assess western/eastern/venezualean equine encephalitis rsisk to human health

A

Horses are sentinel hosts so can be used to predict risk to humansS

92
Q

Signs of western/eastern/venezualean equine encephaliti

A

Pyrexia, dullness, cirlcing/head pressing, dysphagia, paralysis, death

93
Q

What causes western/eastern/venezualean equine encephaliti

A

Togavirus
Primary reservoir in birds/rodents

94
Q
A

Equine (18 decks)

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