Neurology Flashcards

(100 cards)

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
what are the differentials for peracute onset brain disease?
vascular (stroke) trauma (RTA...) toxic
26
what primary injuries are associated with head trauma?
concussion contusion laceration (physical disruption of parenchyma)
27
what secondary injuries are associated with head trauma?
inflammatory mediator release haemorrhage (raised ICP)
28
what is used to assess head trauma?
modified Glasgow coma scale
29
what is the modified Glasgow coma scale based on?
signs of raised ICP
30
how does the score of the modified Glasgow coma scale compare to the prognosis?
low the score the worse the prognosis
31
how can the modified Glasgow coma scale be used to monitor ICP?
do every couple of hours, if it is getting worse then ICP is increasing
32
what is done to treat head trauma patients?
fluid therapy
33
what is the aim of fluid therapy for head trauma cases?
restore intravascular volume to ensure adequate cranial perfusion pressure
34
what fluid should be avoided for fluid therapy of head trauma cases?
glucose containing fluid - hyperglycaemia is associated with poor outcome
35
what fluid should be given as an initial bolus in head trauma cases?
7.5% saline
36
what are the advantages of 7.5% saline boluses in head trauma cases?
treats shock decreases intracranial pressure increases blood flow and oxygen delivery to the brain
37
what fluids are indicated for head trauma with raised ICP?
mannitol or hypertonic saline
38
what needs to be monitored in head trauma cases?
blood pressure oxygenation pain temperature
39
what pain management should be avoided in head trauma cases?
morphine - vomit resulting in raised ICP and herniation
40
why does temperature need monitoring in head trauma cases?
hyperthermia - affects metabolic rate hypothermia - shivering/oxygen demand
41
in terms of general care, what are some good things to do to head trauma cases?
keep head elevated catheterise bladder nutritional support
42
should steroids be given to head trauma patients?
no - hyperglycaemia, increased infection risk, lactic acid production
43
what are the main differentials for acute/subacute onset brain disease?
inflammatory infectious metabolic (wax and wane)
44
what are the three main routes of infection of bacterial meningitis?
haematogenous direct invasion (eyes, ear, nose, bone, trauma) CSF
45
what is the prognosis for bacterial meningitis?
guarded
46
what are the main two infectious brain disease?
Neospora caninum FIP
47
what are the two main metabolic diseases of the brain?
hepatic encephalopathy hypoglycaemia
48
what is the main cause of hepatic encephalopathy?
portosystemic shunts
49
what causes the clinical signs of hepatic encephalopathy?
hyperammoneaemia neuroinflammation deranged neurotransmission cerebral oedema
50
what are the ways of treating hepatic encephalopathy?
lactulose antibiotics diet seizure control
51
why is lactulose used in hepatic encephalopathy cases?
traps ammonia as non-diffusible ammonium in intestines to decrease the absorption into blood
52
what is the aim of altering diet to treat hepatic encephalopathy?
restrict protein and amino acids to reduce ammonia in blood
53
what are the clinical signs of hypoglycaemia?
lethargy, ravenous appetite, anxiety weakness/tremors reduced vision and seizures (all wax and wane)
54
why is hypoglycaemia seen in the brain?
has no storage for glucose
55
why does care need to be taken when correcting hypernatraemia?
do it too rapidly and the cells will burst - permanent brain damage
56
what are the differentials for chronic brain disease?
neoplasia anomalous degenerative
57
what primary neoplasms can be seen in the brain?
intra-axial - glioma extra-axial - meningioma, chord plexus tumour
58
what is the median survival time of infratentorial and supratentorial tumours?
infratentorial - 28 days supratentorial - 178 days
59
what should be done to treat brain neoplasia?
analgesia (paracetamol) anti-inflammatory dose of prednisolone
60
what are the most common anomalous brain diseases?
hydrocephalus hydranencephaly
61
what is storage disease of the brain due to?
lysosomal hydrolase enzyme defect
62
what are the functions of the vestibular system?
maintain balance maintain normal orientation relative to gravitational field maintain position of eyes, neck, trunk, limbs in relation to the head
63
what makes up the peripheral vestibular system?
