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VASC 335 > Cerebrovascular > Flashcards

Cerebrovascular Flashcards

1
Q

What are some risk factors for cerebrovascular pathophysiology? (14)

A
  • Hypertension
  • Diabetes
  • Age
  • Smoking
  • Male
  • Obesity
  • Inactivity
  • Cardiac disease
  • Patent foramen ovale
  • Previous TIA or stroke
  • Dyslipidemia
  • Hypercholesterolemia
  • Genetics/Family history
  • Homocystinaemia
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2
Q

If a bruit is found during carotid auscultation, what does this indicate?

A

Abnormal flow (turbulent)

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3
Q

How is a bruit formed?

A

Turbulent blood flow vibrates the vessel wall

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4
Q

What is a palpable bruit known as?

A

A thrill

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5
Q

Why may a bruit not be detected in the case of a severe stenosis?

A

Due to significantly diminished flow

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6
Q

If there is a difference of >20mmHg between sides, what could this indicate?

A

Possible subclavian steal

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7
Q

What is ataxia?

A

A lack of muscle coordination which can affect walking, swallowing, eye movement, speech etc.

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8
Q

What is diplopia?

A

Double vision

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9
Q

What are drop attacks?

A

A sudden fall while walking or standing that is recovered from quickly.

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10
Q

What is dysphagia?

A

Difficulty swallowing

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11
Q

What is Amaurosis fugax?

A

A complete or partial loss of vision

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12
Q

When someone has weakness or complete loss of function to one limb or one side of the body, what is this known as? (2)

A

Hemiparesis/Hemiplegia

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13
Q

When some experiences a tingling, numb, or burning sensation, what is this known as?

A

Paresthesia

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14
Q

What is aphasia/dysphasia?

A

Inability to speak or comprehend language

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15
Q

If someone has blindness or a visual defect in half of the field of vision, what is this known as?

A

Homonomous hemianopia

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16
Q

Visual disturbances are caused from what kind of symptoms?

A

Ipsilateral - Vision disturbances will occur on the same side as the side of the brain with a lack of blood supply.

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17
Q

Body disturbances are caused from what kind of symptoms?

A

Contralateral - Body disturbance will occur on the opposite side of the brain that has the lack of blood supply.

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18
Q

What is associated with irritation of the endothelial lining of the vessel?

A

Smoking

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19
Q

What are the signs and symptoms of the anterior circulation? (6)

A
  • Behavioural abnormalities
  • Amaurosis fugax
  • Hemiparesis/hemiplegia
  • Paresthesia
  • Aphasia/dysphasia
  • Homonomous hemianopia
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20
Q

What are the signs and symptoms of the posterior circulation? (8)

A
  • Ataxia
  • Bilateral vision blurring
  • Diplopia
  • Drop attacks
  • Dysphagia
  • Motor/sensory disturbances
  • Vertigo
  • Subclavian steal syndrome
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21
Q

What are signs of a subclavian steal? (3)

A
  • Supraclavicular bruit
  • Arm weakness
  • Arm pressures that differ more than 20 mmHg
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22
Q

What are signs and symptoms that are non-localizing to anterior or posterior circulation? (5)

A
  • Dizziness
  • Syncope
  • Dysarthria
  • Headache
  • Confusion
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23
Q

What is arteriosclerosis?

A

Condition of hardening of the arteries resulting in loss of elasticity and thickening of intima over time

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24
Q

What is arteriosclerosis directly related to?

A

Age

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25
Q

What is atherosclerosis?

A

A form of arteriosclerosis referring to the hard and soft build-up of plaque beyond the intimal thickening of arteriosclerosis

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26
Q

What is the most common arterial disease?

A

Atherosclerosis

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27
Q

Atherosclerotic plaque can narrow the lumen and is called a?

A

Stenosis

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28
Q

Atherosclerotic plaque can block the artery which is called what?

A

Occlusion

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29
Q

What diameter reduction is required in a vessel to notice hemodynamic changes (hemodynamically significant)?

A

> 50%

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30
Q

The CCA supplies the ICA with what percentage of blood?

A

70%

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31
Q

What type of resistance should be seen in a normal CCA, ICA, Vertebral and ECA?

A

CCA, ICA, Vert = low resistance

ECA = High resistance

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32
Q

In a normal carotid, the EDV us above the baseline except for when? (2)

A
  • CCA or ECA may have short period of reversed flow at end systole
  • Flow reversal in bulb
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33
Q

If aortic regurgitation is present, what should be visualized in the carotids?

A

Longer period of reversed flow in the CCAs bilaterally

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34
Q

A stenosis is usually caused by plaque deposits but can also be due to what?

A

Extrinsic compression

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35
Q

As flow goes through the stenotic zone, it must what?

A

Increase in velocity to maintain blood volume

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36
Q

Through a stenosis, what principle is used?

A

Bernoulli

High velocity/low pressure through stenosis and low velocity/high pressure distal to stenosis

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37
Q

A critical stenosis does what?

A

Reduces both flow and pressure

50% diameter reduction and 70% area reduction

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38
Q

What has a greater hemodynamic effect than a single lesion?

A

Tandem stenoses due to energy losses that occur at the entrances and exits of stenotic segments

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39
Q

Why does a tandem stenosis have a greater hemodynamic effect than a single lesion?

A

Due to energy losses that occur at the entrances and exits of the stenotic segments

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40
Q

Most carotid stenoses occur where?

A

First 1-2 cm of the ICA

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41
Q

What are factors that affect stenosis velocity? (7)

A
  • Length and diameter of the narrowed segment
  • Endothelial roughness
  • Edge irregularity of narrowing (abrupt/gradual)
  • Flow rate
  • BP/CO/peripheral resistance
  • Collateral presence
  • Vessel anatomy (Size)
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42
Q

What is the best method for accurately assessing the stenotic zone?

A

Spectral analysis

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43
Q

What is color Doppler of the carotid stenosis limited by?

A

Vessel tortuosity and acoustic shadowing from calcific plaque

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44
Q

What are we assessing the vertebrals for?

A

Flow direction and possible obstruction

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45
Q

What is the most important parameter on the spectral display?

A

Peak systolic velocity (critical to search lumen for the HIGHEST velocity).

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46
Q

What does a significant stenosis sound like?

A

High pitched hissing

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47
Q

What happens with a diameter reduction >50-60%?

A

Volume flow decreases rapidly

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48
Q

What happnes with a diameter reduction >70%?

A

Velocities decrease rapidly

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49
Q

With a diameter reduction >80% what happens to the PSV?

A

Reduces below normal levels

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50
Q

What happens to the EDV with <50% diameter reduction?

A

Remains within normal range

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51
Q

What happens to the EDV with >50% diameter reduction?

A

Increase in diastolic velocity

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52
Q

What happens to the EDV with >70% diameter reduction?

A

Rapid rise in diastolic velocity

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53
Q

What factors affect the systolic velocity ratio?

A

Physiologic factors

Ex.
Hypertensive = higher velocities
Diminished CO = lower velocities

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54
Q

What is the systolic velocity ratio (VR)?

A

Ratio = PSV in ICA / PSV in CCA

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55
Q

When can the systolic velocity ratio be used?

A

Only if there is a stenosis in the ICA

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56
Q

When is the VR invalid?

A

If the CCA or Bulb have a stenosis

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57
Q

How can a possible total occlusion be assessed for low/trickle flow? (5)

A
  • Lower wall filter
  • Lower PRF/scale
  • Increase colour gain
  • Increase sample size
  • Use power doppler
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58
Q

With total occlusion, what is the sonographic appearance?

A

Vessel is isoechoic or slightly echogenic to surrounding tissue an no flow is detected with colour or spectral doppler

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59
Q

The string sign means that the vessel is?

A

Nearly occluded

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60
Q

Between the ICA and CCA, which is more likely to become occluded?

A

ICA 10:1

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61
Q

If the ICA is occluded, what may be seen in the ECA and what is this called?

A

Increased flow with high diastolic velocity than normal

Termed “internalization of the ECA”

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62
Q

Bilaterally diminished CCA velocities may indicate what?

A

Poor cardiac output

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63
Q

Unilaterally diminished CCA velocities may indicate what?

A

Ipsilateral proximal disease

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64
Q

What on the spectral display will increase with the severity of the stenosis?

A

Spectral broadening

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65
Q

A distal occlusion can be indicated by what kind of waveform?

A

Staccato

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66
Q

If there is an occlusion in the ICA, what may be seen in the CCA?

A

Absent diastolic flow

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67
Q

How does a waveform appear proximal to a severe stenosis and what is this termed?

A
  • Increased pulsatility
  • Sharp, narrow systolic peak
  • Low systolic velocity
  • Little diastolic flow
  • Reversal in early diastole

“Staccato”

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68
Q

What is heard with a staccato waveform, indicating a severe distal stenosis?

A

Thump

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69
Q

A pre-stenotic waveform may look normal, what would give it away?

A

PSV would be very low

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70
Q

Immediately distal to the stenosis, flow spreads out resulting in what?

A

Turbulence

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71
Q

Where is maximum disturbance seen in a stenosis?

A

1 cm distal

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72
Q

At what point distal to a stenosis does turbulence diminish?

A

2 cm

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73
Q

At what point distal to a stenosis does laminar flow resume?

A

3 cm

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74
Q

Potential energy is higher or lower post stenosis?

A

Lower

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75
Q

What may the only clue to a severe stenosis be if the stenosis is obscured by calcific plaque?

A

Post-stenotic turbulence

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76
Q

What waveform will be seen distal to a severe stenosis (3 qualities) and what is this called (3 names)?

A

A dampened waveform

  • PSV reduced
  • Blunted systolic peak
  • Diastolic flow increased

Called Tardus parvus/pulsus parvus/ pulsus tardus

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77
Q

A low to zero EDV may indicate what if seen in the CCA?

A

A Distal CCA, carotid bifurcation and/or prox ICA high grade stenosis or occlusion

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78
Q

What should be considered if a ≥30 cm/s difference between the right and left CCA velocities is observed at multiple levels? (4)

A
  • Proximal obstruction
  • Vessel tortuosity
  • Tight distal CCA stenosis
  • Compensatory flow due to a contralateral occlusion
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79
Q

What velocities would indicate a >50% stenosis in the ECA?

A

PSV >150-200cm/s with plaque and post-stenotic turbulence

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80
Q

In the presence of a severe ICA stenosis/occlusion, what will be seen in the ECA?

A

Low resistance flow pattern due to it acting as a collateral

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81
Q

When the CCA is occluded, ECA flow direction will do what?

A

Reverse to supply blood to the ICA

82
Q

Arterial occlusion alters flow in collaterals. Some changes include what? (4)

A
  • Increase velocity
  • Increased volume flow
  • Flow reversal
  • Decreased pulsatility
83
Q

What is the primary cause of vertebral basilar insufficiency? (VBI)

A

Atherosclerosis

84
Q

What are the common sites for atherosclerosis? (4)

A
  • Origin of vertebral artery at subclavian artery through to it’s entrance into foramina at C6
  • Transcranial just beyond C1 arch (large curve)
  • Transverse foramina
  • Intracranial segments of VA and VA
85
Q

What are some causes of posterior circulation ischemia? (5)

A
  • Atherosclerosis
  • Emboli
  • Cardiac dysrhythmia
  • Impingement from osteophytes
  • Artery to artery steal syndromes (subclavian)
86
Q

Vertebral artery flow should be what?

A

Antegrade and low resistance

87
Q

Which vertebral artery is often more dominant and what does this mean?

A

Left

Flow velocities can vary from side to side in normal patients

88
Q

Subclavian steal syndrome may be indicated by reverse flow where?

