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phase 2a > Neuro > Flashcards

Neuro Flashcards

1
Q

at what age does epilepsy usually develop?

A

before 20 or over 65

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2
Q

what are focal seizures?

A

in an isolated part of the brain (usually temporal lobe)

affect speech/motor/hearing/memory

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3
Q

do partial seizures impair consciousness?

A

some do - partial complex - do not know you are having eg psychomotor (automatisms)
some don’t -partial simple - myoclonic, jacksonian

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4
Q

what are secondary generalised seizures?

A

begin in one part of the brain and spread to both sides

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5
Q

what is a generalised seizure?

A

affecting both hemispheres of the brain

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6
Q

what is an atonic seizure?

A

‘drop attack’, muscles go floppy

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7
Q

what is a tonic-clonic seizure?

A

generalised
loss of consciousness
muscles stiff (tonic)
violent muscle contractions (clonic)

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8
Q

some features of an epileptic seizure?

A 
prodromal phase - irritability/confusion 
aura 
post ictal confusion, drowsiness, headache lasting 5-30 mins 
seizure lasts for 30-120 secs 
stereotypy 
cyanosis 
can occur from sleep
lateral tongue bite
positive ictal symptoms eg head turning
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9
Q

some features of non epileptic seizures?

A

situational
longer duration
very fast or very slow post ictal recovery
eyes closed
pelvic thrusting
ictal crying
no cyanosis, tongue biting, incontinence or injury

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10
Q

investigations for ?epilepsy?

A

EEG
MRI
ECG
serology

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11
Q

2 drugs for focal epilepsy?

A

carbamazepine

lamotrigine

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12
Q

2 drugs for generalised seizures?

A

sodium valproate

lamotrigine

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13
Q

how does lamotrigine work?

A

decreases sodium currents and glutamate transmission

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14
Q

how does carbamazepine work?

A

prevents repeated firing through sodium channels

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15
Q

how does sodium valproate work?

A

potentiates GABA activity

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16
Q

side effect of sodium valproate?

A

teratogenic
liver damage
hair loss

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17
Q

side effect of carbamazepine?

A

agranulocytosis

aplastic anaemia

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18
Q

side effect of lamotrigine?

A

stevens johnson syndrome

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19
Q

how is status epilepticus defined?

A

seizure for more than 5 mins

or 3 seizures in 1 hour

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20
Q

treatment of status epilepticus?

A

ABCDE
secure airway
oxygen (high flow)
check cardiac, resp function, glucose

IV lorazepam
repeat after 10 mins if not successful
IV phenytoin or phenobarbitol

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21
Q

what is the pathophysiology of parkinsons?

A

death of dopaminergic cells in the substantia nigra

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22
Q

what is a lewy body?

A

collection of alpha synuclein

in lewy body dementia and also sometimes parkinsons

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23
Q

classic 3 features of parkinsons?

A

bradykinesia
tremour - pill rolling
rigidity - cogwheel

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24
Q

what is the gait/posture like in parkinsons?

A

stooped posture

shuffling ‘festinant’ gait with decreased arm swing

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25
Q

what is hypomimia?

A

lack of facial expression

sign of parkinsons

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26
Q

autonomic symptoms of parkinsons?

A

urinary frequency (not incontinence)
dribbling
postural hypotension
constipation

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27
Q

how is parkinsons diagnosed?

A

usually clinical

DATSCAN to visualise DA-ergic activity in striatum

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28
Q

what is first line for parkinsons, how does it work?

A

levodopa (DA precurser) with carbidopa (peripheral decarboxylase inhibitor)

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29
Q

some side effects of levodopa w/ carbidopa?

A 
dystonia
chorea
dyskinesia
nausea 
psychosis
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30
Q

what are ripinirole & bromocriptine? a side effect?

A

DA agonist
used in parkinsons
pulmonary fibrosis

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31
Q

what is selegiline, how is it used?

A

MOA-B inhibitor - stops breakdown of DA and NA

used for depression & parkinsons

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32
Q

what is entecapone?

A

COMT inhibitor
similar to carbidopa
carbidopa + entecapone may extend ‘on’ time of levodopa

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33
Q

what can be given to help tremour? what is a side effect?

A

anticholinergic eg procyclidine

anti cholinergic burden = confusion

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34
Q

what happens when drugs for parkinsons stop working?

A

on dyskinesias = hyperkinetic movement
off dyskinesias = painful dystonic posturing

unpredictable freezing

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35
Q

is parkinsons symmetrical?

A

no

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36
Q

how to distinguish parkinsons from pressure hydrocephalus? (produces a magnetic gait)

A

parkinsons doesnt have incontinence

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37
Q

how to determine parkinsonian tremour from essential tremour?

A 
PD = pill rolling 
essential = worse on intention, better with alcohol and more family history
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38
Q

define stroke?

A

acute sudden onset neurological deficit
due to cerebrovascular pathology
symptoms persisting for more than 24hrs or death

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39
Q

what are the main vessels in the anterior cerebral circulation? - 6

A 
posterior communicating 
middle cerebral
- anterior choroidal 
internal carotid 
anterior cerebral 
anterior communicating
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40
Q

what main arteries branch off basilar?

A 
posterior cerebral
superior cerebellar
pontine
anterior inferior cerebellar 
-- vertebral arteries - posterior inferior cerebellar & spinal are branches
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41
Q

what are brocas & wernickes area?

A 
wernicke = understanding words
brocas = forming words/speaking
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42
Q

where is wernickes area? what is it supplied by?

A

parietal/temporal lobe
opposite side to dominant hand
supplied by middle cerebral artery

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43
Q

where is brocas area, what is it supplied by?

A

frontal lobe
opposite side to dominant hand
supplied by middle cerebral artery

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44
Q

what parts of the brain does the anterior cerebral artery supply?

A

front & top - so frontal cortex and some of the motor cortex (esp upper limbs)

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45
Q

what does the middle cerebral artery supply?

A

sides of brain inc brocas, wernickes, motor (esp lower limbs) and sensory

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46
Q

what is the most common artery to have a stroke in?

A

middle cerebral

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47
Q

what does the posterior circulation supply, what are the symptoms of a stroke there?

A

cerebellum and brainstem

dysarthria, dysphasia, diplopia, dizziness, ataxia, quadrantanopia, reduced GCS

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48
Q

what is a lacunar infarct & how does it present?

A

of the deep ppenetrating arteries
produces an isolated deficit, eg one hand weakness
no visual field defect or cortical malfunction

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49
Q

how do you differentiate stroke from bells palsy?

A

stroke = lower face weakness but forehead spared

bells palsy = forehead affected

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50
Q

are the motor symptoms ipsilateral or contralateral to the infarct?

A

contralateral

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51
Q

what is the bamford classification?

A

for ischaemic stroke, total anterior = 3/3 and partial anterior = 2/3

hemiplegia
homonymous hemianopia
higher cortical dysfunction eg speech

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52
Q

what is the first investigation in suspected stroke?

A

non contrast CT head to exclude haemorrhagic

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53
Q

if you are going to do a thrombectomy how will you find the clot?

A

CT angiogram

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54
Q

what is gold standard for ischaemic stroke investigation?

