neuro top tier Flashcards
what investigation can be done to assess type of stroke
what does this affect
CT stroke - allows you to see if haemorrhagic.
if not (=embolic) then lytic medicine given so embolus broken down and damage reduced. but if it is haemorrhagic, then lytic medicine should be avoided as this would increase the bleed
effect on ischaemia to broca’s area
expressive dysphasia (motor)
effect on ischaemia to wernicke’s area
receptive dysphasia (sensory) - misinterpret own speaking and you think it is wrong \+ can't understand other people's communication
is someone more likely to recover from a large ischaemic (embolic) or haemorrhagic stroke?
haemorrhagic
in haemorrhagic- the axons are disturbed (lenticular striate arteries cross internal capsule) but cell bodies are not affected- so necrosis. so as the haemorrhage resolves (With macrophages ), the pressure on axons decreases allowing recovery
with embolic blockage- there is necrosis of cell bodies. these are unable to regenerate and so are non-recoverable
in terms of the motor homunculus- which areas are supplied to which arteries (and so which areas would suffer from a stroke blockage in this artery)
anterior cerebral arteries = medial of cerebrum and homunculus
– lower limb
middle cerebral arteries = lateral of cerebrum
– upper limb and face
which is more common, embolic or haemorrhagic stroke?
85% embolic
15% haemorrhagic
which side of the brain is more likely to be affected by embolus from heart / carried in heart and why
right brain
R common carotid comes of before L from arch of aorta
name 3 significant causes of embolic stroke
1 heart failure (AF –> stasis –> embolus –> ejected when sinus rhythm returns)
2 blood pressure (stretches artery /longer –> turbulent blood flow –> clot embolus)
3 also kidney/lung/liver failure
what drugs may be given to AF patient for stroke prophylaxis
warfarin - prevent clot formation
where may a clot form with AF
in auricular appendage of atria in heart (Stasis of blood)
where does external carotid supply
dura
skull
face
neck
where does internal carotid supple
circle of willis
which vessels lie extradurally
meningeal arteries
which vessels lie subdurally
bridging veins
which vessels lie subarachnoidly
circle of willis
what symptoms is associated with a subarachnoid haemorrhage
thundeclap headache
what is the main cause of a subarachnoid haemorrhage
berry anerysrm in circle of willis
which haemorrhage type would cause dura to be pushed away from bone
extradural - meningeal
which groups are more suscpetible to subdural haemorrhage
elderly
children
alcoholics
they have brains smaller than their ckulls
epidemioloogy of migraines
common
f>m
<40y. most have 1st in adolescence
epidemiology of tension headaches
very common
f>m
epidemiology of cluster headaches
m>f
<40y
disabling
triggers for migraine
chocolate:
chocolate hangover orgasm cheese oral contraceptuve lie ins alcohol tumult exercise
triggers for tension headache
stress sleep deprivation bad posture hunger eyestrain anxiety noise
red flags for headaches patient
thunderclap headache seizure+ new headache red eye (gllaucoma) immunosuppressed prev malignancy recent trauma fever neck stiffness papilloedema - swollen optic discs
classification of headaches
Primary (migraine, cluster, tension)
Secondary (meningitis, subarachnoid haemorrhage, Giant cell arteritis, idiopathic intracranial HTN, medication overuse headache)
painful cranial neuroptahies, facial pains and othe headaches (trigeminal neuralgia)
pathophysiology of migraines
Changes in brainstem blood flow → unstable trigeminal nerve nucleus and nuclei in the basal thalamus → release of vasoactive peptides (CGRP and substance P)→ inflammation, vasodilation and plasma protein extravasation
migraine
severity
features
uni/bilateral
moderate to severe
aura disrupt daily activity naus/vom photo/phonophobia throbbing
unilateral
tension
severity
features
uni/bilateral
mild-modeate. continue with activities
squeezing/tightening
no naus/vom
none/one of phot/phonophobia
scalp tenderness
bilateral
cluster
severity
features
uni/bilateral
v/ severe
pain around eye/ temporal cranial autonomic features, ipsilateral --red eye --- lactimation --swollen lid -- facial flushing -- blocked nose -rhinnorhea agitated frequent but short may but nocturnal- wake u up
unilateral
rhinnorhea
= blocked nose
trigeminal neuralgia
uni/bilateral
features
unilateral
facial pain
severe
electric shock/shooting/stabbing
triggor= eating, talking
trigeminal neuralgia treatment
