Cerebral Vasculature Flashcards
(24 cards)
perfusion demands of brain
brain makes up 2% of body weight but uses:
- 10-20% of cardiac output
- 20% of body O2 consumption
- 66% of liver glucose
it is therefore very vulnerable if the blood supply is impaired
blood supply to the brain
brachiocephalic trunk -> common carotid and subcalvian arteries
common carotid -> internal carotid and (external carotid)
subclavian -> vertebral artery and (others)
common carotid, internal carotid, vertebral arteries
arteries of the brain
circle of willis
venous drainage of the brain
blood in great cerebral vein -> dural venous sinuses -> superior sagittal sinous -> drains to back of head into occipital area -> confluence of sinuses -> drains laterally into transverse then sigmoid sinus -> internal jugular vein
intracranial haemorrhage
bleeding within the cranial cavity
important to know where exactly bleed is to manage symptoms and inform treatment
types of haemorrhage
- extradural
- subdural
- subarachnoid
- intracerebral
extradural haemorrhage
trauma
immediate clinical effects
arterial, so high pressure
acute emergency, can cause dura to peel away from skull due to pressure
commonly seen in pterion fractures, as middle meningeal artery runs behind
subdural haemorrhage
trauma
delayed clinical effects
venous, so lower pressure
can take hours or days to develop
subarachnoid haemorrhage
ruptured aneurysms (weaknesses in vessel walls that are generally congenital) causes increased intercranial pressure most relevant at base of skull in circle of willis
intracerebral haemorrhage
spontaneous hypertensive
usually close to the origin of the middle cerebral artery
chronic hypertension can cause these bleeds
stroke
cerebrovascular accident - rapidly developing focal disturbance of brain function of presumed vascular origin and of >24 hours duration
85% thrombo-embolic
15% haemorrhagic
transient ischaemic attack
rapidly developing focal disturbance of brain function of brain function of presumed vascular origin that resolves completely within 24 hours
infarction
degenerative changes which occur in tissue following occlusion of an artery
cerebral ischaemia
lack of sufficient blood supply to nervous tissue resulting in permanent damage if blood supply is not restored quickly
thrombosis
formation of a blood clot (thrombus)
embolism
plugging of a small vessel by material carried from a larger vessel e.g thrombi from the heart or atherosclerotic debris from the internal carotid (can also be blocked by air)
public health statistics for stroke
3rd commonest cause of death
100,000 deaths in the UK per annum
50% of survivors are permanently disabled
70% show obvious neurological deficit
risk factors for stroke
age hypertension (haemorrhage risk) cardiac disease (blood clot risk) smoking (general effects on vasculature) diabetes mellitus (general effects on vasculature)
anterior cerebral artery perfusion field
midline portions of the frontal lobes
superior medial parietal lobes
middle cerebral artery perfusion field
lateral portion of the frontal lobe
lateral surface of the temporal and parietal lobes (including the primary motor and sensory areas of the face, throat, hand and arm)
areas for speech (in the dominant hemisphere)
most subcortical deep structures
posterior cerebral artery perfusion field
occipital lobe
inferior part of the temporal lobe
various deep structures (including the thalamus and the posterior limb of the internal capsule)
ACA stroke symptoms
paralysis/hemiplegia of contralateral structures (leg > arm, face)
disturbance of intellect, executive function and judgement (abulia)
loss of appropriate social behaviour
MCA stroke symptoms
“classic stroke”
paralysis/hemiplegia of contralateral structures (arm > leg)
contralateral hemisensory deficits
hemianopia
aphasia/inability to comprehend or formulate language (only if brocas area affected, usually in left sided lesions)
PCA stroke symptoms
visual deficits:
homonymous hemianopia
viisual agnosia (unable to identify objects)
prosopagnosia (unable to recognise faces)