M4: Cerebrovascular Pathophysiology Flashcards
risk factors for carotid disease that can be related to life style
HTN diabetes smoking obesity dyslipidemia physical inactivity
risk factors for carotid disease related to the heart and blood
homocystinaemia
cardiac disease
previous TIA or stroke
genetic and/or uncontrollable risk factors for carotid disease
sex age hypercholesterolemia genetic predisposition/fam Hx patent foramen ovale
carotid disease is most common in which gender
male
what is hypercholesterolemia
genetic defect in the LDL receptors
3 parts to a physical exam to assess for carotid disease
- carotid auscultation for bruits - indicates if abnormal flow is present, caused by turbulent blood flow due to a stenosis, that creates a vibration in the surrounding tissue
- palpate for a thrill - thrill is a bruit that is felt
- bilateral BP - difference of > 20 mmHg b/w sides indicates possible disease/subclavian steal
what are the 2 types of circulation to the brain
- Hemispheric/anterior
2. vertebrobasilar/posterior
in general, what types of symptoms will a stenosis in the Hemispheric/anterior and vertebrobasilar/posterior circulations cause
- Hemispheric/anterior: lateralizing, symptoms on one side of the body
- vertebrobasilar/posterior: non-lateralizing, symptoms on both sides of the body
if an artery supplying anterior circulation to the brain was diseased, where would symptoms be experienced
what can be an exception to this rule and why
on the contralateral side of the diseased artery…
….since the body is often controlled by the cerebral hemisphere on the contralateral side
unilateral vision problems, due to the ophthalmic artery
which arteries supply the anterior circulation of the brain
ICAs
cerebral hemispheres are supplied by which circulatory system of the brain
anterior
general symptoms of disease effecting the hemispheric/anterior circulation (ICA)
hemiparesis/hemiplegia - weakness or loss of function to 1 limb or one side of the body
paresthesia - tingling, numb or burning sensation
aphasia/dysphasia - inability to speak or understand language
if a patient has aphasia/dysphasia, which side of anterior circulation is always effected
always the left
vision symptoms of disease effecting the hemispheric/anterior circulation (ICA)
amaurosis fugax (transient monocular blindness TMB) - black curtain coming over 1 eye vertically, if its a vascular cause
homonomous hemianopsia - blindness or visual defect in half the field of vision in both eyes
if amaurosis fugax is occurring due to a vascular cause, which eye will be affected
ipsilateral
why does homonomous hemianopsia occur
b/c the R brain has visual control for the L side of both eyes, and vice versa
rule for unilateral visual disturbances for anterior circulation
they are always an ipsilateral symptom (artery on same side affected)
can bilateral visual disturbances be due to either anterior or posterior disease
yes
general symptoms of disease effecting the vertebrobasilar/posterior circulation
ataxia - lack of muscle coordination drop attacks - sudden fall that is recovered from quickly dysphagia - difficulty swallowing motor/sensory disturbances vertigo subclavian steal syndrome
vision symptoms of disease effecting the vertebrobasilar/posterior circulation
diplopia - double vision
bilateral visual blurring
define a subclavian steal
reversal of a vertebral artery to collateralize the ipsilateral SCA
localized signs and symptoms of a subclavian steal
supraclavicular bruit
arm weakness
decreased arm pulse
arm BP discreptent by > 20 mmHg
is the patient usually asymptomatic w/ a subclavian steal
yes, so no treatment
non-localized signs and symptoms of a subclavian steal
dizziness syncope dysarthria headache confusion
norm LDL/HDL cholesterol level
3:1
describe arteriosclerosis
directly related to which factor
hardening of arteries leading to degenerative changes
directly related to age
describe the degenerative changes of arteriosclerosis
loss of elasticity and thickeneing of intima over time, may lead to atherosclerosis
describe atherosclerosis
hardening of arteries along w/ the formation of plaque
plaque builds up in the artery wall and limits or stops blood flow by narrowing (stenosis) or occlusion
whats the most common arterial disease
atherosclerosis
what is considered a hemodynamically significant lesion
a stenosis or occlusion that reduces the diameter of an artery by 50% or >, leading to decreased BP or flow distal to the obstruction
4 stages of development of atherosclerosis
stage 1: early atherosclerosis and injury
stage 2: inflammatory response
stage 3: atheromatous thickening - plaque formation
stage 4: advanced atherosclerosis - late changes
describe stage 1 of atherosclerosis
injury to the endothelial that can be due to a variety of causes
what is vasculitis
swelling or a vein or artery wall
describe stage 2 of atherosclerosis
the injury to the endothelial lining leads to an inflammatory response which leads to fatty streaking.
