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Stroke - Coggle Diagram
Stroke
general
^risk with age
but 1/4 are<65yo
20-25% die within 2yrs
10% restroke in first year
40% dependent at 6mths
symptoms and exam tell you where has occurred
definition
sudden onset
localised.specific
functional neurological deficit
presumed vascular cause
persistent for >24hrs/causing death within 24hrs
clinical diagnosis
scans to
rule out haemorrhage/pseudostroke
blood supply
when decreased survival depends on modifying factors
availability of collateral circulation
adequacy of homeostatic response
duration of the ischaemia
magnitude&rapidity of the reduction of blood flow
metabolic needs
defects related to artery affected
anterior
hemiparesis
leg>arm
frontal
apathy
apraxia
cortex affected
problems with synthetic higher cortical functions
middle
hemiparesis
face/arm> leg
hemisensory loss
dominant
dysphagia
non-dominant
hemisensory neglect
cortex affected
problems with synthetic higher cortical functions
posterior
visual problems
memory problems
Therapeutic considerations
different for haemorrhagic vs ischaemic
see haemorrhagic earlier on ct than ischaemic
Ischaemic
possible secondary haemorrhagic transformation
responsible for 85%
occlusion
reduced blood flow
ischaemia+/- infarction
focal
stroke causing
embolic
maximal at outset
risk of later haemorrhagic transformation
cardiac, aortic arch, extracranial vessels
more common than thrombi
middle cerebral artery is most commonly affected
cardiac sources
mural thrombus
patent foramen ovale
valvular heart disease
prosthetic valve
endocarditis
atrial myxoma
cardiac risk factors
ischaemic heart disease
atrial fibrillation
rheumatic heart disease
infective endocarditis
prosthetic heart valves
non-bacterial thrombotic endocarditis
mitral valve prolapse
cardiomyopathy
cardiac aneurysm
myxoma
non-cardiac
atheroembolism
thrombotic
evolves
large vessel stenosis
atheroma branch points
mostly atherosclerosis
common sites for thrombosis
carotid bifurcation
origin of middle cerebral
basilar artery
small vessel stenosis
lipohyalinosis
HTN
arteriosclerosis-hypertension
DM
vasculitis
infl.
immunosuppressed with o.inf.
autoimmune vascular disease
hypercoagulability states
perforating vessels
thrombotic occlusions are usually superimposed on atherosclerotic plaques
symptoms
motor weakness/paralysis
sensory numbness/loss of sensation
loss of higher cortical functions
difficulty speaking
understanding
recognising
sequencing/constructing/performing
visual
loss of balance
nausea and vomiting
sudden death
many have none
if extensive
severe headache
loss of consciousness
convulsions
Transient ischaemic attack
brief episode of neurological dysfunction
due to temporary cerebral/retinal ischaemia
no infarction
less than 60mins
complete recovery
act within an hour
address risk factors for stroke
30% go on to stroke in 5yrs
15% get MI in 5yrs
usually emboli to internal carotid
usually middle cerebral artery
sometimes retinal artery
amaurosis fugax
Hollenhurst plaque
Global cerebral ischaemia
outcome of severe hypotensive episode
anatomy
watershed zones
physiology
vulnerable cells
mild case
only transient post ischaemic confusional state
complete recovery
no irreversible tissue damage
severe case
widespread brain infarction
irreversible damage
whats suggestive
bilateral cortical visual loss
memory loss
proximal limb weakness
sparing of face and hands
Hypoxic ischaemic encephalopathy
can result in
coma/persistent vegetative state
brain death
if kept on ventilator
brain tissue starts to undergo autolysis&become liquid like
Risk factors
age
atheroma
HTN
Hypercoagulable states
serum lipids, obesity, diet
DM
heart disease
diseases of neck arteries
drugs
smoking
haemorrhagic
possible 2° ischaemia due to
vasospasm
SOL decreased perfusion pressure
10-15%
2° to rupture of blood vessel/aneurysm disruption
intracerebral: 7-10%
subarachnoid haemorrhage:5%
infarcts
Nonhaemorrhagic
from acute vascular occlusions
may evolve into haemorrhagic infarcts
when there is reperfusion of ischaemic tissue
usually due to in situ thrombosis
occlusion less likely to undergo fibrinolysis as occluded vessel is abnormal
Haemorrhagic
usually manifest as
multiple
sometimes confluent
petechial haemorrhages
usually due to embolism
subsequently thromolysed by healthy endothelium where lodged
Borderzone
watershed
cortical
internal white matter
regions lying at most distal portions of arterial territories
Features
Gross
Non-haemorrhagic infarct
first 6hrs
little to see
by 48hrs
tissue is pale/soft/swollen
grey-white matter junction is indistinct
infarct very large
potentially ^ICP
2-10days
brain is gelatinous/friable
oedema resolves
10-21 days
tissue liquifys leading to fluid filled cavity
cavity lined by dark grey tissue
gradually expands as dead tissue is removed
Haemorrhagic infarct
multiple petechial haemorrhages
the haemorrhage is presumed to be 2° to reperfusion of damaged vessels/tissues
Global cerebral ischaemia
brain swollen
oedema
gyri widened
sulci narrowed
cut surface shows poor demarcation between grey-white matter
laminar necrosis
Microscopic
Non-haemorrhagic
less than 12hrs
oedema
endothelial/astrocyte swelling
12-48hrs
red dead neurons
eosinophilia/pyknosis
myelin breakdown
neutrophils
48hrs
macrophages start to phagocytose dead cells/blood
up to week 3 post infarct
macrophages are predominant cell type
then liquefaction&angiogenesis?
from week 1
reactive gliosis
after a few mths
healing infarct
shrunken/depressed
cystic
GCI
12-24hrs
neurons become red
areas susc. to irreversible damage
hippocampus
cerebellum
cerebral cortex
24hrs-2wks
cell apoptosis
tissue necrosis
influx of macrophages
vascular proliferation
more than 2 wks
repair
removal of necrotic tissue
loss of normal organised appearance CNS structure
gliosis
Hypertensive cerebrovascular disease
effects
hypertensive encephalopathy
oedema
headaches
nausea&vomiting
agitation
seizures
massive hypertensive intracerebral haemorrhage
Lacunar infarcts
usually few millimetres
in thalamus/internal capsule/caudate nucleus/pons/deep white matter
focus of tissue loss+macrophages
clinically silent or cause neurological impairment
multi infarct dementia/pseudobulbar palsy/marche a petits pas