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Small animal (fourth year) > Neurology > Flashcards

Neurology Flashcards

1
Q

what locations of the brain can a lesion be localised to?

A

forebrain
brainstem
cerebellum
vestibular system (central/peripheral)

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2
Q

what mnemonic can be used to generate a differential diagnosis list?

A

Vascular
Inflammatory/infectious
Trauma
Anomalous
Metabolic
Idiopathic
Neoplasia
Degenerative

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3
Q

what are the main four clinical signs that would localise the lesion to the forebrain?

A

seizure
disorientation
contralateral blindness (normal PLR)
circling

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4
Q

what clinical signs would suggest a forebrain lesion?

A

seizures
behavioural changes
disorientation, depression
contralateral blindness (normal PLR)
facial hypoasthesia
normal gait
circling (ipsilateral), head pressing, pacing
decreased postural response (contralateral limb)

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5
Q

what are the two main clinical signs that suggest a cerebellar lesion?

A

hypermetria
tremors (intention)

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6
Q

what clinical signs suggest a forebrain lesion?

A

normal mentation
abnormal menace (normal vision/PLR)
vestibular signs - head tilt…
ataxia, broad stance, hypermetria
intention tremors
decerebellate rigidity
hypermetric postural response

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7
Q

what are the main three clinical signs of a brainstem lesion?

A

cranial nerve deficits
vestibular signs
paresis (all four/ipsilateral limbs)

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8
Q

what are the clinical signs of brain stem lesions?

A

depression, stupor, coma
cranial nerve deficits
vestibular signs
paresis
decerebrate rigidity
decreased postural response
respiratory/cardiac abnormalities

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9
Q

what are the differentials for a focal/lateralised brain lesion?

A

neoplasia
vascular

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10
Q

what are the differentials for a multifocal brain lesion?

A

inflammatory
infectious

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11
Q

what are the differentials for a diffuse/symmetrical brain lesion?

A

metabolic
toxic

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12
Q

what contributes to intracranial pressure (ICP)?

A

brain
blood supply to brain
cerebrospinal fluid

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13
Q

what is compliance in relation to intracranial pressure?

A

can accommodate mild changes in ICP as when one factor contributing to it (eg. blood supply) increases the others with decrease

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14
Q

what happens when ICP gets too high?

A

herniation underneath the tentorium of through foramen magnum

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15
Q

what structure of the brain does formen magnum herniation effect?

A

cerebellum

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16
Q

what are the signs of raised ICP?

A

mental status (ARAS)
bushings reflex
pupil size and PLR
vestibular eye movement
posture - decerebrate/decerebellate

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17
Q

why does raised ICP effect the mental status of patients?

A

(ARAS - ascending reticular activation system)
awakeness centre in brainstem will decrease in activity with raised ICP causing depression, stupor and coma

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18
Q

what is bushings reflex?

A

very unwell patients with bradycardia and hypertension due to cerebral ischaemia (end stage sign)

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19
Q

how can pupil size change with raised ICP?

A

anisocoria
miosis
mydriasis

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20
Q

what is anisocoria?

A

pupils are different sizes

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21
Q

what is miosis?

A

excessive constriction (shrinkage) of pupil

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22
Q

what is mydriasis?

A

excessive dilation of pupils

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23
Q

how does physiological nystagmus change with raised ICP?

A

eyes don’t move due to a delay in connection between vestibular system and cranial nerves

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24
Q

what is a peracute presentation?

A

extremely sudden onset (change from one second to the next)

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25
Q

what are the differentials for peracute onset brain disease?

A

vascular (stroke)
trauma (RTA…)
toxic

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26
Q

what primary injuries are associated with head trauma?

A

concussion
contusion
laceration (physical disruption of parenchyma)

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27
Q

what secondary injuries are associated with head trauma?

A

inflammatory mediator release
haemorrhage
(raised ICP)

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28
Q

what is used to assess head trauma?

A

modified Glasgow coma scale

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29
Q

what is the modified Glasgow coma scale based on?

A

signs of raised ICP

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30
Q

how does the score of the modified Glasgow coma scale compare to the prognosis?

A

low the score the worse the prognosis

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31
Q

how can the modified Glasgow coma scale be used to monitor ICP?

