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Neuromuscular System Flashcards

NM01-04

1
Q

start of NM01

name the 5 steps of the neurological exam of horses

A
  1. head
  2. neck & trunk
  3. Perineum
  4. gait & posture
  5. autonomous zones
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2
Q

name 2 diseases that could cause ‘dirty tongue’ in horses

A
  1. botulism (weak tongue)
  2. choke
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3
Q

list the 7 structures involved in the pupillary light reflex (PLR) in order

A
  1. optic nerve
  2. optic chiasm
  3. optic tract
  4. pretectal nucleus
  5. oculomotor nucleus
  6. oculomotor nerve
  7. ciliary ganglion
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4
Q

what will the pupil of an eye affected with an optic nerve lesion do in response to indirect light stimulation

A

constrict

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5
Q

what will the pupil of an eye affected with an optic nerve lesion do in response to direct light stimulation

A

dilate

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6
Q

should you remove an eye that can elicit an indirect PLR in the other eye?

A

no! it is still functional

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7
Q

name the 10 structures involved in the menace response in order

A
  1. optic nerve
  2. optic chiasm
  3. optic tract
  4. lateral geniculate nucleus
  5. optic radiation
  6. occipital cortex
  7. motor cortex
  8. internal capsule
  9. facial nucleus
  10. facial nerve
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8
Q

name the 2 cranial nerves involved in the palpebral reflex

A
  1. afferent CN 5
    efferent CN 7
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9
Q

name the 3 cranial nerves that innervate extraocular muscles

A
  1. CN 3
  2. CN 4
  3. CN 6
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10
Q

what spinal cord segments are included in cervical intumescence

A

C7-T2

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11
Q

list the 3 part pathway of the cuntaneous trunci reflex

A
  1. dorsal route into spinal cord
  2. cervical intumescence (C7-T2)
  3. lateral thoracic nerve
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12
Q

name the part of the horse

consists of:
sacrococcygeal spinal cord segments, spinal nerve rootlets and roots, sacral plexus and peripheral nerves to the bladder, rectum, anus, tail and perineum

A

cauda equina

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13
Q

name 2 sites where CSF can be collected from the subarachnois space at

A
  1. atlanto-occipital site
  2. lumbosacral site
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14
Q

which location should be used forCSF location if brain lesion is suspected

A

atlanto-occipital site

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15
Q

which location should be used forCSF location if spinal lesion is suspected

A

lumbosacral site

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16
Q

what will be the clinical signs of a spinal cord lesion in C1-C5

A

increased tone and ataxia of all limbs

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17
Q

what will be the clinical signs of a spinal cord lesion in C6-T2

A

increased tone and ataxia of pelvic limbs ;
paresis of thoracic limbs

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18
Q

what will be the clinical signs of a spinal cord lesion in T3-L3

A

normal thoracic limbs ;
incr tone and ataxia of pelvic limbs

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19
Q

what will be the clinical signs of a spinal cord lesion in L4-S3

A

normal thoracic limbs;
paresis of pelvic limbs

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20
Q

what will be the clinical signs of a spinal cord lesion in Cd1-5

A

perineal paresis and hypalgesia

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21
Q

start of NM02

what kind of deficit causes ataxia

A

proprioceptive deficit

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22
Q

name the type of ataxia

due to loss of conscious and subconscious proprioceptive pathways;
compression lesions always UMN paresis also

A

spinal cord ataxia

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23
Q

name the type of ataxia

loss of balance, ipsilateral antigravity muscle paresis (nystagmus, circling)

A

vestibular ataxia

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24
Q

name the type of ataxia

loss of subconscious proprioception only (hypermetria)

A

cerebellar ataxia

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25
Q

name 5 causes of spinal cord ataxia “wobblers”

A
  1. cervical vertebral malformation
  2. trauma
  3. EHV-1 myeloencephalopathy
  4. EPM
  5. West Nile virus encephalomyelitis
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26
Q

name the grade of spinal cord ataxia

just evident

A

grade 1

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27
Q

name the grade of spinal cord ataxia

owners can spot

A

grade 2

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28
Q

name the grade of spinal cord ataxia

severe

A

grade 3

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29
Q

name the grade of spinal cord ataxia

about to fall over

A

grade 4

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30
Q

this is a structural narrowing of the spinal canal due to a variety of vertebral malformations and potentially trauma that leads to spinal cord compression;
horses exhibit clinical signs of general proprioceptive deficits and UMN spasticity and paresis

A

cervical vertebral malformation

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31
Q

why is pelvic limb ataxia invariably worse in cervical vertebral malformation (CVM)?