there is endothelial thickening
what is fatty streaking
do we see it on US
collection of fat and monocytes inside the vessel wall
no
describe stage 3 of atherosclerosis
muscle cells become infiltrated w/ fat…
repair leads to the formation of scar tissue/fibrosis that leaves a fibrous cap over the soft fatty plaque
how does stage 3 of atherosclerosis appear on US
hypoechoic thickened wall and echogenic cap
does plaque for on or in the vessel wall
inside
describe stage 4 of atherosclerosis
- hemorrhage and/or calcification leading to possible ulcerative plaque, emboli, and further narrowing
- there can be hemorrhage from the vasa vasorum into the plaque which will lead to the breakdown of the fibrous cap and endothelium
why is ulcerative plaque concerning
its unstable and can embolize
is atherosclerosis reversible
no
after a vasa vasorum hemorrhage, can the artery repair itself
no
what determines plaque echogenicity
its composition - lipids, collagen, hemorrhage and/or calcifications
what causes plaque to be anechoic
lipids or hemorrhage
what causes plaque to be hypo
fibrofatty plaque
what causes plaque to be hyper
fibrous plaque
US appearance of intraplaque hemorrhage
hypo regions w/ thin fibrous cap… eggshell pattern
what should you include when describing plaque
location, echogenicity, echotexture, surface contour, composition (sometimes)
can we confirm plaque ulcerations on US
no
describe a thrombus
formation of blood clot over the plaque site which further restricts the lumen and contributes to ischemia or infarction
describe an emboli
thrombus that breaks off into the blood streak, can cause ischemia or infarction if it travels to an area too narrow for it to pass
if patients are asymptomatic but have disease, what is the most common indication for a duplex US
auscultation of a bruit
describe a TIA
brief neurological event that lasts 1-30 minute… cell death do not occur… due to a reduction of blood flow
how long to neuro deficits last w/ a TIA
< 24 hrs
what is RIND
resolving/reversing ischemic neurological deficits… a neurological event w/ symptoms lasting b/w 24 hrs - 3 wks w/ no permanent damage
what is a cerebrovascular accident (CVA/stroke)
loss of blood supply that results in some permanent brain damage including a loss of motor, sensory or cerebral function
how can CVAs be classified
- acute
- unstable evolution, symp come and go….
- completed, no progression or resolution and stable
if AR is present, how will this effect flow in the CCAs
bilaterally, there will be a longer period of reversed flow
what are the NASCET trials
north american symptomatic carotid endarterectomy trial
-study that showed benefit of endarterectomy versus medical treatment in symp patients severe stenosis
what is ACAS
what did it show
asymptomatic carotid atherosclerosis study
showed that endarterectomy reduced stroke risk by 6% over 5 years in asymp patients w/ >60% diameter stenosis
how did NASCET and ACAS measure the diameter of a stenosis
measured the norm lumen distal to the stenosis, and the diameter at the stenosis
see diagram on pg 50
/
factor effecting stenosis velocity
length and diameter roughness/irregularity flow rate physiological factors (BP, CO, etc) collateral circulation norm vessel anatomy
what 2 factors that limit colour doppler assessment of carotid stenosis
vessel tortuosity and shadowing from calcific plaque
what other diagnostic imaging can US be correlated w/ for carotid stenosis
MRA (MR angio), CTA (CT angio)
which parameter is the most important for carotid stenosis
peak systolic velocity….. its important to search the lumen for the highest velocity
a significant stenosis will produce what type of sound on PW
high pitched hissing
w/ carotid stenosis, when will EDV remain in the normal range…. when will it increase