A

do every couple of hours, if it is getting worse then ICP is increasing

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32
Q

what is done to treat head trauma patients?

A

fluid therapy

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33
Q

what is the aim of fluid therapy for head trauma cases?

A

restore intravascular volume to ensure adequate cranial perfusion pressure

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34
Q

what fluid should be avoided for fluid therapy of head trauma cases?

A

glucose containing fluid - hyperglycaemia is associated with poor outcome

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35
Q

what fluid should be given as an initial bolus in head trauma cases?

A

7.5% saline

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36
Q

what are the advantages of 7.5% saline boluses in head trauma cases?

A

treats shock
decreases intracranial pressure
increases blood flow and oxygen delivery to the brain

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37
Q

what fluids are indicated for head trauma with raised ICP?

A

mannitol or hypertonic saline

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38
Q

what needs to be monitored in head trauma cases?

A

blood pressure
oxygenation
pain
temperature

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39
Q

what pain management should be avoided in head trauma cases?

A

morphine - vomit resulting in raised ICP and herniation

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40
Q

why does temperature need monitoring in head trauma cases?

A

hyperthermia - affects metabolic rate
hypothermia - shivering/oxygen demand

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41
Q

in terms of general care, what are some good things to do to head trauma cases?

A

keep head elevated
catheterise bladder
nutritional support

42
Q

should steroids be given to head trauma patients?

A

no - hyperglycaemia, increased infection risk, lactic acid production

43
Q

what are the main differentials for acute/subacute onset brain disease?

A

inflammatory
infectious
metabolic (wax and wane)

44
Q

what are the three main routes of infection of bacterial meningitis?

A

haematogenous
direct invasion (eyes, ear, nose, bone, trauma)
CSF

45
Q

what is the prognosis for bacterial meningitis?

A

guarded

46
Q

what are the main two infectious brain disease?

A

Neospora caninum
FIP

47
Q

what are the two main metabolic diseases of the brain?

A

hepatic encephalopathy
hypoglycaemia

48
Q

what is the main cause of hepatic encephalopathy?

A

portosystemic shunts

49
Q

what causes the clinical signs of hepatic encephalopathy?

A

hyperammoneaemia
neuroinflammation
deranged neurotransmission
cerebral oedema

50
Q

what are the ways of treating hepatic encephalopathy?

A

lactulose
antibiotics
diet
seizure control

51
Q

why is lactulose used in hepatic encephalopathy cases?

A

traps ammonia as non-diffusible ammonium in intestines to decrease the absorption into blood

52
Q

what is the aim of altering diet to treat hepatic encephalopathy?

A

restrict protein and amino acids to reduce ammonia in blood

53
Q

what are the clinical signs of hypoglycaemia?

A

lethargy, ravenous appetite, anxiety
weakness/tremors
reduced vision and seizures
(all wax and wane)

54
Q

why is hypoglycaemia seen in the brain?

A

has no storage for glucose

55
Q

why does care need to be taken when correcting hypernatraemia?

A

do it too rapidly and the cells will burst - permanent brain damage

56
Q

what are the differentials for chronic brain disease?

A

neoplasia
anomalous
degenerative

57
Q

what primary neoplasms can be seen in the brain?

A

intra-axial - glioma
extra-axial - meningioma, chord plexus tumour

58
Q

what is the median survival time of infratentorial and supratentorial tumours?

A

infratentorial - 28 days
supratentorial - 178 days

59
Q

what should be done to treat brain neoplasia?

A

analgesia (paracetamol)
anti-inflammatory dose of prednisolone

60
Q

what are the most common anomalous brain diseases?

A

hydrocephalus
hydranencephaly

61
Q

what is storage disease of the brain due to?

A

lysosomal hydrolase enzyme defect

62
Q

what are the functions of the vestibular system?

A

maintain balance
maintain normal orientation relative to gravitational field
maintain position of eyes, neck, trunk, limbs in relation to the head

63
Q

what makes up the peripheral vestibular system?

A

3 ducts at right angles to each other with endolymph within
vestibulocochlear nerve (CN8)

64
Q

what triggers nerve impulses in the vestibulocochlear nerve?

A

hair bending due to fluid

65
Q

what makes up the central vestibular system?

