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neuro Flashcards

1
Q

patients with parkinsons can also have what

A

POTS- even more increased risk of fall on top of the shuffle gait, bradykinesia

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2
Q

whats symtpoms of psychosis

A

delusions
hallucinations

like short term schitzopherenia

not looking after self, pull away from family

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3
Q

what can cause psychosis

A

drug induced
stress
long use of corticosteroids

can go but can remain

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4
Q

whatsthe two types of stroke

A

ischemia/ infarction
intracranial haemorrahgic

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5
Q

what can cause a disruption of blood supply to the brain

A

thrombus formation/ embolus
athelerosclerosis
shock
vasculitis

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6
Q

whats a tia

A

transient ischemic attack
symtpoms resolve wothing 24 hrs- no lasting issues
new defiition = transient neurological dysfunction secondary to ischemia without infarction

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7
Q

what does having a tia mean and what score do you use

A

means often preced a full stroke
crescendo tia = have 2 or more tia within 1 week increase progression to stroke

use the ABCD2 score to see the risk of the having a storke within 48 hrs

rosier score to see how likely going to have a stroke = above 0 is stroke likely

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8
Q

whats the causes/ risk factors of stroke/TIA

A

hypertension
AF
cv disease- mi, angina, peripheral vascualr disease
carotid artery disease
diabetes
smoking
vasculitis
thrombophila
COCP
blood disorders
cerebal anyersm
brain tumour
atherloscleoris
ADPKD- formaition of anyrsm more liekly
small vessel disease

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9
Q

what can cause disru[tion to nlood supply

A

thrombus/ embolism
shock
vasculitis
athelrosclerosis

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10
Q

whats the presentation of a stroke

A

sudden onset!
sudden…
typically asymmetrical
weakness of limbs
facial weakness
speech - dysphasia
visual/sensory loss
thundeclap headache- more subarachmoid hameorrahge
headache
nausea
vomiting
stiff enck
nyastamus

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11
Q

on examination how would ypu examine a pt wiht suspected stroke

A

focused neuro exam
vitals- bp, saturation, hr
FAST
cv- got any arrhtmia murmurs. pulmoanry odedmea, heart failure

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12
Q

what differential diagnosis are there for signs and symptoms that are stroke like

A

hypoglycemia!!!
alchol / drug toxicity

dizzy condtions=> syncope, labrythine disroders= menieres disease, vertigo, labyrthinitis

neuro =
sizures
migraine with aura
demyelineation- ms
peripheral neuropahty
spinal epidural haematoma

trauma

infection=
sepsis
encephalitis
cns abscess

encephalopathies=
wernickes encephalopthy
hypertenisve encephalopathy

others=
dementia
acute confucsional state
vasculitis
somatoform/conversion disorder

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13
Q

how do you manage a suspected stroke

A

exclude hypoglycemia
immediate brain CT
once had CT and not haemorragic give 300mg aspirin stat then for 2 weeks

if ischmic = thrombolysis with alteplase = can do within 4.5 hrs
thrombectomy within 24 hrs if accesible
if over 4.5 hrs five 300mg asprin OD for 14 days. if asprin contraindicated give clopidogrel

stroke rehab

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14
Q

whats tia managemnt

A

secondary prevention
aspirin 300mg
see specialist within 24 hrs
do ABDC2 score to see risk of having stroke within 48 hrs

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15
Q

what imaging do you do for suspect stroke / tia

A

Diffusion weighted MRI = gold standard
or CT
carotid us TO ASSES IF CAROTID STENOISS

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16
Q

what do you do if ther eis carotid stenosis on US

A

endarterectomy pr carotid steniting

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17
Q

what can you do for secondary prevention for stroke/tia

A

75mg OD clopidegrel or if not ok then use dipyrimdamole 200mg BD
atorvastatin 80mg - dont start immediately
carotid endarectomy / stent if got carotid stenosis
treat modifiable facotrs= ht, diabtetes, smoking, af, diet, alcohol etc

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18
Q

if someone has a stroke/tia can they drive

A

no need to infrom dvla. look on cks website about how long cant drive for etc

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19
Q

whats the percentage of harmoragic stroke

A

10-20% of strokes are intracranial bleeds

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20
Q

whats the types if intraranial bleeds

A

extradural
subdural
subarachnoid
intracerebral

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21
Q

whats the risk factors/causes of burstin a blood vessel and causing a haemorrhagic stroke

A

hypertension
anyerusm
ADPKD
head injury
old
alcholic
ischemic strokes can progress to haemorrhagic
brain tumours- have own bv that arnt as good
anticoagulants -warfarin

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22
Q

sudden onset headache is a key sign of what

A

haeorhagic stroke

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23
Q

whats the s and s of haemorhagic stroke

A

sudden onset of headache
vomiting
seizures
neurological aytmpoms
weakenss- fast
reduced consiousness

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24
Q

a patient has a gcs of 8/15. what do you need to start to consider

A

do they require secruing the airway open- ventilation, intubation, icu ?
8 and below thinji airway

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25
Q

on a ct scan there is a crescent shape. and the shape isnt limited by cranial sutures
what is this

A

subdural haemorrahge

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26
Q

what causes subdural bleeds

A

bridging veins rupture

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27
Q

an alcholic hit his head - minor- and felt funny but then was fine. later on he lost consiouness, was sick and felt dizzy and diffifuclt to speak . what is this

A

subdural haemorrhage
the symtpms can come on quick if severe head injury

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28
Q

who are commonly to have subdural haemorrahes and why

A

elderly and alcoholics
brain atrophies and briding veins are strethced so more easily rupture

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29
Q

whats the common artery to rupure in extra dural haemorahge

A

middle menigeal artery

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30
Q

what does extra dural hameorahge look like on ct

A

bi convex and limited bu crnaial sutures
like half a lemon- pushes into the brain (its a bit extra it wants to show itsslef and its a bit fat so round where as subdrual are sub so they half and skinny so crescent shape)

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31
Q

a patient fractures his temoral bone what arteyr may be affects and waht can this lead to

A

middle menigela artery may have been ruptured leading to a extra dural haemorrahge

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32
Q

a young paitent has a traumatic head injury and has an ongoing headache
he has a period of imprive neruo symtpoms and consiousness but then he rapidly declines over few hrs

what is the cause

A

extra dural haemroage

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33
Q

how does an intracerebal haemorage present

A

similar to ischemic stroke
sudden onset

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34
Q

why do intracerebal haemoeages occur

A

spontaneous
anyrsm rupture
tumour
bleeding due to an ischemia infarct

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35
Q

a patient was lifiting a weigh / having sex and he suddenly got a realy awful headache at the bacl of his head like being hit by a brick so sudden
what is this

A

subarachnoid hameorraghe

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36
Q

whats the casue of subarachnoid haemrroage

A

cerebal anyurseum rupture

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37
Q

what can subarachnoid hameorages be associated with

A

cocaine use
sickle cell aneamia

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38
Q

how do you manage an intracranial bleed

A

immediate ct see what cause
FBC and clotting
stroke unit
recued hypertension but avoid hypotension- brian needs o2
correct clotting abnormality
consider intubation, ventialtion, icu if 8 and below gcs

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39
Q

find blood in the CSF what haemoragic stroke is this

A

subaracnoid

this is where the csf is in the subaracnhoid space

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40
Q

whats the major symtpom of subarachnoid ahemorrage

A

sudden onset of v painful occipital headache
= thurnde clap
= hit on back of head