A

Vertebral artery

89
Q

The loss of the end diastolic component in the vertebral artery may indicate what?

A

Distal occlusion

90
Q

What kind of waveforms indicate a subacute subclavian steal (pre-steal)?

A

Pendulum waveforms (bunny ears)

91
Q

What type of waveform does the subclavian artery have?

A

Triphasic

92
Q

Describe a biphasic waveform: (3)

A

Triphasic without reversal

  • Strong forward flow (Sharp upstroke) in systole
  • No reversal in early systole
  • Forward or no flow in late diastole
93
Q

Describe a monophasic waveform: (4)

A
  • Decreased pulsatility
  • Blunted upstroke
  • May or may not have diastolic flow
  • Continuous forward flow (above baseline)
94
Q

What does the velocity ratio (V2 and V1 of PSV) represent?

A

V1 is the PSV of the prox normal segment and V2 is the max PSV of the stenosis

95
Q

What is a focal velocity increase?

A

≥ double that of the proximal arterial segment

96
Q

What are the basic routes for collateral circulation intracranially?

A
  1. Large inter-arterial connections through circle of willis (pathways between two carotids or between basilar and right or left carotid)
  2. Intracranial to extracranial anastomoses or Pre-Willisian anastomoses
  3. Leptomeningeal
97
Q

What are the intracranial-extracranial anastomoses or Pre-willisian anastomoses? (5)

A
  1. ECA to ICA (ophthalmic)
  2. ECA (occipital) to vertebral (atlantic)
  3. Cervical branches of subclavian to verterbral upper and lower branches
  4. Cervical branches to occipital of ECA
  5. ECA across midline to peri-orbital branches
98
Q

The leptomeningeal connect what?

A

Terminal cortical branches of main cerebral arteries across vascular border zones

99
Q

For extracranial collateral circulation, what happens when the vertebral becomes occluded?

A

Enlargement of opposite vertebral and flow shunted to thyrocervical and costocervical branches

100
Q

For extracranial collateral circulation, what happens when the large aortic branches become occluded?

A

Intercostals and internal mammary arteries will connect to subclavian

101
Q

Name the medical treatments of carotid artery disease: (5)

A
  • Modify risk factors (quit smoking, lose weight etc.)
  • Statin therapy
  • Anti-thrombotics
  • Tissue plasminogen activator (TPA)
  • Anti-coagulants - warfarin, heparin
102
Q

What does tissue plasminogen activator (TPA) do?

A

Treats ischemic stroke within 3 hours of the onset of symptoms

103
Q

Name the surgical treatments of carotid artery disease: (6)

A
  • Carotid endarterectomy
  • ICA resection and re-anastomosis (for kinking)
  • Carotid Thrombectomy
  • Bypass (SCA to Carotid or Carotid to Carotid)
  • Vertebral transposition to CCA
  • Direct focal repairs (SCA, VA)
104
Q

What does endovascular treatment include?

A

Carotid angioplasty and carotid stent

105
Q

After a patient has an endarterectomy, when is their first duplex and what artifact may be seen in this time frame?

A

Within 30 days of the procedure

Shadowing from air entrapment associated with a synthetic patch or graft

106
Q

What are some complications of an endarterectomy? (7)

A
  • Re-stenosis/Occlusion due to intimal hyperplasia (2-3 years) and atherosclerosis (over 3 years)
  • Residual plaque
  • Tissue flaps may cause re-stenosis
  • Vessel narrowing
  • Hematoma
  • Endovascular leak
  • Pseudoaneurysm associated to synthetic patch
107
Q

If a person gets myointimal hyperplasia post endarterectomy what would it be associated with within the first 2-3 years?

A

Increased flow velocity and post-stenotic flow disturbance

108
Q

Where are tissue flaps post-endarterectomy usually seen?

A

Distal end of the endarterectomy

109
Q

What is neointimal hyperplasia?

A

Smooth muscle and fibrous overgrowth of the tissue later that replaces the intima following carotid intervention

110
Q

What is NOT seen within the repair site of an endarterectomy?