3 ducts at right angles to each other with endolymph within vestibulocochlear nerve (CN8)
64
what triggers nerve impulses in the vestibulocochlear nerve?
hair bending due to fluid
65
what makes up the central vestibular system?
brainstem - 4 nuclei cerebellum (inhibits nuclei)
66
what are the clinical signs of vestibular disease?
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
what causes a paradoxical head tilt?
cerebellar disease causes head tilt contralateral to lesion (loss of inhibition)
68
how can the lesion of vestibular disease be localised using nystagmus?
lesion on the slower side
69
what does vertical nystagmus suggest about the location of the lesion?
central vestibular disease
70
what is positional strabismus?
when the head is lifted the eye will drop
71
can paresis be a clinical sign of peripheral or dental vestibular disease?
central - yes peripheral - no
72
can proprioceptive deficits be a clinical sign of peripheral or dental vestibular disease?
central - yes peripheral - no
73
how can mentation be affected by peripheral or central vestibular disease?
central - may be altered peripheral - alert
74
can cranial nerve deficits be a clinical sign of peripheral or dental vestibular disease?
central - V-XII may be affected peripheral - VII may be affected
75
can Horners be a clinical sign of peripheral or dental vestibular disease?
central - rare peripheral - yes
76
how does nystagmus indicate central or peripheral vestibular disease?
vertical is always central horizontal or rotary can be either
77
what are the most common differentials for central vestibular disease?
cerebrovascular disease MUEs, FIP brain tumour
78
what are the most common differentials for peripheral vestibular disease?
otitis media/interna idiopathic
79
what are the two types of strokes?
ischaemic (obstruction) haemorrhagic (rupture)
80
how does cerebrovascular disease present?
stroke or cerebrovascular accident
81
what are the most common underlying diseases causing cerebrovascular disease?
chronic kidney disease hypertension hyperadrenocorticism
82
what does MUO stand for?
meningoencephalomyelitis of unknown origin
83
what type of disease are MUOs?
auto-immune disease of the brain
84
what are the subtypes of MUOs?
granulomatous ME necrotising ME necrotising leukoencephalitis
85
what breeds are granulomatous MEs most common in?
toy/terrier breeds
86
how old are dogs with granulomatous ME?
3-8 years old
86
how are granulomatous MEs distributed?
multifocal distribution
87
what is the prognosis for MUOs?
very poor (progressive chronic disease)
88
how are MUOs treated?
corticosteroids (immunosuppression)
89
what causes CNS involvement of FIP?
immune-complex-mediated vasculitis
90
what are the most common neurological signs of FIP?
tetra paresis, ataxia, nystagmus, loss of balance (cerebellomedullary region)
91
why is FIP causing neurological signs difficult to diagnose?
usually wet form of disease
92
why does otitis media/interna cause peripheral vestibular disease?
CN VII and VIII pass through the middle ear
93
what are some clinical signs of otitis media/interna?
facial paralysis peripheral vestibular signs Horner syndrome pain opening mouth
94
how is idiopathic vestibular disease treated?
spontaneous recovery without treatment
95
what are the clinical signs of idiopathic vestibular disease?
acute onset peripheral signs - rolling, falling, vomiting, ataxia, head tilt, nystagmus
96
what supportive treatment can be given to idiopathic vestibular disease patients?
maropitant (nauseous) reduce stimulation but keep active
97
what are the clinical signs of facial nerve paralysis?
face drooping widening of palpebral fissure food dropping from mouth reduced/absent palpebral relfex
98
what is the most common cause of deafness?
congenital sensorineural deafness
99
what can cause acquired deafness?
chronic otitis interna/media ototoxicity noise trauma anaesthesia associated