carbamazepine
non pharmocological headache management
lifestyle modification
trigger management
psychological and behaviour treatment
surgical treatment (rare)
migraine preventative treatment
B blocker- propanolol
acupuncutre
topiramate - anticonvulsant
botulinum toxin injections
Riboflavin (vit B2)
amitriptyline- tricyclic antidepressant
BAT BRA
migraine relief treatment
triptan (eg sumatriptan) + NSAID
antiemetics (naus/vom)
what should NOT be given to headache patients
opioids/ergots
tension headaches treatment
analgesics - aspirin, NSAIDs tricylci antidepressant (amitryptilline)
cluster headaches treatment for acute attack
triptan
- sumatriptan
- (zolmitriptan)
100% oxygen
cluster headache prevention treatment
verapamil (CCB)
corticosteroids
avoid alcohol
lithium
visual fortification spectra
visual patterns seen withiin aura of migraine
- zig zags
- lines
- flashing lights
non-visual aura experiences do exist – tingling, weakness, dysphasia
meningitis management that is not to do with patient
notify public health
how is neisseria meningitidis spread
droplet
glasgow coma scale
a measure of consciousness
eye/verbal/motor response
neonatal causes of menigitis
e coli
strep b
listeria
infant causes of menigitis
hemophilius influenzae b
neisseria menigitidis
strep pneumonia
adults causes of meningitis
neisseria meningitidis
strep pneumoniae
listeria if immunocompromised
name some complications of meningitis
death amputation scars (from rash) seizures hearing loss (from brain swelling) brain damage, neurological dysfunction
meningitis and encephalitis risk factors
immunosuppression
travel
name 2 causes of chronic meningitis
TB
syphillis
cryptococcal – fungus!
parasitic
what are non-infective causes of meningitis and encephalitis
cancer
drug side effects
autoimmune - vasculitis, SLE
what is different about the presentation of chronic menigitis (compared to acute)
triad = absent/ late
anorexia
menigitis triad
other symptoms
headache
stiff neck
fever
photophobia rash malaise, vomitting irritable wants to lie still papilloedema -- due to increased ICP -- usuaully bilateral
encephalitis symptoms
preceding
- flu like illness (headache, sore throat, myalgia, malaise, runny nose)
then: - fever altered GCS - seizures - memory loss - headache
+/- meningism
kernigs sign
resistnace to extension of the leg while hip flexed (thigh at 90 degrees and calf straightened)
sign of menigism
- specific but not sensitive
brudzinki’s sign
neck in lifted (flexion) and there is reflex flexion of hips and knees in response (in order to relieve meninges discomfort)
sign of menigism
- specific but not sensitive
CSF biochemistry results for menigitis
bacteru, TB, cryptococcus (fungus):
- HIGH in protein and LOW in glucose
virus:
- HIGH in protein and NORMAL in glucose
(virus does not use glucose in order to replicate whereas the others do)
antibiotic treatment for bacterial meningitis
most = cefotaxime and ceftriaxone (3rd gen cephlosporin)
listeria = amoxycillin
non antibiotic treatment for menigitis
steroids - IV dexamethosone –> reduces brain swelling
call public health
treatment for encephalitis
mainly supportive
- fluid/nutrients
- protect, keep on wards
- painkillers
- physio and neuro rehab
antiobiotics for potential menigitis
if herpes simplex virus or varicella zoster virus –> ACICLOVIR
when is aciclovir given to encephalitis
if the cause is herpes simplex virus or varicella-zoster virus
which prophylactic antibiotics are given to close contacts of meningitis
ciprofloxacin
rifampicin
what might GP have to get meningitis started on treatment asap
IM benzylpenicillin (long shelf life)
varicella zoster virus – shingles
- cause
- preeruptive
- eruptive phase
- investigation
- treatment
varicella zoster virus reactivated after lying dormant in the sensory nervous system. when flares up, travels down affected nerve
no skin lesion. but burning and itching in one dermatome
eruption 2 days later: skin lesions appear
- red, swellen plaques. rash within dermatome. these lesions are infectious
sample fluid –> culture. + history and symptoms
oral aciclovir
watershed stroke
due to low BP -low cerebral blood flow
vulnerable areas of brain at the water shed area between arterial territories are the first to be deficient in perfusion lead to infarcts
what is obstructive hydrocephalus
complication…
Blood (haemorrhagic stroke), pus (meningitis) or mass (tumour) around the brainstem/cerebellum - squashes /covers 4th ventricle and exiting foramen
…. raise ICP!!!