A

brainstem - 4 nuclei
cerebellum (inhibits nuclei)

66
Q

what are the clinical signs of vestibular disease?

A

ipsilateral head tilt
head sway (both sides of system effected)
ataxia and wide base stance
leaning/falling
nystagmus
tight circling (less common)
positional strabismus

67
Q

what causes a paradoxical head tilt?

A

cerebellar disease causes head tilt contralateral to lesion (loss of inhibition)

68
Q

how can the lesion of vestibular disease be localised using nystagmus?

A

lesion on the slower side

69
Q

what does vertical nystagmus suggest about the location of the lesion?

A

central vestibular disease

70
Q

what is positional strabismus?

A

when the head is lifted the eye will drop

71
Q

can paresis be a clinical sign of peripheral or dental vestibular disease?

A

central - yes
peripheral - no

72
Q

can proprioceptive deficits be a clinical sign of peripheral or dental vestibular disease?

A

central - yes
peripheral - no

73
Q

how can mentation be affected by peripheral or central vestibular disease?

A

central - may be altered
peripheral - alert

74
Q

can cranial nerve deficits be a clinical sign of peripheral or dental vestibular disease?

A

central - V-XII may be affected
peripheral - VII may be affected

75
Q

can Horners be a clinical sign of peripheral or dental vestibular disease?

A

central - rare
peripheral - yes

76
Q

how does nystagmus indicate central or peripheral vestibular disease?

A

vertical is always central
horizontal or rotary can be either

77
Q

what are the most common differentials for central vestibular disease?

A

cerebrovascular disease
MUEs, FIP
brain tumour

78
Q

what are the most common differentials for peripheral vestibular disease?

A

otitis media/interna
idiopathic

79
Q

what are the two types of strokes?

A

ischaemic (obstruction)
haemorrhagic (rupture)

80
Q

how does cerebrovascular disease present?

A

stroke or cerebrovascular accident

81
Q

what are the most common underlying diseases causing cerebrovascular disease?

A

chronic kidney disease
hypertension
hyperadrenocorticism

82
Q

what does MUO stand for?

A

meningoencephalomyelitis of unknown origin

83
Q

what type of disease are MUOs?

A

auto-immune disease of the brain

84
Q

what are the subtypes of MUOs?

A

granulomatous ME
necrotising ME
necrotising leukoencephalitis

85
Q

what breeds are granulomatous MEs most common in?

A

toy/terrier breeds

86
Q

how old are dogs with granulomatous ME?

A

3-8 years old

86
Q

how are granulomatous MEs distributed?

A

multifocal distribution

87
Q

what is the prognosis for MUOs?

A

very poor (progressive chronic disease)

88
Q

how are MUOs treated?

A

corticosteroids (immunosuppression)

89
Q

what causes CNS involvement of FIP?

A

immune-complex-mediated vasculitis

90
Q

what are the most common neurological signs of FIP?

A

tetra paresis, ataxia, nystagmus, loss of balance (cerebellomedullary region)

91
Q

why is FIP causing neurological signs difficult to diagnose?

A

usually wet form of disease

92
Q

why does otitis media/interna cause peripheral vestibular disease?

A

CN VII and VIII pass through the middle ear

93
Q

what are some clinical signs of otitis media/interna?

A

facial paralysis
peripheral vestibular signs
Horner syndrome
pain opening mouth

94
Q

how is idiopathic vestibular disease treated?

A

spontaneous recovery without treatment

95
Q

what are the clinical signs of idiopathic vestibular disease?

A

acute onset peripheral signs - rolling, falling, vomiting, ataxia, head tilt, nystagmus

96
Q

what supportive treatment can be given to idiopathic vestibular disease patients?

A

maropitant (nauseous)
reduce stimulation but keep active

97
Q

what are the clinical signs of facial nerve paralysis?

A

face drooping
widening of palpebral fissure
food dropping from mouth
reduced/absent palpebral relfex

98
Q

what is the most common cause of deafness?

A

congenital sensorineural deafness

99
Q

what can cause acquired deafness?

A

chronic otitis interna/media
ototoxicity
noise trauma
anaesthesia associated

Small animal (fourth year) (26 decks)

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