A

peripheral location of spinocerebellar tracts

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32
Q

name 6 clinical signs of cervical vertebral malformation (CVM)

A
  1. knuckling, stumbling and toe dragging (paresis)
  2. lack of coordination in foot placement
  3. delayed corrective response when limbs in abnormal location
  4. tight circling reveals both circumduction and pivoting on inside limb
  5. dysmetria
  6. worse pelvic limb ataxia
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33
Q

name the type of cervical vertebral malformation (CVM)

large, younger horses;
various manifestations of developmental orthopaedic disease;
vertebral canal stenosis/wedging/angular fixation;
often C3-C4

A

type 1 cervical vertebral malformation (CVM)

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34
Q

name 4 characteristics/morphologies of type 1 cervical vertebral malformation (CVM)

A
  1. angulation
  2. OCD lesions of articular process joints (not ‘facets’)
  3. epiphysitis
  4. caudal extension of dorsal arches
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35
Q

what size must the vertebral canal be in relation to the width of the vertebra

A

more than 50% of the width of the vertebra

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36
Q

name the type of cervical vertebral malformation (CVM)

large, older horses;
arthritis of caudal cervical vertebrae;
compression of spinal cord by bone and soft tissues

A

type 2 cervical vertebral malformation (CVM)

37
Q

how to treat cervical vertebral malformation (CVM) via surgery?

A

fusion of vertebral bodies

38
Q

this is a disease caused by equine alphaherpes 1 virus (EHV-1);
spread from horse to horse through contact with nasal discharge, aerosol droplets or fomites;
incubation period ranges from 2-10d;
worldwide outbreaks of abortion and resp disease;
reservoir is latently infected horses (trigeminal ganglia)

A

equine herpes myeloencephalopathy (EHM)

39
Q

name 5 clinical signs of equine herpes myeloencephalopathy (EHM)

A
  1. acute onset symmetrical ataxia and paresis
  2. signs progress rapidly ~2d, then stabilise
  3. pelvic limb ataxia > thoracic limbs
  4. CSF often xanthochromic
  5. cauda equina signs
    .
40
Q

what is the diagnostic test of choice for equine herpes myeloencephalopathy (EHM)

A

quantitative PCR of nasal swabs and anticoagulated blood

41
Q

how to treat equine herpes myeloencephalopathy (EHM)?

A

early dexamethasone and antiviral agents (Valacyclovir)

42
Q

name 4 places vestibular nuclei project to

A
  1. extraocular nuclei
  2. spinal cord
  3. cerebellum
  4. cerebrum
43
Q

what muscles does the vestibular system facilitate?

A

ipsilteral antigravity muscles

44
Q

what muscles does the vestibular system inhibit?

A

contralateral antigravity muscles

45
Q

what cells in the cerebellum inhibit UMNs?

A

Purkinje cells

46
Q

what clinical sign will cerebellar pathology result in?

A

hypermetria
(incoordination with big movements)

(no paresis)

47
Q

start of NM03

name 3 inflammatory/infectious causes of forebrain disease

A
  1. viral diseases
  2. meningitis in foals
  3. polyneuritis equi
48
Q

name 2 metabolic forebrain diseases

A
  1. hepatic encephalopathy
  2. neonatal hypoxia/ischaemia
49
Q

name 2 toxic causes forebrain diseases

A
  1. leukoencephalomalacia
  2. intracarotid injections
50
Q

name the bacterial CNS infection

failure of passive transfer;
gram neg organisms;
forebrain signs/head held lowered in rigid extension;
depressed mental status;
recumbency, weakness, abnormal PLRs, decr suckling reflex, seizures

A

foal septicaemia-meningitis

51
Q

this is the most common cause of diffuse brain disease of horses in UK;
pyrrolizidine alkaloids (ragwort)

A

hepatic encephalopathy

52
Q

what are the clinical signs of hepatic encephalopathy due to?