A

diffusion weighted MRI head

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55
Q

what is endarterectomy? what inv for it?

A

to remove atherosclerotic plaques

doppler

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56
Q

what screening programme for stroke in the community?

A

FAST

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57
Q

what is first line for stroke if presented within 4.5 hrs of onset?

A

alteplase (tissue plasminogen activator)

+ aspirin

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58
Q

contraindications for thrombolysis? 5

A 
hypertension
bleeding elsewhere
surgery in the last 3 months
brain malignancy 
over 4.5 hrs since onset
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59
Q

when should you do a thrombectomy in ischaemic stroke?

A

within 6hrs or if you can prove the tissue is viable

there is a risk of reperfusion injury so only do if it will be worthwhile

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60
Q

should you lower BP in stroke?

A

no, this increases the risk of hypoperfusion

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61
Q

secondary prevention after stroke?

A

aspirin for 14 days
clopidogrel
atorvastatin
bp control

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62
Q

risk factors for ischaemic stroke/TIA?

A 
age
hypertension
diabetes 
hypercholesterolaemia
smoking
AF
thrombophilia 
sickle cell
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63
Q

what is a crescendo TIA?

A

2 or more TIA within a week

high risk of stroke

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64
Q

what is the definition of TIA?

A

symptoms of a stroke with complete resolution within 24hrs

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65
Q

what is the pathophysiology of TIA?

A

ischaemia without infarction (the tissue does not die)

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66
Q

what score assesses risk of another TIA or stroke?

A 
ABCD2 
Age (over 60 = 1)
BP (over 140 or 90 = 1)
Clinical features (speech impaired = 1, unilateral weakness =2)
Duration (10 mins+ = 1, 1hr + = 2)
Diabetes

if more than 4 admit

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67
Q

surgical treatment for TIA?

A

endarterectomy if 70% or more stenosis

stent eg carotid stent

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68
Q

long term treatment for TIA?

A

aspirin + clopidogrel for 2 weeks - then just clopidogrel
statins
BP control

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69
Q

what is the usual epidemiology of extradural haemorrhage?

A

young patient with traumatic head injury esp skull fracture

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70
Q

what are the 3 layers of meninges?

A

outer: dura mater - tough fibrous - periosteal and meningeal
middle: arachnoid mater: loose connective tissue
inner: pia mater - thin, tightly adhered to brain
PADS

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71
Q

in an extradural haemorrhage where is the blood?

A

between the skull and the dura mater - usually tightly stuck!

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72
Q

where are the dural venous sinuses?

A

between the two layers of dura, the periosteal and meningeal layers

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73
Q

what artery is most commonly implicated in an extradural haemorrhage?

A

meningeal artery rupture

at the pteron (frontal bone joins parietal bone)

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74
Q

typical history of extradural haemorrhage?

A

blow to side of head
lucid period for a few hours (these vessels bleed slowly)
– loss of consciuosness

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75
Q

what does an extradural haemorrhage look like on CT?

A

hyperdense bright white
lemon shaped
doesnt cross suture lines
skull x ray may also show fracture

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76
Q

management of extradural haemorrhage?

A

ICU / intubate
mannitol - to decrease ICP
craniotomy

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77
Q

where is the blood in a subdural haemorrhage?

A

between the dura and arachnoid

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78
Q

typical history in subdural haemorrhage?

what vessels are typically affected?

A

acute - car crash with accelleration-deceleration
chronic - elderly or alcoholic with trivial fall weeks ago
tear of bridging veins - in elderly/alcoholic this is more likely as brain is shrunken
veins so bleeding can be slow – chronic

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79
Q

what do you see on CT in a subdural haemorrhage?

A

crescent/banana shaped bleeding - all way to midline at each side
acute (white) or chronic (grey) blood
midline shift

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80
Q

presentation of subdural haemorrhage?

A 
acute = reduced worsening GCS 
chronic = progressive confusion 
focal neurological symptoms 
raised ICP (vomitting/reduced ICP/blurred vision)
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81
Q

treatment for subdural haemorrhage?

A

burr hole
craniotomy
mannitol

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82
Q

where is the bleeding in a subarachnoid haemorrhage?

A

between the arachnoid and pia mater

where the CSF should be

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83
Q

what vessels are most often implicated in subarachnoid haemorrhage?

A

usually caused by ruptured berry anneurysm

in circle of willis, esp junctions, in anterior comm/ int carotid/ MCA

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84
Q

typical history/epidemiology for subarachnoid haemorrhage?

A

sudden onset thunderclap headache
while playing sport
female 45-60/connective tissue disorders

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85
Q

symptoms of subarachnoid haemorrhage?

A

sudden onset worse ever headache, occipital (at back)
meningism - photophobia, neck stiffness
vision/speech changes
confusion

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86
Q

what do you see on CT in subarachnoid haemorrhage?

A

star shaped

hyperattenuation in subarachnoid space

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87
Q

apart from CT head, what other investigations might be helpful in subarachnoid haemorrhage?

A

lumbar puncture for xanthochromia - yellow colour indicates bilirubin from blood in csf space

angiography to find the source

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88
Q

treatment for subarachnoid haemorrhage?

A

endovascular coiling/clipping to stop bleeding
nimodipine (calcium channel blocker) to prevent vasospasm secondary to bleeding
lumbar drain for CSF, if hydrocephalus develops

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89
Q

what is the Cushing reflex?

A

in ischaemic stroke
increasing BP, decreasing heart rate, erratic breathing
BP increases in response to hypoperfusion in brain
carotid sinus baroreceptors detect increased BP – slow heart rate
irregular breathing because brainstem is compressed by raised ICP

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90
Q

what does agonal breathing suggest?

A

herniation of the brainstem

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91
Q

some triggers for migraine in susceptible people?

A 
chocolate/wine/cheese/caffeine
oral contraceptive
menstruation
bright lights
strong smells 
lack of sleep
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92
Q

how long does a migraine last?

A

4-72 hours

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93
Q

what is the pain like in migraine?

A

unilateral
throbbing/pulsating
moderate-severe

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94
Q

apart from pain, some presentations of migraine?

A 
prodromal fatigue/mood changes 
nausea
photophobia 
phonophobia 
aura
cannot carry out daily activities, want to lie in a dark room
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95
Q

what is a hemiplegic migraine?

A

unilateral weakness, ataxia, altered consciousness

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96
Q

some common features of migraine aura?

A

flashing lights
zig zag lines in vision
ringing in ears

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97
Q

what is a silent migraine?

A

aura but no headache

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98
Q

acute management of migraine? 3

A

NSAIDS/paracetamol
triptans eg sumatriptan
antiemetic eg metoclopramide

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99
Q

what are triptans for & how do they work?

A 
for acute treatment of migraine 
5ht agonist
causes vasoconstriction 
inhibits peripheral pain receptors 
reduces CNS activity
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100
Q

prophylaxis of migraine?

A

propanolol
topiramate
amitriptyline
riboflavin

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101
Q

some triggers for tension headache?

A 
stress
posture
lack of sleep
eye strain
depression
alcohol
skipping meals
dehydration
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102
Q

what is the pain like in tension headache?

A

bilateral
mild-moderate
pressing/tight sensation
photophobia or phonophobia but not both and no nausea

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103
Q

10 headache red flags?

A 
new onset over 50
immunosupressed
neck stiffness 
history of cancer
history of trauma 
jaw claudication
visual disturbance
changes with posture
started by coughing/laughing etc = increased ICP 
fever
seizure
papilloedema 
vomitting 
change in personality
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104
Q

epidemiology of cluster headache?

A

male
20-50
smoker

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105
Q

what is the pathophysiology of cluster headache?

A

hyperactivity of trigeminal-autonomic reflex arc
vasodilation and trigeminal stimulation
histamine & mast cells
autonomic nervous system activated

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106
Q

presentation of cluster headache?

A 
severe 'boring' 'hot poker' pain over one eye 
myosis, ptosis, red/swollen eye
nasal discharge and tears 
sweating on one side of face 
photophobia
agitation/restlessness
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107
Q

how long does a cluster headache last?

A

15 min - 3hrs

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108
Q

episodic vs chronic cluster headache?

A 
episodic = pain free for 1 month +
chronic = no pain free months
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109
Q

management of cluster headache?

A

neuro referral
acute - sumatriptan, high flow oxygen
prophylaxis - verapamil, prednisolone, lithium

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110
Q

what medications cause medication over use headache?

A

10 days/month: ergotamine
triptans
opioids

15 days/month: nsaid
paracetamol
aspirin

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111
Q

what is the pain like in trigeminal neuralgia?

A 
in one or more distributions of the trigeminal nerve 
no radiation
severe stabbing pain
unilateral 
secs-mins 
triggered by stimuli
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112
Q

management of trigeminal neuralgia?

A

carbamazepine

surgery to decompress or damage the nerve

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113
Q

Some factors that contribute to the epidemiology of MND?

A

smoking
pesticides
SOD1 & C90RF genes

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114
Q

what are upper motor neurones?

A

go from cortex to anterior horn of spinal cord

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115
Q

what are lower motor neurones?

A

go from the spinal cord to the muscle

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116
Q

does MND affect upper or lower motor neurones?

A

can be either or both

if it is affecting only upper motor neurones it is called primary lateral sclerosis
if it affecting only lower motor neurones it is called primary muscular atrophy
if it is affecting upper and lower it is called amyotrophic lateral sclerosis (this is most common)

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117
Q

what is the most common onset of MND?

A

limb

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118
Q

features of upper MND affecting the limbs?

A

pyramidal weakness
– extensors in arms and flexors in legs
spasticity
brisk reflexes

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119
Q

features of lower MND affecting the limbs?

A

weakness
wasting
fasciculations

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120
Q

some features of bulbar MND?

A

dysarthria - speech is slurred or quiet
excessive saliva
choking
jaw spasm

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121
Q

what type of respiratory failure is seen in MND?

A 
type 2 
(because it is a problem with the muscles so you are unable to both breathe oxygen in AND co2 out)
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122
Q

when is the breathlessness worst in MND?

A

at night or when lying flat

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123
Q

some general symptoms of MND?

A 
foot drop
tripping/falling
difficulty using hands 
fatigue, sleep disturbance 
anorexia
frontotemporal dementia
emotional lability
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124
Q

is MND symmetrical?

A

no

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125
Q

3 signs that suggest it is not MND?

A

Symmetry
incontinence
sensory disturbance (MND is specifically of the MOTOR neurones)
relapsing-remitting pattern (MND is gradually worsening)

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126
Q

investigations for MND affecting upper neurones?

A

MRI brain and spine - need to exclude other things

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127
Q

investigations for lower motor neurone pathology? (eg in MND)

A

nerve conduction studies - test how well the nerve conducts the signal

EMG (electromyography) - tests how well the muscle responds to impulses

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128
Q

what is riluzole?

A

antioxidant, may improve symptoms in MND or extend life by a few months

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129
Q

motor neurones that are spared in MND?

A 
oculomotor nerve 
onufs nucleus (controls bladder/continence)
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130
Q

most common cause of meningitis in neonates?

A

group B strep

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131
Q

most common cause of meningitis in adults?

A

s pneumoniae

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132
Q

n meningitidis is a common cause of meningitis, especially in which populations?

A

adults/students

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133
Q

h influenzae is a cause of meningitis, most commonly affecting ____

A

children

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134
Q

listeria monocytogenes is a cause of meningitis, most commonly in which populations?

A 
immunocomp
elderly
neonates 
cancer 
diabetic
pregnant
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135
Q

some viral causes of meningitis?

A

HSV

VZV

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136
Q

define meningitis?

A

inflammation of the meninges, which cover the brain and spinal cord

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137
Q

why is a rash associated with meningitis?

A

n meningitidis is a common cause of meningitis

meningococcal sepsis = disseminated intravascular coagulation, the ‘rash’ is the red spots produced by the tiny clots

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138
Q

classic triad of meningism?

A

photophobia
neck stiffness
headache

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139
Q

apart from meningism, some features of meningitis?

A 
vomitting
fever
impaired consciousness 
seizures 
kernigs sign
brudzinskis sign
non blanching purpuric rash, if meningoccoccal
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140
Q

what is kernigs sign?

A

meningitis
patient lying on back
flex hip and straighten knee
= back pain

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141
Q

what is brudzinskis sign?

A

patient lying on back

flex neck – knees and hips with flex too

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142
Q

what is the CSF like in bacterial meningitis?

A

cloudy
neutrophils/granulocytes
high protein
low glucose

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143
Q

what is the CSF like in viral meningitis?

A

lymphocytes
high protein
normal glucose

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144
Q

what is the CSF like in fungal meningitis?

A

lymphocytes
high protein
low glucose

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145
Q

do you need to send a CSF if you have meningism + rash?

A

no, you can do a blood test for n meningitidis instead

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146
Q

if a CSF contains gram pos cocci what is it most likely to be?

A

strep pneumoniae

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147
Q

if a CSF contains gram pos bacilli what is it likely to be?

A

h influenzae

listeria

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148
Q

what empirical antibiotics should you give for ?meningitis while you are waiting for results?

A

cefotaxine / ceftriaxone

+ amoxicillin if you suspect listeria

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149
Q

what should you give to contacts of someone known to be infected with n meningitidis?

A

ciprofloxacin

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150
Q

what drug reduces the risk of developing complications after meningitis?

A

dexamethasone

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151
Q

potential complications of meningitis?

A 
hearing loss
epilepsy 
cognitive impairment 
memory loss 
focal neurological deficits
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152
Q

some differentials for MND?

A

MS
spinomuscular atrophy
muscular dystrophy
myasthenia

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153
Q

what is the most common cause of encephalitis?

A

HSV

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154
Q

what is encephalitis?

A

inflammation of the brain parenchyma

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155
Q

features of encephalitis?

A 
fever
headache
fatigue
confusion
change in behaviour/psychosis
focal neurological defect eg aphasia/hemiparesis/cerebellar 
seizures
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156
Q

investigations for encephalitis?

A

MRI head to see inflammation - frontal/temporal
CSF

throat swab for virus
serology
blood culture 
FBC, CRP, UE 
EEG - non specific
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157
Q

what can the EEG show in encephalitis?

A

periodic lateralised discharges at 2Hz (not specific)

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158
Q

empirical management for encephalitis?

A

aciclovir

gancyclovir

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159
Q

what virus causes chickenpox/shingles?

A

varicella zoster – chickenpox
lies dormant –
reactivates – shingles – now called herpes zoster

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160
Q

what can happen if you develop chickenpox for the first time in adulthood?

A

pneumonitis (can be fatal)

foetal varicella syndrome, if you catch it in pregnancy – causes maldevelopment of foetus

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161
Q

what is a chickenpox rash classically like?

A

macule-papule-vesicle-pustule-crust

centrifugal distribution

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162
Q

where does the chickenpox virus usually lay dormant?

A

dorsal route ganglion
trigeminal nerve
olfactory nerve

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163
Q

presentation of shingles?

A 
macular -- vesicular rash in dermatomal distribution, one side of midline, thoracic 
pain/itching/tingling/neuropathy 
malaise, myalgia
headache
fever
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164
Q

investigations for shingles?

& a specific stain?

A

serology
viral PCR
tzank - confirms presence of herpesvirus but doesnt differentiate which

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165
Q

management of shingles?

A

aciclovir or valaciclovir

iv immunoglobulin

166
Q

what is ramsey-hunt syndrome?

A 
complication of shingles
paralysis of facial nerve
rash on ear/mouth
tinitus 
hearing loss
167
Q

what is the epidemiology of MS?

A

under 50
more females
more further from the equator
may be related to EBV exposure in teenage

168
Q

is MS in the CNS or PNS?

A

CNS

169
Q

what is the pathophysiology of MS?

A

autoimmune
lymphocytes cross the BBB – destroy oligodendrocytes
demyelination & loss of axons
remyelination – remission for a period (but symptoms may reappear eg when axons stretched by a hot shower)

170
Q

some presenting features of MS?

A 
optic neuritis
nystagmus
focal weakness - face/arms/legs
spasticity
vertigo
paresthesia
cerebellar ataxia 
sensory loss
171
Q

what is optic neuritis & why can it happen in MS?

A

painful unilateral visual loss
demyelination of optic nerve
relative afferent pupillary defect: consensual but not direct constriction

172
Q

what is internuclear opthalmoplegia in MS?

A

dysfunction of the fibre than connects CN 3, 4 and 6 for co ordinated eye movement

173
Q

where is the problem in a conjugate lateral gaze disorder?

A

CN6 - affected eye cannot abduct

174
Q

what are two ‘pre-MS’ syndromes?

A

radiologically isolated: changes apparent on MRI, but no symptoms

clinically isolated: 1 episode of symptoms but you need at least 2 to call it MS

175
Q

3 patterns of disease course in MS?

A

relapsing-remitting
– partial or full recovery between, minimal disability

secondary progressive

    • relapsing-remitting which becomes progressive,
    • or, gradually worsening with relapses superimposed

primary progressive
– gradually worsens from onset

176
Q

what is Lhermitte’s sign?

A

sensations shooting down spine when bending neck

associated with MS

177
Q

investigations for MS?

A

MRI w/ contrast - shows immune activity in CNS

lumbar puncture : oligoclonal bands in CSF
indicates immune activity in CSF

178
Q

what signs might you find on a bedside examination of a patient with MS?

A 
brisk reflexes
eyes don't move together
pyramidal weakness 
unco-ordinated 
babinskis sign 
lhermittes sign
179
Q

what is 1st and 2nd line acute treatment for MS relapses?

A

1st – oral methylprednisolone

2nd – IV steroids

180
Q

treatment for MS symptoms?

A 
amitryptiline 
baclofen 
anti cholinergics (to treat incontinence)
181
Q

drugs that prevent MS relapses?

A 
natalizumab - stops lymphocytes crossing BBB 
alemtuzumab: anti CD20 
betaferon/IFN1beta
daclizumab 
stem cell transplant
182
Q

are brain tumours generally malignant or benign?

A

55% are malignant

183
Q

are brain tumours usually primary or secondary?

A

secondary / metastatic more common

184
Q

what grading system do brain tumours follow, how does it work?

A

WHO classicification

1 - slow growing benign
2 - cytological atypia eg large hyperchromic nuclei
3 - anaplasia, mitotic
4 - microvascular proliferation or necrosis

185
Q

what is the most common type of brain tumour?

A

glioma

186
Q

what is an empendymoma?

A

from lining of ventricle/central canal

a glioma

187
Q

what is oligodendroglioma? how can it be identified? what does it cause?

A 
40s and 50s 
frontal cortex = behavioural changes 
grade 2 or 3 
calcification 
deletion of 1p1qq
glioma
188
Q

what is glioblastoma mutliformae?

A

glioma
from astrocytes
very malignant, grade 4
de novo or develop from grade 2 astrocytoma

189
Q

what is a diffuse astrocytoma?

A

grade 2
type of glioma
can develop into glioblastoma multiformae which is much more malignant

190
Q

what is an anaplastic astrocytoma?

A 
grade 3 (anaplastic)
type of glioma
191
Q

what is a pilocytic tumour?

A

glioma
grade 1
in children
good prognosis

192
Q

what is mengingioma?

A

generally benign

cause symptoms because take up space = nerve lesions & raised ICP

193
Q

what is a hemangioblastoma?

A

brain tumour from blood vessels
develops in cerebellum in middle age
usually low grade

194
Q

what is acoustic neuroma?

A

aka schwanoma - cn 8

195
Q

what is medulloblastoma?

A

brain cancer
small blue cell
cerebellum in children
grade 4

196
Q

focal neurological manifestation of a frontal cortex problem?

A

hemiparesis

personality change

197
Q

focal neurological manifestation of a temporal lobe problem?

A

dysphasia

amnesia

198
Q

focal neurological manifestation of a occipital lobe problem?

A

contralateral visual defect

199
Q

focal neurological manifestation of a parietal lobe problem?

A

hemisensory loss

200
Q

in brain tumour what is the headache like?

A

worse on coughing/bending/lying/in morning
constant
disturbs sleep

201
Q

some symptoms of raised ICP?

A 
headache
vomitting
seizures 
papilloedema 
3rd and 6th CN palsies 
visual field defects
202
Q

investigations for ?brain tumour?

A

MRI (then maybe fMRI)
CT contrast
stereotactic biopsy for histology
– MGMT methylation predicts response to treatment
–IDH-1 mutation indicates glioma replication

203
Q

what chemotherapy is commonly used for brain tumour?

A

PCV - procarbazine, lomustine, vincristine

temozolamide

204
Q

what is usually 1st line for glioma?

A

radiotherapy

205
Q

which tumours are most likely to metastasise to the brain?

A 
lung
breast
prostate
colorectal
renal
malignant melanoma
206
Q

in lateral tentorial herniation what is compressed?

A

posterior cerebral and superior cerebellar arteries
cerebellum and midbrain
CN 3

207
Q

how is peripheral neuropathy defined?

A

axonal or demyelinating damage to several nerves

208
Q

5 aetiology of peripheral neuropathy?

A 
Diabetes 
Alcohol
Vit b12 deficiency
Infective eg guillian barre, lyme 
Drugs - isoniazid, amiodarone

gluten sensitivity
CKD
amyloid, sarcoid
paraneoplastic

209
Q

schwann cells vs oligodendrocytes?

A

both produce myelin
schwann - peripheral
oligodendrocytes - cns

210
Q

5 mechanisms of damage in peripheral neuropathy?

A

demyelination / schwann cell damage
axonal degradation - eg charcot marie tooth
compression
wallerian - trauma - axon separated from cell body
infarction - eg diabetes, arteritis
infiltration - leprosy, cancer

211
Q

what are the 4 types of sensory fibre?

A

A alpha
A beta
A delta
C

212
Q

what are A alpha fibres?

A 
sensory neurones
large 
myelinated
proprioception
if there is damage to them you fall over when you close your eyes
213
Q

what are A beta fibres?

A

large, myelinated

fine touch, vibration

214
Q

what are A delta fibres?

A

small
myelinated
pain & cold
damage = loss of sensation or severe neuropathic pain

215
Q

what are C fibres?

A 
sensory
unmyelinated
slow pain
very small so vulnerable to damage
damage = loss of pain or neuropathic pain
216
Q

what motor neurones are affected in peripheral neuropathy, & when?
what symptoms?

A

lower motor neurones, motor neurone involvement is a late sign
muscle cramp
weakness
atrophy - distal muscles - foot arches, pes cavus
fasciculations

217
Q

what pattern of neurones are affected in symmetrical sensorimotor neuropathy?

A

longest first - so starts in toes and ascends
sensory then motor
sensory - pain, tingling, numbness

218
Q

what pattern of neurones are involved in asymetrical sensory peripheral neuropathy?
what causes this?

A

patchy
dorsal route ganglion

paraneoplastic
sjorens
gluten

219
Q

what is mononeuritis multiplex?

A

peripheral neuropathy aka asymmetrical sensorimotor

loss of motor & sensory in two separate areas

220
Q

what is assymetrical sensorimotor peripheral neuropathy most associated with?

A

systemic vasculitis

221
Q

what will you see on clinical examination of someone with peripheral neuropathy?

A

decreased reflexes
sensory deficits
weakness
wasting

222
Q

investigation of peripheral neuropathy?

A

nerve conduction studies

    • if demyelination, conduction will be slow
    • if the axon is damaged, impulse will be smaller
223
Q

treatment for cramps in neuropathy?

A

quinine

224
Q

treatment for pain in peripheral neuropathy?

A

amitryptiline

gabapentin

225
Q

what is myasthenia gravis?

A

autoantibodies to the Ach receptor, causing muscle weakness

226
Q

what condition is myasthenia gravis associated with?

A

thymoma and thymic hyperplasia

227
Q

what normally happens at the neuromuscular junction to trigger muscle contraction?

A

depolarisation of lower motor neurone = calcium channels open
calcium influx into LMN
calcium = exocytosis of Ach from vesicles
Ach crosses synapse and binds to postsynaptic receptors
ach binding opens the intrinsic channel, potassium out sodium in
voltage gated sodium channels open = depol along t tubule
depol = opening of calcium stores in sarcoplasmic reticulum
calcium = contraction

228
Q

as well as anti-AchR antibodies, what other antibodies might (less commonly) be found in myasthenia gravis?

A

anti-musk (muscle specific kinase)

229
Q

some ocular manifestations of myasthenia gravis?

A

ptosis
upward gaze
complex opthalmoplegia
double vision (because of difficulty with eye movement)

230
Q

some general features of myasthenia gravis?

A 
fatiguability
muscle weakness
dysarthria 
dysphagia
shortness of breathing
fatigue when chewing 
head drop
231
Q

are antibodies always present in myasthenia gravis?

A

no, in fact anti-AchR antibodies only present in 80% pts and only 50% of ocular

232
Q

what are 2 investigations for myasthenia gravis?

what will you see?

A

single fibre EMG
decremental potentiation - response decreases as stimulus is repeated
- this will tell you there is fatiguability

tensilon test
tensilon = ach esterase inhibitor
this will tell you if the symptoms are caused by myasthenia or not (definitive/confirm)

233
Q

what is the treatment for myasthenia gravis?

A

1st line - pyridostigmine (Ach esterase inhibitor)

2nd line - azathiopurine
other immunosuppressants eg prednisolone, methotrexate
rituximab good for MuSK Ab +ve

234
Q

what is myasthenic crisis?

A 
complication of myasthenia gravis 
respiratory difficulty 
SOB, reduced breath sounds, reduced chest expansion
normal saturation, normal ABG 
decreased FVC
235
Q

how to treat myasthenic crisis?

A

IV immunoglobulin
steroids
plasma exchange

236
Q

how is Huntingtons inherited?

A

autosomal dominant

anticipation so if parents are borderline but dont have symptoms, their child could still have it

237
Q

what kind of mutation is seen in Huntingtons?

A 
trinucleotide repeat (CAG)
on chr 4, huntingtin / HTT gene
238
Q

what does the mutation in Huntingtons code for & what is the effect of the mutation?

A

CAG codes for glutamine
too many CAG repeats = build up of glutamine
= misfolding/aggregation
= loss of GABA producing cells, loss of inhibitionn

239
Q

how is movement affected in Huntingtons?

A

it can be initiated but then is hard to stop or change

240
Q

clinical presentation of Huntingtons?

A 
cognitive / mood changes 
chorea - involuntary abnormal movements 
eye movement disorders
dysarthria
dysphagia
dementia
infections
241
Q

management of Huntingtons disease?

A

antipsychotic eg olanzapine
tetrabenazine - DA depleting
benzodiazepine

242
Q

what infections does guillian barre follow?

A

GI eg campylobacter jejuni
EBV
CMV

243
Q

what is the pathophysiology of guillian-barre?

A

autoimmune
molecular mimicry
antibodies to nerves eg myelin sheath or axon
= peripheral neuropathy

244
Q

is guillian barre symmetrical?

A

yes

245
Q

presentation of guillian barre?

A 
following an infection
ataxia
ascending flaccid motor weakness, starts at feet 
hyporeflexia
facial weakness 
reduced sensation
neuropathic pain
respiratory involvement
246
Q

timeframe of guillian barre?

A

develops within 4 weeks of infection
peaks 2-4 weeks after that
takes months to years to recover

247
Q

how is guillian barre diagnosed?

A

clinical diagnosis
Brighton criteria
CSF - high protein, normal glucose and white cells
nerve conduction studies - low signal

248
Q

treatment for guillian barre?

A

heparin/apixaban
plasma exchange
IV immunoglobulins

249
Q

3 causes of spinal cord compression?

A 
cancer (metastatic myeloma, bone tumour, glioma)
disc herniation
infection eg epidural abscess
haematoma 
spinal stenosis
250
Q

what part of the spine is most commonly compressed by tumours?

A

thoracic

251
Q

3 classifications of spinal cord compression caused by tumour?

A

intramedullary - in the vertebral canal
leptomeningeal - where the meninges should be
extradural - compressing the dura from the outside

252
Q

what is the pain like in spinal cord compression?

what makes it worse?

