Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

NEU2 > Equine neurology: central and peripheral > Flashcards

Equine neurology: central and peripheral Flashcards

1
Q

What conditions may lead to collapse due to failure of the muscles in the horse?

A
  • Exercise induced collapse
  • Other metabolic disorders of muscles
  • Electrolyte abnormalities interfering with conduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is idiopathic hypersomnia in horses?

A

Inappropriate sleep in standing adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the characteristics of idiopathic hypersomia in horses

A
  • Rapid or slow onset of recumbency
  • No REM
  • Wake spontaneously
  • May cause trauma
  • May be triggered by specific stimuli
  • Epistaxis may be seen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Explain the cause of idiopathic hypersomnia in horses

A
  • Is not a neurological condition, is due to lack of sleep

- Sleep deprivation can be due to: thoracolumbar pain, bilateral lameness, behavioural/herd dynamic issues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are teh common consequences of head trauma in the horse?

A
  • Often involve vestibular and facial nerves leading to head tilt
  • Brain injuries lead to seizures, coma, recumbency, blindness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What conditions is DMSO used for in the horse?

A

PAS, EHC, EPM, WNV and trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Outline the management of head trauma in horses

A
  • Need to control seizures if present
  • Consider lfuid status/nutrition
  • Patience
  • May require decompressive craniotomy
  • Corticosteroids: no evidence for benefit or negative effect
  • DMSO: little evidence
  • Mannitol: reduces ICP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Evaluate the use of DMSO in the treatment of head trauma in the horse

A
  • Osmotic diuretic so reduces ICP
  • Stabilises lysosomes
  • Free radical repair
  • Little evidence base
  • No immunosuppressive effects as seen in corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe the assessment and management of a down horse with suspected spinal injury

A
  • Give time
  • Lesion localisation important
  • Determine prognosis
  • Request second opinion before euthanasia where possible
  • Need to manage recumbent horse - nutrition, turning, prevention of co-morbidities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

List the indications for euthanasia as a result of spinal injury

A
  • Recumbent for >5days
  • Worsening clinical signs
  • Muscle pathology (myoglobinuria)
  • Colic, uncontrollable pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What approach (in terms of euthanasia) should be taken for a horse that has suffered:

a: pelvic fractures and is recumbent
b: Wobbler’s syndrome (grade 5)
c: Hind limb paralysis/paresis following spinal fractures
d: neuritis of cauda equina
e: non responsive neuropathy of one or more peripheral nerves
f: recumbent non responsive post trauma
g: laminitis, non-responsie
h: lameness associated with prolonged periods of recumbency

A

a: Immediate euthanasia, no second op. required
b: Immediate euthanasia, no second op. required
c: Immediate euthanasia, no second op. required
d: Second opinion required prior to euthanasia
e: Second opinion required prior to euthanasia
f: Immediate euthanasia with second opinion
g: Second opinion required prior to euthanasia
h: second opinion required prior to euthanasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Give a peripheral cause of neurological diseases that falls into the “degenerative” category

A

Equine grass sickness (NB could also be inflammatory/infectious)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Give a peripheral cause of neurological diseases that falls into the “anomalous” category

A
  • Hyperkalaemic period paralysis

- Polysaccharide storage myopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Give a peripheral cause of neurological diseases that falls into the “metabolic” category

A

Synchonous diaphragmatic flutter aka Thumps

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Give a peripheral cause of neurological diseases that falls into the “nutritional” category

A

Equine motor neurone disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Give a peripheral cause of neurological diseases that falls into the “neoplastic” category

A

Mediastinal neoplasia (Horner’s syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give a peripheral cause of neurological diseases that falls into the “inflammatory-infectious” category

A
  • Guttural pouch empyaema

- Vestibular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Give a peripheral cause of neurological diseases that falls into the “inflammatory-inflammatory” category

A

Polyneuritis equi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Give a peripheral cause of neurological diseases that falls into the “idiopathic” category

A
  • Equine recurrent laryngeal neuropathy
  • Shivering
  • Stringhalt
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Give a peripheral cause of neurological diseases that falls into the “toxic” category

A
  • Botulism

- Tetanus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Give a peripheral cause of neurological diseases that falls into the “trauma” category

A
  • Postanaesthetic neuropathies

- Facial nerve damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe the typical appearance of unilateral facial nerve dysfunction

A
  • Ipsilateral ear paralysis
  • Droopy ipsilateral eyelid
  • Ipsilateral muzzle paralysis (nose deviates to the contralateral side )
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the apperance of vestibular disease in horses

A
  • Head tilt and circle in ipsilateral direction
  • Nystagmus “fast phase” away from lesion
  • May be exacerbated by blindfolding as may be compensating with vision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe the common underlying cause of vestibular disease in horses

A
  • Ear disease
  • E.g. trauma: basisphenoid fracture due to rearing and falling backwards
  • Or otitis media/interna: may also lead to facial nerve paralysis and Horner’s, infection in guttural pouch may progress to otitis media
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is polyneuritis equi?