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41
Q

where is the bleeding in a subarachnoid haemorrhage

A

between the pia mater and arachnoid matre= in subarachnoid space

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42
Q

what is n the subarachnoid space

A

csf

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43
Q

patient has
thunderclap headahce sundenly come on whilst lifting weights
stiff neck
photophobia
has some visual changes, speech changes and then has a seizure
and looses consuoisness

what is this

A

subarachnoid hameorrhage

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44
Q

whats the riskk factors of subarachnoid haemorrahge

A

smoking
hypertension
excessive alchol use
cocaine use
fam hist
asiccoated with:
cocaine use, sickle cell anemia, connective tissue disorders= marfans sundrome, ehlers-danlos, neurofibromatosis

more commen in black pt, women, 45-70

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45
Q

what investigations do you do if pt has v bad sudden onset occipital headache, stiff neck, ohotophibia, vision gone blurry

A

subarachnoid haemorrhage=

ct head immediately

if negative then do lumbar puncture if do suspect it

once subarachnoid haemorrhage confirmed do angiography ct/mri to find source of bleeding

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46
Q

a patient has a lubar puncture and fine raised red cell count in the csf and its yellow

the patient has a sudden onset occiital headache

A

subarachnoid haemorrhage= in csf cus in same space get raised red cells in the csf and the csf goes yellow because billirubin in csf= xanthochromia - billirubin by product of red blood cell

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47
Q

what managemnt is there for subarachnoid haemorrhage

A

if dec consiousness inutbtion and ventialtion
MDT - everyone involved, nutrtion, ohysio etc
surgical intervention to treat anyerusm- coiling (catheter) or clipping (cranial surgery)

nimodipine = ccb to prevent vasospasm which is a complication of a subarachnoid heamorrage that would cause ishcemia to the brain

lumbar puncurue or shunt t treat hydrocephalus if there

anti epileptics for seixures

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48
Q

whats a common complication of subarachnoid haemorrhage

A

vasospasm causing ishemia to the brain

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49
Q

whats this

intense pain around one eye. Attacks occurs once a day, each episode lasting 1 hour for the past 8 weeks. Associated with a red and watery eye and a constricted pupil

A

Cluster headache

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50
Q

constant headache with nausea worse in the morning and on coughing suggest what

A

raised intracranial pressure

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51
Q

decreased GCS
headache
nausea and vomiting asociated with what

A

haemorrhagic stroke

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52
Q

what drug is most commonly first line used to to terminate acute seizures

A

benzodiazapines

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52
Q

how do you treat trigeminal neuralgia

A

carbamazepine - first line
surgery to decompress the nerve or can intentionally damage the nerve

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53
Q

a patient comes with a headache. what are all the differentials is could be

A

cluster heaache
tension headache
hormonal headache
analgesic headache
secondary headache
sinusitis
raised intra cranial pressure
brain tumour
giant cell arteritis
glaucoma
intracranial hameorrhage
subarachnoid haemorrhage
carbon monoxide poisoning
meningitis
encephalitis
trigeminal neuralgia
cervical spondylosis
migraines

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54
Q

whats the red flags you need to ask for headache

A

fever, stiff neck?= menigitis/encephalitis
ne neuro symptoms?= stroke, haemorrhage, malignancy
dizziness?= stroke
visual disrurbance?= glaucoma, stroke, giant cell arteritis
sudden onset occipital headache?= subarachnoid haemorrhage
worse on coughing/straining/ in morning?= raised intracranial pressure
vomiting?= raised intra cranial pressure, co poisoning
postural/ worse on stadning, worse lying, benidng over= raised intracranial pressure
severe enough to wake up from sleep?
jistory of trauam= intracranial haemorrhage
pregancy?- last 6 months?- pre-ecampsia

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55
Q

when do you need to consider pre eclampisa when a pt has a headache - what stage in pregancy

A

if got headache in second half of pregnacy investigate for pre-eclampsia

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56
Q

patient has mild ache across forehead which is band like that comes on gradually

A

tension headache

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57
Q

what signs and symptoms of tnesion headache

A

band like
mild ache across forehead
no visual disrubance
come on and resolve gradually

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58
Q

what associations are there with tension headaches

A

dehydration
alcohol
stress
depression
skipping meals

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59
Q

what treatment for tension headache

A

simple analgesia
reassurance
warm towel to area
relaxtion techniques

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60
Q

what headaches have stumpoms like a tension headache- band like across forehead mild ache gradual onset

A

horomonal headache
analgesia headahce
secondary hedaches

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61
Q

whats secondary headaches

A

tension headaches with clear cause
- alcholol
head injurt
CO poisoning
medical condition- infection, pre eclampisa, obstructive sleep apnoea

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62
Q

a patient has a headache,
they have facial pain over the eyes, nose and forehead
its tender to touch over the cheek bone they say
what is this

A

sinusitis- tneder to touch over sinus area is giveaway if they have this
resolves 2-3 weeks

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63
Q

is sinusitis mainly viral or bacterial?

A

viral

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64
Q

what treatment for sinusitis?

A

nasal irrigation with saline
if prolonged symptoms - over 2-3 weeks should have reoslved- then nasal steroid spray
antibiotics occasionally

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65
Q

what is sinusitis

A

headache with inflammation of one/more sinuses

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66
Q

a patient has a band like headache that they keep having for ages
they have been taking pain killers ofr over 3 months for aches and pains of their body and now for the ehadache too

what is this

A

analgesia headache
= long term analgesia use/excessive use

treat by withdrawing from alagesia- reasure pt that its the analgeisa that is causing the pain

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67
Q

a female patient comes in becasue she keeps having refular headaches. they happen about 2 days before her period and then for the forst 3 days of her period but it then stops. what is this

A

hormonal headahce

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68
Q

what the cause of hormonal headaches

A

low oestrogen

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69
Q

whats the s and s of hormonal headaches

A

2 days before period and first 3 days of period have the pain
generic non specific- tension like
may ne going through the menopause/pre menopausal
can get it in first few weeks of pregancy but will improve over last 6 months

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70
Q

a patient is pregant and keeps getting headaches. shes in her first 4 weeks in
shpuld you be concerned about pre ecalmpsia?

A

no.
be concrned if headaches in last half of pregancy

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71
Q

patient is preganct and is getting headaches that are getting worse and shes 6 months into pregancy
should you be worried?

A

yes. considere pre eclampsia

headaches in forst few weeks that get better in last 6 months are hormonal headaches. if get worse or get headaches in last half of pregancy then investigate for pre ecampsia

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72
Q

how do you treat hormonal heaaches

A

contrceptive pill can help
HRT

if getting the headaches when off the pill in the week off can have packs back to back to help

some people find that pill can make them worse though

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73
Q

a patient has a headache and neck pain. what could this be? and need to exclude?

