Blood supply and stroke Flashcards
how many segments does the internal carotid artery have
7
where does the internal carotid originate at
C3-4 at bifurcation of common carotid
where does the ICA enter the skull
at the base via carotid canal
passes through petrous temporal bone
emerges from internal opening of carotid canal
passes OVER f. lacerum
passes through cavernous sinus, piercing rood at the anterior clinoid process, enters sub arachnoid space
what does the ICA give off
ophthalmic artery, then posterior communicating and anterior choroidal arteries
bifurcates into middle and anterior cerebral arteries
what makes up the anterior circulation
the ICA
what branches off the subclavian arteries
vertebral arteries
what is the journey of the vertebral arteries
course posterior-superiorly from the subclavian
enter deep to trasverse process of C6/7
runs in the transvers foramina of the cervical vertebrae
pass across the posterior arch of C1 before entering the skull and the foramen magnum
what branches off the vertebral arteries
anterior spinal arteries
what forms from the union of vertebral arteries
basilar artery
where is the basilar artery formed
between medulla and pons at the levels of abducens nerve root
what are the different parts of the vetebral arteries
cervical (not in foramina)
vertebral (within foramina)
occipital (just before goes through foramen magnum
what branches does the basilar artery give off
hind brain branches
pons, cerebellum, labyrinth, posterior cerebral arteries
what does the posterior inferior cerebellar artery give off
posterior spinal artery
what is the lateral geniculate body involved in
visual pathway
what is the circle of willis
anterior and posterior circulation meet
anastomotic network from meeting of supply to hindbrain and forebrain
what supplies the posterior circulation of the circle of willis
basilar, vertebrals
is variation in the circle of willis common and if so what does this imply
yes
variatation may be involved in an increased risk of ischaemic stroke
what are the most common variants of the circle of willis
most common in the posterior communicating and anterior cerebral arteries
HYPOPLASIA of one or both PCO 30%
HYPOPLASTIC/ ABSENT A1 SEGMENT 15%
ORIGIN OG PCA from ICA with ABSENT, HYPOPLASTIC P1 SEGMENT 20%
INFUNDIBULAR DILATION OF PCOM 10%
what is the relation of CoW to optic chiasm
very close
what is the relation of the vertebral union to the brain stem
very close
what does the anterior cerebral artery supply
medial frontal parietal lobes
what is the route of the anterior cerebral artery and what does it supply
passes over corpus callosum and terminates close to parieto-occipital sulcus (overlaps with PCA branches)
medial parts of primary motor and somatosensory cortices
supplementary motor cortex and corpus callosum
what does the middle cerebral artery supply
most of frontal, parietal, temporal lobes
small part of occipital
2/3 LATERAL SURFACE OF THE BRAIN
primary motor and somatosensory, prefrontal cortex, wernickas, brocas, primary auditory, insular cortex
what is the route and branches of the MCA
gives of central branches to diencephalon
travels along depth of lateral fissure of sylvius
lateral striate arteries are branches which supply corpus striatum, internal capsule and thalamus
what is the course of the PCA
course around midbrain with the optic tract and gives off medial and lateral branches
what does the PCA supply
medially- calcarine cortex, cuneus, precuneus, splenium of the corpus callosum
laterallly-anterior/posterior temporal and occipital cortex
what does the calcarine cortex do
location of primary visual cotex
what does the cuneus and precuneus do
basic visual processing, integration
what does the corpus callosum do
interlobar somatosensory communication between parietal and occipital lobes
what is the order of the homunculus
lateral to medial the body descends
much space is given to movements of the face and hand relative to lower limb and there is more fine movement needed
are ACA specific strokes more likely to affect the arms or the legs
the legs!