A

Non-suppurative neuritis of the proximal spinal, cranial sensory, motor nerveroots and sacral nerves. Can progress to proliferative granulomatous perineuritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the pathogenesis of polyneuritis equi

A
  • Demyelination of teh sacrococcygeal roots of the caudal equina
  • May be secondary to viral disease, autoimmune in some cases, unknown if viral or bacterial
  • Anti-p2 myelin anitibodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe the clinical signs of polyneuritis equi

A
  • Occasionally cranial nerve disease (head tilt)
  • Tail, anal penile, perineal, areflexia and atonia
  • Require analgesia
  • Surrounded by areas of hypersensitivity
  • EMG dhows denervation potentials
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is a key differential for polyneuritis equi?

A

Spinal fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Outline the treatment of polyneuritis equi

A
  • Prognosis is hopeless, no recovery
  • No improvement with steroids or gold salts
  • Nursing, in particular re. bladder required
  • Analgesia
30
Q

What is equine grass sickness?

A

Generalised dysautonomia affecting primarily theenteric nervous system

31
Q

Compare acute, subacute and chronic equine grass sickness based on survival time

A
  • Acute: die rapidly
  • Subacute: survive >2 days
  • Chronic: survive >7 days
32
Q

Describe the epidemiology of equine grass sickness

A
  • Young male on pasture, no prev. exposure to EGS
  • Change of pasture in previous 2 weeks
  • Cool, dry weather, frost
  • Previous cases on same pasture
  • Seasonal bias for April to July
33
Q

List the gastrointestinal signs of Equine grass sickness

A
  • Abdominal pain
  • Nasogastric reflux
  • Dysphagia
  • Empty looking abdomen, very dry faeces
34
Q

What causes the abdominal pain seen in Equine grass sickness?

A
  • Ileus due to myenteric neuronal degeneration (loss of parasympathetic control)
  • Dehydration of colonic contents (impaction)
  • Liver pathology
35
Q

Explain the cause and effects of nasogastric reflux in equine grass sickness

A
  • Loss of lower oesophageal sphincter tone and ileus
  • “vomit” through nose
  • Can lead t oesophageal ulcers
36
Q

Explain the cause and effects of dysphagia in equine grass sickness

A
  • Loss of parasympathetic control to pharynx (CN IX)

- Unable to swallow

37
Q

List the non-GI clinical signs of equine grass sickness

A
  • Tachycardia
  • Ptosis
  • Rhinitis sicca (snuffles)
  • Muscle fasciculations and weakness (narrow based stance)
38
Q

Explain the cause and effect of tachycardia in equine grass sickness

A
  • Loss of vagal control, increased sympathetic outflow

- Heart rate often higher than expected for degree of pain or hypovolvaemia of patient (HR>100)

39
Q

Explain the cause ptosis in equine grass sickness

A
  • PSNS dysfunction to CN III/VII (suply to levator palpebrae superioris, levator anguli oculi)
  • Mullers muscle (sympathetic innervation)
  • Non-specific debilitating disease
40
Q

Explain the cause and effect of rhinitis sicca in equine grass sickness

A
  • Loss of PSNS supply to mucosal glands of nasal mucosa
  • Seen in late subacute/chronic disease
  • Dry crusty nasal discharge, poor prognostic sign
41
Q

Compare the pathology in acute and chronic equine grass sickness

A
  • Localised to ileum in chronic

- Generalised intestinal pathology in acute

42
Q

Describe and evaluate the best diagnostic test for equine grass sickness

A
  • Ileal biopsy
  • requires laparotomy (midline/flank): decreases survival
  • May see neuronal degeneration within ganglia, depletion of ganglia, vacuolation
43
Q

List the differential diagnoses for dysphagia in the horse

A
  • Equine grass sickness
  • Botulism
  • Lead toxicity
  • Anatomical pharyngeal abnormalities e.g. sub-epiglottic cyst, cleft palate
  • Foreign body (pharyngeal, oesophageal)
  • Guttural pouch disease
  • Neurological disease (EPM, rabies, EEE, WEE, trauma)
44
Q

Outline the aspects of treatment of equine grass sickness

A
  • Nursing care
  • Analgesia
  • Management of each clinical sign
45
Q

Describe the nursing care required for equine grass sickness

A
  • Feeding: small feeds every 30-60mins, hand feeding, hand grazing, varied diet
  • Appetite stimulation: diazepam 0.02mg/kg IV BID-TID (nt as successful as in cats)
  • Prokinetics e.g. cisapride
46
Q

Describe analgesia in the management of equine grass sickness

A
  • Promotes voluntary feeding, reduces pain associated with swallowing and abdominal pain
  • Oesophageal/gastric ulceration - H2 blockers, sucralfate
47
Q

What is the prognosis for equine grass sickness?

A

50% recover, 50% of those normal within a year, rest have ongoing problems with colic etc.

48
Q

Identify the poor prognostic factors for equine grass sickness

A
  • Surgery (hence make a clinical diagnosis)
  • Dysphagia
  • Colic
  • Ponies (vs cobs)
  • Rhinitis
49
Q

Explain the significance of equine grass sickness relating to other horses

A
  • EGS thought to be related to pasture toxin
  • Often several cases from same pasture
  • Horses exposed to EGS less likely to develop the condition
  • Naiive animals most likely to be affected
50
Q

What is equine motor neuron disease (EMND)?