A

could be cervical sponylosis but need to exclude:
inflammatory, maligancy, infection, spinal cord/nerve root lesions

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74
Q

whats cervical spondylsosis

A

degenrative changes of the cervical spine

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75
Q

a patient has intense facial pain on one side of his face ocver his cheek and to the ear and down to the jaw. feels like electricity shooting. sometimes last seconds sometime shours but it seems to be getting worse

A

trigeminal neuralgia

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76
Q

whats trigeminal neurlagia and the s ans s

A

can affect combo of branches
cause isnt certain but could be due to compression of nerve

90% are unilateral
5-10% of patients with multiple sclerosis ahve this
intense pain - like electricity shooting
spontaneous
can last seconds - hrs
attacks often worsen in severity over time
triggers can be cold weather, citrus fruit, spicy food, caffeine

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77
Q

what triggers can casue trigeminal neuralgia

A

cold weather
spicy foods
caffeine
citrus fruit

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78
Q

how do you treat trigeminal neuralgia

A

carbamazepine - first line
surgery to decompress the nerve or can intentionally damage the nerve

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79
Q

a patient comes with a headache. what are all the differentials is could be

A

cluster heaache
tension headache
hormonal headache
analgesic headache
secondary headache
sinusitis
raised intra cranial pressure
brain tumour
giant cell arteritis
glaucoma
intracranial hameorrhage
subarachnoid haemorrhage
carbon monoxide poisoning
meningitis
encephalitis
trigeminal neuralgia
cervical spondylosis
migraines

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80
Q

whats the types of migraine

A

migraine with aura
migraine without aura
silent migraine- no headahce just aura
hemiplegia migraine

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81
Q

whats s and s of migraine

A

headache an last 4-72hrs
moderate to high interensty
pounding/throbbing
usually unilateral
photophobia
phonophobia
with/without aura
nausea and vomiting

aura= visial changes
blurred vision
sparks in vision
lines across vision
loss of different visual fields

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82
Q

whats the stage of migraine

A

not all pt have all 5 and vary
prodromal = can being 3 dyas before headache- yawn, fatigue, mood changes

aura- lasts up to 60 mins

headahce- last 4-72hrs

resolution- fades and can be relived by vomiting/sleeping

recovery/postdromal

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83
Q

what triggers can casue migraine

A

vary
can be har d to identify

stress
dehydration
certain foods-caffeine, chocolate, cheese
mesturation
abnormal sleep patterns
trauma
birhgt lights
strong smells

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84
Q

what acute managemnt can a patient have when expeirivning migraine

A

dark room and sleep
paracetamol
NSAIDs= naproxen, ibruprofen
antiemetcis if vomiting- metaclopramide
triptans - sumatriptan 50mg as migrain starts

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85
Q

what do triptans do that could help with migraine

A

act on smooth muscle of arteries and casue vasoconstiction

inhibit pain receptors

decrease neuronal acitivty in CNS

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86
Q

what prophylaxis can be done for migraines

A

propanolol
topiramate - teratogenic!!
amitriptyline

if migraine triggered by menstruation then can use triptans or NSAIDs = mefanamic acid
frovatriptan / zolmitriptan

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87
Q

what drug do you use for prophalxis of migraines that is teratogenic

A

topiramate

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88
Q

red swollen watering eye
nasal discharge
facial sweating
severe pain around eye

A

what is this
cluster headache

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89
Q

whats s and s of cluster heaache

A

get cluster of attacks then non for a while

red, swollen, watering eye
nasal discharge
intolerable exrely sever epain usually around eye
typically unilateral
miosis
ptosis
facial sweating
attacks last 15 mins to 3 hrs

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90
Q

what triggers can there be of clustr headache

A

alchol
strong smells
exercise

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91
Q

what treatment is there for pt exeprinceing a cluster ehadache

A

triptans- sumatriptan 6mg injected subcutaneously

high flow 100% oxygen for 15-20 mins- can be done at home

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92
Q

what prophylaxis is there for cluster headaches

A

varapamil
lithium
prednisolone - 2-3week course to try and break the cycle in the cluster

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93
Q

what happens in brown-sequards syndrome

A

unilateral spastic paresis and loss of proprioception/vibration sensation with loss of pain and temperature sensation on the opposite side

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94
Q

whats this
bilateral spastic paresis and loss of pain and temperature sensation

A

anterior spinal artery occlusion

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95
Q

whats a benign essential tremor

A

fine tremor affecting all voluntary musclees

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96
Q

where can the fine tremor be seeen in benign essentail tremor

A

commonly in hands but can the tremor in head, jaw, vocal temor

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97
Q

whats the features of benign essential tremor

A

5-8hertz
associated with older age
worse on voluntary movment- imporves wit rest
worse when tired, stressed, after caffeine
improves with alcohol
absent during sleep

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98
Q

what do you need to exclude before clinically diagnosing benign essential tremor

A

parkinsons
huntington chorea
ms
hyperthyroidism
fever
med- anti psychotics

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99
Q

how do you manage beningn essential tremor

A

only give med if causing functional/ pscyholigical problems

propanolol - non selective beta blocker
primidone - barbituate ant epipleptic

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100
Q

whats the difference between benign essential tremor and parkinsonian tremor

A

PT, 4-6hertz= BT 5-8 hertz
PT, worse at rest= BT improves at rest
PT asymmetrical = BT symmetrical
PT imrpoves with intentional movement = BT worse with intentional movement
PT other parkinson features =BT no parkisnon features
PT does not change with alcohol = BT improves with alcohol

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101
Q

a patient is 70
they have a tremor
they pick up a cup of tea and the tremor in that hand worsens
they sometimes have a beer in the evening which helps the tremor a bit

what is this

A

benign essential tremor

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102
Q

whats parkinsons

A

progresive reduction of dopamine in the basal ganglia causing disorders of movement

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103
Q

what neurotransmitter is lacking in parkinsons

A

dopamine

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104
Q

where does dpoamine get produced

A

substantia nigra

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105
Q

whats the signs and symtpoms of parkinsons

A

resting tremor
bradykinesia
rigidity - cogwheel

bradykinesia= slow movements that get slower and smnaller
handwriting gets smaller and smaller
shuffling gait
hard to inititate movement
difficult to turn around when standing
hypomimia - mask like face

tremor usually asymmetrical - one side worse than other
depression
sleep disrubance and insomnia
postural instability - hypotension makes thi worse and increased risk of falls
cogmitive impairement and memory problems

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106
Q

what parkinsons - plus syndromes

A

dementia with lewy bodies
multiple system atrophy
progressive supranuclear palsy
corticobasal degeneration

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107
Q

what signs and symtpoms are there with lewy body dementia

A

parkinsonism features
progressive cognitive delcine
visual hallunciations
disturnaces with rem sleep
fluctuating consiousness
delusions

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108
Q

whats multiple system atrophy

A

parkinson features
where neurones of multiple systems degenerate
have also autonomic dysfucntion= postural hypotension, consitpation, abnormal sweating, sexual dysfunction
cerebellar dysfucntion= ataxia

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109
Q

what management is there for parkinsons

A

levodopa = synthetic dopamine
- try use last as efectiveness wears off over time
use a peripheral decarboxylase inhibitor with levopdopa to stop it being broken down before get to brain - carbidopa and benserazide
= co-careldopa
= co-benyldopa

COMT inhibitors = entacapone take with the combo of levodopa and pdi to extend effectiveness of leveodopa

dopamine agonist = bromocryptine, pergolide, carbergoline
use to delay use of levodopa then use with levodopa to reduce dose needed

mao b inhibitors = specifiv to dopamine
use on own and then with levodopa to recduce dose of levodopa needed
= selegiline, rasagiline

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110
Q

whats the side effects of leveodopa

A

dyskinesias due to too much dopamine
dystonia = excessive muscle contraction=> abnormal posture, exagerated movement
chorea= abnormal involuntary movements - jerking and random
athetosis= involuntary twisting/ wrtighing movements usally in fingers, hands and feet

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111
Q

entacapone is what type of drug and use when

A

comt inhibitor used in parkinon treatment

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112
Q

co-benyldopa is what and used when

A

levodopa and benserazide used in parkinsons treatment

113
Q

bromocryptine
pergolide
carbergoline
what drugs are these and used when

A

dopamine agonsots used in parkisnons treatment

114
Q

what side efect of dopamine agonsits are there

A

pulmonary fibrosis

115
Q

a patient has parkinsons disease and also pulmonary fibrosis
what could be the cause of the pulmonary fibrosis

A

medication
dopamine agonist

116
Q

selegiline
rasagiline
what drugs are these and used when

A

MAO b inhibitors
parkinson treatment

117
Q

whats neuropathic pain

A

caused y abnormal functioning of the sensory nerves delvering abnormal and painful signals to the brain

118
Q

whats paresthesia

A

burning, tingling, oins and needless and numbness

119
Q

whats the signs and symptoms of neuropathic pain

A

burning
tingling
pins and needles
electric shocks
loss of sensation to touch of afected area

120
Q

what investgation can be done if suspect neuropathic pain

A

DN4 questionaire
asses character of pain
score 4 over

121
Q

whats the causes of neuropathic pain

A

post herpetic neuralgia = shingles
in distribution of dermatome

nerve damage from surgery

MS

diabetic neuralgia- esp foot

trigeminal neurlagia

complex regional pain syndrome

122
Q

whats complex regional pain syndrome

A

area ffected by abnormal nerve funcioning
causes neuro[athic pain and abnormal sensation
usually isolated to one limb
often triggered by injury to area
can be very painful- even wearing clothes can hurt
can intermittently swell, change colour, change temp, flush and abnormal sweating

123
Q

whats the management of neuropahtic pain

A

amitriptyline
duloxetine
gabapentin
pregabalin

these are frist line so use one then if doesnt work use another - except trigeminal neuralgia is carbamazapine first line

other options
tramadol- ony use toshort term to try control flares
capsaicin cream - to localised area
phsyio.- maintain strength
pschycological - understanding and coping

124
Q

whats motor neurone disease

A

progressive degeneration of motor neuones both upper and lower - no sesnory symptoms

125
Q

whats the most common type of MND

A

amylotrophic lateral sclerosis

126
Q

whats the second most common type of MND

A

progressvie bulbar palsy

127
Q

whats the types of mnd

A

how they present
Amylotrophic lateral sclerosis
progressive bulbar palsy
primary lateral scleorisis
progressive muscular atrophy

128
Q

whats risk facotrs for mnd

A

fam hist of it
smoking
exposure to heavy metals
certain pesticides

129
Q

whats this

60 year old man with progressive weakness throughout his body
keeps tripping on things
slurs his speech a bit

A

MND

130
Q

whats the possible presentatios of mnd

A

weaknes of msucles throughout body
weakness usually first noted in upper limbs
slurred speech
increased fatigue when excerising
tripping/clumsy/dropping things
stiff/cramp
muscle wasting, fasciculations, reduced reflexes, reduced tone= lmn

increased tone/spacitisity, brisk reflexes, upgoing plantar relfex= umn

131
Q

how to manage mnd

A

support fam and pt= MDT, break bad news well, advaned directives to document pts wishes, end of life planning

riluzole= can slow progression and extend survival in AML

NIV- help breahting at night

132
Q

what investigations do you do if suspect mnd

A

excluded other causes of motor neurone issues
clinical diagnosis by specialist

133
Q

what medication do you give for bells palsy within 72hrs of symptom onset

A

corticosteroid- prednisolone

134
Q

whats ms

A

chronic progressvie condition
demeylienation of CNS neurones
immune mediated inflammatory condition

135
Q

32 year old woman
double vision for few weeks thrn went
now got numbness in right arm
gets headaches that are over the right jaw and right top head

what is this

A

MS
neurological signs= trigeminal neurglagia is last thing

136
Q

whats signs and symptoms of MS

A

symtpoms usually progress over 24 hrs
early on in disease the symptoms fully resolve later on become more permanent and symptoms worse
stymptoms last days to wees intitally
optic neuritits
eye movement abnormalitites= internuclear opthalmoplgia
conjugate lateral gaze disorder
(look laterally in direction of affected eye and the affected eye wont abduct)
focal weakenss: bells palsy, horners syndrome, limb paralysis, incontinence
focal sensory symptoms: trigeminal neuralgia, numbness, paraestheisa, postive lhermittes sign
cerebellar- ataxia,, vertigo, clumsiness, dysmetria

sensory ataxia- positive romberg test and gait disturbance

137
Q

how can ms be descirbed in patterns

A

relapsing and remitting -active and / worsening
secondary progressive - starts off relapsing and remitting then worsens and symptoms dont fully resolve- incomplete remissions
primary progressive
- active and/progressing

138
Q

how manage relapse of ms

A

methylprednisolone 500mg oraly daily for 5 days
or iv 1g daily 3-5 days if severe

manage symtpoms
exercise
neuropathic pain- gabapentin/amitriptyline
depression- SSRI
urge incontinence- tolterodine/oxybutyrin
spasiticity- physio/ gabapentin/ baclofen

139
Q

investigations for ms

A

lumbar puncture- oligocolonal bands in csf
mri see lesions

140
Q

causes for ms

A

vit d deficiency
smoking
obesity
EBV
genes

141
Q

what age and gender get ms

A

female
20-50s

142
Q

whats a v common sign/symptom of ms

A

optic neuritis

143
Q

s and s optic neurtis

A

unilateral reduced vision
develop over hrs - days
central scotoma- enlarged blind spot
pain on eye movment
impaired colour vision
relative afferent pupillary defect

144
Q

es of opitic neuritits

A

ms- most common - 50% get optic neuritis likkely develop ms
diabetes
siphilis
measles
mumps
lymes disease
sle
sarcoidosis

145
Q

treatment opitic neurtits

A

steroids
2-6 week recovert

146
Q

eye drooping and mouth drooping on left side of face

what nerve is affeced and upper or lower?

A

left sided lower motor neruone
facial nerve

147
Q

how do tyou know if its upper motor neruone ornmlower motor neurone in facial nerve pasly

A

upper motor neurone the forehead is spared
lower motor neurone all the face affeted

upper facial nucleus has bilateral innervcation from both sides of brain
lower facial nucleus has contrlateral innervation

if stroke on right side of brain
the left side of lower half will droop and spare left forehead cus the top left forehead is innervated also by the left side of the brain too

148
Q

rash round ear and unilateral drooping of mouth and eyes and forehead
what is this

A

ramsay hunt syndrome

149
Q

what innervation does the facial nerve supply

A

motor= facial expresion
stylohyoid
platsyma
stapedius of inner ear
posterior digastric

sensory= anterior 2/3 tast of tongue

para= supply para to sublingual and submandibular glands and lacrimal gland

150
Q

whats bells palsy

A

idiopathic
unilateral lmn facial nerve pasly= enitre side of face affected - same side of lesion

151
Q

treat bells pasly

A

within 72hrs of onset can give prednisolone - 50mg for 10 days or 60mg for 5 days then 5 day of reducing by 10mg each day
lubricating eye drop give no matter time
most will get better several weeks some take a year to get better
- 1/3 have lasting weakness

152
Q

whats the cause of ramsay hunt syndrome and whats and s

A

herpes zoster virus

unilateral lmn facial nerve pasly- affect entire side of face
vesciular rash around ear / in esr canal/ pinna. can extend to anterior 2/3 of tongue and hard patlate
rash same side as affectedface

153
Q

treat ramsay hunt syndrome

A

initiated within 72hrs
prednisolone and
aciclovir
lubricating eye drops

154
Q

what causes are there of lmn lesion causing facial nerve palsy

A

bells palsy- idiopathic
ramsay hunt syndrome- herpes zoster virus
infection= otitis media, malignat otis externa, HIV, lymes disease

systemic= diabetes, sarcoidosis, MS, lukaemia, guillian barre syndrome

tumors= parotid, acoustic neuroma, cholesteatoma

trauma= direct nerve trauma, damage in surgfery, base of skull fracture

155
Q

where does the facial nerve leave the skill and what does it go through

A

exits at brainstem at cerebellopontine angle
passes through temporal bone and parotid gland

156
Q

whats the branches of the facial nerve

A

temporal
zygomatic
cervical
buccal
marginal mandibular

157
Q

whats presentation of brain tumours

A

neurological symptoms to location
signs and symptoms of raised intracranial prssure

158
Q

erson has headaches thats be continuous for 4 days and its worse when they wake up

what could this be a sign of
what simple test can you do

A

raised intracranial pressure
measure bp - ht?
fundoscopy- look for papilloedema

159
Q

signs and wymptoms of raised intracranial pressure

A

papilloedema
headaches–> constatn
nocturnal
wonrse on waking
worse on coughing, straining, leaning forwards
vomiting

altered mental state
visual field defect
sizures- esp focal
unilateral ptosis
cranial nerve 3 and 6 palsies

160
Q

whats the types of brain tumours

A

metasates from lung, breast, colorectal and prostate

gliomas= tumout of glial cells
these are graded 1-4
4 being most maligant
astrocytoma- glioblastoma multiforme most malignant
oligodendroglioma
ependymoma - benign

meningiomas- usually benign but bad cus raised icp

acoustic neuroma= tumour of schawann cells aroud the auditory erve of the inner ear

pituiatary tumours

161
Q

sign and symptoms of acoustic neuroma

A

occur at cerebellopontine angle
slow growing
usually unilateral
hearing loss
tinnitus
balance problrms
cn 7 pasly

162
Q

if aucstic neuroma is bilateral what type of tumour is it

A

neurofibromatosis type 2

163
Q

signs and symptoms of pituitary tumour

A

bitemporal hemianopia
hormone deficiences or hormones in excess–>
acromegaly= inc GH
hyperprolactinaemia = inc prolactin
cushings disease = inc ACTH and cortisol
thryotoxicosis= inc TSH and thyroid hormone

164
Q

treat pituitary tumour

A

transphenoidal surgery
radiotherpay
meds to supress if excess hormones=
somatostatin analouges if excess GH= ocreotide
bromocriptine to block prolactin secreting tumours

165
Q

whats huntingtons chorea

A

autosomal dominant progressive degenration of neurones

166
Q

whats the cause of huntingtons chorea

A

autosomal dominant
trinucelotide repeat disorder of the HTT gene on chromosome 4
shows anticipation - each sucesssive generation has increased repeatitions and so has early age of onset and increase severity of symtpoms
CAG repeats

167
Q

hats anticipation

A

a feature of trinucelotide repeat disorderes
each sucessive generation has increased repeats of the gene and so increase severity of disease and earlier age of onset

168
Q

30 yr old
has progressive worsening of symtoms
habing mood changes lots
then started having movement problems where was making involutary movements and struggling to swalloe

what is this

A

huntingtons chorea

169
Q

s and s of huntingtons chorea

A

gradual and progressive symotms
starts around 30s-50s
starts with cognitive (including demetia) , pscyiatric, mood disorders
then moves onto movement disorders
chorea= abnormal andinvoluary movements
dysarthia= issue speaking
dysphagia
eye movement disorders
behavioural problems - issues with family, job loss etc

170
Q

diagnosis of huntingtons

A

genetic testing
have pre and post counselling

differnetials- other causes of dementia
other causes of chorea

171
Q

treatment for huntingtons

A

no tratment just symtpomatic relief
MDT
speech and language therapy if needed
genetic cousnelling for fam, preg, childnren
adavance directives
plan end of life
supress movement disorders= antipsycotics- olanzapine
benzodiazapines= diazapam
dopamine depelting agents= tetrabenazine

172
Q

whats cause of death and life expecatncy in huntigtons chorea

A

suicide more common
often other ilnnes =cus more suspetible to illness= pneumonia
life expectancy 15-20yrs after onset. ofsymptoms

173
Q

whtas myasthenia gravis

A

autoimmune condition that casues muscle weakness that gets worse on muscle use and improves with rest

174
Q

cause of myasthenia gravis

A

strong link between thyoma and this
AchR antibodies= bind to ach r at nmj and so ach cant bind so cant stimulte r so cant illicit muscle contraction

10% of patietns due to MuSK auto antibodies

5% of patients due to LRP4 auto antibodies

last 2 auto antibodies are for proteitns that are respo sible for creaition and organisation of Ach r = not enough AchR

antibodies can also activcate complement system in the nmj and so damage the cells at the post synaptic membrane

175
Q

patiet has LRP4 autoantibodie
what does this cause

or
patient has MuSK antobodies

A

mysathenia gravis

176
Q

whats s and s of myasthenia gravis

A

muscle weakness worse in evening

women under 40
men over 60
thyoma
mostly affects proximal muscles and muscles of head and neck =
extraocular m weakness= diplopia
eyelid weaknes= ptosis
diff swallowing
fatige in jaw when chewing
weakness in facial movements
slurred speech

177
Q

what can you do on examination to test for myasthenia gravis

A

want to elict muscle fatiguiability

repeated blinking- can exaserbate ptosis

prolonged upward gaze can ellicit diplopia
repeated abduction of arm 20 times then when compare find unilateral weakness to that arm
check to see if thymectomy scar
test FVC

178
Q

how to diagnose myasthenia gravis

A

antibodies test- AchR antibodies
LRP 4 antibodies
MuSK antibodies
ct/mri of thymus gland to look for thyoma
edrophonium test- give IV edrophonium chloride/ neogstimine = this blocks acetylcholinesterase so more ach in the nmj so more availble. tobind to temporaily and briefly relives weakness

179
Q

what certainly estabilsh a diagnosis of myasthenia gravis

A

edrophonium test

180
Q

what treamtent is there. for myasthenia gravis

A

neostigmine/ pyridostigmine = achesterase inhibitors

prednisolone/ azathioprine = supress antobody production

thymectomy= even if no thyoma can help
rituximab if nnothing else works- monoclonal ab agaisnt b cells

181
Q

patient has sudden inability to breath they have had an upper resp trsct infection and are on neostigmine
what is this

A

myasthenic crisis

have myasthenia gravis and have acute worsening of symptoms often trifgfered by another illnes eg. upper res tract infecction

can casue resp failure as the resp muscles weaknes

give niv/ bipap/ intubation/ ventilation
give immunomodulatory therapy= iv immunoglobulins and plasa exchange

182
Q

whtas lamber eaton myasthenic syndrome

A

similar to myasthenia gravis
autoimmune agaisnt voltage gated calcium channels.