A

radicular (spreading down spinal root to legs) or local

worse when lying/coughing

253
Q

presentation of spinal cord compression?

A

back pain
progressive motor weakness - umn and lmn
sensory loss
bladder/bowel dysfunction, retention

254
Q

describe the motor impairment in a spinal cord lesion?

A

LMN signs at the level of the lesion – wasting, weakness, hyporeflexia

UMN signs BELOW the level of the lesion – hyperreflexia, contralateral spasticity, extensor plantar reflex

255
Q

describe the sensory impairment in spinal cord compression?

A

ascending numbness
parasthesia
1-5 caudal levels below the lesion
less common than motor symptoms

256
Q

what is the gold standard investigation for spinal cord lesion?

A

MRI

257
Q

some differentials for spinal cord compression?

A

MS
MND
guillian barre
spinal cord compression

258
Q

treatment of spinal cord compression?

A

IV dexamethasone
surgical decompression - eg remove tumour, discectomy etc
epidural steroid injections

259
Q

3 places that can be stenosed in spinal cord stenosis & the names for them?

A

central spinal canal = central stenosis
nerve root canals = lateral stenosis
intervertebral foramina = foramina stenosis

260
Q

3 causes of spinal stenosis?

A 
congenital
age related degeneration
herniated disk
thickening of ligaments eg ligamentum flavum 
fractures
tumour
spondylolisthesis (slipped disk)
261
Q

presentation of spinal cord stenosis?

A 
gradual
intermittent neurogenic claudication
leg weakness worse when standing 
saddle anaesthesia
lower back/buttock/leg pain
262
Q

investigations for spinal stenosis?

A

MRI

CT angiogram and ABPI to exclude peripheral artery disease

263
Q

what is cauda equina syndrome?

A

compression of the bundle of nerves at the bottom of the spinal column, ‘the cauda equina’

264
Q

what is the most common cause of cauda equina syndrome?

A

herniated lumbar disk

265
Q

what is the piece of dura in the middle of the cauda equina called?

A

conus medullaris

266
Q

what happens to the nerves in the cauda equina?

A

they still exit the spinal cord at their respective vertebral level
for the cauda equina nerves this is L3-L5, S1-S5, C0

267
Q

what do the nerves of the cauda equina supply?

A

sensation to bladder rectum & perineum
parasympathetic to bladder & rectum
motor to anal & rectal sphincters
motor to lower limbs

268
Q

clinical presentation of cauda equina?

A

saddle anaesthesia
urinary retention and/or urinary incontinence
faecal incontinence
bilateral sciatica
bilateral severe motor weakness in legs #
erectile dysfunction
loss of anal tone on PR exam

269
Q

how can you distinguish cauda equina from spinal cord compression?

A

cauda equina only affects lower motor neurones
spinal cord compression affects both UMN and LMN so you will also see some hyperreflexia

depending on the cause spinal cord compression could be gradual onset (eg in spinal stenosis), cauda equina is always a sudden onset

270
Q

what investigations for cauda equina?

A

urgent MRI spine

bladder USS to check for urinary retention
check reflexes and anal tone

271
Q

treatment for cauda equina?

A

emergency lumbar decompression surgery

272
Q

what nerve is compressed in carpal tunnel syndrome?

what is the function of this nerve?

A

palmar digital cutaneous branch of the median nerve

    • sensory function to first 3.5 fingertips (not the palm though, this is a different branch that doesnt go through the carpal tunnel)
    • thumb motor function (thenar muscles) – abductor pollicis brevis, opponens pollicis, flexor pollicis brevis (not the adductor!)
273
Q

the carpal tunnel is formed by what?

A

flexor retinaculum, aka transverse carpal ligament

274
Q

clinical presentation of carpal tunnel syndrome?

A

gradual onset, intermittent, worst at night, wakes you up
sensory changes to first 3.5 fingers - numbness, paraethsia, burning, pain
reduced thumb grip strength/difficulty with fine movements

275
Q

what relieves carpal tunnel syndrome?

A

shaking the hand

276
Q

what is phalins test?

A

for carpal tunnel

fully flex the wrist and hold it - pos if it causes symptoms

277
Q

what is tinnels test?

A

for carpal tunnel

tap the carpal tunnel- pos if it produces symptoms

278
Q

what is the kameth and stoddart questionnaire?

A

shows the likelihood of carpal tunnel

279
Q

what is gold standard investigation for ? carpal tunnel syndrome?

A

nerve conduction studies

280
Q

risk factors for carpal tunnel?

A 
diabetes
hypothyroid
obesity
repetitive strain 
acromegaly 
perimenopause 
RA
281
Q

management of carpal tunnel syndrome?

A

rest
wrist splints
steroid injection
cut the flexor retinaculum

282
Q

what do the dorsal spinal columns transmit?

A

proprioception

fine touch

283
Q

which spinal cord pathway has gracilis and cuneate nuclei and what are these for?

A

dorsal spinal column
gracilis = medial = legs
cuneate = lateral = arms

284
Q

what does the spinothalamic tract transmit?

A

pain

temperature

285
Q

where do the dorsal spinal columns decussate?

A

medulla

286
Q

where do the spinothalamic tracts decussate?

A

spinal cord

287
Q

what does the corticospinal tract transmit?

A

motor

288
Q

where does the corticospinal tract decussate?

A

85% decussates in the medulla, this is the lateral tract
15% decussates in the spinal cord, this is the medial tract

remember that corticospinal tract is motor so impulses travel down from brain to spine
thus the lateral tract is contralateral to the brain but ipsilateral to the muscles it innervates

289
Q

damage to the anterior spinal artery causes what effect?

A

damages the lateral spinothalamic tract

– lose pain and temperature sensation

290
Q

how does B12 deficiency affect the spinal cord and what is the effect of this lesion?

A

B12 deficiency = posterior spinal cord syndrome

affects dorsal columns = bilateral loss of proprioception and fine touch

291
Q

what does syringomyelia cause?

A

syringomyelia = development of fluid filled cyst in spinal cord
cape like distriibution - loss of sensation over arms

292
Q

does spinal cord lesion affect upper or lower motor neurones?

A

usually both

293
Q

how is continence affected in spinal cord lesions?

A

UMN pathology
increased sphincter tone
retention and constipation

294
Q

is there is a spinal cord lesion above the level of T6 what happens?

A

autonomic dysreflexia
hypertension
bradycardia
sweating and flushing

295
Q

if all limbs are affected where is the spinal cord lesion?

A

cervical

296
Q

if only the legs are affected where is the spinal cord lesion?

A

thoracic

297
Q

if the diaphragm is affected where is the spinal cord lesion?

A

above C3

298
Q

investigation for ?spinal cord lesion?

A

MRI whole spine

299
Q

what kind of nerves are carried in spinal nerves? (ie sympathetic, motor etc)

A

all kinds - autonomic, sensory and motor

300
Q

what is an afferent fibre?

A

afferent = sensory

annie is sensitive

301
Q

what is an efferent fibre?

A

efferent = motor

has an effect on the muscle

302
Q

what nerve is damages in elbow trauma and what functions does this nerve provide?

