Blood supply and stroke Flashcards

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
Q

what is the course of the PCA

A

course around midbrain with the optic tract and gives off medial and lateral branches

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26
Q

what does the PCA supply

A

medially- calcarine cortex, cuneus, precuneus, splenium of the corpus callosum
laterallly-anterior/posterior temporal and occipital cortex

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27
Q

what does the calcarine cortex do

A

location of primary visual cotex

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28
Q

what does the cuneus and precuneus do

A

basic visual processing, integration

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29
Q

what does the corpus callosum do

A

interlobar somatosensory communication between parietal and occipital lobes

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30
Q

what is the order of the homunculus

A

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

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31
Q

are ACA specific strokes more likely to affect the arms or the legs

A

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
Q

what hemisphere dominance do most people have

A

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
Q

what are other symptom categories of stroke

A

visual symptoms
higher cortical- language, speech, attention, neglect, cognition symptoms
coordination

brain stem pathologies also produce
conscious level/coma
swallow
eye movements

34
Q

what are the three components involved in speech and language
what are the deficits generated via stroke

A

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
Q

what is non fluent aphasia

A

generation deficit
inability to produce words and sentences mentally
eg. brocas

36
Q

what is dysarthria due to

A

facial paresis

37
Q

what is an example of fluent aphasia

A

wernickes aphasia

38
Q

where is brocas area located
what supplies it

A

inferior frontal gyrus
MCA

39
Q

where is wernicke found
what supplies it

A

dorsal end of superior temporal gyrus
MCA

40
Q

what is the difference between brocas and wernickes

A

brocas helps to produce language in a fluent way
wernickes helps to make sure the language makes sense

41
Q

what is hemi-spatial neglect and the potential mechanism behind it

A

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
Q

describe what happens to patients who are left dominant individuals with hemi-spatial neglect from non-dominant hemisphere lesion

A

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
Q

how do you remember which quadrant is affected in quadrantopias

A

PITS
Parietal lobe lesion – INFERIOR parts affected
Temporal lobe– SUPERIOR parts affected

44
Q

what is a notable feature of post-chiasmal lesions

A

homonymous hemianopia
thrombosis of PCA can produce cortical homonymous hemianopia
infarction of tissue in V1 and macular cortex

45
Q

what is antons syndrome

A

cortical blindness (bilateral infarction of V1) with no insight and confabulation

46
Q

what is the definition of stroke

A

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
Q

what are modifiable risk factors

A

hypertension
t2dm
hyperlipidaemia
smoking
heart disease
ex alcohol
oestrogen containing drugs
polycythaemia

48
Q

what are non modifiable risk factors

A

age
men>women
face (black>asian>white)
previous vascular event
heredity
high fibrinogen

49
Q

what is a transient ischaemic attack

A

<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
Q

what causes ischaemic stroke

A

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
Q

what are watershed arteries

A

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
Q

what two things might atherosclerotic plaques in large vessels do

A

cause thrombus formation which might embolise (eg. mca thrombosis to carotid artery)
cause hypoperfusion of border territories

53
Q

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

A
54
Q

what are lacunar stroke

A

• 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
Q

describe basilar artery strokes symptoms

A

brainstem lesions
cranial nerve signs
cerebellar signs- ataxia
some quadriplegia- locked in syndrome
facial weakness, dysarthria, dysphagia, dysphonia

56
Q

what is lateral medullary syndrome

A

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
Q

what is medial inferior pontine syndrome

A

foville syndrome
abducens nerve palsy with contralateral hemiplegia

58
Q

what is weber’s syndrome - ventromedial midbrain

A

ipsilateral oculomotor palsy
contralateral spastic hemiparesis

branches of posterior cerebral artery, basilar artery

59
Q

what is the patient pathway for stroke

A

examination
scoring - ROSIER/ NHSS
imaging
immediate management
thrombolysis/thrombectomy
rehab- speech and language therapy, clinical psyhchology, PT/OT. dedicated stroke unit

60
Q

what investigations do you do for stroke

A

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
Q

What are hyperacute signs

A

0-24 hours
hyperdense sign
loss of grey-white matter differentiation
cortical hypodensity
parenchymal welling and gyral effacement

62
Q

what are acute signs (24 hours to 1 week)

A

infarct with lower attenuation tissue visible, mass effect due to swelling
CT brain with contrast scans are better

63
Q

what are subacute signs (1-3 weeks)

A

CT fogging- cortical petechial haemorrhages
hypoattenuation reverses as the oedema settles- almost normal appearance

64
Q

what is chronic signs

A

hypodense at its peak- DENSELY DARK INFARCT SIGN
may be negative mass effect where unaffected side pushes against affected side

65
Q

what is teh ROSIER score

A

recognition of stroke in the emergency room

enable assessment of stroke in a time limited scenario

66
Q

what is the NIHSS

A

National institutes of health stroke scale
enable assessment of stroke in a time-limited scenario

67
Q

what is the immediate treatment

A

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
Q

what is the penumbra

A

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
Q

what is the criteria for thrombectomy

A

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
Q

what is thrombolysis

A

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
Q

what is secondary prevention and post-stroke care

A

treat hypertension with normal targets
antithrombotics
in AF- direct oral anticoagulation
statins on discharge if total cholesterol >4mmol/L
aftercare and rehab

72
Q

what is subarachnoid heamorrhage

A

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
Q

what is the most important treatment for subarachnoid haem

A

Nimodipine 60mg 6x day for 3 weeks

74
Q

what are surgical procedures for subarach haem

A

endovascular coiling
craniotomy and clipping for difficult to access aneurysms - riskier

75
Q

what mimics a stroke

A

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