183
Q

whats the casue of lambert eaton myasthenic syndrome

A

antibodies agasint voltage gated calcium channels
these are in presynatoic termials of nmj and so the channels are destroyed so less Ach can be released into the synapse

VGCC are found. in small cell lung cancer so antibodies produced= small cell lug cancer major casue

184
Q

if patient has lambert eaton myasthenic sydrome what do you need to consider to investigate for

A

small cell lung cancer

185
Q

signs and symptoms of lambert eaton myasthnic syndrome

A

slower pregression and less pronounced symtoks of myasthenia gravis

proximal muscles affected most- gait affected more than in MG (mg is more face issues)
weakness increased with prolonged use (although some say can have improvement) - worse in evening

ptosis
diplopia
slurred speech
dysphagia

186
Q

what investigations of LEMS

A

ct/mri to see if malignacy the cause - consdier small cell lung cancer esp if older smoker with symtpoms
VGCC antibodies

screen for underlying malignacy after 2 years of diagnosis of lambert eaton myasthenic syndrome

187
Q

treatment for lambert eaton myasthenic syndrome

A

amifampridine = blocks voltage gated potassium channels in presynaptic termianl of nmj = prolongs depolarisation = ca channels able to work more= increased acetylcholine releasd into synapse

immunosupressants= prednisolone/ azathioprine

iv immunoglobulins
plasmapheresis

188
Q

what casues are there of peripheral neuropathies

A

charcot marie tooth disease
A- alcohol
B- B12 deficiency
C- cancer and CKD
D- diabetes and drugs- isonazid, amidarone, cisplatin
E- every vasculitis

thyroid disease
infection - hiv, syphilis, leprosy

189
Q

whats chacot marie tooth disease

A

iheirted peripheral neuropthy- motor and sensory

vasrious types of it
most genetic mutations are autosomal dominant
causes dysfunction to mylein or axons
mutations can arise. denovo

190
Q

high foot arch
bilateral foot drop
reduced tendon relfexes
peripheral sensory loss
symmetrical atrophy to the muscle below the knees - inverted champage bottle legs

A

charcot marie tooth disease

191
Q

s and s of charcot marie tooth disease

A

slowly progressive
weakness of feet and anles
depressed or absent tendon relfexes
weakness of dorsiflexion
bilateral foot dtop
symmetrical atrophy of muscles below the knees- inverted champagne bottle legs
atrophy of muscles of hands- esp thenar muscle
high foot arch- pes cavus
weakness in lower legs
weakness in hands
decreased muscle tone
peripheral sensory loss

192
Q

what ages does charcot marie tooth disease present

A

before 10 usulay
can be delayed to age 40 though

193
Q

what investigfations to do for susepcted charcot marie tooth disease

A

mri/ct of brain and sc
exclude other neuropathies- blood test for b12, folate, lft, ck, antinucelar ab
muscle biopsy
csf
nerve conduction studies - can show got cmt disease

194
Q

managemnt of charcot marie tooth disease

A

supportive
orthopdeics
podiatrist
ot
physio
neuro and geneticits for diagnosis

195
Q

patient has sudden onset of weakness in both feet and now in lower legs
had a tummy bug 3 weeks ago

what is this

A

guillain barre syndrome

196
Q

whats guillain bare syndrome

A

scute paralytic polyneuropathy affectig periperal nervous sytem = autoimmune demyelination and axonal degenration

197
Q

cause of guillain barre syndrome

A

molecular mimicry =
have infection so b cells produce antibodies agaionst antigen of pathogen
thieese antiboides also match for protiens in nerve cells - mylien sheath, axon

get degenration. ofthe nerves

198
Q

what infections are strongly linked to guillain barre syndrome

A

camplyobacter jejuni
cytomegalovirus
epstein barr virus

199
Q

signs and symptom of guillain barr syndrime

A

hypotonia
symmetircal ascending weakness starting in feet and moving up body - can also start in hands and move up
redcued relfexes
can have periperal loss of sensation
can have neuropathic pain
can progress to cranial neres-> facial nerve pasly (all of face)
can in sevre cases get resp failure due to paralysis. of resp muscles

200
Q

when do symtoms of guillain barre syndrome start

A

within 4 weeks of previous infection
symptoms peak at 2-4 weeks and then recovery period is motnhs - years

201
Q

how to diagnose guillain barre syndrome

A

lumbar puncture- csf have high protein, normal gluocse and cell count

nerve condcution studies- redcues signal

think other casues ofacute paralysis

202
Q

what casues are there of acute apralysis

A

guillain barre syndrome
brain- stroke, encephalitius, brainstem compression
sc- sc compression, infection
anterior horn cell= enterovirus, poliovirus
nerve root- CMV, HIV
peripheral nerve- vasculitis, lead poisoning, lyme disease, thyamine def, diptheria
nmj= myasthenia gravis(more slow though and worse when moving ), lambert eaton myastheinc syndrome, botulism
muscle- hypokalemaie, polymyositis

203
Q

management of guillain barre syndrome

A

iv immuoglobulins
plasma exchange
suportive care
vte prophylaixis

204
Q

hats a leading cause of death in guillain barre dynsrome

A

PE

205
Q

hat medication is given for men with epilelpsy

A
  • generalised seizure: sodium valproate
    focal seizure: lamotrigine or levetiracetam
206
Q

How does cushings syndrome casue hypokalaemia and metabloc alkalosis

A

high cortisol can act as a mineralcoritcioid
potassium is therofre excreted as na reabsorbed

hydroen ions swapped for na so secrete h ions

So get cushing sydnrome features and muscle cramps, tremor, weakness = hypokaelmiea

207
Q

How does cushings syndrome casue hypokalaemia and metabloc alkalosis

A

high cortisol can act as a mineralcoritcioid
potassium is therofre excreted as na reabsorbed

hydroen ions swapped for na so secrete h ions

So get cushing sydnrome features and muscle cramps, tremor, weakness = hypokaelmie

208
Q

whats the cushing reflex

A

bradycardia and hypertension
The Cushing reflex is a physiological nervous system response to increased intracranial pressure that results in hypertension and bradycardia. Cerebral perfusion pressure (CPP) = mean arterial pressure (MAP) - intracranial pressure. Therefore if intracranial pressure is high, the only way the body can compensate to increase CPP is by increasing MAP. A sympathetic reflex therefore results in hypertension. This results in a counter parasympathetic reflex by stimulation of the baroreceptors resulting in bradycardia.

Bradycardia and hypertension with a wide pulse pressure is the correct answer. Cushing’s triad, compromised of widening pulse pressure, bradycardia and irregular breathing, is a late sign indicating impending brain herniation. Systolic hypertension occurs as a reflex to maintain cerebral perfusion pressure in the presence of raised intracranial pressure.

209
Q

ptient hit laterally in head with cricket ball
what worry about

A

The mechanism of injury, loss of consciousness and ‘lucid interval’ should ring alarm bells for an extradural haematoma.