long term stroke treatment
clopidogrel (antiplatelet)
secondary prevention –
statin,
warfarin (if AF)
antihypertensives
haemorrhagic stroke treatment
monitor GCS
reverse any anticoagulants (vit k for warfarin)
control hypertesnion
manual and medical decompression of high ICP (diuretics, raise head etc)
how do you reverse warfarin
vitamin K)
contraindication for thrombolysis for ischaemic stroke. name 5
1 Recent surgery (3m) 2 Recent arterial puncture 3 History of active malignancy 4 Brain ansyursm 5 Patient is on anticoagulation 6 Severe liver disease 7. Acute pancreatitis 8 Clotting disorder 9 If time of onset not unknown. Don't give thrombolysis -- give aspirin for 2w than clopidogrel after
ischaemic stroke treatment
thrombolysis tissues plasminogen activator = ALTEPLASE antiplatelet therapy = CLOPIDOGREL/ASPIRIN
general stroke supportice treatment
oxygen
hydration inc glucose
CHADVASC=
calculates risk of stroke for patients with AF
ABCD score
calculates risk of stroke for TIA patients
age diabetes high BP clinical features (of TIA/stroke) duration (longer than 1h = 2 points, less =1)
calculates risk of stroke for TIA patients
ABCD score
calculates risk of stroke for patients with AF
CHADVASC=
stroke investigation
** CT/MRI head – see if haemorrhagic or ischemic (ischaemi = less dense)
look for AF - pulse, BP, ECG
look for thrombocytopenia/polycythaemia (highrbc) – FBC
look for hypoglycaemia – serum glucose
can also do doppler ultrasound of carotid
lenticulostriate artery haemorrhagic stroke
- these are small vessels off the anterior cerebral artery that supply mid brain, and cross internal capsule
- theyre prone to rupture due to thin adventitia
- this disturbs all motor and sensory axons - cant transmit (internal capsule)
- but the cellbodies are not affected so there is no necrosis. this means there is the possibility of recovery as pressure on axons decreases
amaurosis fugax
transient visual distubrance - sudden temporary sight loss in one or both eyes. painless (stroke/TIA)
Due to atherosclerosis / thromboembolism in Internal carotid artery Ophthalmic artery Retinal artery -leading to temporary retinal hypoxia
symptoms of PCA stroke
Visual issues - peripheral vision, face recognition, colour naming, can’t interpret what they can see, cortical blindness
Headache
–Rare in ischaemic stroke! Think PCA!
symptoms of MCA stroke
upper limb and face
face droop
hemianopia
if L stroke:
brocas (expressive dysphasia)
wernickes (receptive dysphasia + cant understand others)
symptoms of ACA
lower limb -- gait incontinence drowsiness decrease in spontaneous speech and movement