A

Normal intimal-media stripe

111
Q

Wall thickening post-endarterectomy is normal unless what?

A

It’s associated with a lumen reduction and increase in PSV

112
Q

When is the first duplex done after a patient gets a carotid stent?

A

Within 30 days

113
Q

What are the complications of a cartoid stent? (5)

A
  • Poor stent placement (gap betwwen stent and wall)
  • Re-stenosis via hyperplasia
  • Progressive stenosis distal to stent due to athero disease
  • Stent shift
  • Stent kinking
114
Q

What would be some normal duplex findings with a carotid stent? (3)

A
  • Smooth velocity increase into stent
  • Slight lumen narrowing at ends of stent with no significant velocity elevation
  • Laminar or only slightly disturbed flow
115
Q

How can you tell the difference between a stent and endarterectomy sonographically?

A

A stent is on bottom and top and an endarterectomy appears more speckly due to sutures and will only be on one side

116
Q

What would a mesh appearance of the vessel walls indicate?

A

Carotid stent

117
Q

What is a carotid artery dissection?

A

Tear in the intimal lining

118
Q

What is a false lumen?

A

Where blood enters from dissection, travelling between intima and media

119
Q

How does carotid artery dissection happen?

A

Trauma, iatrogenic complication or it can be spontaneous (conditions that weaken wall).

120
Q

How can the false lumen appear on US? (5)

A
  • Reconnected to distal origin or blind ended
  • Patent or occluded
  • Intimal flutter with cardiac cycle
  • Duplicated lumen
  • Disturbed flow distally
121
Q

What can the expansion of the false lumen in a dissection cause?

A

Obstruction due to the true lumen narrowing leading to stroke or TIA symptoms

122
Q

Where does ICA dissection typically start?

A

First 2-4 cm

123
Q

What may CCA dissection be due to? (2)

A
  • Typically an extension of aortic dissection or:

- Blunt trauma

124
Q

What can the false lumen of a dissection progressively dilate into?

A

Pseudoaneurysm

125
Q

What are risk factors for spontaneous dissection? (6)

A
  • Hypertension
  • Fibromuscular dysplasia
  • Marfan’s syndrome
  • Elhers-Danlos symdrome
  • Cystic medial necrosis
  • Other: Strenuous exercise, rapid neck motion, spine compression
126
Q

How is carotid artery dissection treated?

A

Anticoagulation therapy

127
Q

What are direct tests for artery dissection?

A

Ultrasound, MRA, angiogram

128
Q

What does FMD stand for?

A

Fibromuscular dysplasia

129
Q

What is fibromuscular dysplasia?

A

Non-atherosclerotic arterial disease

130
Q

What does fibromuscular dysplasia resemble on US?

A

String of beads/pearls = multiple tandem stenosis and dilations followed by a significant increase in PSV with extensive turbulance

131
Q

What vessels does FMD typically affect?

A

Medium and large sized (ICA and renal artery)

132
Q

Who is most likely to develop FMD and where?

A

Women >90% and usually in the mid-section of the ICA becoming apparent in the 4th or 5th decade of life

133
Q

What does fibromuscular dysplasia typically involve?

A

2-6 cm segment of mid extra-cranial ICA

134
Q

What is the treatment of FMD for symptomatic patients?

A

Dilatation of artery through angioplasty

135
Q

What is a CBT?

A

Carotid body tumor

136
Q

What is a carotid body tumor?

A

Small cluster of chemoreceptor cells

137
Q

Where is a carotid body tumor located?

A

Split of the carotid bifurcation (part of the autonomic nervous system)

138
Q

CBT is a tumor of ganglioma comprised of chromaffin, also known as?

A

Paraganglioma

139
Q

Where does a CBT arise from?

A

Off the ganglion of the glossopharyngeal nerve

140
Q

Who and how likely is someone to get a CBT? (3)

A
  • Rare
  • Females 3-5x more often
  • People living at high altitudes
141
Q

What supplies blood to a CBT?