A

Spontaneous neurodegenerative disease with insidiuous onset preogressing over one to several months

51
Q

Describe the cause of equine motor neuron disease

A
  • Associated with vit E/Se deficiency

- Oxidative damage of peripheral nerves leading to weakness and other sigsn

52
Q

What is an “elephant on a barrel” stance pathognomic of in horses?

A

Equine motor neuron disease

53
Q

Describe the clinical signs of equine motor neuron disease

A
  • Weight loss + ravenous appetite
  • Symmetrical neurogenic muscle atrophy (LMN signs)
  • Triceps, biceps, quadriceps atrophy
  • Fine fasciculations adn coarse trembling
  • Frequent recumbency
  • Wekaness
  • Worse standing than walking
  • Continuously shift weight on hindlimbs, unabe to lock stifles
  • Excessive sweating
  • Low head carriag
  • Tail elevation
  • Short strided gait
  • No ataxia
  • Black teeth (highly suggestive, but not pathognomic)
54
Q

Which methods are used in the diagnosis of equine motor neuron disease?

A
  • Clinical signs
  • Muscle biopsy
  • Blood biochem and haematology
  • EMG
  • Retinal examination
55
Q

Describe the results on muscle biopsy that would indicate equine motor neuron disease, and state which muscle is used

A
  • Sacrocaudalis dorsalis medialis muscle used (top of tail head)
  • Shows severe denervation, atrophy and fibrotic contraction
56
Q

Describe the results on retinal examination that would indicate equine motor neuron disease

A

Mosaic pattern of brown pigment in the tapetal fundus (lipofuscin deposition)

57
Q

Describe the pathology that occurs with equine motor neuron disease

A
  • No gross lesions, but may see pale vastus muscle
  • Neuronal degeneration with depletion of motoro neurons in the ventral horns of the spinal cord
  • Axon degeneration in ventral roots and peripheral nerves
  • Neurogenic muscle atrophy of type 1 muscle fibres
  • Lipopigment deposition in capillaries of spinal cord
58
Q

How does the neurogenic muscle atrophy of type 1 fibres that occurs in EMND relate to the clinical signs?

A
  • Cannot lock stay apparatus, so cannot stay standing for long periods of time
  • No issues at walk or trot so see constant shifting and recumbency, but no ataxia when moving
59
Q

Outline the treatment for equine motor neuron disease

A
  • Unrewarding
  • Vit E supplementation-
  • Green grass
  • Euthanasia
60
Q

Discuss the prognosis of EMND

A
  • Poor, may show minimal slow improvement

- Will always remain weak and thin

61
Q

Explain how vitamin E deficiency may lead to EMND

A
  • Inadequate access to green pasture

- Vit E protects membranes by scavening free radicals and preventing peroxidation of lipid membranes

62
Q

Describe idiopathic head shaking in horses

A
  • Vertical movements of head in repeated fashion
  • May rub nasal areas on legs
  • Occasionally strike out at muzzle while ridden
63
Q

Discuss the causes of idiopathic head shaking in horses

A
  • Multifactorial, not consistent between horses
  • Behavioural/stereotypical component
  • Allergic rhinitis
  • Photic
  • Trigeminal stimulation
64
Q

Describe the diagnosis of idiopathic head shaking in horses

A
  • Frustrating
  • Rule out obvious causes such as trauma, foreign body
  • Assess response to therapy e.g. cyproheptadine, carbemazepine, steroids, sunglasses if photic
  • Perinerualanalgesia (infraorbital nerve)
65
Q

Describe the treatment of idiopathic head shaking in horses

A
  • Depends on underlying cause
  • Medical therapy: cyproheptadine, carbamazepine, steroids
  • Physical therapy: nose nets, fly shields
  • Surgery (nerve compression)
66
Q

What is cauda equine neuritis?

A

Rare and sporadic disease in horses that involves the nerves on the cauda equina

67
Q

Which cranial nerves are affected in cauda equina neuritis?

A

CN VII, VIII, and rarely V

68
Q

What causes cauda equina neuritis?

A

Likely autoimmune or post infectious origin (herpes, adenovirus)

69
Q

Which group of horses is most affected by cauda equina neuritis?

A

Adult females

70
Q

Describe the clinical signs of cauda equina neuritis

A
  • Tail paralysis, incontinence, gait deficits

- Cranial nerve deficits

71
Q

Describe the progression of cauda equina neuritis

A
  • Inflammation starts in intradural portion fo the nerve root (lymphoplasmacytic)
  • Inflammation continues in the extradural portion forming large “masslike” lesions (granulomatous)
72
Q

Describe the method for the diagnosis of cauda equina neuritis and the prognosis

A
  • Compatible clinical signs
  • CSF shows non-suppurative pleocytosis and elevated total protein
  • Post mortem
  • Prognosis poor

NEU2 (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions