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18- SA- Neurology > Neurology > Flashcards

Neurology Flashcards

1
Q

Define Parapesis

A

partial loss of voluntary motor ability in 2 limbs - most commonly affecting the hindlimbs

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2
Q

define paraplegia

A

complete absence of any voluntary motor ability in 2 limbs - most commonly affecting the hindlimbs

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3
Q

List 7 common clinical conditions causing parapesis/ paraplegia in dogs/cats

A

IVDD
ischaemic myelopathy
FCE
spinal fracture
neoplasia
MUO
degenerative myelopathy

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4
Q

what is MUO

A

meningoencephalomyelitis of unknown origin

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5
Q

define tetraparesis

A

partial loss of voluntary motor ability - weakness in the ability to generate gait - in all 4 lilmbs

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6
Q

Define tetraplagia

A

complete absence of any voluntary motor ability in all 4 limbs

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7
Q

List 6 common clinical conditions causing tetraparesis/ tetraplegia/ cervical pain in dogs and cats

A

IVDD
MUO
SRMA
FIP
discospondylitis
atlantoaxial subluxation

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8
Q

what is SRMA

A

steroid responsive meningitis arteritis

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9
Q

List 3 common clinical conditions that cause generalised neuromusclular weakness in dogs/ cats

A

clostridial diseases
poly myositis
IPRN-idiopathic polyradiculoneuritis

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10
Q

what is IPRN

A

idiopathic polyradiculoneuritis

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11
Q

Describe the presentation of MUO

A

usually chronic, painful, progressive and multifocal

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12
Q

Describe how MUO occurs

A

autoimmune idiopathic inflammation of the meninges in the brain and spinal cord

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13
Q

Decsribe how to diagnose MUO

A

non definitive but:
MRI
bloods
CSF tap

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14
Q

Describe how to treat MUO

A

high immunosuppressive dose of steroids and/or immunosuppressive agents

variable prognosis

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15
Q

Describe the pathophysiology of FCE

A

is a focal embolus of fibrocartilage within the ascending artery of the spinal cord- can be bilateral or unilateral

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16
Q

Decsribe how to diagnose FCE

A

MRI

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17
Q

Describe how to treat FCE

A

conservative management - assess bladder and bowel function

they usually recover with time and physio

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18
Q

Describe the presentation of FCE

A

sudden onset non-painful paresis/paralysis, especially if unilateral - highly suspicious of FCE

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19
Q

Describe the 3 manifestations of IVDD

A

type 1 - nuclear extrusion (disc bursts an pushes out

type 2 - protrusion (disc shifts upwards)

disc cyst - small amount of nuclear material comes out of the spinal cord and is very hydroscopic which causes a build up of water around the disc

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20
Q

Describe how to diagnose IVDD

A

radiography or MRI

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21
Q

Describe the presentation typically seen with IVDD type 2

A

= protrusion
usually progressive in onset, clinical signs predominantly by compression

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22
Q

Describe the typical presentation of IVDD type 1

A

= extrusion
usually sudden onset pathology (but can get multiple episodes which can resolve spontaneously without intervention)

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23
Q

Describe how to treat IVDD

A

referral for surgical removal

conservative - rest and NSAIDs

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24
Q

Describe the pathophysiology of degenerative myelopathy

A

progressive degeneration of the spinal cord

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25
Q

Describe the presentation of degenerative myelopathy

A

chronic progressive hindlimb ataxia
non-painful condition

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26
Q

Describe how to diagnose Degenerative Myelopathy

A

is by exclusion (IVDD protrusion) there are no signs yet identified on MRI

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27
Q

which breed commonly gets Degenerative Myelopathy

A

GSDs

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28
Q

Describe how to treat Degenerative Myelopathy

A

no effective therapy
physio been shown to slow the rate of progression but not prevent

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29
Q

Describe the pathophysiology of spinal fracture

A

needs significant trauma unless there is a pathological fracture

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30
Q

Describe the presentation of spinal fractures

A

acute onset of clinical signs- can be exacerbated by movement of unstable structures

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31
Q

Describe how to diagnose a spinal fracture

A

conscious radiography

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32
Q

Describe how to treat a spinal fracture

A

conservative management if fracture is stable - rest and analgesia

euthanasia

refer for surgical stabilisation

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33
Q

what is the prognosis of a spinal fracture

A

determined by the degree of concussion, compression or laceration damaged sustained by the spinal cord

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34
Q

Describe ischaemic myelopathy

A

loss of blood supply to the spinal cord - caused by some form of blockage

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35
Q

Describe how neoplasia affecting CNS generally present

A

progressive with focal presentation
can be painful or non-painful

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36
Q

Describe how to treat neoplasia that affect the CNS

A

no effective chemo protocol
corticosteroids at anti-inflammatory doses
Surgical excision is unlikely to be curative due to the inability to remove a surgical margin

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37
Q

Describe the pathophysiology of discospondylitis

A

is infectious inflammation within the nucleus pulposus of the disc

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38
Q

Describe how discospondylitis presents

A

chronic progressive spinal pain without obvious neurological deficits that may be focal on palpation of difficult to localise.

Chronic pain but can occasionally progress to ataxia or some paresis

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39
Q

Describe how to diagnose discospondylitis

A

radiography- in chronic cases
CT/MRI

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40
Q

Describe how to treat discospondylitis

A

systemic antibiotics (for 6 weeks)

can perform surgey to lance the abscess

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41
Q

Describe the pathophysiology of polymyositis

A

autoimmune inflammation within the muscles leads to large amounts of pain

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42
Q

Describe how polymyositis presents

A

chronic lameness or lethargy secondary to generalised pain

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43
Q

Describe how to treat polymyositis

A

corticosteroids at an immunosuppressive dose

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44
Q

Describe how to diagnose polymyositis

A

definitive on muscle biopsy

45
Q

why do toy breeds more commonly get atlantoaxial subluxations

A

they have laxity of the tendons holding C1 and C2

46
Q

Decsribe how to diagnose an atlantoaxial subluxation

A

radiography - conscious or GA with careful dynamic views
CT/MRI

47
Q

How does atlantoaxial subluxation present

A

Variable:
- cervical pain
- intermittent collapse
- tetraparesis

48
Q

DEcsribe how to treat a atlantoaxial subluxation

A

immobilise the joint for 6 weeks and provide analgesia

neck brace and cage rest

some cases will need surgical stabilisation

49
Q

what are atlantoaxial subluxations associated with

A

significant trauma incident (eg dogs running into patio doors with forced head ventroflexion)
OR
in young toy breed dogs where anatomical factors will predispose.

50
Q

Name a common spinal tumour seen in cats

A

lymphosarcoma

51
Q

what neurological signs can metronidazole cause at high doses

A

vestibular signs

52
Q

How does wet FIP present

A

oedema in tissues

53
Q

Describe how dry FIP presents

A

rapidly progressive - causes granulomas in tissues (can occur in nervous system)
sudden hindlimb ataxia which can progress

54
Q

Describe how to diagnose neurological FIP

A

bloods
MRI

55
Q

Describe how to treat FIP

A

Supportive care: anti-inflammatories, appetite stimulants (mirtazapine), vitamin B12, s/c fluids at home, anti-oxidants
Remdesivir
Euthanasia?

56
Q

Describe how to diagnose clostridial disease

A

CSF tap
MRI
bloods

57
Q

Describe how botulism presents

A

sudden onset neuromuscular weakness affecting all limbs- flaccid paralysis

58
Q

Describe how to treat botulism

A

remove the animal from the source of the toxin (generally dead animal) - should be recover after this

59
Q

Describe how tetanus presents

A

varies from mild stiffness to severe spasm and inability to stand

60
Q

Describe how to treat tetanus

A

clean wounds
supportive therapy
anti-toxin- not as important as in horses

61
Q

Describe the pathophysiology of IPRN

A

inflammation of the nerve roots, travels from the back legs forwards - stops at cervical region of goes further and takes out the diaphragm

62
Q

Describe how IPRN presents

A

progressive ascending lower motor neurone weakness, initally of the distal himdlimbs progressing to all limbs

63
Q

Describe how to treat IPRN

A

usually left limiting
no specific treatment- conservative therapy with support and physio

64
Q

Describe the pathophysiology of SRMA

A

is an autoimmune condition with inflammation targeted towards the arteries in the meninges.

65
Q

Describe how SRMA presents

A

in young dogs around 12 months old
acute onset severe neck pain without evident neuro deficits

66
Q

Describe how to diagnose SRMA

A

CSF tap - will see neutrophils
MRI- to rule out other differentials

67
Q

Describe how to treat SRMA

A

extended course of corticosteroids at immunosuppressive doses - 6 weeks min

68
Q

How does neospora present

A

generalised muscle issue not paralysis
hindlimb rigidity in young dog
muscle pain

69
Q

describe central vestibular syndrome

A

lesions affecting nerve roots within the brain

70
Q

describe peripheral vestibular syndrome

A

lesions affecting peripheral nerve roots

71
Q

List 4 common clinical conditions causing central or peripheral vestibular syndrome in dogs or cats