A

The ECA

142
Q

What will a CBT be supplied by if it grows very large?

A

ICA, vertebral artery, or thyrocevical trunk will help the ECA supply

143
Q

What are the symptoms of a CBT? (4)

A

Palpable mass, headache, neck pain, hoarseness

144
Q

What are complications of having a CBT?

A

Compression of laryngeal nerve or invasion of surrounding vessels

145
Q

What is the treatment for a CBT?

A

Surgical resection, embolization with angiography

146
Q

What are pseudoaneurysms caused by?

A

Decreased or weakened wall

147
Q

There is an increased risk of pseudo-aneurysms post what?

A

Post-endarterectomy

148
Q

What are the causes of an aneurysm and what is the most common? (4)

A
  • Atherosclerosis = most common
  • Dissection
  • Trauma
  • Prev. Surgery
149
Q

Where is an aneurysm most common?

A

CCA (fusiform located at bifurcation of CCA or prox ICA)

150
Q

What is arteritis/vasculitis?

A

Inflammation of the arterial walls resulting in blood vessel damage

151
Q

What is known as the pulseless disease?

A

Takayasu’s arteritis

152
Q

What is Takayasu’s arteritis?

A

Concentric inflammation of aorta and its branches

153
Q

What is known as giant cell arteritis?

A

Temporal arteritis

154
Q

What is temporal arteritis?

A

Inflammation of medium sized vessels of the head, neck, eyes, and optic nerve. Affects the extracranial branches of the carotid.

155
Q

What is known as periarteritis nodosa?

A

Polyarteritis

156
Q

What is polyarteritis?

A

Multiple sites of inflammation in small and medium sized arteries of the body

157
Q

What is known as thromboangitis obliterans?

A

Buerger’s disease

158
Q

What is Buerger’s disease?

A

Occurs in distal arteries of young male smokers

159
Q

Radiation therapy causes what kind of injury?

A

Injury to the vasa vasorum and necrosis of the vessel wall

160
Q

What are tests to aid in the diagnosis of carotid pathology? (6)

A
  • Physical exam
  • Doppler
  • OPG-GEE (indirect)
  • CT (Computed Tomography)
  • Cerebral arteriography (angiography) - xray w/dye
  • MRA/MRI - magnetic fields w/ or w/o contrast
161
Q

What is a normal ICA PSV?

A

<125 cm/s

162
Q

What is a normal ICA/CCA PSV ratio?

A

<2.0

163
Q

What is a normal ICA EDV?

A

<40 cm/s

164
Q

What is the PSV of the ICA with <50% stenosis?

A

<125 cm/s

165
Q

What is the plaque estimate with a stenosis <50%?

A

<50%

166
Q

What is is the ICA/CCA PSV ratio with a stenosis <50%?

A

<2.0

167
Q

What is the ICA EDV with a stenosis <50%?

A

<40 cm/s

168
Q

What is the PSV of the ICA with 50-69% stenosis?

A

125-230 cm/s

169
Q

What is the plaque estimate with a 50-69% stenosis?

A

> 50%

170
Q

What is the ICA/CCA PSV ratio with a 50-69% stenosis?

A

2.0-4.0

171
Q

What is the EDV of the ICA with a 50-69% stenosis?

A

40-100 cm/s

172
Q

What is the PSV of the ICA with a stenosis >70% but less than near occlusion?

A

> 230 cm/s

173
Q

What is the plaque estimate with a stenosis >70% but less than near occlusion?

A

> 50

174
Q

What is the ICA/CCA PSV ratio with a stenosis >70% but less than near occlusion?

A

> 4.0

175
Q

What is the EDV of the ICA with a stenosis >70% but less than a near occlusion?

A

> 100 cm/s

176
Q

What is the ICA PSV with a near occlusion?

A

High, low, or undectable

177
Q

What is the plaque estimate for a near occlusion?

A

Visible

178
Q

What is the ICA/CCA PSV ratio with a near occlusion?