A

imbalance of GABA and glutamate

53
Q

name 8 clinical signs of hepatic encephalopathy

A
  1. icterus
  2. weight loss
  3. diarrhoea
  4. abdominal pain
  5. head pressing
  6. yawning
  7. leaving food in mouth
  8. seizures
54
Q

name 4 clinical signs of neonatal encephalopathy - usually delayed few hours to 2 days

A
  1. reduced awareness of environment
  2. failure to find udder and suck
  3. funny ‘barking’ noises
  4. lack of affinity for mare
55
Q

name 2 important causes to r/o when diagnosing neonatal encephalopathy

A
  1. failure of passive transfer
  2. sepsis
56
Q

this nerve contains somatic fibres that innervate the muscles of facial expression & parasympathetic fibres that stimulate tear production;
courses through middle ear, dorsal aspect of guttural pouch, ventral ramus of mandible and ventral to the facial crest

A

facial nerve

57
Q

name 3 clinical signs of guttural pouch mycosis

A
  1. CN VII/VIII
  2. horners syndrome
  3. dysphagia
58
Q

name 4 clinical signs of temporohyoid osteoarthropathy (when the petrous temporal bone fuses with the temporohyoid joint)

A
  1. CN VIII
  2. CN VII
  3. head shaking
  4. dysphagia
59
Q

what is the surgical treatment of temporohyoid osteoarthropathy

A

removal of one of the bones of the hyoid apparatus
(ceratohyoidectomy)

60
Q

this is chronic granulomatous inflammation of the extradural nerve roots of many peripheral nerves;
can present first with cranial nerve signs (VII/VIII);
progressive disease and early euthanasia should be considered

A

polyneuritis equina

61
Q

name 2 exercise-related myopathies

A
  1. spradic exertional rhabdomyolysis
  2. chronic exertional rhabdomyolysis
62
Q

name 9 key clinical signs associated with weakness

A
  1. narrow base stance
  2. low head carriage
  3. weight loss
  4. incr periods of recumbency
  5. dyaphagia
  6. weight shifting
  7. muscle tremors
  8. reluctance to move
  9. toe dragging

(NO ATAXIA)

63
Q

name 6 generalised neuromuscular diseases causing weakness/myasthenia

A
  1. myopathies
  2. botulism
  3. EMND
  4. electrolyte disorders (HPP & hypocalcaemia)
  5. EGS
  6. myaesthenia gravis
64
Q

name 5 generalised neuromuscular diseases causing stiffness/spasticity/hypertonia

A
  1. myopathies
  2. electrolyte disorders (HPP & hypocalcaemia)
  3. tetanus
  4. shivering
  5. stiff horse syndrome
65
Q

name the disease causing classic myaesthenia

found ubiquitously in soil;
grows and produces toxin in anaerobic environments (decaying veg and animal carcasses);
silage provides suitable growth medium;
horses most susceptible to B and C toxins;
toxins block acetylcholine release and cleaves proteins required for vesivle release

A

Clostridium botulinum
(Botulism)

66
Q

name 3 locations where botulism toxin blocks acetylcholine release at

A
  1. neuromuscular junctions
  2. peripheral cholinergic nerve terminals in autonomic ganglia
  3. post-ganglionic parasympathetic nerve endings
67
Q

name 3 modes of intoxication with botulism

A
  1. ingestion of preformed toxin (forage poisoning)
  2. growth of organism in GIT (toxicoinfectious botulism)
  3. contamination of wounds (wound botulism)
68
Q

name 3 clinical signs of Botulism in the early stages

A
  1. depression
  2. inappetence
  3. exercise intolerance
69
Q

name 3 cranial nerve signs seen in a horse with Botulism

A
  1. sluggish PLR
  2. dysphagia (V, VII, IX, X), salivation
  3. reduced tongue tone
70
Q

name 5 clinical signs associated with gait and posture in a horse with botulism

A
  1. weak
  2. fasciculation
  3. sloppy, short gait
  4. low head carriage
  5. symmetrical and predictable