A

ulnar nerve
(C7-T1 via brachial plexus)
for wrist flexion, crossing fingers, sensory to little and 4th fingers
lesion = claw hand

303
Q

wrist drop indicates damage to which nerve?

what else is the nerve for?

A

radial nerve

for spreading hands and opening fist
sensation to dorsal thumb

304
Q

a heavy rucksack or broken rib commonly causes damage to the ___

A

brachial plexus

305
Q

what happens when the phrenic nerve is damaged?

A

loss of innervation to diaphragm

= orthopnoea and diaphragm is raised on CXR

306
Q

lung cancer, thymoma and TB commonly damage which nerve?

A

phrenic

307
Q

foot drop indicates damage to which nerve?

A

common peroneal (branch of sciatic), aka common fibular nerve

308
Q

pelvis fracture commonly damages which nerve?

A

sciatic

L4 - S3

309
Q

common peroneal nerve is from which spinal levels and could be damaged by what?

A

L4-S1

trauma to fibular head

310
Q

which nerve innervates plantar flexion and sensation on the sole of the foot?

A

tibial

311
Q

damage to what nerve causes burning thigh pain?

A

lateral cutaneous L2-L3

312
Q

what condition is highly associated with Alzheimers?

A

Down’s, everyone with Down’s will get Alzheimer’s

313
Q

what is the most common type of dementia?

A

Alzheimer’s

314
Q

pathological features of Alzhiemer’s? (histology etc)

A

beta amyloid plaques
tau containing tangles
synaptic degradation
atrophy of the centre of the brain

315
Q

presentation of Alzheimers?

A 
MEMORY - short term and make new 
language 
attention/concentration
personality change eg aggression
disorientation time and place
316
Q

investigations for Alzheimers?

A

MRI
MMSE

to rule out other causes:
U&E
thyroid tests
B12

317
Q

what is pyridostigmine?

A

Ach esterase inhibitor

used for myasthenia gravis and alzheimers

318
Q

who is frontotemporal dementia more common in?

A

under 65s

319
Q

what is the pathophysiology of frontotemporal dementia?

A

frontal and temporal atrophy

no plaques, but tau positive & TD43 negative inclusions

320
Q

what is the presentation of frontotemporal dementia?

A

behavioural problems
progressive aphasia - difficulty forming language
semantic dementia - loss of vocabulary

321
Q

how is frontotemporal dementia inherited?

A

dominant

322
Q

drugs for frontotemporal dementia?

A

SSRI

323
Q

what is the pattern of onset in vascular dementia?

A

stepwise

stable symptoms with a sudden increase which you do not recover from

324
Q

presentation of vascular dementia?

A 
visual disturbance 
UMN signs 
attention deficit 
depression 
incontinence
emotional disturbance 
if the original infarct was subcortical, may get dysarthria, parkinsons
memory loss
325
Q

investigations for vascular dementia?

A

MRI to look for previous infarcts
cognitive impairment screen
have they had strokes before?

326
Q

what is in a cognitive impairment screen?

A 
orientation
attention
language 
visuospatial
motor
327
Q

what is an eosinophyllic intracytoplasmic neuronal inclusion body?

A

lewy bodies

328
Q

how is lewy body dementia diagnosed?

A 
dementia 
\+ 2 of:
fluctuating concentration
visual hallucinations 
spontaneous Parkinsonism 
SPECT/PET scan shows low DA transmission
329
Q

what are red flags for spinal cord compression? - 3

A

loss of bowel/bladder function
UMN in lower limbs
LMN in upper limbs

330
Q

what is brown sequard syndrome?

A

hemisection of the spinal cord

in exams is typically A&E knife injury + loss of sensation

331
Q

presentation of brown sequard syndrome?

A

ipsilateral hemiplegia (loss of proprioception, vibration sensation and potentially spastic pareparesis)
contralateral pain and temperature loss below lesion
complete loss of sensation at site of penetration

332
Q

first line investigation for brown-sequard (or any penetrating trauma?)

A

plain radiograph

can do MRI/neuro exam later

333
Q

treatment for brown sequard?

A

spine immobilisation
steroids
physio

334
Q

what is charcot marie tooth?

A

inherited peripheral neuropathy

335
Q

the 4 types of charcot marie tooth syndrome?

A

1 - unstable myelin - children, weakness and loss of sensation starting from feet and going up
2 - axonal - like type 1 but later onset
3 - marked segmental demyelination - floppy baby
4 - demyelination - males more common

336
Q

how is duchenne muscular dystrophy inherited?

A

x linked - males

337
Q

what is the problem in duchenne muscular dystrophy?

A

lack of dystrophin (which should strengthen muscle)

338
Q

presentation of duchenne muscular dystrophy?

A 
cannot run, hop or jump 
fatigue
recurrent falls 
under 3 
milestones delayed 
speech is slurred
339
Q

investigation for duchenne muscular dystrophy?

A

raised serum creatinine kinase

muscle biopsy

340
Q

complications of duchenne muscular dystrophy?

A 
learning difficulties 
resp failure
cardiomyopathy 
osteoporosis 
infections
341
Q

what is clozepine?

A

an antipsychotic, dopamine antagonist

important because can cause Parkinsonism

342
Q

what is CN1?

A

olfactory nerve

for smelling!

343
Q

how can the olfactory nerve be damaged?

A

trauma to cribriform plate

344
Q

a left parietal lesion of the optic radiation causes what kind of vision deficit?

A

Quadrantanopia
of inferior right quadrant

PITS - parietal lesion = inf loss, temporal lesion = superior loss)

345
Q

optic nerve vs optic tract?

A

optic nerve is from the eye to the optic chiasm

optic tract is from the chiasm to the lateral geniculate body

346
Q

if one pupil is not constricting to direct or consensual light stimulation to the other eye, where is the problem?

A

CN3 - the pupil is not constricting

347
Q

if the right pupil constricts in response to light shone in the left eye, but when you shine the light on the right neither constrict - where is the problem?

A

CN2 - the optic nerve

as the pupil is not detecting the light

348
Q

what does CN3 innervate?

A

CN3 is the occulomotor nerve

superior and inferior and medial rectus
inferior oblique

pupillary sphincter
lps to lift eyelid

349
Q

signs of a lesion to CN3?

A

ptosis
pupil does not accomodate to light
absent pupillary light reflex
outward deviation - as there is function of the lateral rectus to look out (CN6) but not inf oblique (CN3) to counteract it

350
Q

what does CN4 innervate?

how does damage to it present?

A

CN4 = trochlear nerve
innervates superior oblique - looks in and down
damage = diplopia when walking downstairs

351
Q

what does the superior oblique muscle do and what is it innervated by?

A

looks in and down (even tho is superior oblique)

trochlear nerve CN4

352
Q

what does the superior rectus muscle do and what is it innervated by?

A

looks up

occulomotor nerve CN3

353
Q

what does the inferior oblique muscle do and what innervates it?

A

looks up and in

cn3 occulomotor nerve

354
Q

what are the 3 branches of the trigeminal nerve?

A

v1 - opthalmic - forehead sensation
v2 - maxillary - cheeks sensation
v3 - mandibular - chewing + sensation on anterior 2/3 tongue

355
Q

how can the trigeminal nerve be damaged?