210
Q

water deprivation test of primary polydipsia show what

A

Water deprivation test: primary polydipsia
urine osmolality after fluid deprivation: high
urine osmolality after desmopressin: high

211
Q

whats the difference in primary polydipsia and dehydration in water deprivation test

A

Dehydration . This patient would have a high urine osmolality to begin with and he is not clinically showing signs of dehydration (e.g. dry mucous membranes and prolonged capillary refill time) based on the hydration status assessment. Further investigations would also be needed to assess the cause of his dehydration as he is drinking water and it is not addressing his thirst.

212
Q

what would high stepping gait indicate

A

A high-stepping gait develops to compensate for foot drop. If found unilaterally then a common peroneal nerve lesion should be suspected. Bilateral foot drop is more likely to be due to peripheral neuropathy.

213
Q

A 64-year-old female with a history of rheumatoid arthritis presents with increased difficulty in walking. On examination there is weakness of ankle dorsiflexion and of the extensor hallucis longus associated with loss of sensation on the lateral aspect of the lower leg. What is the most likely diagnosis?

A

common peroneal n pasly
The sciatic nerve divides into the tibial and common peroneal nerves. Injury often occurs at the neck of the fibula

The most characteristic feature of a common peroneal nerve lesion is foot drop.

Other features include:
weakness of foot dorsiflexion
weakness of foot eversion
weakness of extensor hallucis longus
sensory loss over the dorsum of the foot and the lower lateral part of the leg
wasting of the anterior tibial and peroneal muscles

214
Q

child comes with epilepsy with cafe au lait spots, angiofibromas over the nose and cheeks and a gew shagreen pathces.
what is this

A

tuberous sclerosis

215
Q

mutation of TSC1 gene on chromosome 9 causes what

A

this produces hamartin
mutaztion of this causes tuberous scleorosis

216
Q

what genes cause tuberous scleorisis

A

TSC1 gene- chromosome 9- hamartin

TSC2 gene- chromosome 16- tuberin

217
Q

s and s of tuberous scleorisi

A

main feature is hamartomas = benign neoplastic growths of the tissue it orginates in

can affect: lungs, brain, heart, eyes, kidneys, skin

skin signs=
cafe au lait spots
angiofibromas across nose and cheeks
ash leaf spots
shagreen patches
poliosis - white hair patch in any hair
subungual fibromas

neuro=
epiplepsy
learning disability and developmental delay

othes:
rhabdomyomas in heart
gliomas
polycystick kidnneys
lymphangioleimyomatosis - often in lungs
retinal hamartomas

218
Q

s and s of lymphangioleimyomatosis

A

oftens affects lungs
seen in tuberous sclerosis
lungs:
coguh, sob, haemoptysis, chest pai, pneumothroax

219
Q

treat tuberous sclerosis

A

supportive
monitoring
treat compliations

220
Q

what is the most common type of nneurofibrosmatosis

A

type 1

221
Q

s and s of idiopathic intracranial ht

A

This is evidenced by the presence of diffuse headaches, blurred vision, pulsatile tinnitus (the ‘woosh’ sound she describes) and the bilateral papilloedema.

headache
blurred vision
papilloedema (usually present)
enlarged blind spot
sixth nerve palsy may be present

222
Q

what class of antibiotics can increase risk of idiopathic intracranial haemorrhage

A

Lymecycline is in the tetracycline class of antibiotics - a class known to increase risk of developing this condition.

223
Q

rf for idiopathic intracranial ht

A

young, overweight females.

Risk factors
obesity
female sex
pregnancy
drugs
combined oral contraceptive pill
steroids
tetracyclines
retinoids (isotretinoin, tretinoin) / vitamin A
lithium

224
Q

management for idiopathic intracranial haemorrhage

A

weight loss
diuretics e.g. acetazolamide
topiramate is also used, and has the added benefit of causing weight loss in most patients
repeated lumbar puncture may be used as a temporary measure but is not suitable for longer-term management
surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve. A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure

225
Q

what imaging would you use to look for demyelinating lesions eg. MS

A

MRI with contrast

226
Q

whats wernickes dyspahsia

A

Wernicke’s dysphasia: speech fluent, comprehension abnormal, repetition impaired
Important for meLess important
Wernicke’s dysphasia is correct. This results from damage to Wernicke’s area in the temporal lobe and impairs language comprehension, repetition of words and phrases. In Wernicke’s dysphasia speech is fluent with intact sentence structure, but is lacking meaning.

227
Q

whats brocas dysphasua

A

dysphasia where the speech is non-fluent, unlike in this case, because Broca’s area in the frontal lobe connects with the motor cortex to produce the movements required to articulate the words. As a result, repetition of words is also poor. Comprehension is normal in patients with frontal lobe damage, as the language comprehension centres found in the temporal lobe, Wernicke’s area, are intact.

228
Q

whats steven johnson syndrome and what drugs can casue the adverse affect

A

fevers
photophobia
rash

lamotrigine
NSAIDs
cephlasporins
sulphonomides
allopurinol
other anticonvulsants

229
Q

whats webers syndrome

A

Weber’s syndrome is a midbrain stroke syndrome that involves the fascicles of the oculomotor nerve resulting in
ipsilateral CN III palsy and contralateral hemiplegia or hemiparesis.

230
Q

the empty delta sign is seen on venography
pt has bilateral papilloedema and headache

what is it

A

sagittal sinus thrombosis is associated with raised ICP and the ‘empty delta sign’ on venography.

231
Q

lucid interval after injury- eg. awake 30 mins then collapse
biconvex on imaging of brain

what is this

A

acute extradural haermorrhage

its biconvex so not with the shape. ofthe head. like you throw a ball at someones head and its leaving a dent in it

cause often middle menigeal artery

232
Q

acute subdural haemorrhage occurs due to what and what shape on imaing

A

due to shake of head
bridging veins
crescent shape- shape sape as the way the skull goes (cus its inside the mater so with the brain and skull)

Acute subdural haemorrhage occurs due to vein’s rupture and results in the collection between brain and dura mater. These veins rupture due to sudden jolts or shake to the brain. It usually appears as crescent-shaped on CT scan.

233
Q

what would wubarachnoid haemorrhage lead to

A

Sub-arachnoid haemorrhage would lead to stroke. The patient would usually present with sudden severe headache and vomiting.

234
Q

whats cerebral contusion caused by and is

A

Cerebral contusion is a bruise of the brain tissue and usually occurs due to small blood vessel leaks into the brain tissue. It usually result in increase intracranial pressure. It usually occurs due to the brain coming to sudden stop against the inner surface of the skull. The typical causes include motor vehicle accidents or when the head strikes the ground.

235
Q

what prophylaxis for cluster headaches
what use for acute attak

A

Verapamil is used for cluster headache prophylaxis. Sumatriptan is used as an acute rescue therapy (along with high-flow oxygen),

236
Q

how does syringomyelia present

A

Syringomyelia classically presents with cape-like loss of pain and temperature sensation due to compression of the spinothalamic tract fibres decussating in the anterior white commissure of the spine

237
Q

imporntant cisual field defects

A

Visual field defects:
left homonymous hemianopia means visual field defect to the left, i.e. lesion of right optic tract
homonymous quadrantanopias: PITS (Parietal-Inferior, Temporal-Superior)
incongruous defects = optic tract lesion;
congruous defects= optic radiation lesion or occipital cortex

238
Q

Deficiency of what vitamin can cause Wernicke’s encephalopathy and if left untreated can lead to irreversible Korsakoff’s syndrome.

