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blood flow determines
which neural systems remain functional
brain cant effectively store
oxygen or glucose
continuous perfusion is required to
sustain neuronal signaling
the cerebral cortex is especially vulnerable to
hypoxia
right and left internal carotid arteries
anterior circulation
right and left vertebral arteries, which join to form the basilar artery
posterior circulation
anterior and posterior circulation systems communicate through the
circle of willis
vertebral arteries ascend and supply the
spinal cord and medulla
vertebral arteries give rise to
posterior inferior cerebellar arteries
vertebral arteries joint to form the
basilar artery
basilar branches supply the
pons and cerebellum
basilar artery divides into the
anterior inferior cerebellar and superior cerebellar arteries, posterior cerebral arteries
internal carotid arteries supply most of the
cerebral hemispheres
major branches of internal carotid artery
anterior cerebral aa., middle cerebral aa., anterior choroidal artery
anterior communicating artery connects the
2 ACAs
anterior circulation of the brain
internal carotid arteries
middle cerebral aa
anterior cerebral aa
posterior circulation of brain
vertebrobasilar aa
posterior cerebral aa
components of circle of willis
Posterior cerebral arteries, posterior communicating arteries, internal carotid arteries, anterior cerebral arteries, anterior communicating artery
circle of willis supplies
cerebral hemispheres
allows blood to reach tissue through alternative routes over time
circle of willis
connected by posterior communicating arteries
PCA and internal carotid
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?
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
deficits persist for longer than 1 day and are stable
completed stroke
deficits worsen intermittently b/c of continuing thrombosis or repeated emboli
progressive stroke
mini stroke, silent stroke, or temporary clot or amyloid cells
TIA
obstruction of blood flow to the brain
ischemic stroke
rupture of flow of blood to the brain and preventing BF to the brain
hemorrhagic stroke
increased BP means more
stress on arterial wall
80% of strokes
ischemic
-can be thrombotic or emboli
vessel rupture causes loss of downstream perfusion plus pressure from extravascular blood
hemorrhagic
Types of Hemorrhagic Stroke
intracerebral and subarachnoid (aneurysm- barry or saccular)
clot forms elsewhere, travels, and abruptly occludes a cerebral vessel
embolus
clot forms at the site of vascular disease; onset may be abrupt or progressive
thrombus
clinical deficits reflect the
tissue deprived of blood (stroke)
small vessel lesions
lacunar infarcts
occlusion of small, deep arteries creates small cavities after necrotic tissue is cleared
lacunar infarcts
common locations of lacunar infarcts
basal ganglia, internal capsule, thalamus, and brainstem
findings are often purely sensory or purely motor
lacunar infarcts
blood outside vessel compresses surrounding brain tissue
hemorrhagic stroke
deficits may be severe at onset and change as edema evolves
hemorrhagic stroke
sudden, excruciating headache
subarachnoid hem.
possible brief loss of consciousness
subarachnoid hem.
initial findings may be nonfocal
subarachnoid hem.
complications of subarachnoid hem. include
continued bleeding, vasospasm, infarction, and hydrocephalus
bleeding into CSF-filled subarachnoid space, often w sudden severe headache
subarachnoid hem.
sequence to localize stroke
artery
tissue supplied
disrupted function
movement and examination findings
produces massive infarction in both MCA and ACA arteries
ICA
supplies the entire lateral aspect of the cerebral hemispheres (frontal, temporal, and parietal lobes) and subcortical structures
MCA
supplies the medial aspect of the cerebral hemispheres (frontal and parietal lobes) and subcortical structures including basal ganglia
ACA
supplies the cerebellum and medulla (vertebral artery) as well as pons, internal ear and cerebellum (basilar artery)
VBA
supplies the corresponding occipital lobe and medial and inferior temporal lobe, upper brainstem, midbrain, posterior diencephalons, and most of thalamus
PCA
homunclus
how much brain space dedicated to each body part
post central gyrus
parietal lobe
precentral gyrus
frontal lobe
central sulcus
lies b/t the post central and pre central gyri
2 parts of homunclus
somatosensory cortex and motor cortex
ACA supplies
medial frontal and parietal lobes
contralateral weakness and fine touch loss are greater in the lower limb than the upper limb or face
ACA
possible personality change, impulsiveness, perseveration, and gait apraxia
ACA
supplies most of the lateral cerebral hemispheres and parts of the basal ganglia/internal capsule
MCA
contralateral face and upper limb weakness and sensory loss are often greater than lower limb involvement
MCA
optic radiation involvement can cause contralateral homonymous hemianopia
MCA
occipital involvement: contralateral visual-field loss or cortical blindness
PCA
secondary visual cortex involvement: visual agnosia
PCA
thalamic involvement:
hemisensory loss and possible severe pain (PCA)
hippocampal involvement:
declarative memory impairment (PCA)
supplies brainstem/cerebellum
VBA
cranial nerve involvement, equilibrium disturbances, possibility of locked in syndrome
VBA
lie between distal branches of major cerebral arteries
watershed regions
systemic hypotension can reduce perfusion to
watershed areas
upper limb weakness and paresthesias may occur when
ACA-MCA border areas are affected (watershed areas)
abnormal vascular formation, arteries connect to veins through abnormal thin-walled vessels rather than normal capillaries
arteriovenous malformation
may stay silent till rupture
AVM
rupture can cause hemorrhage, loss of perfusion, and mass effect; presents like stroke
AVM
dilation of wall of artery or vein
aneurysm
swollen area has thin walls- prone to rupture
aneurysm
most common, outpouching of vessel wall
saccular (berry) aneurysm
small sac connected by a thin connection to the artery increases the risk for bleeding
saccular aneursym
treatment via clipping or coiling
saccular aneurysm
common sites of berry aneurysm
at bifurcations of vessels
specialized permeable barrier b/w the capillary endothelium of CNS and extracellular space
BBB
assists in preventing many pathogens from entering the CNS
BBB
blocks certain drugs and protein antibodies from accessing the brain (dopamine)
BBB
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
cerebral arteries auto regulate local blood flow, primarily depending on 2 factors:
bp and metabolites
is vitally important to ensure adequate BF and to prevent brain edema
autoregulation
accumulation of excess tissue fluid in brain
edema
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
pressure w/in skull
ICP
normal ICP
5-15 mm Hg
ICP above 20 is
pathologic
potential causes of ICP include
edema, hydrocephalus, tumor, hemorrhage, and other space-occupying lesions
increased ICP symptoms
vomiting, nausea, headache, drowsiness, frontal lobe gait ataxia, and visual and eye movement problems
BF to brain can be evaluated by
PET scan or angiography
based on metabolism of injected radioactively labeled substances
PET scan
major venous system of the brain consists of
cerebral veins
veins drain into
dural sinuses and the internal jugular vein
2 sets of veins drain the cerebrum:
superficial and deep
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