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Blood supply and stroke Flashcards

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1
Q

how many segments does the internal carotid artery have

A

7

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2
Q

where does the internal carotid originate at

A

C3-4 at bifurcation of common carotid

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3
Q

where does the ICA enter the skull

A

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

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4
Q

what does the ICA give off

A

ophthalmic artery, then posterior communicating and anterior choroidal arteries
bifurcates into middle and anterior cerebral arteries

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5
Q

what makes up the anterior circulation

A

the ICA

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6
Q

what branches off the subclavian arteries

A

vertebral arteries

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7
Q

what is the journey of the vertebral arteries

A

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

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8
Q

what branches off the vertebral arteries

A

anterior spinal arteries

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9
Q

what forms from the union of vertebral arteries

A

basilar artery

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10
Q

where is the basilar artery formed

A

between medulla and pons at the levels of abducens nerve root

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11
Q

what are the different parts of the vetebral arteries

A

cervical (not in foramina)
vertebral (within foramina)
occipital (just before goes through foramen magnum

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12
Q

what branches does the basilar artery give off

A

hind brain branches
pons, cerebellum, labyrinth, posterior cerebral arteries

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13
Q

what does the posterior inferior cerebellar artery give off

A

posterior spinal artery

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14
Q

what is the lateral geniculate body involved in

A

visual pathway

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15
Q

what is the circle of willis

A

anterior and posterior circulation meet
anastomotic network from meeting of supply to hindbrain and forebrain

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16
Q

what supplies the posterior circulation of the circle of willis

A

basilar, vertebrals

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17
Q

is variation in the circle of willis common and if so what does this imply

A

yes
variatation may be involved in an increased risk of ischaemic stroke

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18
Q

what are the most common variants of the circle of willis

A

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%

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19
Q

what is the relation of CoW to optic chiasm

A

very close

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20
Q

what is the relation of the vertebral union to the brain stem

A

very close

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21
Q

what does the anterior cerebral artery supply

A

medial frontal parietal lobes

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22
Q

what is the route of the anterior cerebral artery and what does it supply

A

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

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23
Q

what does the middle cerebral artery supply

A

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

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24
Q

what is the route and branches of the MCA

A

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

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25
what is the course of the PCA
course around midbrain with the optic tract and gives off medial and lateral branches
26
what does the PCA supply
medially- calcarine cortex, cuneus, precuneus, splenium of the corpus callosum laterallly-anterior/posterior temporal and occipital cortex
27
what does the calcarine cortex do
location of primary visual cotex
28
what does the cuneus and precuneus do
basic visual processing, integration
29
what does the corpus callosum do
interlobar somatosensory communication between parietal and occipital lobes
30
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
31
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
32
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
33
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
34
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
35
what is non fluent aphasia
generation deficit inability to produce words and sentences mentally eg. brocas
36
what is dysarthria due to
facial paresis
37
what is an example of fluent aphasia
wernickes aphasia
38
where is brocas area located what supplies it
inferior frontal gyrus MCA
39
where is wernicke found what supplies it
dorsal end of superior temporal gyrus MCA
40
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
41
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
42
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
43
how do you remember which quadrant is affected in quadrantopias
PITS Parietal lobe lesion -- INFERIOR parts affected Temporal lobe-- SUPERIOR parts affected
44
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
45
what is antons syndrome
cortical blindness (bilateral infarction of V1) with no insight and confabulation
46
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.
47
what are modifiable risk factors
hypertension t2dm hyperlipidaemia smoking heart disease ex alcohol oestrogen containing drugs polycythaemia
48
what are non modifiable risk factors
age men>women face (black>asian>white) previous vascular event heredity high fibrinogen
49
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)
50
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
51
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
52
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
53
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
54
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
55
describe basilar artery strokes symptoms
brainstem lesions cranial nerve signs cerebellar signs- ataxia some quadriplegia- locked in syndrome facial weakness, dysarthria, dysphagia, dysphonia
56
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
57
what is medial inferior pontine syndrome
foville syndrome abducens nerve palsy with contralateral hemiplegia
58
what is weber's syndrome - ventromedial midbrain
ipsilateral oculomotor palsy contralateral spastic hemiparesis branches of posterior cerebral artery, basilar artery
59
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
60
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
61
What are hyperacute signs
0-24 hours hyperdense sign loss of grey-white matter differentiation cortical hypodensity parenchymal welling and gyral effacement
62
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
63
what are subacute signs (1-3 weeks)
CT fogging- cortical petechial haemorrhages hypoattenuation reverses as the oedema settles- almost normal appearance
64
what is chronic signs
hypodense at its peak- DENSELY DARK INFARCT SIGN may be negative mass effect where unaffected side pushes against affected side
65
what is teh ROSIER score
recognition of stroke in the emergency room enable assessment of stroke in a time limited scenario
66
what is the NIHSS
National institutes of health stroke scale enable assessment of stroke in a time-limited scenario
67
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
68
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
69
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
70
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
71
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
72
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
73
what is the most important treatment for subarachnoid haem
Nimodipine 60mg 6x day for 3 weeks
74
what are surgical procedures for subarach haem
endovascular coiling craniotomy and clipping for difficult to access aneurysms - riskier
75
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

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