A

b1= thiamine

239
Q

L3 nerve root compression

A

L3 nerve root compression
Sensory loss over anterior thigh
Weak hip flexion, knee extension and hip adduction
Reduced knee reflex
Positive femoral stretch test

240
Q

L4 nerve root compression

A

Sensory loss anterior aspect of knee and medial malleolus
Weak knee extension and hip adduction
Reduced knee reflex
Positive femoral stretch test

241
Q

L5 nerve root compression

A

Sensory loss dorsum of foot
Weakness in foot and big toe dorsiflexion
Reflexes intact
Positive sciatic nerve stretch test

242
Q

S1 nerve root compression

A

Sensory loss posterolateral aspect of leg and lateral aspect of foot
Weakness in plantar flexion of foot
Reduced ankle reflex
Positive sciatic nerve stretch test

243
Q

contralateral hemiparesis and sensory loss
lower extremity> upper extremity

which artery affected in stroke

A

anterior cerebral artery

244
Q

contralateral hemiparesis and sensory loss
upper extremity> lower extremity
contralaterla homonymous hemianopia
aphasia

which artery affected in this stroke

A

middle cerebral artery

245
Q

contralateral homonymous hemianopia with macula sparing
visual agnosia
which artery affected in this stroke

A

posteror cerebral artery

246
Q

ipislateral CN3 palsy
contralateral weakness of upper and lower extrmitits

whats this and what affected

A

webers syndrome
branches of posterior cerebral artey that suply midbrain

247
Q

ispilateral facial pain and temp loss
contrlateral limb/torso pain and temp loss
ataxia, nystagmus

A

posterior infeferior cerebellar artey
= lateral medullary syndrome/ wallenburg syndrome

248
Q

ipislateral facial paralsyis and deafness

A

with also similar to posterios infeerior this is anterior infererior cerebellar artery = lateral pontine syndrome

249
Q

amacurosis fugax= darkening of the vision in area casue

A

rentinal / opthamic artery stenosis
carotid artery stenosis

250
Q

locked in syndrome casue

A

where they cant move/speak but can blink eyes and move eyes up and down

casue = basiliar artery affected

251
Q

lacunar strokes present with what

A

either
isolated hemiparesis, hemisensory loss
or
hemoparesis with limb ataxia

strong association with ht
common sites: basal ganglia
thalamus
internal caspule

252
Q

idiopathic intracranial ht treatment

A

acetazolamide- carbonic anhydrase inhibitor = reduce production of CSF

topiramate is another med to use in IIH

253
Q

frontal lobe epilepsy

A

jackasonian march
clonic movements starting in one extremity and moving proximally through the body is typical of a Jacksonian March. This, combined with post-ictal weakness usually indicates a frontal lobe origin.

254
Q

temporal lobe epilepsy

A

usually presents with automatisms, such as lip-smacking, grabbing, or plucking at clothes, along with sudden emotional disturbance or a feeling of deja vu

May occur with or without impairment of consciousness or awareness

An aura occurs in most patients
typically a rising epigastric sensation
also psychic or experiential phenomena, such as déjà vu, jamais vu
less commonly hallucinations (auditory/gustatory/olfactory)

Seizures typically last around one minute
automatisms (e.g. lip smacking/grabbing/plucking) are common

255
Q

parietal lobe epilepsy

A

sensory disturbances, such as paraesthesia, electric shock type sensations, hallucinations, or dizziness

256
Q

occipital epilepsy

A

typically visual, presenting with flashers and floaters, or lines in the vision

257
Q

cerebellum indirectly cause epilepsy symptoms

A

the cerebellum can indirectly cause epileptic seizures, they are unlikely to originate in the cerebellum itself. Symptoms of cerebellar damage include gait disturbance, jerky movements, and speech disturbance

258
Q

alzheimers dementia main feature

A

memory

259
Q

vvascualr dementia main feature

A

mood
stepwise fashion of progression
ht major risk facotr

260
Q

frontotemporal dementia main feature

A

earlier onset 45-65yrs
personaility, social, decsion,empathy= frontal lobe

speech, language and memory loss= temporal lobe

261
Q

differntials for dementai

A

HIV related dementia
prion protien disease - CJD
depression!!
normal pressure hydrocephalus
mild cognitive impairment

262
Q

confusion screen

A

calcium
FBC
U &E
LFT
CRP and ESR (urine test can be sent to labs if conufusion in elderly uti)
TFT- hypothryoidism
B12 and folate
glucose

263
Q

blood test to differentiate between seixure and non-epileptic pseudo seizure

A

prolactin
true epileptic= raised prloactin

264
Q

webers syndrome

A

Weber’s syndrome is a form of midbrain stroke characterised by the an ipsilateral CN III palsy and contralateral hemiparesis

265
Q

ipsilateral CN3 palsy and contralateral hemiparesis

A

webers syndrome

266
Q

biceps reflex

A

C5,C6

267
Q

internucelar opthamplegia

A

Internuclear ophthalmoplegia (INO) occurs due to a lesion of the medial longitudinal fasciculus (MLF), a tract that allows conjugate eye movement. This results in impairment of adduction of the ipsilateral eye. The contralateral eye abducts, however with nystagmus.

same eye cant adduct
other eye can abduct but nystagmus when it does

268
Q

no matter waht the realpse is in what rx for MS relapse

A

oral methylprednisolone

269
Q

foot drop

A

common peroneal nerve damage

270
Q

analgesia headache managemnt

A

stop nsaids, triptans and paracetmaol immedisately
withdraw opiates sloewly (codeine)

271
Q

contralteral homonymous hemianopia with macula sparing and visual agnosia

A

posterior cerebral artery

272
Q

pituitary gland tumour eye changes

A

Bitemporal hemianopia, upper quadrant defect

273
Q

stroke what side eye changess

A

same side as the parlasyis
the homonymous hemianopia is always on the same side as the paresis.

274
Q

Primary open angle glaucoma in right eye

A

Unilateral peripheral visual field loss

275
Q

bitemporal hemianopia

A

lesion of optic chiasm
upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour
lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma

276
Q

locked in syndrome - cant move or speak but can follow eye commands
which artery in this affected

A

basillar artery

blood vessel supplies the cerebellum, thalamus, occipital lobe, and brainstem. These strokes are rare and often devastating. There are 3 main presentations of patients experiencing a basilar artery infarct:
An acute decreased GCS and advanced motor symptoms.
Insidious, gradual deterioration in GCS and motor symptoms with a subsequent sudden advanced decrease in GCS and motor symptoms.
A ‘herald hemiparesis’ with associated headache and vision changes prior to the onset of permanent symptoms of motor loss

277
Q

Ipsilateral oculomotor palsy and contralateral weakness of the upper and lower extremity

A

branches of the posterior cerebral artery that supply the midbrain

278
Q

sensation of fine touch, proprioception and vibration are all conveyed in the

A

dorsal column

279
Q

brown sequard syndrome

A

tracts affeced:
1. Lateral corticospinal tract
2. Dorsal columns
3. Lateral spinothalamic tract

casues:
1. Ipsilateral spastic paresis below lesion
2. Ipsilateral loss of proprioception and vibration sensation
3. Contralateral loss of pain and temperature sensation

Medicine (11 decks)

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