norm if theres a diameter reduction of <50%
> 50% reduction will cause an increases in diastolic velocity…. >70% there will be a rapid rise in EDV
…. valuable for detecting high grade stenosis
what is the systolic velocity ratio
what physiological factors can effect this ratio
ratio of the PSV in the ICA / PSV in the CCA
HTN, reduced CO
when will the systolic velocity ratio be invalid
if theres stenosis in the CCA or the bulb
describe trickle flow
occurs when a stenosis is so severe that the blood trickles through the residual lumen
another term for trickle flow
pre-occlusive stenosis
to confirm occlusion, or when it’s being considered, how must we alter the machines controls
set the controls for low flow…. low wall filter, low PRF, increase colour gains, power doppler, increase sample size
scan distal to the bulb w/ PW and colour if occlusion in the CCA
describe a total occlusion
when no flow is detected by colour or spectral doppler w/ appropriate settings
what can happen to arterial pulsations w/ total occlusion
they can be absent
how may the vessel appear w/ total occlusion
- isoechoic or slightly echogenic to the surrounding tissue, making it hard to see the walls
- reduction of vessel size w/ longstanding occlusion
when is the string sign seen
w/ nearly occluded vessels
ratio of ICA to CCA occlusion
10 : 1
what is internalization of the ECA
when the ECA has increased flow w/ a higher diastolic velocity than norm
w/ total occlusion in the CCA, how would flow in the contralateral and ipsilateral CCA change
what sound will you hear on the ipsilateral CCA
contralateral: may have increased compensatory flow w/ increased velocities
ipsilateral: will show decreased PSV and an absent or reversed diastolic flow, will have a thump sound
w/ ICA occlusion, what happens to diastolic flow in the CCA
a downstream occlusion of the ICA is indicated by what type of waveform
may be absent
staccato
describe the waveform proximal to a significant stenosis
this type of waveform is often accompanied by what sound
staccato… increased pulsatility, decreased systolic velocity, little diastolic flow and reversal in early diastole
thump
describe the waveform distal to a significant stenosis
post stenotic turbulence directly after the stenosis, flow retunrs to laminar 3 cm distal to stenosis
where is max disturbance experienced distal to a stenosis
1 cm
if a stenosis is obscured by calcific plaque, what may be the only clue to a severe stenosis
post stenotic turbulence
what waveform is seen more distal to a significant stenosis
tardus parvus… slow to peak and lower PSV increased diastolic flow
other terms for tardus parvus
pulsus tardus
pulsus parvus
is there an abnorm velocity value for the CCA
no
what might low or no EDV in the CCA indicate
distal CCA, bulb or prox ICA severe stenosis
if theres a velocity difference of >/= 30 cm/s b/w the bilateral CCAs, what 3 things should be considered
prox CCA obstruction
the vessel is tortuous
compensatory flow due to contralateral occlusion/stenosis
norm PSV and EDV for ICA
abnorm?
PSV: <125 cm/s
EDV: <40 cm/s
anything above these values indicated stenosis
W/ severe ICA stenosis or occlusion, what can happen to the blood flow in the ECA
Why
It may have a low resistance waveform as the ECA would be acting as a collateral to supply the brain
How can you tell the ECA from the ICA if both have a low resistance waveform due to ECA collateralization to supply the brain
Look for branches from the ECA
OR
Do a temporal tap (tapping the superficial temporal artery), and the spectral tracing will oscillate if you’re in the ECA
If the CCA is occluded what often happens to the direction of flow in the ECA
It will reverse in order to supply blood to the ICA and profuse the brain
Is a healthy patient, should waveforms be fairly symmetrical on both sides
If not?