A

Variable

179
Q

What is the EDV of the ICA with a near occlusion?

A

Variable

180
Q

What is the ICA PSV with total occlusion?

A

Undectable

181
Q

What is the plaque estimate with total occlusion?

A

Visible with no lumen detectable

182
Q

What is dyslipidemia?

A

Abnormal levels of plasma lipids closely associated with the development of atherosclerosis

183
Q

What is hypercholesterolemia?

A

A genetic defect in the LDL receptors

184
Q

Why is a patent foramen ovale a risk factor for cerebrovascular pathology?

A

If there is a clot in the blood travelling in the right side of the heart it can pass through the PFO, enter the LA and travel up to the brain (stroke) or coronary artery (heart attack).

185
Q

What is homocystinaemia?

A

An elevation of the homosysteine level in blood linked to strokes, stenosis and thicker plaque.

186
Q

What is TIA?

A

Transient Ischemic Attack (TIA)

A brief episode of neurologic symptoms where cell death does not occur (lasts less than 24 hrs)

187
Q

What is syncope?

A

Transient loss of consciousness (fainting)

188
Q

What is dysarthria?

A

Abnormal speech or difficulty with speech

189
Q

Describe the stages of the development of atherosclerosis?

A

Stage 1: Endothelial injury

Stage 2: Inflamm response - lipids enter wall (fatty streak) and platelets respond (foam cells) consuming muscle cells with fat

Stage 3: Scar tissue/fibrosis - fibrous cap covers fatty portion of plaque

Stage 4: - Ulcerative plaque - Hemorrhage, calcification and thinning can cause plaque to become unstable and be at risk to embolize

190
Q

Describe intra-hemorrhage/lipid, fibrofatty, fibrous and calcific plaque on US.

A

Intra Hemorrhage/lipid plaque = anechoic

Fibrofatty plaque = hypoechoic

Fibrous plaque = Hyperechoic

Calcific plaque = Highly reflective with shadowing

191
Q

What is a berry aneurysm?

A

An aneurysm in the circle of willis vessels caused by congenital weakness

192
Q

What is the most common indication for a duplex US in asymptomatic patients?

A

Auscultation of a bruit

193
Q

What is RIND?

A

Resolving/Reversing Ischemic Neurologic Deficit

A neurologic event with symptoms lasting 24 hrs - 3 wks with no permanent damage

193
Q

What is CVA?

A

Cerebrovascular accident (stroke)

Loss of blood supply causing permanent damage (loss of motor, sensory or cerebral function)

193
Q

What can CVA be classified as? (3)

A
  1. Acute-sudden onset
  2. Unstable evolution (symptoms come and go)
  3. Completed/stable (no progression or resolution)
194
Q

What is VBI and what are the symptoms? (5)

A

Vertebrobasilar Insufficiency

Causes bilateral symptoms of visual blurring, paresthesia, vertigo, ataxia and drop attacks

195
Q

What are the treatments of cerebrovascular disease? (8)

A
  • Stop smoking
  • Exercise
  • Weight control and low cholesterol diet
  • Aspirin therapy - decreases platelet aggregation
  • Trental (drug) - decrease blood velocity
  • Anti-hypertensive drugs - decrease forces on vessel wall
  • Surgery - endarterectomy/stent placement
  • Administer TPA within 24 hrs of stroke onset
196
Q

What other tests are correlated with positive US results?

A
  • Angiographic studies

- MRA

197
Q

What is a temporal tap and what is it used to assess?

A

Tapping the superficial temporal artery (STA) to visualize the spectral trace oscillating in order to identify the ECA

198
Q

When may a low resistance flow pattern be observed in the ECA?

A

In the presence of a severe ICA stenosis or occlusion (ECA acts as collateral to supply the brain).

199
Q

Where is a tortuous/coiled ICA most often seen, what does it produce and who most often has them?

A
  • Usually seen within the first 2-3 cm
  • May produce a bruit
  • Occur 4x more often in women than men

VASC 335 (9 decks)

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