because the MCA supplies 2/3 of the lateral brain from hand upwards (on the motor homunculus)
as we know from lateral to medial the body is descended on the motor homunculus
therefore the ACA does the rest, like the legs
the arms are still being supplied by the MCA
ACA supplies medial aspect of primary motor and somatosensory cortices
what hemisphere dominance do most people have
left and so language is localised to the left hemisphere
90% of right handed people have a left lateralising –> if someone has lesion in left hemisphere they would have difficulty with language
most left handed people have mixed dominance (both hemispheres involved)- 50% lateralise to the right hemisphere
what are other symptom categories of stroke
visual symptoms
higher cortical- language, speech, attention, neglect, cognition symptoms
coordination
brain stem pathologies also produce
conscious level/coma
swallow
eye movements
what are the three components involved in speech and language
what are the deficits generated via stroke
generation- NON-FLUENT APHASIA
articulation- DYSARTHRIA (due to facial paresis)
reception- FLUENT APHASIA- word salad
we generate the words in out brain before producing sounds via mechanical means
what is non fluent aphasia
generation deficit
inability to produce words and sentences mentally
eg. brocas
what is dysarthria due to
facial paresis
what is an example of fluent aphasia
wernickes aphasia
where is brocas area located
what supplies it
inferior frontal gyrus
MCA
where is wernicke found
what supplies it
dorsal end of superior temporal gyrus
MCA
what is the difference between brocas and wernickes
brocas helps to produce language in a fluent way
wernickes helps to make sure the language makes sense
what is hemi-spatial neglect and the potential mechanism behind it
reduced awareness of stimulus on one side of space, even with no sensory loss
THOERIES
1. deficit in attention (pay more attention to one side of the visual field)
2. representation is affected- unable to generate idea of left/right side- direct stimuli to the ipsilateral side
describe what happens to patients who are left dominant individuals with hemi-spatial neglect from non-dominant hemisphere lesion
in left dominant patients (majority of people):
left hemisphere provides attention for the right side
right hemisphere provides attention for both side, with a preference to the left
if lesion in non-dominant hemisphere (not responsible for language)
left hemisphere only providing attention for right side of visual fields.
right is affected therefore cant visualise left side
how do you remember which quadrant is affected in quadrantopias
PITS
Parietal lobe lesion – INFERIOR parts affected
Temporal lobe– SUPERIOR parts affected
what is a notable feature of post-chiasmal lesions
homonymous hemianopia
thrombosis of PCA can produce cortical homonymous hemianopia
infarction of tissue in V1 and macular cortex
what is antons syndrome
cortical blindness (bilateral infarction of V1) with no insight and confabulation
what is the definition of stroke
clinical syndrome characterised by sudden onset of rapidly developing focal or global neurological disturbance, persistent for greater than 24 hours or leads to death.
what are modifiable risk factors
hypertension
t2dm
hyperlipidaemia
smoking
heart disease
ex alcohol
oestrogen containing drugs
polycythaemia
what are non modifiable risk factors
age
men>women
face (black>asian>white)
previous vascular event
heredity
high fibrinogen
what is a transient ischaemic attack
<24 hour neurological dysfunction
from focal brain, spinal cord or retinal ischaemia without evidence of cute infarction
most less than an hour 60%
some still result in infarction 33%
CRESCENDO TIA (sign of further stroke- show poor vascular supply)
what causes ischaemic stroke
85% of cases
from large vessel thrombosis (maybe with embolism)
cardiac emboli- AF, Endocarditis, replacement valve thrombus
lacunes
arterial dissection
vasculitis
illicit drugs
haematological cause
what are watershed arteries
ischemic lesions which are situated along the border zones between the territories of two major arteries
area supplied by two major arteries
therefore get some supply
so get dark hypodense areas on ct
what two things might atherosclerotic plaques in large vessels do
cause thrombus formation which might embolise (eg. mca thrombosis to carotid artery)
cause hypoperfusion of border territories
BAMFORD STROKE CLASSIFICATION
what are the symptoms and causes of
1. total anterior circulation stroke
2. partial anterior circulation stroke
3. posterior circulation stroke
4. lacunar stroke
what are lacunar stroke
• small infarctions of the internal capsule, thalamus, striatum, brainstem
Occlusion of perforating arteries
such as the lenticulostriate of the
MCA and thamalic branches of
the PCA
• They lack higher cortical signs
• Specific modality of lesion?
Think Lacunar!