Yes
if no apparent cause, use other modalities to determine cause
3 basic routes for intracranial collateral circulation
- Large inter-arterial connections through the circle of willis
- Intracranial-extracranial anastomoses or Pre-willisian anastomoses
- Leptomeningeal
Large inter-arterial connections through the circle of willis connect which vessels in the event of occlusion
Provide path b/w both carotids or b/w the basilar A and the R or L carotid
Intracranial-extracranial anastomoses or Pre-willisian anastomoses connect which vessels in the event of occlusion
ECA to ICA (ophthalmic)
Or
ECA (occipital) to vertebral (Atlantic)
Which Intracranial-extracranial anastomosis is the most common
ECA to ICA
Leptomeningeal collaterals connect which vessels in the event of on occlusion
main cerebral arteries
If the vertebrals are occluded what are the most common extracranial collaterals
The opposite vertebral which will become enlarged
Or flow is shunted to the thyrocervical and costocervical branches
(on exam)
If the larger AO branches are occluded what are the most common extracranial collaterals
Intercostal and internal mammary arteries connecting to the subclavian
(On exam)
When assessing the parameters for stenosis, why is it important to look at both the velocites and ratios
Velocites can be falsely elevated due to compensatory flow
Would an endarterectomy ever be done on an fully occluded ICA
No
When the ICA is occluded, how can the path of the vessel change
Where in the vessel are these changes usually seen
Is this more common in W or M
Can become tortuous or coiled and appear S or C shaped…. usually seen W/in first 2-3 cm of occlusion
W, 4x more common
Causes of posterior circulation ischemia (vertebral basilar insufficiency)
Which is most common
Atherosclerosis
Emboli
Extrinsic compression
Subclavian steal
Heart dysfunction
Most common site for stenosis in the vertebral A
2nd most common
Origin of vertebral A/proximal portion, up to C6 where the vertebrals enter the vertebrae
Intracranially, just past C1 before the vert form the basilar A
Other DI to identify occlusion/stenosis in the vertebrals (since US for vert are limited)
Angiography
MRAngio
Norm flow in vert A
Low resistance, laminar flow
Why is US for vert stenosis limited
We don’t directly image the prox portion of the vert and we can’t see around the shadowing of the vertebrae
Is there a ratio we use for the vert to indicate disease
No
Can flow in the vert velocities vary from L to R?
Why or why not
Yes
One side is usually dominant, often the L side
Most obvious finding in the vert for subclavian steal syndrome
Reversal of flow in the vert A to feed the arm
How is a subclavian steal confirmed (3 ways)
Abnorm subclavian waveform
Reversed flow in vert
Or bilateral BP >/= 20 mmHg different (lower BP will be on the affected side)
What kind of waveform in the vert indicates a subacute or pre-subclavian steal
Pendulum waveform/bunny ears where ONLY the systolic portion of the waveform with me reversed.
Review triphasic/multiphasic, etc
Page 100 of notes
Norm waveform of the Subc A
Is there a norm value for PSV
Triphasic or multiphasic, can be biphasic in older adult
No, but the velocity is usually higher than the carotids
A hemodynalically significant stenosis of >50% is defined by which parameters
Focal velocity increas (at least double)
Post stenotic turbulence
Possible colour bruit
What ratio can you use for assessing the subc A for disease
V2 PSV/V1 PSV
V2: PSV of stenosis
V1: PSV of prox norm segment
Which 3 indirect signs of subc steal are important to identify when a proximal velocity of the vert are hard to obtain
- Compare the arterial waveforms at the same site on both arteries (for test)
- spectral waveform changes (for any vessel)
- increased velocities with lumen reduction and post stenotic turbulence
If the prox vert A is occluded, what will the flow direction be in it’s collaterals
Reversed to feed the vert
What is it called if a patient has neurological deficits or symptoms due to subclavian steal
subclavian steal syndrome/phenomenon
Which artery other than the vert, may have reversed flow w/ a subclavian steal
Reversal of the basilar artery
Medical treatment for carotid artery disease
Reduce risk factors
Tissue plasminogen activator (to treat ischemic stroke)
Anticoagulants
Surgical treatment for carotid artery disease
Endarterectomy (most common)
Thrombectomy
Focal repairs
Bypass
Endovascular treatment for carotid artery disease
Carotid angioplasty
Carotid stent
These are often done w/ an endarterectomy
When is the first US done after a endarterectomy
W/in 30 days
Complications from an endarterectomy
-Re-stenosis/occlusion: myointimal/neointimal hyperplasia (w/in 2-3 years) primary atherosclerosis (after 3 years)
- residual plaque