A

idiopathic vestibular disease
otitis interna
MUO
neoplasia

72
Q

List 3 common clinical conditions causing cranial nerve dysfunction in dogs and cats

A

trigeminal neuropathy
facial paralysis
trigeminal neoplasia

73
Q

what is a notifiable disease causing neurological signs in dogs and cats

A

rabies

74
Q

DEfine seizure

A

abnormal electrical activity within the brain causing episodes and neurological deficits and the disruption of the autonomic nervous system during episodes

75
Q

List 4 common clinical presentations producing seizures in dogs and cats

A

idiopathic epilepsy
metabolic brain disease
structural brain disease
neurotoxicity

76
Q

what are head tilts commonly associated with

A

vestibular disease
OR
ear infections

77
Q

define nystagmus

A

involutary rapid eye movements

78
Q

List the clinical signs of vestibular disease

A

head tilt
ataxia
wide-based stance
circling
leaning
falling
positional strabismus

79
Q

will bilateral vestibular disease have a head tilt or nystagmus

A

no

80
Q

List the clinical signs seen with central vestibular disease

A

possible paresis or proprioceptive deficits

consciousness may be depressed, stuporous or comatose

CN 5-7may be affected

horizontal, rotary or vertical nystagmus may be present

81
Q

List the clinical signs seen with peripheral vestibular disease

A

alert
CN 7 affected
possible horner’s syndrome
horizontal or rotary nystagmus

82
Q

Describe how to differentiate central from peripheral vestibular disease

A

both will have head tilt towards lesion, nystagmus, circling, nausea

central will have other neurological signs

83
Q

Describe how to diagnose idiopathic vestibular syndrome

A

by exclusion

84
Q

Describe how to treat idiopathic vestibular disease

A

conservative management- if nausea significant part of presentation can try anti-emetic
no specific treatment

85
Q

Describe presentation of trigeminal neuropathy

A

sudden onset dropped jaw
can maually close jaw with no pain

86
Q

Describe how to diagnose trigeminal neuropathy

A

by exclusion (TMJ problems and masticatory myositis)

87
Q

Describe how to treat trigeminal neuropathy

A

conservative therapy (support eating and drinking)- return to function in 4-6 weeks

88
Q

Describe how facial paralysis presents

A

facial asymmetry
absence of blink
lateral deviation of the nose

89
Q

Describe presentation seen with trigeminal neoplasia

A

progressive head assymmetry secondary to atrophy of temporal and masseter muscle unilaterally

90
Q

Describe how to diagnose trigeminal neoplasai

A

CT/MRI

91
Q

Describe how to diagnose neospora

A

serology

92
Q

Describe how to treat neospora

A

Clindamycin if caught early
PTS -

93
Q

a case present with its first seizures with no known aetiology - what is the first diagnostic test?

A

biochem and haematology

94
Q

a cat present with a right head tilt and nystagmus - where is the lesion ?

A

right vestibular lesion

95
Q

what do seizures with altered mentation mean between them mean

A

forebrain lesion

96
Q

what drugs are used to control seizures

A

benzodiazapeam and phenobarbitone

97
Q

List the side effects of using phenobarbital to control seizures

A

risk of hepatic damage
sedative effect
PU/PD

98
Q

how long does phenobarbital take to get to a therapeutic dose to control seizures

A

2 weeks

99
Q

why would we use imepitoin instead of phenobarbital to control seizures

A

if worried about liver pathology

100
Q

why don’t we do blood test with imepitonin

A

it has a big therapeutic range

101
Q

what seizure case is phenobarbitone licensed in

A

progressive cases
frequent seizures
cluster seizure

102
Q

when is imepiton licensed in small animal seizures

A

idiopathic epilepsy

103
Q

why can we us Benzodiapazerm as an anticonvulsant in cats but not dogs

A

dogs develop a tolerance

104
Q

what can we give if diazepam hasn’t stopped a seizures

A

phenobarbital
CRI propofol

105
Q

what is the lesion is you have a vestibular disease plus any neurological deficits

A

central vestibular lesion

106
Q

what are signs of bilateral vestibular disease

A

head swings side to side
shifting nystagmus

107
Q

what cranial nerves effect swallowing

A

CN 9, 10, 12

108
Q

dog present with dysphagia - how do you decide if it bilateral or unilateral

A

the tongue will hang out of one side if unliateral

109
Q

is dysphagia is profoundly bilateral - where must the lesion be

A

brainstem- effecting multiple CN

18- SA- Neurology (11 decks)

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