(NO ATAXIA)

71
Q

name the disease characterised by stiffness

found in soil and GIT;
requires anaerobic conditions;
consider sites of contamination - puncture wounds!
produces potent endotoxins

A

Clostridium tetani
(Tetanus)

72
Q

name 2 potent exotoxins produced by C. tetani

A
  1. tetanolysin
  2. tetanospasmin
73
Q

name the C. tetani exotoxin

promotes necrosis and spread of infection

A

tetanolysin

74
Q

name the C. tetani exotoxin

inhibits exocytosis of GABA and glycine

A

tetanospasmin

75
Q

name 6 clinical signs of tetanus

A
  1. change in gait (stilted action)
  2. difficulty eating
  3. spastic muscle contractions
  4. head and neck extension
  5. elevated tail head
  6. anxious expression
76
Q

name 3 features of an anxious expression in horses

A
  1. flared nostrils
  2. retracted eyelids
  3. erect ears
77
Q

name 5 therapeutics for a horse with tetanus

A
  1. ACP
  2. sodium benzyl penicillin
  3. procaine penicillin
  4. antitoxin
  5. hydrogen peroxide (1%)
78
Q

how to prevent tetanus?

A

VACCINATION

79
Q

name the exercise related neuromuscular disorder

classic ‘tying up’/set fast;
generally one-off incidents;
associated with training/feeding mismanagement;
easily managed and treated;
unclear metabolic dysfunction within muscle leading to muscle hypoxia;
hindlimbs especially affected

A

sporadic exertional rhabdomyolysis

80
Q

name 5 clinical signs of sporadic exertional rhabdomyolysis

A
  1. painful muscles
  2. sweating
  3. elevated rectal temp
  4. red/brown urine!
  5. stiff stilted gait
81
Q

name 2 laboratory findings in a horse with sporadic exertional rhabdomyolysis (ER)

A
  1. elevation in muscle-derived enzymes (CK, AST)
  2. myoglobinuria
82
Q

name 4 differential diagnoses for sporadic exertional rhabdomyolysis (ER)

A
  1. laminitis
  2. colic
  3. injuries to pelvic region
  4. aorto-iliac thrombosis
83
Q

name 4 parts of treatment for sporadic exertional rhabdomyolysis (ER)

A
  1. rest
  2. analgesia (NSAIDs)
  3. sedatives (acepromazine)
  4. fluids (in severe cases)
84
Q

name 4 key give aways for acute severe myopathy (atypical myopathy)

A
  1. time of year (autumn)
  2. signs of myopathy
  3. brown urine
  4. high CK/AST
85
Q

name the exercise related neuromuscular disorder

mainly thoroughbreds, fillies, and those with nervous temperaments;
pathophysiology unknown - altered intracellular calcium balance may be involved;

A

recurrent exertional rhabdomyolysis (RER)

86
Q

name 3 glycogen storage disorders

A
  1. Glycogen Branching Enzyme Disease (GBED)
  2. Polysaccharide Storage Myopathy (PSSM)
  3. Equine Polysaccharide Storage Myopathy (EPSM)
87
Q

name the glycogen storage disorder

quarter horse and related breeds (morgan, appaloosa, paints);
recurrent episodes of ‘tying up’;
CK and AST raised disproportional to amount of work and remains elevated for considerable time

A

Polysaccharide Storage Myopathy (PSSM)

88
Q

this is a specific mutation in the glycogen synthase gene (single base pair substitution);
autosomal dominant (N/N vs P/N vs P/P)

A

Polysaccharide Storage Myopathy (PSSM) type 1

(all other types of PSSM denoted type 2)

89
Q

this is a transient event caused by cerebral hypoperfusion

Equine (11 decks)

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