cranial blood supply

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Last updated 8:30 PM on 8/19/26
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101 Terms

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blood flow determines

which neural systems remain functional

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brain cant effectively store

oxygen or glucose

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continuous perfusion is required to

sustain neuronal signaling

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the cerebral cortex is especially vulnerable to

hypoxia

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right and left internal carotid arteries

anterior circulation

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right and left vertebral arteries, which join to form the basilar artery

posterior circulation

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anterior and posterior circulation systems communicate through the

circle of willis

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vertebral arteries ascend and supply the

spinal cord and medulla

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vertebral arteries give rise to

posterior inferior cerebellar arteries

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vertebral arteries joint to form the

basilar artery

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basilar branches supply the

pons and cerebellum

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basilar artery divides into the

anterior inferior cerebellar and superior cerebellar arteries, posterior cerebral arteries

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internal carotid arteries supply most of the

cerebral hemispheres

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major branches of internal carotid artery

anterior cerebral aa., middle cerebral aa., anterior choroidal artery

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anterior communicating artery connects the

2 ACAs

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anterior circulation of the brain

internal carotid arteries

middle cerebral aa

anterior cerebral aa

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posterior circulation of brain

vertebrobasilar aa

posterior cerebral aa

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components of circle of willis

Posterior cerebral arteries, posterior communicating arteries, internal carotid arteries, anterior cerebral arteries, anterior communicating artery

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circle of willis supplies

cerebral hemispheres

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allows blood to reach tissue through alternative routes over time

circle of willis

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connected by posterior communicating arteries

PCA and internal carotid

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3 things you need to know when blood flow in brain is impaired

-how quickly it happened

-size of lesion (how much blood flow is cut off)

-collateral circulation?

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brief focal neurologic dysfunction w/ full recovery w/in 24 hours, typically due to ischemia; medical emergency even though symptoms resolve; pt education, stroke prevention intervention

transient ischemic attack

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deficits persist for longer than 1 day and are stable

completed stroke

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deficits worsen intermittently b/c of continuing thrombosis or repeated emboli

progressive stroke

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mini stroke, silent stroke, or temporary clot or amyloid cells

TIA

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obstruction of blood flow to the brain

ischemic stroke

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rupture of flow of blood to the brain and preventing BF to the brain

hemorrhagic stroke

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increased BP means more

stress on arterial wall

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80% of strokes

ischemic

-can be thrombotic or emboli

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vessel rupture causes loss of downstream perfusion plus pressure from extravascular blood

hemorrhagic

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Types of Hemorrhagic Stroke

intracerebral and subarachnoid (aneurysm- barry or saccular)

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clot forms elsewhere, travels, and abruptly occludes a cerebral vessel

embolus

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clot forms at the site of vascular disease; onset may be abrupt or progressive

thrombus

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clinical deficits reflect the

tissue deprived of blood (stroke)

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small vessel lesions

lacunar infarcts

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occlusion of small, deep arteries creates small cavities after necrotic tissue is cleared

lacunar infarcts

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common locations of lacunar infarcts

basal ganglia, internal capsule, thalamus, and brainstem

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findings are often purely sensory or purely motor

lacunar infarcts

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blood outside vessel compresses surrounding brain tissue

hemorrhagic stroke

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deficits may be severe at onset and change as edema evolves

hemorrhagic stroke

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sudden, excruciating headache

subarachnoid hem.

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possible brief loss of consciousness

subarachnoid hem.

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initial findings may be nonfocal

subarachnoid hem.

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complications of subarachnoid hem. include

continued bleeding, vasospasm, infarction, and hydrocephalus

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bleeding into CSF-filled subarachnoid space, often w sudden severe headache

subarachnoid hem.