A

trigeminal neuralgia
herpes zoster
nasopharyngeal carcinoma
acoustic neuroma

356
Q

medial deviation of eyes at rest indicates a problem with which nerve?

A

abducens CN6
abducens innervates lateral rectus
abducens damaged = unopposed medial rectus

357
Q

what is CN7?

A

facial nerve - facial expression

358
Q

what are the parasympathetic functions of the facial nerve?

A

lacrimation

salivation

359
Q

causes of facial nerve dysfunction?

A

bells palsy
temporal bone fracture
herpes zoster

360
Q

what is CN8?

A

Vestibulocochlear - hearing and balance

361
Q

aminoglycosides cause damage to which nerve?

A

vestibulocochlear CN 8

362
Q

what is CN9?

A

glossopharyngeal
sensory to pharynx, taste on post 1/3 tongue
parasympathetic - parotid gland

363
Q

which cranial nerves innervate the tongue?

A

facial - taste on ant 2/3
glossopharyngeal - taste on post 1/3
trigeminal - sensation
hypoglossal - motor

364
Q

how can you test the glossopharngeal nerve?

A

gag reflex

365
Q

what is CNX?

A

vagus nerve
sensory and motor to pharynx and larynx
speech, cough
parasymp to GI tract and viscera

366
Q

which cranial nerve innervates the accessory muscles?

A

CN 11, accessory

367
Q

how can you test the accessory nerve?

A

ask pt to shrug their shoulders or turn head

368
Q

how can you test CN12?

A

CN 12 is hypoglossal

ask pt to stick tongue out, it will deviate to weak side

369
Q

some general causes of cranial nerve damage?

A 
polio
guillian barre
MS 
tumour
vasculitis 
stroke
lupus 
syphilis 
TB/fungal meningitis
370
Q

in ischaemic stroke how does the hemiplegia change over time?

A

initially flaccid, then becomes spastic as UMN lesion

371
Q

where is the clot if there is hemianopia?

A

posterior circulation

372
Q

risk factors for intracerebral haemorrhage?

A

hypertension
age / smoking // alcohol / diabetes
anticoagulation/ thrombolysis
microanneurysms

373
Q

what is hydrocephalus caused by?

A

CSF obstruction

raised ICP

374
Q

when can you test CSF for xanthrochromia?

A

after 12hrs

only if ICP is fine

375
Q

when there has been a latent period after subdural haemorrhage why does it suddenly get worse?

A

clot starts to autolyse = draws water in

376
Q

when is sumatriptan contraindicated?

A

heart disease

377
Q

what is wernickes encephalopathy?

A

ataxia
opthalmoplegia
confusion

vitamin B1 deficiency - thiamine
chronic alcoholics
flapping tremour
management - B vitamin infusion

378
Q

most common origin of secondary brain tumour?

A

non small cell lung cancer

379
Q

what is korsakoffs?

A

ecephalopathy can develop from wernickes

380
Q

what kind of acteylcholine receptors are affected in myasthenia gravis?

A

nicotinic

381
Q

if there is automatisms where is the seizure?

A

temporal lobe

382
Q

if there is motor features eg jacksonian march where is the seizure?

A

frontal lobe

383
Q

presentation of progressive bulbar palsy?

A 
dysarthria
dysphagia 
nasal regurg of fluids
choking 
lmn lesions of tongue
'trouble initiating swallow'
384
Q

acute vision loss suggests suggests stroke in

A

posterior circulation

385
Q

what is the most common cause of meningitis in pregnancy?

A

listeria

386
Q

what is 1st line for ?meningitis?

A

blood cultures

lumbar puncture = gold standard
use when CT shows is fine

387
Q

what is the prophylactic antibiotic for contacts of listeria?

A

ciprofloxacin

388
Q

3 contraindications for lumbar puncture?

A

raised ICP
focal neurology
haemodynamically unstable eg bradycardia, hypotension
decreased GCS

389
Q

how is sumatriptan given in acute cluster headache?

A

subcutaneous

390
Q

what are risk factors for Alzheimer’s?

A

Down’s syndrome
depression
reduced physical activity
lonliness

391
Q

3 causes of guillian barre?

A

camp
CMV
EBV
mycoplasma

392
Q

how is guillian barre diagnosed?

A

CSF shows raised proteins with no immune cells

393
Q

what ABCD2 score is high risk?

A

6

394
Q

as well as paralysis of facial muscles, what might you see in bells palsy?

A 
loss of taste 
hearing loss (as cn7 innervates the stapedius muscle)
395
Q

locked in syndrome is caused by damage to which vessels?

A

pontine

396
Q

signs of raised ICP?

A 
papilloedema 
vomitting
seizures 
extensor posturing 
pupil dilation (cn3 palsy)
cn6 palsy 
headache 
decreased consciousness
397
Q

3 symptoms of frontotemporal dementia?

A 
change in speech
disinhibition
social withdrawal
impulsivity
loss of personal awareness 
primitive hyperreflexia
stereotypy
398
Q

what treatment is first line for MS?

A

methylprednisolone

399
Q

what is delirium tremens?

A

alcohol withdrawal

400
Q

what is Romberg’s test?

A

for peripheral neuropathy
ask patient to close their eyes
and stand on one leg
if either proprioception or vestibular function is compromised they will fall over –> pos rhombergs test
pos rhombergs indicates peripheral neuropathy eg vit b12 deficiency, ehlers danlos, or vestibular dysfunction

if they sway but dont fall over this indicates cerebellar pathology

401
Q

progressive weakness that gets better with exertion is

A

lambert eaton myasthenic syndrome

related to small cell lung cancer

402
Q

apart from the neuropathy, how does vit B12 deficiency present?

A 
anaemia
yellow tinge 
angular cheilitis 
depression etc 
fatigue 
glossitis
403
Q

what kind of motor neurones are found in the anterior horn cells?

A

lower

404
Q

what is gowers sign?

A

in duchenne muscular dystrophy

use arms to get up from sitting

405
Q

if you suspect MS is it best to do an MRI or lumbar puncture?

A

MRI is best
it is less invasive

CSF to look for oligochromal bands is reserved for atypical cases

406
Q

which dementia is associated with hallucinations & recurrent falls / syncope?

A

lewy body

407
Q

gambling is linked with what parkinsons drugs?

A

dopamine agonists eg ropinarole

408
Q

what cranial nerves are involved in the reflex that makes you blink when something touches the cornea?

A

sensing - trigeminal nerve. if this is damaged the opposite eye wont blink either

motor - facial nerve. if this is damaged one eye will not blink, when you touch it or the other one. but the other eye will respond in both situations

409
Q

nystagmus is a problem with which cranial nerve?

A

vestibulocochlear

410
Q

of the 6 eye movement muscles, which 2 are not innervated by CN3?

A

LR6 SO4 (lardy arse sofa)

lateral rectus - 6 (abducens)
superior oblique - 4

411
Q

who gets Felty’s syndrome?

A

50-70s white with long standing rheumatoid arthritis

412
Q

what are the 3 components of charcots neurological triad and who does it affect?

A

MS
dysarthria (scanning/stuccato speech)
intention tremour
nystagmus

phase 2a (10 decks)

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