10.1 strokes Flashcards

1
Q

what is a stroke?

A

a serious life threatening condition that occurs when blood supply to part of the brain is cut off

symptoms and signs persist for more than 25 hours

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2
Q

what is a transient ischaemic attack (TIA)?

A

a mini stroke

similar clinical features to a stroke, but completely resolves within 24 hours

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3
Q

what are the types of stroke?

A
  • ischaemic. usually thromboembolitic.
  • haemorrhage. intecerebral with vessel rupture in brain parenchyma or subarachnoid.
  • others include dissection, hypoxic brain injury and venous sinus thrombi.
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4
Q

what is the emergency management for a stroke?

A
  • thrombolysis within 4 hour window

- CT to determine if its a bleed. if it is, can’t do thrombosis. pupuose of CT is to exclude a haemorrhage cause.

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5
Q

how would a stroke appear on a CT/MRI?

A

CT - ischaemic area of brain not visible early on, as infarct becomes more established the ischaemic area will become more hypodense

MRI - sometimes performed, ischaemia shows up as a high signal area

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6
Q

what circulations form the circle of willis?

A

anterior cerebral circulation

the vertebral arteries

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7
Q

what are the classic stroke syndromes of an anterior cerebral artery infarct?

A
  • contralateral weakness in lower limb
  • lower limb affected worse than upper limb and face
  • contralateral sesnsory changes in same pattern as motor deficits (because sensory homunculus is similar to motor homunculus)
  • urinary incontinence due to paracentral lobules being affected (medial part of cortices and supply perineal area)
  • apraxia from L frontal lobe damage. Cant complete motor planning e.g can’t dress themselves even when power is normal.
  • alien hand syndrome/split brain from corpus callosum involement
  • aphasia = can’t speak. Dysarthia = don’t make sense. more likely in MCA infarcts than ACA infarcts.
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8
Q

how to MCA infarcts correlate to mortality in strokes?

A

MCA supplies a large area of brain
can have widespread effected
are associated with 80% mortality if the main trunk of the MCA is affected due to resulting cerebral oedema and swelling

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9
Q

how can MCA infarcts become haemorrhagic?

A

can occur if the vessels in the infarcted area break down

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10
Q

what branches are effected if the MCA is occluded proximally at the main stem (before the leticulostriate arteries come off)?

A

all branches of the MCA will be affected, including lenticulostriates and distal branches to cortical areas

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11
Q

why do you get contralateral hemiparesis in a proximal MCA infarct? how does this differ in a distal MCA infarct?

A

contralateral full hemiparesis (face arm leg)

as internal capsule has been affected which carries fibres to face, arm and leg (through the leticulostriate arteries) so even tho MCA supplies face and arm area of motor homunculus, this is irrelevant (anterior cerebral supplies the most medial portion of the motor homunculus = the leg)

however, in a distal infarct, the internal capsule is spared so only the area of the motor homunculus supplied by the MCA will be affected

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12
Q

what visual field defects are experienced in proximal MCA infarcts?

A

visual field defects

(homonymous hemianopia with no macula sparing due to destruction of superior and inferior optic radiations through superior temporal and parietal lobes. more distal can lead to quadrantinopias as only one radiation affected)

no macula sparing as taking out the whole tract

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13
Q

why Is contralateral neglect experienced in proximal MCA infarcts?

A

usually in lesions of right parietal lobe

essentially don’t acknowledge that the usually left side of space or even your own body exists. Visual fields normal.

other features:

  • tactile extinction (touch both sides at the same time, won’t feel the affected side)
  • visual extinction
  • anosognosia (won’t acknowledge they had a stroke)
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14
Q

is aphasia experienced in proximal MCA infarcts?

A

yes
global if dominant (left) hemisphere affected
therefore, can’t understand or articulate words. This is if the main trunk of MCA if affected.

otherwise broca’s and wernickes areas are supplied by branches of the MCA.

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15
Q

what are the symptoms of a proximal MCA infarct?

A
  • aphasia
  • contralateral hemiparesis
  • visual field defect
  • contralateral neglect
  • contralateral sensory loss
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16
Q

how is contralateral sensory loss experienced in proximal MCA infarcts?

A

usually in distribution of primary sensory cortex supplied by MCA = face and arm, but could involve larger areas if sensory fibres in internal capsule affected

17
Q

what is a lacunar stroke?

A

where the lenticulostriate arteries are occluded

causes destruction of small area of internal capsule and basal ganglia
dont cause cortical features e.g neglect or aphasia

18
Q

what are the types of lacunar strokes?

A
  • pure motor. Face, arm, leg damaged due to damaged motor fibres travelling through internal capsule due to occlusion of lenticulostriate arteries. contralateral hemiparesis
  • pure sensory. face arm and leg, due to damage to sensory fibres travelling through internal capsule.
  • sensorimotor (mixed, caused by infarct occurring at boundary between motor and sensory fibres)
19
Q

how does the MCA divide and what do its divisions supply?

A

distally, MCA splits into a superior and inferior division

superior division supplies lateral and frontal lobe including primary motor cortex and Broca’s area. occlusion = contralateral face and arm weakness and expressive aphasia if left hemisphere affected

inferior division supplies lateral parietal lobe and superior temporal lobe, including primary sensory cortex, wernickers area and both optic radiations. occlusion will cause contralateral sensory changes in face and arm, receptive aphasia and contralateral visual defect without macula sparing (homonymous hemianopia as both radiations damaged)

20
Q

what symptoms are experiences in a posterior cerebral artery infarct?

A

somatosensory and visual dysfunction typical

contralateral homonymous hemianopia (with macula soaring due to collateral supply from MCA)

contralateral sensory loss due to damage to thalamus

21
Q

what are the signs of a cerebellar infarct?

A

Ipsilateral signs
DANISH

D- dysdiadochokinesia
A- Ataxia
N -  Nystagmus 
I - intention tremor
S - slurred speech 
H - hypotonia 

possibly ipsilateral brainstem signs as cerebellar arteries supply brainstem as they loop round to the cerebellum

22
Q

what would you see in brainstem infarcts?

A

ipsilateral cranial nerve signs - as cranial nerve nuclei arise from the brainstem, not the cortex

23
Q

what are dangers of basilar artery infarcts?

A

supplies brainstem, occlusion can cause sudden death

24
Q

what are the properties of a distal (superior) basilar artery infarct?

A

visual and oculomotor deficit (as basilar sends some branches to midbrain which contain oculomotor nuclei)

behaviour abnormalities

somnolence, hallucinations and dream like behaviour - as brainstem contains important centres for sleep regulation e.g reticular activating system

motor dysfunction often absent (if cerebral peduncles can get blood from the PCA which in turn as being filled by posterior communicating arteries)

25
Q

what are the properties of a proximal (inferior) basilar artery infarct (at level of pontine branches)?

A

locked in syndrome =
complete loss of movement of limbs however preserved ocular movement. Eyes still move because midbrain is getting supply from PCA via posterior communicating arteries.

preserved cpnciousness - maybe because reticular formation is still intact.

26
Q

what clinical storm can be used to quickly diagnose stokes?

A

the Bamford Oxford stroke classification