• PURE motor? Think Internal
capsule, corona radiata
• PURE sensory? Think Thalamus
describe basilar artery strokes symptoms
brainstem lesions
cranial nerve signs
cerebellar signs- ataxia
some quadriplegia- locked in syndrome
facial weakness, dysarthria, dysphagia, dysphonia
what is lateral medullary syndrome
wallenberg’s syndrome
ataxia, abnormal eye movements,
involvement of occluded posterior inferior cerebellar artery or vertebral artery
-main symptoms- ipsilateral sympathetics = horner’s syndrome
vestibular nucleus =nausea, vomiting, vertigo nystagmus
inferior cerebellar peduncle= ipsilateral ataxia
what is medial inferior pontine syndrome
foville syndrome
abducens nerve palsy with contralateral hemiplegia
what is weber’s syndrome - ventromedial midbrain
ipsilateral oculomotor palsy
contralateral spastic hemiparesis
branches of posterior cerebral artery, basilar artery
what is the patient pathway for stroke
examination
scoring - ROSIER/ NHSS
imaging
immediate management
thrombolysis/thrombectomy
rehab- speech and language therapy, clinical psyhchology, PT/OT. dedicated stroke unit
what investigations do you do for stroke
CT head with no contrast
-fast, clearly show haemorrhage, clearly show mass effect, infarction, herniation, hydrocephalus, no vascular access
CT head with contrast
-better resolution of BBB as leakage of contrast into parenchyma, clear inflammation, ischaemia, angiogenesis, increased pressure identification, ideal for occlusion identification
Magnetic resonance angiogram
-not favoured in acute- 30 mins, higher sensitivity/ specificity that CT
What are hyperacute signs
0-24 hours
hyperdense sign
loss of grey-white matter differentiation
cortical hypodensity
parenchymal welling and gyral effacement
what are acute signs (24 hours to 1 week)
infarct with lower attenuation tissue visible, mass effect due to swelling
CT brain with contrast scans are better
what are subacute signs (1-3 weeks)
CT fogging- cortical petechial haemorrhages
hypoattenuation reverses as the oedema settles- almost normal appearance
what is chronic signs
hypodense at its peak- DENSELY DARK INFARCT SIGN
may be negative mass effect where unaffected side pushes against affected side
what is teh ROSIER score
recognition of stroke in the emergency room
enable assessment of stroke in a time limited scenario
what is the NIHSS
National institutes of health stroke scale
enable assessment of stroke in a time-limited scenario
what is the immediate treatment
support with o2
exclude hypoglycaemia
if normal glucose
give 300mg aspirin once daily (for all tia suspect)
PPI with aspirin (eg. omeprazole)
- clopidogrel, dipyridamole if allergic
aspirin for 2 weeks before changing to long term anti-thrombotics
what is the penumbra
potential salvageable space
moderately ischaemic
functioning electrophysiological activity
found around ischaemic core
reperfusion aims to restore supply to the penumbra- preventing extension of the core
what is the criteria for thrombectomy
Offer as soon as possible and within 6
hours of onset of symptoms, together
with thrombolysis if within 4.5 hours
to acute ischaemic stroke with
confirmed occlusion of the proximal
anterior circulation demonstrated on
CT cerebral angio or MRA.
• Can be offered within 24 hours
provided proven image findings and
salvageable tissue defined by CT
perfusion or diffusion weight MRI.
• People should previously have good
functional status and NIHSS >5
higher score= worse outcome
what is thrombolysis
tissue plasminogen activation drugs
drugs-
alteplase and tenecteplase
convert plasminogen–>plasmin
plasmin breaks down fibrinogen–>fibrin
must start asap within 4.5 hours of symptom onset
intracranial heamorrhage ruled out
immediate reimaging is accessible
what is secondary prevention and post-stroke care
treat hypertension with normal targets
antithrombotics
in AF- direct oral anticoagulation
statins on discharge if total cholesterol >4mmol/L
aftercare and rehab
what is subarachnoid heamorrhage
form of haem stroke
haem into subarachnoid space between arachnoid and pia mater
thunderclap occipital headache
1/3 die, 1/3 severely disabled, 1/3 recover well
investigations - xanthochromia >12 hours post symptom onset on LP
CT cerebral angiogram- shows haemorrhage
what is the most important treatment for subarachnoid haem
Nimodipine 60mg 6x day for 3 weeks
what are surgical procedures for subarach haem
endovascular coiling
craniotomy and clipping for difficult to access aneurysms - riskier
what mimics a stroke
5 S’s
patient will likely have ischaemic background like previous heart disease, hypertension, type 2, features that are focal, hemiparesis, gaze palsies
poor picture if poor mental status
seizure
sepsis
syncope
space occupying lesions
somatisation