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sequence to localize stroke

artery

tissue supplied

disrupted function

movement and examination findings

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produces massive infarction in both MCA and ACA arteries

ICA

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supplies the entire lateral aspect of the cerebral hemispheres (frontal, temporal, and parietal lobes) and subcortical structures

MCA

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supplies the medial aspect of the cerebral hemispheres (frontal and parietal lobes) and subcortical structures including basal ganglia

ACA

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supplies the cerebellum and medulla (vertebral artery) as well as pons, internal ear and cerebellum (basilar artery)

VBA

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supplies the corresponding occipital lobe and medial and inferior temporal lobe, upper brainstem, midbrain, posterior diencephalons, and most of thalamus

PCA

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homunclus

how much brain space dedicated to each body part

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post central gyrus

parietal lobe

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precentral gyrus

frontal lobe

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central sulcus

lies b/t the post central and pre central gyri

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2 parts of homunclus

somatosensory cortex and motor cortex

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ACA supplies

medial frontal and parietal lobes

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contralateral weakness and fine touch loss are greater in the lower limb than the upper limb or face

ACA

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possible personality change, impulsiveness, perseveration, and gait apraxia

ACA

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supplies most of the lateral cerebral hemispheres and parts of the basal ganglia/internal capsule

MCA

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contralateral face and upper limb weakness and sensory loss are often greater than lower limb involvement

MCA

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optic radiation involvement can cause contralateral homonymous hemianopia

MCA

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occipital involvement: contralateral visual-field loss or cortical blindness

PCA

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secondary visual cortex involvement: visual agnosia

PCA

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thalamic involvement:

hemisensory loss and possible severe pain (PCA)

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hippocampal involvement:

declarative memory impairment (PCA)

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supplies brainstem/cerebellum

VBA

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cranial nerve involvement, equilibrium disturbances, possibility of locked in syndrome

VBA

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lie between distal branches of major cerebral arteries

watershed regions

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systemic hypotension can reduce perfusion to

watershed areas

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upper limb weakness and paresthesias may occur when

ACA-MCA border areas are affected (watershed areas)

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abnormal vascular formation, arteries connect to veins through abnormal thin-walled vessels rather than normal capillaries

arteriovenous malformation

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may stay silent till rupture

AVM

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rupture can cause hemorrhage, loss of perfusion, and mass effect; presents like stroke

AVM

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dilation of wall of artery or vein

aneurysm

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swollen area has thin walls- prone to rupture

aneurysm

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most common, outpouching of vessel wall

saccular (berry) aneurysm

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small sac connected by a thin connection to the artery increases the risk for bleeding

saccular aneursym

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treatment via clipping or coiling

saccular aneurysm

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common sites of berry aneurysm

at bifurcations of vessels

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specialized permeable barrier b/w the capillary endothelium of CNS and extracellular space

BBB

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assists in preventing many pathogens from entering the CNS

BBB

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blocks certain drugs and protein antibodies from accessing the brain (dopamine)

BBB

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oxygen consumption increases from the brainstem to the cerebral cortex, leaving the cerebral cortex

more vulnerable to hypoxia than vital structures in the lower brainstem

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cerebral arteries auto regulate local blood flow, primarily depending on 2 factors:

bp and metabolites

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is vitally important to ensure adequate BF and to prevent brain edema

autoregulation

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accumulation of excess tissue fluid in brain

edema

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edema causes include:

-concussion

-cardiac arrest

-high altitude: fluid pressure results in ischemia, causing arterioles to dilate, increasing the capillary pressure, and producing more edema

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pressure w/in skull

ICP

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normal ICP

5-15 mm Hg

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ICP above 20 is

pathologic

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potential causes of ICP include

edema, hydrocephalus, tumor, hemorrhage, and other space-occupying lesions

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increased ICP symptoms

vomiting, nausea, headache, drowsiness, frontal lobe gait ataxia, and visual and eye movement problems

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BF to brain can be evaluated by

PET scan or angiography

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based on metabolism of injected radioactively labeled substances

PET scan

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major venous system of the brain consists of

cerebral veins

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veins drain into

dural sinuses and the internal jugular vein

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2 sets of veins drain the cerebrum:

superficial and deep

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drain cortex and the adjacent white matter then empty into the superior sagittal sinus or one of the sinuses around the inferior cerebrum

superficial veins