- tissue flaps
- narrowing
- hematoma
- endovascular leak
- pseudoaneurysm
- stent displacement/poor placement/kinking
Describe a myointimal/neointimal hyperplasia
Tissue overgrowth, often a rxn to a stent
Is the normal intimal seen on US after a endarterectomy
How will the sutures appear
No
Bright reflectors
Will you see some normal wall thickening post endarterectomy
Is this important
Yes
No. Unless associated w/ lumen reduction and increased PSV
Are PSV unpredictable w/ a carotid stent
How can we monitor them
Yes
Compare PSV from exam-exam in the same location
Describe a carotid artery dissection
A tear in the intimal lining, blood enters the media of the vessel and creates a false lumen
Causes of carotid artery dissection
Trauma
Medical complications
Spontaneous
Can a false lumen be blind ended or reconnect distal to the origin
Yes
How can a carotid artery dissection obstruction
Expansion of the false lumen which can narrow the true lumen
Where in the ICA does a dissection usually occur
risk factors for spontaneous carotid dissection
In the first 2-4 cm of the ICD
HTN, fibromuscular dysplasia, marfans, ehlers-danlos syndrome, cystic medial necrosis
A CCA dissection can be the extension of what other type of dissection
AO, usually will effect the left CCA
US appearance of carotid dissection
Intimal flutter
Duplicated lumen
Narrowed true lumen, false may be thrombosed
How is carotid dissection treated
Anticoagulation therapy
Describe fibromuscular dysplasia
What’s it characteristic appearance
Non-atherosclerotic disease characterized by tandem stenosis caused by vessel wall abnormalities
-affects medium and large arteries
String of beads/pearls
Which arteries do fibromuscular dysplasia most commonly effect
Renal arteries
ICA
Can coexist in these locations
Fibromuscular dysplasia is most predominant in which gender
Where in the ICA does it most commonly occur
Women
2-6 cm of the Mid, extracranial segment of the ICA
For test
Symptoms of fibromuscular dysplasia
Incidental or TIA
Describe a carotid body tumor (CBT)
Where are they located
Sm cluster of highly vascular chemoreceptor cells that are part of the autonomic nervous sys
at the bulb
What kind of tumor is a CBT
What tissue does it arise from
Paraganglioma
Arises from the ganglion of the glossopharyngeal nerve
Are CBTs usually benign
More common in M or W
Yes
women, 3-5 X
Where does a CBT get its blood supply
ECA usually, if it gets larger, ICA may supply it as well, or the VA or thyrocervical trunk
US appearance of CBT
Ovoid
Widening or bulging of the bifurcation, highly vascular
Symptoms of CBT
Complications of CBT
palpable mass, headache, neck pain, hoarseness
Compression of the laryngeal nerve or invasion of surrounding tissue
2 Treatments for CBT
Surgical removal
Embolization with angiography
Are aneurysms and pseudo aneurysms common or rare in the carotid sys
Rare
Describe a pseudoaneurysm
Weakening/tear in the artery wall, creating a collection of blood b/w the media and Adventitia
What’s the most common cause of aneurysms in the carotid sys
Which location is the most common
Atherosclerosis
CCA
Treatment of extra cranial aneurysms
Surgical resection
Endovascular therapy
Describe vasculitis
Inflammation of the wall of an artery/vein leading to wall damage
Causes and treatment for vasculitis
Causes: genetics, infectious, toxins
Treatment: steroids
4 diseases that cause vasculitis
Takayasu’s arteritis
Temporal arteritis
Polyarteritis
Buergers disease
What types of injuries can radiation cause
Injury to the vasa vasorum, endothelial cells and necrosis of the vessel wall
What are normal duplex and doppler findings after a carotid endarterectomy.
- smooth velocity increase into the stent
- Slight narrowing of the lumen at the ends of the stent with no significant velocity increase
- Laminar or only slightly disturbed flow
Whats the definitive diagnostic test to identify obstructive lesson in the carotid system
angiography
what’s needed to diagnose a subclavian steal
reversal in a vert. A combined with a significant difference in arm pressures
which ares need to be sampled post endarterectomy
prox native artery prox stent attachment site prox, mid, distal within the stent dist stent attachment site native artery distal to the stent
most common complication post endarterectomy within the first 2-3 years
what about 3 + years
restenosis by neointimal hyperplasia
complications from atherosclerosis
US appearance of FMD
tandem stenosis and dilations, with moderate-severe increase is PDV with extensive turbulence
how can arterial flow be altered in collaterals with occlusion
increased flow to compensate
increased velocity to compensate
flow reversal
decreased or changes in pulsatility
What PSV in the ECA indicates 50% or greater stenosis?
Greater than 150-200 cm/s
